TRIGLYCERIDES A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Triglycerides: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84104-7 1. Triglycerides-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on triglycerides. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON TRIGLYCERIDES ......................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Triglycerides ................................................................................. 4 E-Journals: PubMed Central ....................................................................................................... 62 The National Library of Medicine: PubMed ................................................................................ 64 CHAPTER 2. NUTRITION AND TRIGLYCERIDES ............................................................................... 81 Overview...................................................................................................................................... 81 Finding Nutrition Studies on Triglycerides ................................................................................ 81 Federal Resources on Nutrition ................................................................................................... 85 Additional Web Resources ........................................................................................................... 85 CHAPTER 3. ALTERNATIVE MEDICINE AND TRIGLYCERIDES ......................................................... 91 Overview...................................................................................................................................... 91 National Center for Complementary and Alternative Medicine.................................................. 91 Additional Web Resources ........................................................................................................... 96 General References ..................................................................................................................... 103 CHAPTER 4. DISSERTATIONS ON TRIGLYCERIDES ......................................................................... 105 Overview.................................................................................................................................... 105 Dissertations on Triglycerides ................................................................................................... 105 Keeping Current ........................................................................................................................ 106 CHAPTER 5. CLINICAL TRIALS AND TRIGLYCERIDES ................................................................... 107 Overview.................................................................................................................................... 107 Recent Trials on Triglycerides ................................................................................................... 107 Keeping Current on Clinical Trials ........................................................................................... 109 CHAPTER 6. PATENTS ON TRIGLYCERIDES.................................................................................... 111 Overview.................................................................................................................................... 111 Patents on Triglycerides ............................................................................................................ 111 Patent Applications on Triglycerides......................................................................................... 139 Keeping Current ........................................................................................................................ 175 CHAPTER 7. BOOKS ON TRIGLYCERIDES ....................................................................................... 177 Overview.................................................................................................................................... 177 Book Summaries: Federal Agencies............................................................................................ 177 Book Summaries: Online Booksellers......................................................................................... 178 The National Library of Medicine Book Index ........................................................................... 179 Chapters on Triglycerides .......................................................................................................... 180 CHAPTER 8. MULTIMEDIA ON TRIGLYCERIDES ............................................................................ 187 Overview.................................................................................................................................... 187 Bibliography: Multimedia on Triglycerides ............................................................................... 187 CHAPTER 9. PERIODICALS AND NEWS ON TRIGLYCERIDES ......................................................... 189 Overview.................................................................................................................................... 189 News Services and Press Releases.............................................................................................. 189 Newsletter Articles .................................................................................................................... 191 Academic Periodicals covering Triglycerides............................................................................. 191 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 193 Overview.................................................................................................................................... 193 U.S. Pharmacopeia..................................................................................................................... 193 Commercial Databases ............................................................................................................... 194 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 199 Overview.................................................................................................................................... 199 NIH Guidelines.......................................................................................................................... 199
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NIH Databases........................................................................................................................... 201 Other Commercial Databases..................................................................................................... 203 The Genome Project and Triglycerides ...................................................................................... 203 APPENDIX B. PATIENT RESOURCES ............................................................................................... 207 Overview.................................................................................................................................... 207 Patient Guideline Sources.......................................................................................................... 207 Finding Associations.................................................................................................................. 209 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 211 Overview.................................................................................................................................... 211 Preparation................................................................................................................................. 211 Finding a Local Medical Library................................................................................................ 211 Medical Libraries in the U.S. and Canada ................................................................................. 211 ONLINE GLOSSARIES................................................................................................................ 217 Online Dictionary Directories ................................................................................................... 218 TRIGLYCERIDES DICTIONARY .............................................................................................. 221 INDEX .............................................................................................................................................. 307
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with triglycerides is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about triglycerides, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to triglycerides, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on triglycerides. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to triglycerides, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on triglycerides. The Editors
1
From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON TRIGLYCERIDES Overview In this chapter, we will show you how to locate peer-reviewed references and studies on triglycerides.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and triglycerides, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “triglycerides” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
Why Are Triglycerides So Important? Source: Diabetes Self-Management. 12(6): 31-32, 34. November-December 1995. Contact: Available from R.A. Rapaport Publishing, Inc. 150 West 22nd Street, New York, NY 10011. (800) 234-0923. Summary: The author covers triglycerides and stresses their importance in determining risk of heart disease. Topics include noninsulin-dependent diabetes mellitus (NIDDM) and heart disease; how heart disease develops; why triglycerides are so important; treating lipid abnormalities; lipid-lowering medications, including bile-acid sequestrants, nicotinic acid, fibrates, and HMG CoA reductase inhibitors; and reducing the risk of heart attacks. The author stresses that knowing one's total cholesterol level is
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not enough; learning one's triglyceride level and correcting it if it is high can lessen one's risk of heart disease.
Federally Funded Research on Triglycerides The U.S. Government supports a variety of research studies relating to triglycerides. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to triglycerides. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore triglycerides. The following is typical of the type of information found when searching the CRISP database for triglycerides: •
Project Title: ALTERNATIVE THERAPIES FOR MENOPAUSE: A RANDOMIZED TRIAL Principal Investigator & Institution: Newton, Katherine M.; Associate Investigator; Center for Health Studies Seattle, Wa 98101 Timing: Fiscal Year 2002; Project Start 01-JUL-2000; Project End 30-NOV-2004 Summary: (Adapted from Investigator's Abstract) Hormone replacement therapy (HRT: estrogen and progestin) remains the treatment of choice for women with vasomotor symptoms, and long-term HRT has been recommended for prevention purposes. The demand for alternatives to HRT, and the availability and use of over-the-counter products including dietary phytoestrogen supplements and naturopathic medicines, has grown dramatically. Few of these products have faced the rigors of randomized trials and none have been tested to evaluate their effects on long-term outcomes. The purpose of this four-year randomized controlled trial is to evaluate the efficacy and safety of three alternative approaches utilizing phytoestrogens to treat vasomotor symptoms in peri- and postmenopausal women. The treatments were chosen because of the scientific evidence supporting a possible benefit, the availability of products with adequate quality control their frequency of use in naturopathic medicine, and our ability to blind participants to the intervention. The five proposed treatment arms are as follow: 1) esterified estrogen and micronized progesterone: 9) a single herbal product, black cohosh; 3) a multibotanical preparation; 4) a combination regimen that includes the same multibotanical preparation plus soy diet counseling; and 5) placebo. The primary aim is to compare the effects of three alternative treatments, HRT, and placebo on the frequency and intensity of vasomotor symptoms measured by The Wiklund Menopause Symptom Checklist and a daily Vasomotor Symptom Diary. The secondary aims are to compare the effects of three alternative treatments, HRT, and placebo on the following:
2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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1) vaginal cytology (vaginal maturation index); 2) serum lipids (total cholesterol, HDL and LDL cholesterol, triglycerides); 3) bone mineral density (hip and spine dual energy x-ray absorptiometry scan); 4) glucose metabolism (insulin, fasting blood glucose); and 5) coagulation factors (fibrinogen, PAI-1). The hypotheses are that compared to placebo the three alternative treatments tested in this study will have the following effects: reduce frequency of hot flashes and night sweats, improve vaginal maturation and decrease vagina atrophy as measured by maturation index, lower total cholesterol and LDL with no effect on HDL, reduce the rate of decline in bone mineral density (BMD), and have no effect on glucose metabolism or clotting factors. To accomplish the specific aims the investigators propose to do the following: 1) recruit and randomize 400 periand post-menopausal women to one of five treatment arms for one year; 2) collect measurements of primary and secondary outcomes at baseline, three, six, and 12 months; and 3) compare changes in outcomes in the groups taking alternative treatments to those in the HRT and placebo groups. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANALYSIS OF SEX HORMONES AND LIPOPROTEINS IN YOUNG MALES Principal Investigator & Institution: Barton, Bruce A.; Senior Statistician and Vice President; Maryland Medical Research Institute, Inc 600 Wyndhurst Ave Baltimore, Md 21210 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2004 Summary: (Provided by Applicant) This application requests support for secondary analysis of the Sex Hormones and Lipoproteins in Adolescent Males Study (HD/HL18281), a 3-year (1984-1987) study of lipids, blood pressure, weight, fat patterning, and sex steroid hormones (SSH) in adolescent males. A total of 664 black and white males, ages 10-15, were enrolled into a study designed as a series of repeated data collections over 2 years within age cohorts. Cross-sectional analyses have been used to explain differences during adolescence in SSH and SSH-lipid relationships between black and white boys and between boys with and without a family history of CHD. When the data were originally collected for this study, theoretical models of flexible longitudinal analytic techniques had been developed, but were not available for computer use. These techniques, now supported by software, allow a more powerful and complete analysis of these data. The primary aim of these analyses is to explicate the contribution of changes in SSH and fat patterning to changes in plasma concentrations of high (HDL-C) and low (LDL-C) density lipoprotein cholesterol, triglycerides (TG), and apolipoproteins (apo) Al, All, and B occurring during puberty in males. SSH assayed included estradiol (E2) and free testosterone (T). We will test the following hypotheses: (1) increasing free T predicts/leads to decreases in HDL-C and increases in LDL-C, apo B, and the LDL-C/HDL-C ratio in adolescent males; (2) increasing E2 predicts decreases in apo B, LDL-C and the LDL-C/HDL- C ratio, but the resultant effects will vary with adiposity and fat patterning; (3) rapid weight gain predicts increased central adiposity, defined as the ratio of truncal skinfolds to total skinfolds, and with greater decreases in HDL-C and increases in triglycerides, apo B, LDL-C and the LDL- C/HDL-C ratio. Rapid weight gain predicts increased E2, but the atherogenic effects of increased central adiposity on lipids are greater than the antiatherogenic effects of E2. These analyses will provide a better understanding of metabolic factors underlying obesity-hormone-lipoprotein relationships. Given the welldocumented increase in obesity in American youth, these analyses are especially pertinent and address important public health issues.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANCILLARY STUDY DATA ANALYSIS IN VA-HIT Principal Investigator & Institution: Rubins, Hanna; Medicine; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2003 Summary: The VA HDL Intervention trial (VA-HIT) was a multicenter, placebo controlled, randomized trial that showed that gemfibrozil significantly reduced major cardiovascular events in 2531 men with coronary heart disease, low levels of low density lipoprotein (LDL) cholesterol and low levels of high density lipoprotein (HDL) cholesterol. In addition to its unique lipid profile, the VA-HIT population also had a high prevalence of diabetes, impaired fasting glucose, or high fasting plasma insulin; central obesity; and hypertension, which are all components (together with high triglycerides and low ILL-cholesterol) of a constellation of risk factors known as the metabolic syndrome. Since prior clinical trials have not enrolled this type of population, the VA- HIT database is a unique resource. The purpose of the present proposal is to use this database to study additional risk markers that were measured in the study population. Specific proposed analyses are: 1. An analysis of the association between levels of glucose tolerance, insulin resistance and other features of the metabolic syndrome, occurrence of major cardiovascular outcomes, and gemfibrozil efficacy. 2. An analysis of the effect of gemfibrozil on progression of carotid atherosclerosis, as measured by B-mode ultrasound. 3. An analysis of the association between LDL particle size distribution and lipoprotein subclass distribution; homocysteine; lipoprotein(a); Creactive protein, tissue plasminogen activator; fibrinogen; and factor VII; major cardiovascular outcomes, and gemfibrozil efficacy. Written documentation that the data will be available to us is included in the letter from Dr. Peter Peduzzi of the VA Cooperative Studies Program. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ANIMAL MODELS OF DIABETIC VASCULAR DISEASE Principal Investigator & Institution: Breslow, Jan L.; Professor; Lab/Biomed Genetic/Metabolism; Rockefeller University New York, Ny 100216399 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2006 Summary: Since the mayor cause of morbidity and mortality in diabetics is macrovascular disease, we propose creating mouse models in which diabetes worsens macrovascular disease. These models will be of great use for studies of pathophysiology and to design new therapies. To produce such models, we have assembled a multidisciplinary team with expertise in mouse models of diabetes and dyslipidemia and in the evaluation of atherosclerosis progression, atherosclerosis regression/remodeling and injury/restenosis. We propose modern genetic approaches to generate diabetic mouse models in which hyperglycemia can be induced by compromising pancreatic (beta-cell function. This will be accomplished through the conditional expression of dominant-negative mutant forms of HNF-1 alpha or HNF-4 alpha or through the inactivation of HNF-1 beta using beta-cell specific promoters and inducible recombinases in transgenic mice. Mice in which hyperglycemia can be induced will be crossed with genetically manipulated mice that have defects of insulin resistance and /or obesity. This aim, in a novel way, will establish diabetic animal models that recapitulate the clinical history of the most common form of diabetes, type II, which is characterized by a variable period of insulin resistance/obesity (pre-diabetic
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state) followed by P-cell decompensation and the development of overt diabetes. A second challenge will be to mimic in the mouse the diabetic dyslipidemia phenotype, which is characterized by increased triglycerides, small dense LDL and decreased HDL cholesterol. Since we have already shown that this is insufficient to cause atherosclerosis in the mouse, we will also breed in traits to raise the levels of LDL cholesterol. To accomplish this we will use human apo CIII and cholesterol ester transfer, protein transgenes and either the human apo B transgene or the LDL receptor knockout trait. Our strategy will be to cross diabetic models with the diabetic dyslipidemia models to establish new models in which diabetes worsens macrovascular disease, as measured by atherosclerosis progression, regression/remodeling, and/or injury/restenosis. We will then use new genetic technology to combine the various required alleles to make a diabetogenic- macrovascular disease model that is easy to breed and transfer to other investigators. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANTIBODIES TO LIPOPROTEIN LIPASE AND ATHEROSCLEROSIS Principal Investigator & Institution: Reichlin, Morris; Vice President of Research; Oklahoma Medical Research Foundation Oklahoma City, Ok 73104 Timing: Fiscal Year 2002; Project Start 05-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Premature atherosclerosis in patients with Systemic Lupus Erythematosus (SLE) has been recognized for the past 25 years. As much as a 50fold increase in risk for coronary artery disease has been found in SLE patients compared to controls and an increased risk for thrombotic cerebrovascular disease has also been recognized. In the past decade lipid abnormalities have been recognized in SLE patients that are "proatherogenic". These include elevated LDL cholesterol, low HDL cholesterol and elevated triglyceride levels that are not due to nephrotic syndrome. Careful clinical studies suggest that conventional risk factors such as age, sex, smoking, hypertension, etc., do not completely account for the prevalence of premature atherosclerosis. Indeed, there appears to be an element of risk conferred by the lupus process itself We postulate that this mechanism of the SLE associated risk lies in autoimmune events that perturb lipid homeostasis in the direction of elevated triglycerides and cholesterol. We further suggest that part of this effect is due to an immune response to lipoprotein lipase which occurs in 50% of SLE patients and promotes hypertriglyceridemia. In addition, autoantibodies to apolipoprotein A-1, Apo B and Apo E may perturb lipid transport and promote decreased HDL cholesterol and increased LDL cholesterol. Our plan is to combine our expertise in autoantibody research with epidemiologic methods. We will conduct a prospective study of SLE patients and their matched controls to evaluate these immune responses on lipid levels, in the presence of conventional risk factors and confounders, and their association with premature atherosclerosis. Recognition of autoimmune mechanisms that promote elevated triglycerides could lead to specific interventions as therapy or even possibly prevention of premature atherosclerosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: APOE IN CHOLESTEROL AND TRIGLYCERIDE HOMEOSTASIS Principal Investigator & Institution: Zannis, Vassilis I.; Medicine; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-AUG-2005
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Summary: (provided by applicant): Apolipoprotein E (apoE) is an important protein of the cholesterol transport system. ApoE is responsible for the clearance of lipoprotein remnants from the circulation via lipoprotein receptors, contributes to cholesterol homeostasis, and protects from atherosclerosis. ApoE has also been shown to have other functions which contribute to cholesterol and triglyceride homeostasis, including VLDL triglyceride secretion and VLDL lipolysis, two processes which may affect plasma triglyceride levels. It is our hypothesis, which is supported by preliminary data, that the carboxy terminal domain of apoE is responsible for the hypertriglyceridemia which is induced by overexpression of apoE. We also hypothesize that overexpression of carboxy terminal apoE variants may protect from atherosclerosis. Our specific aims are: 1) To use adenovirus-mediated gene transfer as well as transgenic mice to elucidate the role of apoE in triglyceride homeostasis and establish the mechanism of apoE-induced hypertriglyceridemia in vivo. 2) To use adenovirus-mediated gene transfer of different apoE forms (in appropriate receptor-deficient mouse models) to elucidate the role of apoE receptors in cholesterol clearance in vivo and in vitro. The mouse models that will be utilized for gene transfer are apoE-/-, LDLR-/-, liver-specific LRP-/- mice as well as crosses among these The gene transfer and receptor binding studies will define the ligand speciflcities for different receptors. 3) To express long-term apoE forms that do not induce hypertriglyceridemia using adenoassociated viral vectors (AAV-apoE) and transgenic mice in order to correct the hypercholesterolemic and atherogenic profile of apoE-deficient mice. This specific aim will explore the ability of selected truncated and mutant forms of apoE that do not induce hypertriglyceridemia to protect from atherosclerosis. We expect that apoE forms that can clear cholesterol and triglycerides and protect from atherosclerosis may provide new therapeutic tools in the near future for the correction of remnant removal disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ARCH PLAQUES AND STROKE IN AN ETHNICALLY MIXED COMMUNITY Principal Investigator & Institution: Di Tullio, Marco R.; Medicine; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2001; Project Start 01-JUN-1997; Project End 31-MAY-2003 Summary: (Adapted from Applicant's Abstract). Atherosclerotic plaques (atheromas) in the aortic arch are considered a potential cause for ischemic stroke in the elderly. The impact of arch atheromas in different racial-ethnic groups is unknown. Moreover, the association of arch atheromas with lipid disorders or hypercoagulability, that may enhance their embolic potential, has not been investigated. A population-based, casecontrol study is proposed to address the following Specific Aims: 1) to determine if aortic arch atheromas are a risk factor for ischemic stroke in the elderly, and their importance in different racial-ethnic subgroups; and 2) to determine if aortic arch atheromas are associated with lipid abnormalities or hypercoagulable states in elderly stroke patients. Secondary Aims will be to evaluate the 4-year stroke recurrence risk in patients with and without atheromas in the overall group and by racial-ethnic subgroups, and the additional risk associated with morphological characteristics of the atheroma (presence of ulcerations or mobile components). A total of 300 cases of ischemic stroke and 300 stroke-free controls, matched by age, gender and race will be enrolled in this 5-year population-based case-control study. Study subjects will be drawn from the ongoing Northern Manhattan Stroke Study (NoMaSS), which will assure recruitment and provide other data collection. The presence of arch atheromas will be ascertained by transesophageal echocardiography. Lipid tests will include total
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cholesterol, triglycerides, HDL and LDL cholesterol, lipoprotein (a), apolipoproteins A-I and B. Hypercoagulability tests will include fibrinogen, prothrombin fragment F1+2 and lupus anticoagulant. Annual telephone follow-up will be performed on cases and controls to ascertain mortality and stroke. Conditional logistic regression will be used to calculate the adjusted odds ratio for stroke of aortic arch atheromas in the overall study group and stratified by racial-ethnic subgroups. The study will provide important data on stroke pathophysiology and set the ground for clinical trials to assess the efficacy of therapeutic options in treating elderly patients with stroke and aortic arch atheromas. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ASSEMBLY LIPOPROTEINS
&
SECRETION
OF
APO
B
CONTAINING
Principal Investigator & Institution: Ginsberg, Henry N.; Professor; Medicine; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2001; Project Start 01-AUG-1996; Project End 31-JUL-2006 Summary: (provided by applicant): Apolipoprotein B, the major apolipoprotein on atherogenic VLDL and LDL, is essential for the assembly and secretion of these lipoproteins by human livers. Studies in cultured liver cells have provided important insights related to the unique regulation of apoB, including its inefficient translocation, its bitopic topology across the endoplasmic reticulum (ER) membrane, its degradation by the cytosolic proteasome, and some of the characteristics of its association with its lipid ligands to become a lipoprotein. However, several critical aspects of the regulation of the assembly and secretion of apoB-lipoproteins remain undefined. In the proposed studies, we will continue to use cultured hepatocyte cell-lines, particularly HepG2 and McARH7777 cells, to address unanswered questions. We will, however, extend our investigations to include studies using primary mouse hepatocytes as well as in vivo measurements of apoB-lipoprotein secretion in adenovirus-infected, transgenic, and "knockout" mouse models. Four hypotheses will be tested: Hypothesis A: The complex secondary structure of apoB, and in particular the presence of one or more densely hydrophobic b-sheet domains, is the basis for the unique aspects of its translocation across the ER and its predisposition for ubiquitination and proteasomal degradation. Hypothesis B: Newly synthesized core lipids, triglycerides (TG) and cholesteryl esters (CE) are both critical for the efficient initial translocation of apoB across the ER and its targeting for lipoprotein assembly. However, TG is the sole lipid added at the later stages of lipoprotein assembly ("the second step"). Hypothesis C: The transition of apoB from a lipid-poor lipoprotein to a TG-enriched lipoprotein that is targeted for secretion includes the completion of translation and translocation, and transport of the lipid-poor particle to either the ER Golgi Intermediate Compartment (ERGIC) or the Golgi apparatus. It is at one of these two sites that bulk lipid addition (the second step) occurs. Importantly, this trafficking can be regulated by a variety of mechanisms distinct from core-lipid synthesis. Hypothesis D: Fatty acid flux to the liver is the major determinant of the assembly and secretion of apoB-lipoproteins. The impact of fatty acid flux on apoB-lipoprotein secretion may be modulated by the status of insulin signaling in the liver, but the latter plays only a minor role in the overall regulation of apoB-lipoprotein secretion. We believe that completion of these studies will provide the basis for new and innovative approaches to the treatment of human dyslipidemias. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BEHAVIORAL FACTORS AND DIETARY CHANGE IN WHTFSMP Principal Investigator & Institution: Bhargava, Alok; Professor; Economics; University of Houston 4800 Calhoun Rd Houston, Tx 77004 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2004 Summary: (provided by applicant): The primary purpose of the research in this project is to specify and estimate models for dietary intakes of the subjects in the Women's Health Trial: Feasibility Study in Minority Populations (WHTFSMP) taking into account the behavioral factors emphasized in the Social Learning Theory and the Health Belief Model. The comprehensive analysis will incorporate the socioeconomic factors such as education and income, and the physiological aspects such as anthropometric indicators and the current energy intakes that reflect the subjects' energy requirements. In addition, the theories of "habit persistence" in diets from the economics literature will be incorporated in the modeling framework. The subjects in the Intervention group of the WHTFSMP received counseling for adopting diets that were low in fat and high in fruits and vegetables. The research will analyze the proximate determinants of the intakes of carbohydrate, saturated, monounsaturated, and polyunsaturated fats, fiber, calcium, acarotene and ascorbic acid using the data at baseline, six and 12 months from the Control and Intervention groups of the WHTFSMP. The second objective of the research is to estimate dynamic random effects models for the subjects' risk factors for coronary disease and cancer such as plasma LDL and HDL cholesterol, triglycerides, and glucose levels. Behavioral factors, anthropometric indicators, energy derived from saturated and polyunsaturated fats, and dietary cholesterol will be explanatory variables in models for plasma LDL cholesterol. The dynamic model is suitable for plasma cholesterol since 50% of cholesterol is endogenously produced. The comprehensive analysis of the data from the WHTFSMP will be useful for refining educational programs that seek to promote healthful eating. In particular, the incorporation of the various behavioral factors in the analyses of dietary intakes will identify strategies of targeting women who are at greater risk of chronic disease but are less likely to change their behavior and would benefit from enrollment in nutrition education programs. The results from the empirical models for plasma LDL, HDL, triglycerides and glucose will be useful for identifying strategies for lowering the subjects' risks for cardiovascular disease and cancers. Overall, the results will facilitate the design of policies for improving health of especially minority women in the United States and will be useful for analyses of the Women's Health Initiative data. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BIOLOGY OF 12-LIPOXYGENASE ISOZYMES Principal Investigator & Institution: Funk, Colin D.; Professor of Pharmacology; Pharmacology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2001; Project Start 01-FEB-2000; Project End 31-JAN-2004 Summary: Atherosclerosis, chronic inflammatory process progressing from fatty lesions to fibrous and unstable plaques, is the major underlying factor in most cases of coronary heart disease. Clinical disease as a result of atherosclerotic disease remains as the leading determinant for the extensive mortality and morbidity. and exorbitant health care costs in our society. The "LDL oxidation" hypothesis has gained general acceptance as a leading player in atherogenesis and it is recognized that oxidized LDL exhibits many pro-atherogenic properties. properties. The factors that initiate LDL, oxidating in vivo are poorly understood. However, circumstantial evidence has placed the 12/15lipoxygenase in the context of atherosclerosis. Thus, in the first specific aim, the role of
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12/15- lipoxygenase in mouse models of atherosclerosis (apoB editing catalytic polypeptide-1 (apobec-1)/LDL-receptor deficient and apoE deficient) will be assessed by quantitating lesion development throughout the aorta by the "en face" method using appropriately crossbred 12/15-lipoxygenase deficient mice. The combined effects of the anti-oxidant vitamin E with 12/15-lipooxygenase deficiency will also be examined. Total cholesterol, triglycerides, lipoprotein profiles and oxidative stress markers known as isoprostanes will be measured and correlated with lesion development. If specific 12/15-lipoxygenase inhibitors are ultimately to be used in atherosclerotic disease management they will need to be effective in limiting, or causing regression of, preexisting lesion. By using an inducible 12/15-lipoxygenase gene disruption strategy in mice with atherosclerosis at various stages this important matter will be addressed. In specific aim 2, the subset of macrophages expressing 12/15- lipoxygenase will be characterized and purified. The effects of lipid loading and factors regulating 12/15lipoxygenase gene expression will be determined. In specific aim 3, the novel 12(R)lipoxygenase will be characterized and its relevance to atherosclerosis and LDL oxidation discerned. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CELL SIGNALING: MACROVASCULAR COMPLICATIONS OF DIABETES Principal Investigator & Institution: Bornfeldt, Karin E.; Pathology; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2002; Project Start 30-SEP-1998; Project End 30-NOV-2005 Summary: (provided by applicant): A majority of people with diabetes die of cardiovascular disease caused by atherosclerosis that is accelerated by diabetes. The factors that drive diabetes-accelerated atherosclerosis are still poorly understood. Our recent studies on a new porcine model show that diabetes in combination with elevated lipid intake causes increased accumulation and proliferation of arterial smooth muscle cells (SMCs) in lesions of atherosclerosis. The increased SMC proliferation occurs concomitant with hyperglycemia and elevated levels of plasma triglycerides. High glucose levels are not sufficient to induce SMC proliferation, but certain fatty acids common in triglycerides (oleate and linoleate) stimulate SMC proliferation in the presence of insulin-like growth factor I (IGF-I). We propose that diabetes leads to an increased amount of IGF-I and of lipoprotein lipase in lesion macrophages, and that lipoprotein lipase degrades triglycerides into free fatty acids that act in synergy with IGF-I to stimulate SMC proliferation. Our goal for the next five years is to address the following questions: 1. Do oleate and linoleate enhance the growth-promoting effects of IGF-I on SMCs? 2. How do oleate and linoleate synergize with the growth-promoting action of IGF-I in SMCs? 3. Does lipoprotein lipase produced by lipid loaded macrophages increase SMC proliferation by generating oleate and linoleate? 4. Does glucose or lipids associated with diabetes stimulate SMC proliferation, lipoprotein lipase and IGF-I in lesions of atherosclerosis and does lack of macrophage-derived lipoprotein lipase result in reduced SMC proliferation? We will use several animal models of diabetes-associated atherosclerosis, isolated arterial SMCs for signal transduction studies as well as a co-culture model of monocyte derived macrophages and SMCs. Increased understanding of the regulation of SMC proliferation and accumulation in diabetic lesions of atherosclerosis may provide the basis information necessary for development of highly specific drugs that can prevent lesion progression and formation of vulnerable lesions that are likely to cause the clinical symptoms of cardiovascular complications in diabetes.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COGNITIVE BEHAVIOR THERAPY IN ACUTE POST MYOCARDIAL INFARCTION PATIENTS Principal Investigator & Institution: Schneiderman, Neil; Professor and Director of Health Program; University of Miami Coral Gables Box 248293 Coral Gables, Fl 33134 Timing: Fiscal Year 2001; Project Start 01-JUL-1986; Project End 31-JUL-2006 Summary: (provided by applicant): Depression and inadequate social support are risk factors for medical morbidity and morality after acute myocardial infarction (AMI). The Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial is a multicenter, randomized, controlled clinical study of cognitive-behavioral treatment (CBT) for depression and inadequate social support in post-AMI patients. Because the ENRICHD trial did not focus on biological risk factors (e.g., lipoproteins, lipids, glucose tolerance, adiposity, insulin, inflammatory markers, coagulation factors), possible subclinical markers of disease (e.g., coronary calcification, elevated intima-media thickness [IMT] of carotid artery, decreased brachial artery vasodilation, increased left ventricular mass) or putative mediators (e.g., cortisol, catecholamines) of increased coronary heart disease (CHD) risk or putative subclinical markers of disease, we propose to study further some 200 Miami patients previously enrolled in ENRICHD as well as 210 (180 completors) newly-recruited post-acute MI patients. Thus, approximately 100 previously studied ENRICHD patients, who received CBT, and 100 ENRICHD patients who received usual care, would be compared in terms of posttreatment cardiovascular risk factors, possible subclinical markers of disease and other biological and psychosocial variables to determine the effects of CBT. These patients would then be compared with 210 (180 completors) newly recruited post-acute MI patients. Half of these newly recruited subjects would be randomized into the CBT condition and half into usual care. These newly recruited post-MI patients would be assessed both before and after treatment (i.e., CBT or usual care) in terms of psychosocial variables (e.g., depression and social support), putative biological mediators (e.g., elevated cortisol), risk factors (e.g., elevated triglycerides) and possible subclinical markers of disease (e.g., coronary calcification) as well as demographic and medical characteristics. The project would use all of the core units. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CONTROL OF ADIPOGENESIS AND ENERGY METABOLISM Principal Investigator & Institution: Farmer, Stephen R.; Professor; Biochemistry; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 01-JUN-1997; Project End 31-MAY-2002 Summary: (Adapted from applicant's abstract): Adipose tissue plays a central role in controlling energy metabolism within the organism. Its primary function is to store triglycerides during periods of caloric excess and to mobilize these stores as free fatty acids during caloric deprivation. In modern western civilization, individuals usually consume more calories than they expend which can lead to a high incidence of obesity. In humans, obesity is one of the most common metabolic disorders and it is an independent risk factor for several pathological diseases including non-insulindependent diabetes mellitus (NIDDM), hypertension and cardiovascular disease. Recent studies suggest that some of these disorders may be linked to a breakdown in the regulatory mechanisms that control the expression of metabolic genes in mature adipocytes. Some progress towards an understanding of these processes has come from
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studies involving the identification of transcription factors which regulate adipogenesis. Most notable among these factors are members of the family of CCAAT/enhancer binding proteins (C/EBPs) and the peroxisome proliferator activated receptors (PPARs). In the case of the C/EBPs, C/EBPa is expressed in high abundance in a limited number of tissues, including fat and liver, where it plays a central role in regulating energy homeostasis. PPARg2 expression is limited to adipose tissues where it plays a central role in committing multipotential stem cells to the adipogenic lineage, as well as regulating differentiation of preadipocytes into adipocytes. The investigators have recently demonstrated that the conditional ectopic expression of C/EBPb and C/EBP( in multipotential NIH-3T3 fibroblasts induces PPARg expression which in turn stimulates adipogenesis based on the synthesis of triglycerides and their deposition into fat droplets. The specific aims are designed to define the transcriptional events that control adipogenesis. Aim 1 will determine the role of C/EBPb, C/EBP( and PPARg in inducing the early commitment phase of adipogenesis which involves the initiation of C/EBPa transcription. Aim 2 will identify and characterize the regulator elements in the C/EBPa gene and the corresponding nuclear DNA binding proteins that regulate C/EBPa transcription during the differentiation of 3T3-L1 preadipocytes. Aim 3 will determine the role of PPARg and the C/EBPs in regulating the expression of the mature, terminally differentiated adipocyte. This will involve an analysis of how these transcription factors control the expression of the insulin-dependent glucose transport system which include induction of the glucose transporter 4 (GLUT4), the insulin receptor and the insulin receptor substrate 1 (IRS1). Accordingly, mRNAs and proteins of these markers will be analyzed and the ability of NIH-3T3 cells to facilitate glucose uptake in response to insulin will be assessed. These studies should lead to insights into the molecular mechanisms regulating energy homeostasis and the defects underlying obesity and NIDDM. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CONTROL OF GENE TRANSCRIPTION BY ESSENTIAL FATTY ACIDS Principal Investigator & Institution: Clarke, Steven D.; Professor and Love Chair of Nutritional,; Human Ecology; University of Texas Austin 101 E. 27Th/Po Box 7726 Austin, Tx 78712 Timing: Fiscal Year 2001; Project Start 15-FEB-1999; Project End 31-DEC-2002 Summary: Dietary polyenoic (n-6) and (n-3) fatty acids (PUFA) reduces blood VLDL by coordinately: (a) inhibiting fatty acid biosynthesis; (b) reducing fatty acid flux to triglycerides; and (3) enhancing liver and skeletal muscle fatty acid oxidation. In a sense, PUFA are classic fuel partitioners (i.e. direct lipid from storage to oxidation); and in this way may protect against the development of insulin resistance and cardiovascular disease. PUFA regulation of metabolism is often viewed as a simple pleiotropic effect resulting from changes in membrane fatty acid composition. However, fatty acids may also govern gene transcription by functioning as ligand activations for members of the steroid receptor super-family (e.g. PPARs). Although PPARs per se appear not to mediate the PUFA suppression of hepatic lipogenic genes (e.g. fatty acid synthase-FA), the kinetics of the PUFA inhibition are consistent with a ligand mediated event. Thus we hypothesize that, PUFA, or a metabolite, bind to a specific PUFA response factor (RF) which interacts with the PUFA-RE and functions to silence FAS transcription by interfering with the transfactors with the PUFA-RE and functions to silence FAS transcription by interfering with the trans- factors associated with the glucocorticoid (GRE) and/or insulin (IRE) response sequences. Moreover, since PUFA
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appear to activate trans-factors of the steroid receptor super-family, we propose PUFA are dietary humoral factors when consumed t critical periods of development can "imprint" genes in a manner that alters their gene expression throughout the life cycle. The rat FAS gene including 15kbp of 5' flanking will be employed to: (a) functionally map the yet unidentified PUFA-RE and the GRE in the 5'-flanking sequences of the FAS gene; (b) characterize the interaction between the IRE and the GRE which leads to amplification pf FAS transcription; and determine how the PUFA-RE interacts to silence the GRE and IRE of FAS; and (c) identify and characterize the trans-factors responsible for the PUFA regulation of FAS transcription. These Aims will be addressed by a combination of techniques including: transfection analyses with rat liver cells in primary culture; DNAse-I hypersensitivity site mapping and in vivo footprinting of nuclei from rats fed PUFA versus 18:1 (n-9); and in vivo footprinting with hepatocytes monolayuers treated with (n-6)/(n-3) PUFA; UV cross-linking for trans-factor characterization; and yeast one-hybrid system for cloning PUFA-RE trans-factors associated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DHEA EFFECTS ON MOOD IN DEPRESSED HIV+ PATIENTS Principal Investigator & Institution: Rabkin, Judith G.; Professor; New York State Psychiatric Institute 1051 Riverside Dr New York, Ny 10032 Timing: Fiscal Year 2001; Project Start 10-AUG-2000; Project End 31-JUL-2004 Summary: This is a double blind, placebo-controlled clinical trial of the antidepressant effect of DHEA among HIV+ individuals. Secondary goals will include determination of whether DHEA has anabolic effects or androgenic effects on enrolled subjects. The investigators will consider the basic endocrinology of adrenal steroid metabolism in the subjects, and propose to assess the effects of DHEA on immune status and viral activity with regard to the safety of the use of DHEA in HIV infected individuals. The study is an eight week double blind controlled trial of oral DHEA vs. placebo with an eight week maintenance phase for drug responders, and 16 weeks of open treatment offered to placebo non-responders (after the eight week double blind trial). They propose a 1:1 randomization and predict that 114 enrolled individuals will complete the eight week trial. If DHEA ameliorates depressive symptoms, as well as increasing libido and reducing loss of muscle mass, then the investigators will have identified an intervention with a broad spectrum of action suitable for both men and women with HIV infection, that is practical, inexpensive, and accessible. With regard to the endocrine studies, the investigators will assess precursors and metabolites of DHEA before and after oral administration of the compound, and examine effects of cortisol, triglycerides, insulin, cholesterol, growth hormone, IGF-1, and IGF-1 binding proteins. Tests will be administered at study baseline, weeks 4 and 8, including standard dose ACTH, low dose ACTH, CRF, and GNRH stimulation tests to assess the hypothalamic-pituitaryadrenal and hypothalamic-pituitary gonadal function before and after DHEA administration. This will permit the investigators to assess potential underlying mechanisms for the putative therapeutic effects of DHEA on mood, libido, and body composition. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DIABETIC NEUROPATHY: IMPLICATIONS FOR WOUND REPAIR Principal Investigator & Institution: Gibran, Nicole S.; Associate Professor; Surgery; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2003; Project Start 30-SEP-1999; Project End 31-AUG-2007
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Summary: (provided by applicant): This proposal explores cell signaling pathways that occur between cutaneous sensory nerve fibers and endothelial cells in response to cutaneous injury. Our previous data suggest that nerve-derived neuropeptides contribute to the normal wound repair process. In contrast, non-healing chronic ulcers associated with diabetes mellitus are characterized by microangiopathy and decreased innervations. Based on encouraging data during the past funding period we continue to explore our hypothesis that in patients with diabetes mellitus, hyperglycemia and hyperlipidemia impair microvascular endothelial cell response to nerve-derived neuropeptides and endothelial cell production of necessary inflammatory mediators. These abnormalities contribute to impaired response to cutaneous injury. We will test our hypothesis by addressing the following Aims: Aim 1: To determine the effects of hyperglycemia and matrix glycosylation on microvascular endothelial cells responses. Hyperglycemia can directly alter cellular responses and can indirectly alter cellular response by extracellular matrix molecule glycosylation. We will determine whether hyperglycemia and/or matrix molecule glycosylation alters SP-induced endothelial cell mediator synthesis, cytoskeleton organization, integrin expression and intracellular signaling. Aim 2: To determine the effect of elevated fatty acid levels on endothelial cell responses. Hyperlipidemia is strongly associated with complications in diabetes mellitus. We will determine whether elevated fatty acids alone or as Triglycerides alter SP-induced endothelial cell mediator synthesis, cytoskeleton organization, integrin expression or intracellular signaling. Aim 3: To determine the anti-oxidant regulation of microvascular endothelial cell response to hyperglycemia & hyperlipidemia. Oxidative stress due to hyperlipidemia may alter cellular response to injury. We will continue our studies of effects of antioxidants, vitamin E, vitamin C and n-acetyl cysteine on cellular responses under hyperlipidemic and hyperglycemic conditions. Aim 4: To determine whether restoration of neuropeptide activity improves wound repair in diabetic mice. We will use several approaches to evaluate the roles of neuropeptides in wound repair. Using an excisional wound repair model in hyperglycemic db/db mice, we will replace substance P and inhibit neutral endopeptidases activity. We will also test the effects of antioxidants in this murine wound model. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DIET THERAPY IN DIABETES MANAGEMENT OF MEXICAN AMERICANS Principal Investigator & Institution: Briones, Esperanza R.; Univ of Texas-Pan American Edinburg, Tx Timing: Fiscal Year 2002; Project Start 01-JUN-1977; Project End 31-JUL-2006 Summary: (provided by applicant): Diabetes in Hispanic Americans is a serious health problem. It affects 1.2 million or 10.6% of the Mexican American population. Approximately 24% of Mexican Americans in the U.S. between the ages of 45-74 have diabetes. In Hispanic adults, diabetes is primarily type 2, and its incidence is correlated with the occurrence of obesity. The purpose of the study is to conduct a two and half (21/2) year randomized trial of a culturally appropriate dietary and lifestyle education intervention designed for Mexican Americans with type 2 diabetes residing in Rio Grande Valley. Both males and females, with type 2 diabetes will be recruited, with two age subgroups, ages 45-59 and 60 and above. Eligible participants will be randomized into two groups. Group 1 will receive the conventional dietary counseling and group 2 will receive additional sessions and follow-up. The specific objectives of the study are: to assess the effectiveness of a culturally appropriate intervention to improve participants' adherence to dietary modifications, medication schedules, and promote sustained
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improvements in lifestyle behaviors; to assess the anthropometric measurements, health habits, and nutrient consumption of subjects at baseline and after dietary and educational sessions; to determine fasting serum glucose and glycosylated hemoglobin in assessing the level of diabetes control; and to assess the lipid profile (serum cholesterol, triglycerides, high density lipoprotein cholesterol) which are associated with the development of coronary heart disease in diabetes. Statistical calculations will be used to evaluate the differences between the two groups. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DISTINCT HUMAN MACROPHAGE RECEPTOR FOR ABNORMAL VLDL Principal Investigator & Institution: Gianturco, Sandra H.; Prof/Div/Gerontology/Geriatric Medicine; Medicine; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2003; Project Start 01-JAN-1991; Project End 30-JUN-2007 Summary: (provided by applicant): Elevated plasma triglycerides (TG) and TG-rich lipoproteins (TGRLP), especially postprandial (pp) TGRLP, are emerging risk factors for atherothrombotic disease. However, little is known about the molecular basis for their interaction with cells of the artery wall or in the periphery. We identified and cloned a wholly unique receptor for dietary ppTGRLP, the apoB48 receptor (apoB48R), found in human monocyte-macrophages and in foam cells in arterial lesions. Now a mouse model, deficient in this receptor, has been created, and evidence demonstrates that in an atherogenic background the loss of the apoB48R reduces atherosclerosis significantly, further implicating it in macrophage foam cell formation and reduces peripheral uptake in tissues that normally express the receptor and elevates plasma cholesterol and triglycerides (TG). Therefore, using this new mouse model, we plan to determine its role in dietary lipoprotein metabolism and ppTGRLP uptake by cells in the periphery where the receptor is highly expressed (bone marrow, spleen, skeletal muscle and adipose). Furthermore, we will identify the molecular mechanisms and the extent to which ppTGRLP are atherogenic in mouse models of atherogenesis, including the apoEand LDL R-deficient mice, crossed into the apoB48R-deficient mouse and in our newly developed apoB48R transgenic mice with enhanced tissue specific apoB48R expression in macrophages and liver (where it is not normally found) and we will evaluate the impact of the apoB48R on atherogenesis when animals are subjected to atherogenic and TG-elevating diets, thereby altering the postprandial mileau. We further plan to determine in vitro the molecular and cellular mechanisms by which the apoB48 R operates, that is, rapid, efficient accumulation of intracellular lipid. In vitro studies will identify the receptor recycling rates, endosomal/lysosomal trafficking, possible involvement of microtubules and/or microfilaments and rates of synthesis and degradation. The ligand-binding domain of the receptor will be sought as an eventual targeting site for intervention. Finally we will identify potential additional modifiers of macrophage pathobiology that may be exacerbated by the uptake of ppTGRLP via the apoB48R pathway by interfering in the normal cholesterol homeostasis, both production (HMGCoA reductase) and efflux (via ABC A1). The proposal uses the powerful techniques of mouse genetics coupled with dietary manipulations in vivo coupled with cell and molecular biology approaches in vitro aimed to answer key questions about the role of the apoB48 R and its interaction with ppTGRLP in health and disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DYSLIPIDEMIA AND RISK OF CVD IN DIABETIC MEN AND WOMEN Principal Investigator & Institution: Hu, Frank B.; Nutrition; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-JUL-2006 Summary: We propose to assess biochemical markers of dyslipidemia and endothelial dysfunction, and omega-3 fatty acids in relation to risk of CVD among men and women diagnosed with type 2 diabetes in two large ongoing cohort studies, the Nurses? Health Study (NHS) and Health Professionals? Follow-up Study (HPFS). By 1998, 12,600 confirmed type 2 diabetic cases have already accumulated in the two cohorts. By the year 2002, 5,507 blood samples prospectively collected from persons with previously or newly diagnosed type 2 diabetes will be available for analyses. Using this unparalleled resource, we will specifically evaluate (1) The relationship between plasma levels of cell adhesion molecules (i.e. sICAM-1, sVCAM-1, E-selectin), diabetic dyslipidemia, and risk of CVD among diabetics; (2) the association between Lp(a) concentrations and risk of CVD among diabetics, independent of high triglycerides and low HDL; (3) the association between long-term intakes of omega-3 fatty acids and CVD risk in diabetes. The main NHS and HPFS grants will provide follow-up and documentation of CVD in addition to covariate information. Overall, the large size of these cohorts, the prospective design, the high follow-up rates, and the availability of archived blood specimens provide a unique opportunity to study the relationship between diabetic dyslipidemia and risk of CVD in an extremely cost-efficient and timely manner. In addition, these two cohorts provide an unusual opportunity to compare lipid profiles and endothelial markers of CVD between diabetic men and women. We believe that this study will provide new insight into the understanding of the atherosclerotic process in diabetes and may suggest new nutritional and pharmacological means to prevent and treat CVD complications among diabetics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EFFECT OF CAPTOPRIL ON THE DIABETIC-HYPERTENSIVE HEART Principal Investigator & Institution: Heyliger, Clayton E.; Ponce School of Medicine G.P.O. Box 7004 Ponce, Pr 00731 Timing: Fiscal Year 2001; Project Start 30-SEP-1986; Project End 31-MAY-2005 Description (provided by applicant): Hypertension and diabetes mellitus commonly occur together. Unfortunately, very few randomized, controlled trials of antihypertensive treatment have been carried out in diabetic patients. Thus, decisions regarding the efficacy of such treatment must be based upon evidence, often controversial, extrapolated from studies in non-diabetic populations. A classic example can be seen in studies on the effect of antihypertensive therapy on lipids. Although abnormal myocardial lipid metabolism is a serious complication of diabetes mellitus and is strongly implicated in diabetes-induced primary cardiomyopathy, studies on antihypertensive therapy-induced lipid abnormality are confined to the development of atheroscelerosis and ischemic heart disease. We believe that the effect of antihypertensive agents on lipid metabolism in the cardiovascular system is not limited to the blood where they either have no effect, adversely affect or have a beneficial effect on lipid levels, but also extends to the myocardium, where they also influence lipid levels. Further, this alteration in myocardial lipid metabolism is associated with changes in cardiac contractile performance. In this regard, it is our hypothesis that the beneficial
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effect of captopril on lipid metabolism in the circulation is not confined to the blood where it decreased total cholesterol, triglycerides, and low density lipoproteins (LDL) as well as increased high density lipoproteins (HDL), but is also beneficial to the myocardium where it likewise positively influences lipid metabolism. This study will, therefore, provide evidence to support this hypothesis. It will assess the effect of captopril on myocardial lipid metabolism of the diabetic-hypertensive rat. Specifically, it will assess the effect of this agent on myocardial levels of cholesterol, triglycerides and long chain acyl carnitines and CoAs. These lipids and lipid intermediates accumulate in the diabetic heart and are strongly implicated in its depressed contractile performance. The male spontaneously hypertensive rat (SHR) will be the animal model. It will be made diabetic with a single tail vein injection of streptozotocin (60 mg/kg). Captopril will be administered in the drinking water (100 mg/kg) 3 days after diabetes induction. Rats will be sacrificed after 6 weeks of diabetes with sodium pentobarbital (75 mg/kg, i.p.). This study will present new findings about captopril therapy during diabetes plus hypertension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EXERCISE INTERVENTION IN COLORECTAL POLYP PATIENTS Principal Investigator & Institution: Mctiernan, Anne M.; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-JAN-2004 Summary: (Adapted from the Applicant's Abstract): Strong observational evidence points to a link between physical activity and reduction in risk of colon cancer. The mechanisms for this association have not been delineated, nor have the amounts and types of exercise needed for a putative protective effect been determined. We propose a randomized controlled clinical trial of a one-year moderate aerobic/strength training exercise intervention in adenomatous colon polyp patients (n=100 men, 100 women). We hypothesize that polyp patients in an exercise intervention will experience significant biological effects on colorectal epithelium, specifically Ki67 indices of proliferation, bax and bc1-2 markers of apoptosis, and prostaglandin concentrations (PGE2 and PGF2cc). Patients will be recruited on-site from gastroenterology physicians' offices and secondarily from a high-risk colorectal cancer family registry. Sedentary individuals with newly diagnosed (within the past 18 months) adenomatous colon polyp(s) will be screened for eligibility and randomized to either the exercise intervention or a stretching-control group. The exercise intervention will use existing proven methods for adopting and maintaining exercise, taken from our ongoing research program. It will consist of 3 months' facility-based exercise instruction in small groups, followed by 9 months' home-based exercise program supplemented with group behavior change meetings. The goal for exercise will be moderate-level aerobic exercise 5-6 days per week for 30-45 minutes, plus strength training 2 days per week for 15-20 minutes. Colon and rectal biopsies will be taken at baseline and 12-months, and examined for amount and patterns of epithelial cell proliferation (with Ki67 marker) and apoptosis markers (bc1-2 and bax, an inhibitor and an inducer of apoptosis, respectively). Additional potential markers of exercise effect on colon cancer risk will be measured, including rectal mucosal biopsy prostaglandin concentrations, stool frequency, insulin-like growth factor (IGF-1) and IGF binding protein (IGFBP-3), insulin, glucose, C-peptide, triglycerides, and measures of fat mass and fat distribution. Other measures at baseline and 12 months include fitness (V02max), self-reported physical activity, diet, and quality of life. Results from this unique human experimental study
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will provide important information about mechanisms of exercise effects on colon carcinogenesis and about potential Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EXERCISE, DIABETES, AND CORONARY SMOOTH MUSCLE CALCIUM Principal Investigator & Institution: Sturek, Michael S.; Professor; Dalton Research Center; University of Missouri Columbia 310 Jesse Hall Columbia, Mo 65211 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-MAR-2003 Summary: Our long-term goal is to determine if exercise training attenuates the excess coronary artery disease (CAD) in diabetes and the vascular smooth muscle (VSM) Ca (Cam) signaling mechanisms involved. In our porcine model of diabetic dyslipidemia coronary arteries show increases in contraction to prostaglandin F2alpha (PGF) and Cam responses to endothelin-1 (ET). Exercise of normal swine decreases Ca release from the sarcoplasmic reticulum (SR) and increases Ca influx, while decreasing ET-induced contraction and DNA synthesis. However, ET-induced contraction does not require Ca release that is dependent on tyrosine kinase, a signal for cell growth. Overall hypothesis: after exercise training increased ET-induced Ca influx attenuates contraction, while decreased SR Ca release attenuates growth of smooth muscle. Design: low fat control pigs (C), high fat fed (HF), and alloxan diabetic and high fat fed (D) pigs are maintained for 20 and 30 wk to study the progression of CAD and compared to D pigs exercise trained (D plus EX). Specific Aims are to test the hypotheses that in diabetes: 1) Exercise improves glycemic and lipidemic status. Diabetes will be defined by measures of blood glucose, glycated protein, insulin, etc. HDL, LDL, VLDL, triglycerides, apoproteins, glycated LDL, and ET will define features of diabetic dyslipidemia. 2) Exercise attenuates the increase in CAD. Intravascular ultrasound will assess atheroma and vasoconstrictor responses to PGF and ET in vivo. Histology and contractile tension responses of coronary rings to PGF and ET will provide in vitro measures of CAD. 3) Exercise attenuates the conversion of VSM from the contractile (cVSM) to synthetic (sVSM) phenotype. sVSM cell phenotype will be identified using digital imaging microscopy by the Cam response to UTP, perinuclear SR, DNA, smooth muscle actin, desmin, and vimentin. 4) Exercise attenuates the increased contraction of cVSM by increasing ET receptor-dependent Ca influx. Mn and Ba influx used as Ca surrogates will assess Ca influx. Subsarcolemmal Ca localization relative to ryanodine receptors will be digitally imaged. 5) Exercise attenuates the increased ET-induced Cam amplitude and nuclear Ca localization by decreasing tyrosine kinase-dependent Ca release from the SR. Imaging will assay in single cells the relative content and spatial distribution of ET, ryanodine, and IP3 receptors, tyrosine phosphorylation, DNA and Cam. Significance: the first study of Ca localization mechanisms involved in the excess CAD in diabetic dyslipidemia and the therapeutic effects of exercise on CAD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FFA METABOLISM IN DIFFERENT TYPES OF HUMAN OBESITY Principal Investigator & Institution: Jensen, Michael D.; Professor of Medicine; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2001; Project Start 01-AUG-1988; Project End 31-JUL-2003 Summary: Abnormalities of fatty acid metabolisms are considered important contributors to the adverse health consequences of upper body/visceral obesity. Excess hepatic FFA delivery, perhaps originating from visceral adipose tissue lipolysis, could
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account for the reduced ability of insulin to inhibit hepatic glucose production and for the abnormal VLDL kinetics in visceral obesity. The investigators have found that overnight postabsorptive (basal) hepatic FFA delivery is increased in obesity, but that visceral lipolysis increases in proportion to visceral fat mass only in obese women. The abnormalities of hepatic glucose and lipid metabolism attributed to excess FFA would be expected to be more apparent at times of elevated plasma insulin concentrations. However, there is no information regarding the effects of insulin on splanchnic FFA metabolism in visceral obesity. Excess FFA can also impair insulin mediated glucose disposal in muscle. This could occur through direct or indirect mechanisms; increased FFA is associated with increased intramuscular triglycerides, which are independently associated with insulin resistance. The investigators propose to assess the effects of insulin on splanchnic FFA metabolism in visceral obesity and to investigate intramuscular fatty acid kinetics using a newly developed stable isotope technology. The objectives of this proposal are to determine whether: 1) insulin suppression of splanchnic FFA release is impaired in visceral obesity; 2) visceral lipolysis contributes a greater proportion of hepatic FFA delivery in viscerally obese than in non-obese individuals under hyperinsulinemic conditions; 3) intramuscular triglyceride hydrolysis is increased in visceral obesity compared with trained and sedentary lean humans; 4) insulin inhibits both intramuscular triglyceride hydrolysis and the delivery of fatty acids to pre-oxidative intramuscular pool in lean (trained and sedentary) but not viscerally obese humans; and 5) improved insulin action with respect to glucose metabolism, whether accomplished by exercise training/weight loss or via troglitazone treatment, is associated with improvements in insulin action on FFA and intramuscular fatty acid metabolism in viscerally obese humans. Completion of the studies proposed in this application will better define the role of insulin in regulating visceral lipolysis in high risk obesity and will provide novel information regarding intramuscular fatty acid metabolism in insulin resistant and insulin sensitive states. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FLAX: SAFETY & EFFICACY IN REDUCING CARDIOVASCULAR RISK Principal Investigator & Institution: Szapary, Philippe O.; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 26-SEP-2002; Project End 31-MAY-2004 Summary: (provided by applicant): Hypercholesterolemia is an important established risk factor for atherosclerotic cardiovascular disease (ASCVD). The National Cholesterol Education Program (NCEP) has recently estimated that 100 million Americans qualify for treatment of their hypercholesterolemia. Of these Americans, 65 million could be managed with diet and exercise alone, referred to as Therapeutic Lifestyle Changes (TLC) by the most recent NCEP guidelines. The NCEP has already recognized the importance of diet and Complementary Alternative Medicine (CAM) therapies in the management of dyslipidemia by incorporating soluble fiber and plant-based stanol esters as part of TLC. Flaxseed is a unique food as it contains significant amounts of soluble fiber as well as the richest source of both alpha-linolenic acid (ALA) and phytoestrogenic lignans, which have all been implicated in the prevention of ASCVD. Because flaxseed contains these constituents, it may play an important role in TLC in the future, but data is currently lacking. In addition, because lignans can bind to the estrogen receptor and elicit a hormonal response, chronic flaxseed consumption may have undesirable hormonal effects. Thus in this project, we propose to systematically evaluate the safety and efficacy of ground flaxseed ingestion in both men and women
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21
with hypercholesterolemia over the short term. This will be done in a single doubleblind, randomized, placebo controlled clinical trial. Because little is known about the metabolic effects of flaxseed in men, randomization will be stratified by gender. The test dose of flaxseed meal will be 40 grams administered in baked products and compared to a matching wheat bran control. The primary endpoints of this study are to evaluate the effects of flaxseed consumption on lipid metabolism and oxidative stress. The primary response variables in terms of lipid metabolism will include low density lipoprotein (LDL-C) cholesterol and post-prandial triglycerides. For the evaluation of oxidant stress, the primary response variable will be urinary isoprostane secretion, the most sensitive marker of in vivo oxidative damage. Secondary variables of interest will include markers of cholesterol metabolism, vascular inflammation, endocrine function, safety and acceptibility. The results from this study will lay the foundation for several lines of research into the clinical and biochemical effects of flaxseed supplementation in modulating cardiovascular risk. Specifically, the data generated from this project will be used as preliminary data to pursue R01 submissions to NCCAM and NHLBI to investigate the long-term effects and mechanisms of action of the various components of flaxseed on lipid metabolism and clinical endpoints in patients at risk for ASCVD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FUNCTIONAL ARTERIAL CHANGES IN ATHEROGENESIS Principal Investigator & Institution: Kullo, Iftikhar J.; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-JAN-2008 Summary: (provided by applicant): The broad long-term goal of the candidate is to develop new strategies to improve cardiovascular risk assessment. The goal of this proposal is to evaluate the association of two measures of arterial function - endothelial function and arterial compliance - with conventional and novel risk factors on one hand and with sub-clinical atherosclerosis on the other hand. The hypothesis is that these measures of arterial function mediate the deleterious effects of conventional and novel risk factors and are associated with coronary atherosclerosis in asymptomatic individuals. The novel risk factors to be studied include the 'conditional' risk factors (homocysteine, fibrinogen, lipoprotein (a), triglycerides, small dense low density lipoprotein (LDL), and C-reactive protein and polymorphisms in selected candidate genes (endothelial nitric oxide synthase and angiotensin converting enzyme). Endothelial function will be assessed by brachial artery reactivity using vascular ultrasound and arterial compliance assessed by pulse wave velocity using applanation tonometry. Because the effects of novel risk factors on arterial function may depend on the background of conventional risk factors, the measures of arterial function will be obtained in two well-characterized, community-based cohorts with different burdens of conventional risk factors. In both cohorts, coronary artery calcification measured by electron beam computed tomography, a quantitative measure of subclinical atherosclerosis, is available at no cost for the present proposal. Candidate: To obtain additional skills necessary for a career as an independently funded clinical investigator, the candidate will complete courses in research design, biostatistics and genetic epidemiology. Based on the training and experience obtained, the candidate plans to submit an R01 application in year 4 of the award building on the studies proposed in this application. Environment: The candidate is supported by an accomplished team of mentors and consultants and has access to unparalleled resources at Mayo Clinic Rochester for patient-oriented research including one of the finest General Clinical Research Centers in the country.
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Triglycerides
Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GARLIC THERAPY IN HYPERLIPIDEMIA CAUSED BY HAART Principal Investigator & Institution: Standish, Leanna J.; Professor; None; Bastyr University 14500 Juanita Dr Ne Kenmore, Wa 98028 Timing: Fiscal Year 2001; Project Start 13-SEP-2000; Project End 31-MAY-2003 Summary: This is a phase I/II randomized double-blind, placebo controlled trial to study garlic as lipid lowering therapy in hyperlipidemic HIV-infected subjects treated with highly active anti-retroviral therapy (HAART). We will utilize Garlicin/TM, an allicin-standardized dried garlic supplement in three escalating doses (700 mg, 1400 mg, and 2800 mg/day) in HIV- infected subjects (n=102, with 51/arm) who are receiving HAART. The primary aim of this study is to measure the effects of three escalating doses of Garlicin/TM on total serum cholesterol. Secondary aims include determining the tolerability and adverse events associated with three escalating doses of Garlicin/TM and gathering preliminary data on the effects on fasting serum triglycerides, basal glucose and insulin levels as well as serum transaminases (ALT and AST). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC TRIGLYCERIDES
AND
ENVIRONMENTAL
DETERMINANTS
OF
Principal Investigator & Institution: Arnett, Donna K.; Associate Professor; Epidemiology; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2006 Summary: (provided by applicant): Hypertriglyceridemia is emerging as important predictor of atherosclerosis, and recent evidence suggests related phenotypes of triglycerides (TGs), such as TG remnant particles and small LDL particles, are particularly atherogenic. There is considerable variation in the response of TGs and related phenotypes to the environment. The aim of the proposed study is to characterize the genetic basis of the variable response of TGs to two environmental contexts, one that raises TGs (dietary fat), and one that lowers TGs (fenofibrate treatment). We will recruit 2,400 family members from 3-generational pedigrees of the ongoing NHLBI Family Heart Study (FHS) in two genetically homogeneous centers (Minneapolis and Salt Lake City). We will collect measurements before and after a dietary fat challenge to assess postprandial TGs and related atherogenic phenotypes (VLDL TGs, chylomicron TGs, TG remnant particles, HDL and LDL particle sizes, total cholesterol, LDL-C, and HDL-C). In families with 2 or more members in a sibship with TGs >= 130 mg/dl, we will conduct a short-term, placebo-controlled, randomized trial of fenofibrate in all willing and eligible family members (anticipated sample size = 1,200). A two-period crossover design will be executed with a 2-week washout between two 3-week treatment periods (placebo or micronized fenofibrate, 160 mg). About 1,000 family members have a Marshfield genome marker set available as part of NHLBI FHS; the remaining 1,400 will be typed using the same marker set. We will conduct genome-wide linkage analyses using stateof-the-art methods to localize novel genetic loci contributing to TG response in the context of fat loading and fenofibrate treatment. We will type 15 single nucleotide polymorphisms (SNPs) in ten candidate genes known to contribute to the response of TGs to dietary fat and fenofibrate, and create haplotypes for association studies. We will use combinatorial partitioning methods and neural networks to test association of the
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individual SNPs and haplotypes with response to the two environmental interventions. The identification of genetic loci that predict TG response in the presence of two disparate contexts, fat loading and fibrate therapy, may provide insights into genetic pathways (a) predisposing to hypertriglyceridemia, ultimately leading to avenues for primary prevention, and (b) predicting response to TG lowering, leading to new drug targets for hypertriglyceridemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETIC AND GENOMIC ANALYSIS OF APOAV Principal Investigator & Institution: Rubin, Edward M.; Director, Joint Genome Institute; Division of Life Sciences; University of Calif-Lawrenc Berkeley Lab Lawrence Berkeley National Laboratory Berkeley, Ca 94720 Timing: Fiscal Year 2003; Project Start 01-DEC-2002; Project End 30-NOV-2006 Summary: (provided by applicant): Based on human/mouse comparative sequence analysis we have identified a fourth member of the chromosome 11 apolipoprotein (apoAI, apoCIII, apoAIV) gene cluster which we have named apolipoprotein AV (apoAV). Our recent studies in humans and mice indicate that apoAV is an important determinant of plasma triglyceride levels. In mice, the overexpression of a human apoAV transgene resulted in decreased plasma triglyceride concentrations, while inactivation of the mouse apoAV gene led to increased triglyceride levels. Complementing these mouse findings, three independent human studies consistently showed that two minor apoAV haplotypes are strongly associated with increased triglycerides. These initial investigations indicate that the newly discovered apolipoprotein gene, apoAV, is an important modulator of plasma triglyceride levels in mammals. Accordingly, this grant focuses on deciphering several fundamental properties of apoAV that include: 1) determining the mechanism by which apoAV affects plasma triglycerides and its atherogenic consequences using apoAV transgenic and knockout mice, 2) investigating the factors and DNA sequences involved in the regulation of apoAV expression and 3) using a combination of human haplotype studies and defined manipulations of the mouse genome to identify apoAV single nucleotide polymorphisms (SNPs) that directly participate in determining triglyceride levels in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC DETERMINANTS: LOW HDL, HIGH TRIGLYCERIDES, OBES* Principal Investigator & Institution: Mahley, Robert W.; Director; J. David Gladstone Institutes 365 Vermont St San Francisco, Ca 94103 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2004 Summary: (provided by applicant): Over the past 10 years, extensive studies have been conducted in Turkey to determine the risk factors for heart disease. Studies involving approximately 10,000 Turkish men and women from six different regions of Turkey have established that this population is unique in several ways. The Turks have the lowest plasma levels of high density lipoprotein cholesterol (HDL-C) of almost any population in the world (75 percent of the men and 50 percent of the women have HDLC levels 30 kg/M2], and both men and women have a tendency toward hypertriglyceridemia. The low HDL-C, however, is independent of obesity or hypertriglyceridemia. Samples from this well-characterized population provide a unique opportunity to explore the genetic determinants associated with the high
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Triglycerides
prevalence of low HDL-C, hypertriglyceridemia, and obesity (characteristics of the metabolic syndrome). This project will analyze DNA from frozen blood samples to investigate new candidate gene targets that may provide insights into the abnormalities characterizing this population. The samples and extensive biodata are available on all 10,000 participants. In Specific Aim 1, we will identify polymorphisms in acyl CoA:diacylglycerol acyltranferase (DGAT)- I and -2 and in ATP-binding cassette A I (ABCA I) genes that are associated with differences in BMI, HDL-C, and triglyceride concentration, and other parameters such as blood pressure. These studies will focus significantly on promoter and coding sequence polymorphisms in DGAT-I and -2 and ABCAL In Specific Aim 2, we will determine whether the polymorphisms have functional significance by using a luciferase reporter system to determine expression of polymorphic forms of DGAT and ABCAI, a cholesterol efflux measurement to determine the functional significance of ABCAI coding sequence polymorphic sites, and a triglyceride synthesis assay to determine the functional significance of DGAT-I and -2 polymorphic sites. The polymorphic site association studies will be performed on DNA samples from three subgroups of Turks: (a) individuals likely to have the metabolic syndrome, (b) individuals with isolated low HDL-C (normal triglycerides), and (c) normolipidemic unaffected controls. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETICS & REGULATION OF HEPATIC LIPASE Principal Investigator & Institution: Deeb, Samir; Research Professor; Medicine; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-AUG-2003 Summary: The long-term goals of this proposal are to define mechanisms of regulation of hepatic lipase (HL) levels and to determine how genetic variation at the HL gene locus modulates these levels under a variety of physiological and pathological states. HL plays a key role in lipoprotein metabolism by catalyzing the hydrolysis of triglycerides and phospholipids. A high level of HL is associated with two important metabolic risk factors for atherosclerosis: diminished concentrations of plasma high density lipoprotein cholesterol (HDL-C) and an increased prevalence of small, dense low density lipoprotein (LDL) particles. A significant proportion (20-30%) of the total variability in HL activity is explained by the common genetic variation in the regulatory sequences of the HL gene whereby, the variant form was observed to be associated with lower HL and higher HDL2 levels. Gender is another modulating factor since women have, on average, higher levels of HDL2 and lower levels of HL. The underlying hypotheses of this proposal are, first, that one or more of the observed regulatory sequence variants causes diminished HL gene expression which, in turn, results in increased HDL-C levels and expression is regulated by cholesterol and estrogens. Our preliminary in vitro studies indicate that sterols up-regulate and estrogens downregulate activity of the HL gene promoter, respectively. The specific aims are to: 1) Determine by association and linkage analysis whether the observed LIPC promoter variants underlie the observed interindividual variation in levels of hepatic lipase activity and HDL2 estrogens and sterols and assess the role of the regulatory sequence variants modulate the relationships between HL levels and gender, menopause status, estrogen replacement therapy and intra-abdominal fat deposits. The results of these studies will provide insights into the molecular genetic bases for interindividual variation in HL activity and the associated plasma lipoprotein profiles. This will open the door for novel pharmaceutical approaches that target modification of the lipoproteins.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENOMIC DISSECTION OF A QTL AFFECTING THE LIPID PROFILE Principal Investigator & Institution: Olivier, Michael; Physiology; Medical College of Wisconsin Po Box26509 Milwaukee, Wi 532264801 Timing: Fiscal Year 2003; Project Start 10-JUL-2003; Project End 30-JUN-2008 Summary: (provided by applicant): The metabolic syndrome is a common disorder posing a significant major risk for coronary heart disease and early mortality in the Western hemisphere. Central to its cardiovascular complications is the association of the syndrome with the specific abnormalities in plasma lipid and lipoprotein profiles including increased plasma triglycerides, decreased HDL cholesterol, and predominance of dense lipoprotein particles. In search for the genetic etiology of this lipid disorder, we identified a quantitative trait locus (QTL) on human chromosome 7q36 strongly linked to variation in plasma lipid levels. We hypothesize that this QTL contains genetic variants that contribute to alterations in biologic pathways underlying the genesis of the lipid disorder. To test for this hypothesis, we propose a comprehensive approach utilizing established resources and expertise to identify the functional sequence variants within this QTL. Specifically, we will 1.) identify single nucleotide polymorphisms (SNPs) and their haplotype and linkage disequilibrium structure across the entire QTL region; 2.) Analyze association of informative SNPs with plasma triglyceride levels, LDL levels, and lipoprotein density fractions using variance component linkage/disequilibrium analyses; and 3.) Identify potentially functional sequence variants in associated genes or genomic regions using Bayesian quantitative trait nucleotide analysis. This comprehensive application of newly available genomic technologies, novel statistical approaches, the DNA and phenotypic information available, and the consortium of expertise assembled behind this project will ensure the successful elucidation of the genetic etiology of this lipid disorder and consequently the development of effective means for prevention and/or treatment of cardiovascular complications of the metabolic syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GROWTH OUTCOMES IN BRONCHOPULMONARY DYSPLASIA AT 36WKS Principal Investigator & Institution: Steward, Deborah K.; None; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-MAY-2007 Summary: (provided by applicant): The prevalence of bronchopulmonary dysplasia (BPD) in very low birthweight (VLBW) infants continues to be a significant problem as more and more extremely immature preterm infants survive acute respiratory distress. Traditionally, BPD has been defined as continued requirement for supplemental oxygen at 28 days of life. Because of the extreme immaturity of the survivors, BPD is now defined as the need for mechanical ventilation and/or oxygen at 36 weeks postconceptional age (PCA). Poor growth is the most common morbidity experienced by VLBW infants with BPD. While the cause of this poor growth is multifactorial potential causative factors include inadequate nutritional intake, inefficient nutrient utilization, and inflammation associated with BPD. However, the role of these factors in the poor growth of these infants has not been examined. The purpose of this study is to prospectively characterize relationships among nutritional intake, nutrient utilization,
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Triglycerides
inflammation, and growth in VLBW infants with BPD when compared to VLBW infants at high-risk for BPD (on oxygen at 28 days of life). VLBW infants, appropriate for gestational age, will be studied at 28 days of life, 33 weeks PCA, and 36 weeks PCA. Group differences for study variables will be examined at the three time points. Study variables include growth (growth velocity, arm muscle area, and arm fat area), nutritional intake (kcal/kg/day and grams of protein/kg/day), nutrient utilization (nitrogen balance, serum prealbumin, and serum triglycerides), and inflammation (interleukin-1 ra and tumor necrosis factor). Predictors of growth velocity will also be determined by examining the interactive effects of respiratory disease with nutritional factors, nutrient utilization, and inflammatory factors. Methods to be used for data collection of the study variables include review of the medical record, computer software analyses, collection of body fluids for biochemical assays and bomb calorimetry, and anthropometric measures. Characterizing the determinants of poor growth in VLBW infants with BPD will facilitate understanding of this problem and identify promising areas for nutritional intervention. Further, nutritional intervention may also decrease the severity of BPD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HIGH ABNORMALITY
FAT
FEEDING
AND
INTRAMYOCELLULAR
LIPID
Principal Investigator & Institution: Guo, Zengkui; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2006 Summary: It is now known that intramyocellular triglycerides (imcTG) content in skeletal muscle of obese adults is increased and this abnormality is associated with impaired glucose metabolism in the muscle. However, the pathways responsible for the increase and the link between the increased imcTG and insulin resistance have not been studied in detail. The objective of this application is to determine the factors and pathways that are responsible for the imcTG accumulation, and to determine whether the oxidation of imcTG fatty acids is also increased and, if so, whether it directly affects glucose metabolism. It is hypothesized that elevated plasma insulin and fatty acid levels, as commonly seen in human obesity, independently stimulate imcTG synthesis and synthesis is the primary pathway leading to the increased imcTG accumulation; and that a larger imcTG pool leads to accelerated imcTG oxidation thereby interfering with muscle glucose metabolism. To test the hypotheses, three specific aims will be pursued to answer following questions: 1) Is insulin an anabolic hormone stimulating imcTG synthesis? 2) Does elevated plasma fatty acid concentration increase imcTG synthesis by providing abundant precursors? 3) Is a larger imcTG pool associated with accelerated oxidation of imcTG fatty acids, and if so, how this affects muscle glucose metabolism? A new one-pool model will be applied to determine the rates of imcTG synthesis, turnover and oxidation directly (muscle biopsy) at controlled insulin and fatty acid levels in rats made obese by high fat feeding. The oxidation of imcTG fatty acids and muscle glucose uptake, glycolysis and glycogen synthesis will be determined using multiple tracers to determine the effect of imcTG oxidation on glucose metabolism. Stable isotopic tracers (13C) and mass spectrometry (GC/MS and isotope ratio MS) will be used to quantitate the kinetics. These studies are designed to answer the questions whether an enlarged imcTG is a chemical entity that imposes a negative effect on glucose metabolism, and whether plasma insulin and fatty acids are responsible for the increased imcTG, and if so, how. Thus, the proposed research will improve the understanding of the mechanism
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of insulin resistance and imcTG abnormalities in the obese rat that will benefit investigation of human obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HIV PROTEASE INHIBITORS AND ATHEROSCLEROSIS Principal Investigator & Institution: Smart, Eric J.; Professor; Physiology; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506 Timing: Fiscal Year 2002; Project Start 15-APR-2002; Project End 31-MAR-2007 Summary: (provided by applicant) We hypothesize that HIV protease inhibitors alter macrophage class B scavenger receptor-dependent uptake and efflux of cholesterol thereby promoting the formation of lipid-laden macrophages and atherosclerotic lesions. A major drawback to the use of HIV protease inhibitors is that they promote the development of dyslipidemia, which is an established risk factor for the development of atherosclerosis. Numerous reports have suggested a causal link between protease inhibitor therapy and atherosclerosis; however, this has not been unequivocally demonstrated in a large-scale clinical trial. The dyslipidemia, which is primarily an increase in triglycerides, is unlikely to completely account for the development of atherosclerotic lesions in HIV patients because atherosclerosis is a multifactorial disease that is not controlled by a single factor. Our preliminary data demonstrate that HIV protease inhibitors have direct effects on macrophages, which are critical cellular mediators in atherosclerotic lesion development. The generation of lipid-laden macrophages is a key event in atherogenesis and is thought to be due, in part, to unregulated uptake of modified lipoproteins. Such aberrant cholesterol accumulation is influenced by the functions of the class B scavenger receptors, SR-BI and CD36. Both receptors are found in atherosclerotic lesions and on macrophages. In addition, both receptors can mediate the uptake of lipoprotein cholesterol and the efflux of cellular cholesterol. Our preliminary data demonstrate that peritoneal macrophages isolated from LDL receptor null mice given the HIV protease inhibitors, amprenavir, indinavir, or ritonavir, contain more SR-BI and CD36 than aged-matched controls. In addition, all three protease inhibitors increased SR-BI and CD36 levels in THP-1 cells, our macrophage cell model system. The protease inhibitors also increased the cellular cholesterol content in both the in vivo and in vitro model systems, which is consistent with our hypothesis. Importantly, mice given amprenavir, indinavir, or ritonavir had significantly more atherosclerotic lesions than control mice. We will test two Specific Aims. Aim 1 : To determine the effects of HTV protease inhibitors on SR-BI and CD36 dependent cholesterol uptake and efflux. Aim 2: To determine the leukocyte (i.e., macrophages, etc.) specific effects of HIV protease inhibitors on atherosclerotic lesion formation in LDL receptor null mice that have been transplanted with bone marrow from SR-BI x LDLR and CD36 x LDLR null mice. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HYPOTHALAMIC DYSFUNCTION /AGED-RELATED METABOLIC DECLINE Principal Investigator & Institution: Rossetti, Luciano; Professor; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2003; Project Start 01-DEC-2002; Project End 30-NOV-2007 Summary: (provided by applicant): Chronic increases in the availability of nutrients are likely to contribute to several key metabolic features of aging. The latter include (but are not limited to) increased deposition of fat within the abdominal cavity (visceral
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Triglycerides
adiposity), increased tissue levels of triglycerides, insulin resistance, relative decrease in energy expenditure, and augmented risks for atherosclerotic disease (ASCVD) and for type 2 diabetes mellitus (DM2). Under normal circumstances, the deleterious effects of the excessive availability of nutrients are countered by the prompt activation of nutrient "counter regulatory" systems. The latter include (but are not limited to) hypothalamic neuro-circuitries partly under the control of leptin. The activation of these nutrient "counter regulatory" systems should prevent the excessive storage of energy and the onset of insulin resistance. Thus, there appears to be a functional feedback loop, which normally prevents visceral adiposity, insulin resistance, and other metabolic features of aging from developing. However, there is mounting evidence that aging is a state of leptin resistance. Consistent with these recent findings, the operation of this feedback loop is likely to be impaired and leptin may therefore fail to compensate for the deleterious effects of nutrient excess during the aging process. Our proposal will therefore focus on mechanisms responsible for hypothalamic responses to nutrient excess and how they are altered during aging. We also wish to discern impairments in hypothalamic neuro-circuitries, which are due to chronic increases in nutrient availability from those due to the aging process per se. Based on preliminary results and on this overall hypothesis we wish to pursue the following specific aims: Does aging modify the actions of leptin on energy, glucose and lipid metabolism and on insulin action? We will examine the dose-response relationship between central delivery of leptin and biological outcomes. We will particularly focus on the effect of low dose ICV leptin administration on metabolic rather than behavioral end points. Can stimulation of the melanocortin pathway overcome the leptin resistance of aging? We will test the hypothesis that activation of CNS melanocortin receptors bypasses the defect in leptin signaling in aging rats. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INNOVATIVE OBESITY PREVENTION FOR AFRICAN-AMERICAN GIRLS Principal Investigator & Institution: Robinson, Thomas N.; Assistant Professor Of; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2003; Project Start 01-AUG-1999; Project End 30-NOV-2006 Summary: (provided by applicant): We propose a 2-arm parallel group, randomized controlled trial to test the efficacy of an after school dance program and a family-based intervention to reduce television, videotape and video game use to reduce weight gain among lower socioeconomic status African-American preadolescent girls. An active placebo control group will receive an information-based community health education intervention. A total of 260 girls will be randomized to the two conditions and the interventions will last for the full 2-year period of the study. Our interventions and study design are supported by prior studies demonstrating the feasibility and potential efficacy of dance classes and reducing television viewing for reducing weight gain, formative studies, and the success of a 12-week randomized controlled pilot study of the proposed trial. Measures will be collected in girls' homes at baseline and 6, 12, 18 and 24 months. Body Mass Index (BMI) is the primary outcome measure, The primary hypothesis will be tested by comparing individual trajectories of change in the treatment and control groups over the entire two-year course of the trial, using random regression models, Specific Aims include: 1. To participate with NHLBI and the Memphis GEMS investigators to conduct a full-scale, collaborative, 2-year randomized controlled trial, including both site-specific and collaborative measures and site-specific and collaborative analyses. 2. To test the effect of the Stanford GEMS intervention on BMI
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over 2 years (the primary outcome). We hypothesize that, compared to controls, girls in the treatment-group will significantly reduce their weight gain (BMI) over the two-year study period. 3. To test the effects of the Stanford GEMS intervention on secondary outcomes over two years. We hypothesize that, compared to controls, girls in the treatment group will significantly reduce their waist circumference, triceps skinfold thickness, resting blood pressures, resting heart rate, fasting insulin, total cholesterol, LDL-cholesterol, triglycerides, television, videotape and video game use, meals eaten in front of television, total dietary calorie intake, percent of calories from fat, weight concerns, and body disatisfaction, and significantly increase their HDL-cholesterol, after school and daily physical activity, self-esteem, and school performance. 4. To conduct analyses to evaluate potential moderators and mediators of intervention effects on primary and secondary outcomes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IS DHEA REPLACEMENT THERAPY BENEFICIAL? Principal Investigator & Institution: Holloszy, John O.; Professor; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): The major emphasis of our research on the prevention of physical frailty and loss of independence has been on the adaptations to exercise. However, because most Americans are not motivated to exercise, we have started to evaluate other approaches to maintenance of health and prevention of frailty. Of these, the most powerful appears to be DHEA replacement therapy. In this context, the overall goals of this study are to determine whether long term dehydroepiandrosterone (DHEA) replacement therapy has beneficial effects that could (a) delay the development of frailty and disability, (b) protect against development of type 2 diabetes and coronary artery disease, (c) improve quality of life, and d) obtain information on the mechanisms of DHEA action. DHEA and DHEA sulfate (DHEAS) plasma concentrations peak at about 20 yr of age and decline rapidly and markedly after age 25 yr. DHEA is a PPAR-alpha activator. PPAR-alpha plays major roles in regulating lipid metabolism and controlling inflammation. DHEA also appears to have anabolic effects on muscle and bone. The study proposed here is a randomized, double blind, placebo-controlled trial of DHEA replacement. It is designed to determine the effects of 12 mo of DHEA replacement in 65-75 yr old women and men on (a) truncal and visceral fat, (b) insulin resistance and serum triglycerides, (C) muscle mass and strength, (d) bone mineral density, (e) chronic inflammation, (f) arterial-endothelium-dependent vasodilation, and (g) sense of well being. The specific aims of this study are to test the hypotheses that 12 mo of DHEA replacement will (a) Result in significant decreases in truncal and visceral fat by shifting metabolism to fat oxidation and increasing energy wastage; (b) Decrease insulin resistance and decrease serum triglycerides; (c) Increase muscle mass and strength, by decreasing catabolic stimuli and increasing anabolic stimuli; (d) Increase bone mineral density by increasing anabolic stimuli and decreasing catabolic stimuli; (e) Reduce chronic inflammation and decrease pro-inflammatory cytokine production by peripheral blood mononuclear cells; (f) Improve arterial endothelium dependent vasodilation; and (g) Improve general sense of well being. A major emphasis of this research is on the mechanisms responsible for the biological effects of DHEA replacement. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Triglycerides
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Project Title: LIPID METABOLISM IN FAT CELLS Principal Investigator & Institution: Guo, Wen; Boston Medical Center Gambro Bldg, 2Nd Fl, 660 Harrison Ave, Ste a Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAY-2004 Summary: Medium chain fatty acid ingestion (MCFA) results in diminished fat storage in animals and humans, while similar intake of long chain fatty acids (LCFA) results in weight-gain. The goal of our project is to examine the cellular mechanisms underlying this phenomenon. Our hypothesis is that substitution of MCFA for LCFA will downregulate the expression of adipogenic proteins, lower the lipid storage capacity of adipose cells, facilitate fatty acid release from stored fat, and probably also reduce the capacity for differentiation of adipose cell precursors. The specific aims of this study focus on: 1) the metabolic fate of MCFA and how this is influenced by LCFA, glucose and insulin, 2) the effects of MCFA on fat storage and lipolysis, and on membrane lipid composition of sub-cellular components (plasma membrane, mitochondria, and endoplasmic reticulum); 3) the effects of MCFA on the expression of adipogenic proteins during the differentiation process; and 4) changes in fat cell function as a result of longterm MCFA dietary adaptation. An integrated approach will be used to characterize the metabolic end products of MCFA, to search for unidentified end products, and to explain the excess energy expenditure that results from MCFA treatment. We will identify and quantify, the major metabolic end products of fatty acids (lipids and CO2) by NMR. 13C isotope labeled substrates will be used in appropriate experiments. This greatly enhances the selectivity and sensitivity of NMR analysis. We will compare heat generation by cells adapted to MCFA or LCFA by measuring oxygen consumption and redox state; quantify the important metabolites (acetylCoA and acetylcarnitine) by HPLC, and analyze the fatty acid compositions by GLC. If significant changes in subcellular membrane composition are found as a result of MCFA treatment, subsequent effects on membrane structure and fluidity will be analyzed by solid state NMR. Other standard biochemical assays will be used for the measurement of ketone bodies, total triglycerides, cholesterol, DNA, protein, etc. The mRNA products of differentiationdependent adipogenic genes will be determined by Northern analysis. Fat cell morphology will be characterized by phase- contrast microscopy. Using this integrated approach, we anticipate developing important new information to help shed light on the molecular mechanisms of the control of obesity and obesity-related health disorders afforded through MCFA administration. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LIPOPROTEIN LIPASE AND PREECLAMPSIA Principal Investigator & Institution: Hubel, Carl A.; Magee-Women's Hospital of Upmc 300 Halket St Pittsburgh, Pa 15213 Timing: Fiscal Year 2001; Project Start 15-FEB-2000; Project End 31-JAN-2005 Summary: Preeclampsia is a leading cause of maternal death and increases perinatal death five-fold. There is compelling evidence that maternal endothelial dysfunction contributes to the pathogenesis of preeclampsia. Hypertriglyceridemia, decreases in high density lipoprotein (HDL) cholesterol, and abnormally small-sized low density lipoprotein (LDL) particles are characteristic features of preeclampsia. We have proposed that these lipid abnormalities promote endothelial dysfunction in preeclampsia through the generation of oxidative stress. Lipoprotein lipase (LPL) plays a vital role in the clearance of triglycerides from the circulation. The importance of LPL defects in the development of cardiovascular disease is increasingly recognized. Several
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common variations in the LPL gene promote the triad of increased triglyceride, decreased HDL cholesterol, and small-sized LDL. The dyslipidemic effects of these functional variants are accentuated by pregnancy. In our Caucasian population, a sum total of 18.8% of preeclamptics are heterozygous for either the N291S or D9N coding sequence variants of the LPL gene, compared with 4.6% of normal pregnancy controls. Accordingly, Aim 1 is to test whether these observations can be generalized to other populations. We will compare the prevalence of the four most common, functional variants in the LPL gene in Caucasians and African-Americans from western Pennsylvania, and in Icelandic women. Aim 2 is to sequence the coding and promoter regions of the LPL gene to identify other functional variants, which will then be genotyped in cases and controls. We posit that variations in the LPL gene the predispose to dyslipidemia are over-represented in women with preeclampsia. Aim 3 is to compare plasma lipids, lipid peroxidation products, and markers of endothelial dysfunction in women with preeclampsia stratified by genotype. We hypothesize that, among women with preeclampsia, those carrying LPL variants with reduced enzymatic activity will display an especially adverse blood profile. In Aim 4, we will measure plasma LPL enzyme activity in women 12 weeks postpartum to further test the hypothesis that a constitutional deficiency in LPL (hormonally and/or genetically mediated) is associated with preeclampsia. In Aim 5, we will explore the effects of heterozygous LPL deficiency on endothelial regulation of vascular function during pregnancy, using the LPL knockout mouse. This systematic approach will help to clarify the link between dyslipidemia and the pathogenesis of preeclampsia and could provide clues to prevention or treatment of the disorder. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LIPOPROTEIN LIPASE IN FATTY ACID PARTITIONING Principal Investigator & Institution: Capell, Warren H.; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2005 Summary: (provided by applicant): Fatty acids are delivered to cells either circulating as free fatty acids (FFA) or esterified in triglycerides (TG) carried by lipoproteins. Lipoproteins interact with lipoprotein lipase (LPL), hydrolyzing their TG and making lipoprotein fatty acids (LPFA) available to cells. It is widely believed that once fatty acids enter cells, regardless of how they are delivered, they enter a common pool which is then partitioned to storage or oxidation based on the metabolic needs of the cell. However, there are examples in the literature that form a basis for hypothesizing that LPL may impact the uptake and metabolic partitioning of LPFA separately from FFA. In the proposed research, the following hypotheses will be tested: 1) By virtue of their interaction with LPL, LPFA are more likely to be esterified and stored as TG, while FFA are more likely to be partitioned toward oxidation. 2) Active LPL on the cell/endothelial surface is essential for this partitioning of LPFA to occur. 3) The partitioning of LPFA is less dependent on the metabolic environment than is the partitioning of FFA. 4) Overexpression of LPL leads to an intracellular TG pool that is not readily mobilized for oxidation. We plan to test these hypotheses utilizing myoblast and mouse models of LPL overexpression. Simultaneously providing separately labeled fatty acids as LPFA and FFA, we will be able to examine the partitioning toward storage or oxidation of each, and how disrupting normal LPL action affects this partitioning. We will also examine how LPL overexpression affects the mobilization of the intracellular TG pool, as stagnancy of this pool is felt to be associated with the development of insulin resistance.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LP(A) HOMOCYSTEINE AND CARDIOVASCULAR RISK IN ESRD Principal Investigator & Institution: Longenecker, Joseph C.; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 10-JUL-1998; Project End 30-JUN-2005 Summary: (Adapted from applicant's abstract) Dr. Longenecker, who trained in Internal Medicine (IM) at the Johns Hopkins Hospital (1990-1993), served as Associate Program Director for the IM Residency Program at Abington Memorial Hospital (1993-1996). He is seeking this MCSDA to study the epidemiology of atherosclerotic cardiovascular disease (ASCVD) in dialysis patients, complete a Ph.D. in Epidemiology and transition to an independent career in clinical research. Over the past year, he completed a Master of Public Health degree at Hopkins and joined the Welch Center for Prevention, Epidemiology and Clinical Research, one of the premiere sites for mentored clinical research in the country. Under the mentorship of Drs. Michael Klag and Josef Coresh, he received the NIDDK Renal Disease Epidemiology Training Grant, joined the CHOICE study (Choices for Healthy Outcomes in Caring for ESRD, an AHCPR-funded PORT), was appointed as a Clinical and Research Fellow in the Division of General Internal Medicine, co-authored a published paper with Dr. Klag, developed the proposed research plan, and finished writing a book on acid-base disorders to be published next year by Williams and Wilkins. Lipoprotein(a) [Lp(a)], homocysteine (tHcy) and ASCVD are markedly elevated in dialysis patients. However, there is insufficient evidence to establish Lp(a) and tHcy as independent risk factors for the increased incidence of ASCVD in this population. As an ancillary study of CHOICE, Dr. Longenecker plans to conduct a prospective study in 875 incident dialysis patients to investigate serum Lp(a) levels, Lp(a) isoforms and tHcy levels as risk factors for ASCVD. Dr. Longenecker has designed and initiated the ASCVD outcome data collection and validation procedures for the study. He will review the hospitalization records for ASCVD outcomes in the entire cohort. Lp(a) levels, Lp(a) isoforms and tHcy levels will be determined for each participant and will be analyzed as risk factors for ASCVD outcomes. Multivariate analyses will control for confounding by age, race, smoking, history of ASCVD, diabetes, hypertension, alcohol, body mass index, cholesterol, high and low density lipoproteins, triglycerides, and dialysis dose. The study will have sufficient power for a race- stratified analysis of interaction. Dr. Longenecker will later complete a metaanalysis of either Lp(a)- or tHcy-lowering therapies. Based on this quantitative review of the literature, he will conduct a clinical trial to test the efficacy of a promising Lp(a)- or tHcy-lowering therapy in dialysis patients. The combination of observational and experimental research in the supportive context of the Welch Center, CHOICE, and the Department of Epidemiology will give Dr. Longenecker the experience and tools he needs to develop into an Independent clinical scientist. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MACRONUTRIENTS AND CARDIOVASCULAR RISK Principal Investigator & Institution: Appel, Lawrence J.; Associate Professor; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 25-MAY-2002; Project End 31-MAR-2007 Summary: While there is widespread consensus that the optimal diet to reduce cardiovascular risk should be low in saturated fat, the type of macronutrient that should replace saturated fat (carbohydrate, protein or unsaturated fat) is a major, unresolved
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research question with substantial public health implications. The proposed study will evaluate these 3 dietary approaches by studying their effects on established coronary risk factors and a selected group of emerging risk factors. The study design is a randomized, three period cross-over feeding study that will compare the effects on blood pressure and plasma lipids of a carbohydrate-rich diet (the DASH diet) to two other diets, one rich in protein and another rich in unsaturated (UNSAT) fat, predominantly monounsaturated fat. The DASH diet has been shown to reduce blood pressure and LDL-cholesterol substantially, and is currently recommended by policy makers. During a 1 week run- in, all participants will be fed samples of the 3 study diets (DASH, PROTEIN and UNSAT). Using a three period cross-over design, participants will then be randomly assigned to the DASH, PROTEIN OR UNSAT diet. Each feeding period will last 6 weeks; a washout period of at least 2 weeks will separate each feeding period. Throughout feeding (run-in and the 3 intervention periods), participants will be fed sufficient calories to maintain their weight. Trial participants (n=200, approximately 50 percent female, approximately 50 percent African-American) will be 20 years of age or older, with systolic blood pressure of 120-159 mmHg and diastolic blood pressure of 80-95 mmHg. Primary outcomes variables will be blood pressure and the established plasma lipid risk factors (LDL-C, HDL-C and triglycerides). Secondary outcomes will include apolipoproteins VLDL-apoB and VLDL-apoCIII, which should be superior to triglycerides as predictors of cardiovascular events, as well as total apolipoprotein B, non-HDL cholesterol, and lipoprotein(a). In this fashion, the trial should advance our fundamental knowledge of the effects of diet on both traditional and emerging risk factors, and in the process, inform policy makers and health care providers on the relative benefits of carbohydrate, protein and unsaturated fat, predominantly monounsaturated fat, as means to reduce cardiovascular risk. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MAGNETIC RESONANCE OF CARDIAC C13 FLUX & METABOLIC RATE Principal Investigator & Institution: Lewandowski, E Douglas.; Professor; Physiology and Biophysics; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2003; Project Start 01-AUG-1993; Project End 31-JUL-2008 Summary: (provided by applicant): This proposal exploits the opportunity for a comprehensive 13C NMR evaluation of fatty acid handling within the intact, functioning heart. The overall goal is to further develop and apply our kinetic 13C NMR methods to study the reciprocal relationship between the activity of the key regulator of fatty acid oxidation, carnitine palmitoyl transferase I (CPTI) and turnover of the myocardial triglyceride pool in normal and diabetic animal models. New and exciting findings from the previously funded period enable 13C NMR to distinguish between oxidative rates in the mitochondria and the rate of long chain fatty acid transport, via CPT1, as well as detect the incorporation rate of 13C-enriched palmitate into the myocardial triglyceride pool, all in the intact, beating heart. Therefore, this study explores the hypotheses that: 1) changes in the regulation of long chain fatty acid oxidation, via CPT1 activity, mediate the turnover rate of myocardial triglycerides and can be evaluated in whole hearts by a comprehensive examination of 13C enrichment kinetics; 2) Alterations in triglyceride content and turnover in the diabetic myocardium occur due to a combination of hyperlipidemia and changes in the expression of genes encoding enzymes for fatty acid uptake and oxidation pathways and that these can be distinguished via 13C NMR as independent mediators in the pathogenesis of diabetic cardiomyopathy. This hypothesis will be tested in both in both rat and mouse models of
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Triglycerides
normal, diabetic, and genetically altered cardiac phenotypes. Specific aims are: 1) Determine reciprocal effects of fatty acid oxidation rates on triglyceride turnover via cardiac 13C NMR during partial inhibition of CPT1; 2) Examine long chain fatty acid oxidation rates, CPT1 activity, and triglyceride pool turnover in the hearts of rats with type-I (insulin deficient) diabetes and test for a potential link between triglyceride accumulation and turnover and the activation of protein kinase C; 3) Investigate effects of triglyceride pool size on the reciprocal nature of CPT1 activity and triglyceride turnover in a transgenic mouse model, overexpressing peroxisome proliferatoractivated receptor alpha (PPAR-alpha), that mimics the diabetic phenotype for fatty acid and glucose metabolism and allows for dietary control of myocardial triglyceride pool size; 4) Examine long chain fatty acid oxidation rates, CPT1 activity, and triglyceride turnover in a more clinically relevant animal model of type II (insulin resistant) diabetes, the db/db mouse model, versus non-diabetic, wild-type mice. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISM & SIGNIFICANCE OF CUBILIN-MEDIATED HDL UPTAKE Principal Investigator & Institution: Argraves, W Scott.; Associate Professor; Cell Biology and Anatomy; Medical University of South Carolina 171 Ashley Ave Charleston, Sc 29425 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2004 Summary: We have used a unique cell culture model to study in vitro catabolism of high density lipoproteins (HDL) and to identify cubilin as a receptor that mediates endocytosis and lysosomal degradation of holoparticle HDL. The activities of cubilin are distinct from those of the other known HDL receptor, scavenger receptor SR-BI, which mediates selective lipid uptake without facilitating endocytosis and degradation of the whole particle. Cubilin is a 460-kDa peripheral membrane protein that is expressed in kidney, intestine and yolk sac edoderm. The physiological significance of cubilin activity with respect to HDL endocytosis in these tissues is unknown. The vital role served by yolk sac cubilin is indicated by the severe developmental abnormalities observed when cubilin antibodies are administered to pregnant rats or to embryos cultured ex utero. A central hypothesis of this grant application is that cubilin functions in the yolk sac endoderm to mediate uptake of maternal plasma HDL and thereby serves a role supplying the embryo with HDL-associated cholesterol, lipid-soluble vitamins, phospholipids and/or triglycerides. To test this hypothesis, and to characterize fundamental mechanistic features of cubilin function, four aims are proposed. The first aim is to define the molecular basis for ligand binding and endocytotic functions of cubilin and will include mapping binding sites for HDL apolipoproteins A-I and A-II, and establishing the basis for the association of cubilin with the plasma membrane as it lacks a membrane-spanning domain. To accomplish these goals, recombinant fragments of cubilin and monoclonal antibodies will be produced and tested using in vitro binding and cellular uptake assays. The second aim is to determine whether other cell surface proteins function in conjunction with cubilin to mediate HDL endocytosis. These studies will evaluate megalin, a receptor that binds cubilin, and several other proteins that copurify with cubilin in the process of cublilin-mediated HDL endocytosis. The third aim is to test the hypothesis that cubilin not only functions to mediate lysosomal degradation of HDL but also mediates transcytosis as a means to transport HDL or its constituents across certain epithelia. This study will involve measuring transport of radiolabeled HDL across a monolayer of cubilin-expressing cells cultured on a permeable support. The fourth aim is to determine the developmental significance of
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cubilin-mediated uptake of HDL by yolk sac endoderm. Together, these studies should provide new insights into the function of cubilin in processes such as maternalembryonic lipoprotein transport and embryonic development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MENTORED DEVELOPMENT AW
PATIENT-ORIENTED
RESEARCH
CAREER
Principal Investigator & Institution: Kosmiski, Lisa A.; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 30-JUN-2005 Summary: PROPOSAL (Adapted from the applicant's abstract): Treatment of HIVinfected individuals with PIs is associated with changes in body fat distribution and metabolic disturbances similar to those seen in syndrome X. PI use has been variably associated with hypertriglyceridemia, insulin resistance including diabetes mellitus and the development of central obesity which is often accompanied by loss of fat from the extremities and buttocks. It is unclear how these complications relate to each other. Based on the experience of patients with syndrome X, it is highly probable that if these metabolic complications of PI therapy cluster, then they will in turn be associated with an increased risk of coronary artery disease. One hypothesis of this proposal is that patients who develop an increase in abdominal girth as well as those who develop hypertriglyceridemia without a clinically apparent change in body fat distribution will both have significantly more visceral fat and insulin resistance compared to controls. The investigators hypothesize that these changes represent one syndrome rather than several. To test this hypothesis, four groups of HIV-infected subjects will be compared: 1) PI-treated patients who have developed a "protease paunch;" 2) PI-treated patients with hypertriglyceridemia but no clinically apparent change in body fat distribution; 3) PI-treated patients free of these two complications; and 4) PI-naive patients. Body composition and visceral adiposity will be determined by dual energy X-ray absorptiometry (DEXA) and computerized tomography, respectively. Insulin sensitivity will be measured using the frequently sampled intravenous glucose test (FSIGT). A prospective study is also planned to test the hypothesis that, after the initiation of PI therapy, a decline in insulin sensitivity will predict the development of visceral fat accumulation and, therefore, may be casual in its development. This is a unique opportunity to study the development of visceral obesity and its relationship to insulin resistance. Finally, the investigators hypothesize that the decrease in peripheral adipose tissue associated with PI therapy is due to increased mobilization or decreased storage of triglycerides (TGs)in those depots. Other potential mechanisms of adipose tissue loss including apoptosis and dedifferentiation will also be studied. The loss of peripheral fat stores offer a unique opportunity to determine the genes involved in regulating adipose tissue mass and distribution in general. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: METABOLIC PHENOTYPING CENTER FOR MOUSE MODELS OF DIABET* Principal Investigator & Institution: Malloy, Craig R.; Professor of Radiology and Internal Medi; Radiology; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2001; Project Start 15-JUL-2001; Project End 30-JUN-2006 Summary: (Taken directly from the application) This is an application to establish a mouse phenotyping center to quantitatively evaluate liver gluconeogenesis, pyruvate
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recycling, the contribution of glycerol and Krebs cycle intermediates to glucose production, total glucose turnover, and citric acid cycle flux in live animals using a combination of 13C and 2H tracers and NMR spectroscopy. This standard metabolic assay provides the most comprehensive existing analysis of gluconeogenesis. It will be made available to on-campus and off-campus investigators having animal models of NIDDM or related disorders. In addition to the standard metabolic profile described above, a series of other phenotype specific metabolic techniques including a quantitative measure of substrate oxidation, measures of intracellular cations, and citric acid cycle flux using 13C enriched substrates will also be made available for selected animal models. A unique feature of this phenotyping center is that input will come from chemists, physicists, physiologists, computer scientists, physicians, and geneticists. All are recognized experts in 13C isotopomer analysis. A 400 MHz wide-bore NMR spectrometer will be dedicated to this project. All mice selected for phenotyping will be subjected to a standard protocol performed by high-level technicians; the data will be analyzed and interpreted by NMR spectroscopists and biochemists and made available through an interactive web site designed to allow the external investigators to test a fit of their isotopomer data to alternative metabolic models. A basic research core will focus on improving sensitivity through indirect detection of protons, develop an oral glucose tolerance test that includes 13C and 2H tracers, develop methods to measure fat oxidation in vivo, and extend measurements of extramyocellular adipose versus intramyocellular triglycerides in hind-limb mouse skeletal muscle. Finally, an administrative core will coordinate the activities of the three research cores and interface discussions between external investigators and center scientists. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: METABOLISM AND GENETICS OF HYPOBETALIPOPROTEINEMIA Principal Investigator & Institution: Schonfeld, Gustav; Professor of Internal Medicine; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 01-JAN-1998; Project End 31-DEC-2007 Summary: (provided by applicant): This is a competitive renewal application to study the genetics and metabolism of familial hypobetalipoproteinemia (FHBL). Genetic studies: In addition to our families with APOB mutations on chromosome (chr) 2, we reported on seven families with linkage of FHBL to a 2cM region on chromosome 3p21. One of our aims is to find the etiologic gene in the region by positional cloning, using DHPLC (Transgenic Wave) technology and genomic DNA sequencing for mutation detection. A third group of FHBL five families manifests no linkage with either chr 2 or 3. Genomewide genotyping is being performed in these families. Our second aim is to perform linkage analyses to find susceptibility regions and ultimately the gene(s). Metabolic studies: Using magnetic resonance spectroscopy, we found 5-fold increases in liver fat in FHBL subjects bearing apoB truncation mutations compared with matched controls. We have also studied the assembly of VLDL-triglycerides (TG) in these subjects. Infusions of 2H2-palmitate, quantitation of palmitate tracer/tracee ratios in plasma and in VLDL-triglycerides by gas chromatography-mass spectrometry, and kinetic modeling of the data demonstrate that a greater proportion of VLDL-TG is derived from hepatic sources than from plasma palmitate in FHBL subjects than controls. A significant correlation was found between liver fat (by MRI) and the fractional contribution of hepatic sources (r=0.90, p=0.001). Our aim is to extend these studies in our FHBL subjects and to patients with the metabolic Syndrome X, and to evaluate the importance of metabolic "risk factors" such as body weight, insulin resistance on the extent of accumulation of liver fat in these groups.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MODIFIED LDL, AUTOIMMUNITY AND VASCULAR DISEASE IN DIABETES Principal Investigator & Institution: Lopes-Virella, Maria; Medical University of South Carolina 171 Ashley Ave Charleston, Sc 29425 Timing: Fiscal Year 2001; Project Start 30-SEP-1996; Project End 31-AUG-2006 Summary: (provided by applicant) High levels of immune complexes (IC) containing oxLDL predict the development of macrovascular complications in type 1 diabetes (DM) and are associated with coronary artery disease (CAD) in type 2 DM. Data obtained during the on-going funding period shows that the levels of oxLDL-IC are significantly associated with internal carotid intima-medial thickness (p<0.001, n=853) and are significantly increased in type 1 DM with micro/macroalbuminuria and moderate/severe retinopathy, compared with levels of LDL-IC in patients with normalalbuminuria or mild retinopathy (p<0.013 and 0.0006, respectively). The levels of LDL-IC are strongly correlated with serum Apo B levels, serum Lp(a) levels and serum triglycerides (p<0.0001, n=853) and have also a significant direct correlation (p<0.0001, n=854) with C-reactive protein and with soluble ICAM-1 (p<0.02, n=455). LDL-IC correlate as well with Hb A1c (p<0.005, n=888), suggesting that glycemic control will impact the formation of LDL-IC. We have also demonstrated in patients with micro or macroalbuminuria that antibodies (Ab) against ox-LDL isolated from oxLDL-IC have a higher affinity than the free Ab present in sera of the same patients. This suggests that one critical factor determining the pathogenicity of oxLDL-IC is the synthesis of oxLDL Ab of moderate affinity, able to form stable IC with pro-inflammatory potential. Because Chlamydia pneumonia has been shown to have a strong epidemiological correlation with CAD and one of its major antigens is a cell wall lipopolysaccharide (LPS), that when released into circulation is transported by lipoproteins, we plan to investigate whether chlamydia LPS is present in IC purified from sera of diabetic patients. The main goal of this proposal is to compare the levels of soluble adhesion molecules (sCAM) and the levels and characteristics of LDL-IC isolated from the sera of a type 2 DM cohort (Prospective VA Cooperative Trial) under intensive or standard glycemic control. We hypothesize that, similarly to type 1 DM, LDL-IC in type 2 DM have pro-inflammatory characteristics and are associated with micro and macrovascular complications. We further hypothesize that intensive glycemic control will impact the formation of IC and the release of CAMs into the circulation. We also propose to determine whether or not patients from the DCCT/EDIC cohort (type 1 DM) and VA cohort 2 (type 2 DM) that develop macrovascular disease, retinopathy and micro/macro-albuminuria have a higher incidence of chronic C. pneumoniae infection and to characterize the IC present in the serum of patients from both cohort 1 and 2 that develop macrovascular disease/nephropathy/retinopathy for oxLDL, oxLDL-Lp(a), AGE-LDL, Chlamdial-LPS or DNA, as well as Ab against these antigens. We will also determine the affinity and isotype distribution of Ab isolated from IC, to evaluate their pro-inflammatory potential. Finally, we will assess possible pathogenic mechanisms triggered by these IC by investigating their ability to induce accumulation of cholesterol in macrophages, kidney mesangial cells and retinal pericytes and to activate these cells leading to the expression of cytokines, sCAM and metalloproteinases. Incorporation of our study into the Program allows us to compare LDL-IC levels with the inflammatory markers and endothelial cell dysfunction markers measured in other projects and that will result in a better understanding of the significance of auto-immune responses to modified forms of LDL to the pathogenesis of atherosclerosis in diabetes.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR MECHANISMS OF GLYCEROL KINASE DEFICIENCY Principal Investigator & Institution: Dipple, Katrina M.; Pediatrics; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 30-JUN-2006 Summary: (provided by applicant): My long-term career goal is to have an academic position where I will do basic science research on inborn errors of metabolism, diagnose and treat patients with genetic disorders, and teach medical and graduate students. My short-term career goals are to obtain an assistant professor level position with mentoring that will make me an independent physician-scientist. This application is for my transition from genetics fellow and clinical instructor to become an independent physician-scientist and junior faculty member. The research career development plan includes mentoring and course work in the areas of metabolic flux, kinetics analysis and imaging. The courses are in the areas of the mathematics of imaging and kinetic analysis, and represent critical topics that I will need to master to become an independent researcher in this area. I choose to pursue this work at UCLA as I have already begun this research in the laboratory of Dr. Edward R. B. McCabe as a genetics fellow, and because of the resources and reputation of UCLA in imaging, and, in particular, functional imaging. This proposal focuses on understanding the pathogenesis of glycerol kinase (GK) deficiency - an X-linked inborn error of metabolism. GK is expressed at highest levels in the liver and phosphorylates glycerol to glycerol 3phosphate. Glycerol 3-phosphate then serves as a substrate for the glycolytic pathway, glycogenesis, gluconeogenesis, and the synthesis of glycerolipids including triglycerides and plasmalogens. GK deficiency (GKD) occurs as part of an Xp21 contiguous gene syndrome or as isolated GKD which may be symptomatic (episodic metabolic and central nervous system (CNS) decompensation) or asymptomatic (only pseudo-hypertriglyceridemia). We have investigated patients with isolated GKD due to missense mutations, and have showed that there is no correlation between genotype and phenotype. Our goal is to understand the expression of GK and the pathogenesis of GKD. Our first specific aim is to define the GK promoter and the transcription factors important for GK expression. The second specific aim is to determine the effect of the individuals' mutations on the metabolic flux in the cell through use of stable isotope, imaging, and microarray studies in lymphoblastoid cell lines and GK knockout mice. A better understanding of this disease process will improve our ability to diagnose and treat patients with this rare metabolic disorder, while giving us insight into more common disorders that disrupt carbohydrate and fat metabolism, such as diabetes mellitus. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR HYPERLIPIDEMIA
SIGNALING
OF
RAPAMYCIN
INDUCED
Principal Investigator & Institution: Abdel-Fattah, Ghada F.; Medicine; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 30-JUN-2005 Summary: (provided by applicant): Hypertriglyceridemia is a major risk factor for cardiovascular disease (CVD), and is associated with insulin resistance. Rapamycin (RAPA) is a potent antiproliferative and immunosuppressive drug that reduces acute graft rejection. RAPA, however, induces hyperlipidemia by unknown mechanisms.
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Understanding how the Mammalian Target of Rapamycin (mTOR) pathway regulates insulin signaling and triggers hyperlipidemia will help reduce risk of CVD, and insulin resistance. The hypothesis tested is that RAPA induces hypertriglyceridemia via an insulin-dependent signaling pathway. Rapamycin interferes with insulin-mediated triglycerides storage in adipocytes leading to increased release of free fatty acids (FFA) to the circulation. Subsequently, influx of FFA lead to augmented hepatic secretion of VLDL-triglycerides and hypertriglyceridemia. Supportive evidence is provided by our preliminary studies in renal transplant patients, as well as observations that RAPA abolishes insulin signals via the FK506 binding protein (FKBP)/mammalian target of rapamycin (mTOR)/p70s6kinase pathway (13-17).SPECIFIC AIM 1. To characterize in vitro the molecular component(s) of the signal transduction of rapamycin in insulinresponsive 3T3-L1 adipocytes. Studies will utilize both genome-based and biochemical approaches to define the cellular pathways of RAPA-induced signals in 3T3-L1 adipocytes. Gene expression will be analyzed by pathway-specific cDNA microarray and will be correlated to protein levels and phosphorylation state; phosphatase (PP2A) activities; FFA; TG levels; hormone sensitive lipase (HSL), and lipoprotein lipase (LPL) activities.SPECIFIC AIM 2. To determine in vitro if inhibition of mTOR expression will eliminate RAPA-induced effects via an insulin-dependent pathway. Studies will investigate the functional significance of blocking mTOR translation by antisense oligonucleotides in 3T3-L1 adipocytes treated with RAPA, compared to the controls, on the same parameters determined in aim 1. SPECIFIC AIM 3. To define in vivo the mechanisms of RAPA-induced hypertriglyceridemia, and impact of RAPA on hepatic triglyceride secretion, lipid and lipoprotein regulatory enzymes in guinea pigs. Animals will be injected with either RAPA or vehicle and will be used in two parallel studies to determine the effect of RAPA on hepatic triglyceride secretion, insulin signaling and lipid metabolism. Findings from these studies will identify the intermediate molecules altered by rapamycin and will address the cross-talk between mTOR and insulin signaling. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NIACIN, N-3 FATTY ACIDS AND INSULIN RESISTANCE Principal Investigator & Institution: Harris, William S.; Professor; St. Luke's Hospital 4401 Wornall Rd Kansas City, Mo 64111 Timing: Fiscal Year 2003; Project Start 20-FEB-2003; Project End 31-JAN-2008 Summary: (provided by applicant): The insulin resistance syndrome (IRS) afflicts approximately 47 million Americans. Its principal components include central obesity, elevated triglycerides, decreased high density lipoprotein cholesterol (HDL-C) levels, fasting hyperglycemia, and/or hypertension. Individuals with the IRS are at significantly increased risk for developing type 2 diabetes mellitus and/or coronary heart disease (CHD). While diet and exercise can improve some manifestations of the IRS, pharmacotherapy is often needed to normalize other components. In recent studies from our laboratory, niacin and fish oil (n-3 fatty acids, FA) used in combination in individuals with the IRS improved the lipid phenotype, but also, unexpectedly, the mealinduced suppression of free fatty acid (FFA) flux (an important indicator of adipose tissue insulin sensitivity). This project will explore the clinical efficacy of combined (and mono-) therapy with n-3 FA and niacin on CHD risk factors, on triglyceride and FFA kinetics and on glucose disposal rates in subjects with the IRS. We will conduct a single, randomized, parallel-arm, placebo-controlled trial. Subjects with the IRS (per the NCEP ATP-itl guidelines) will be randomly allocated to one of four intervention groups after a one-month dual placebo run-in period. The groups will be: n-3 FA (3.4 g/d), crystalline
40
Triglycerides
niacin (3 g/d), the combination, or duat placebo. The latter two groups will include 20 subjects each while the two-monotherapy arms will have 10 subjects each. Effects on endpoints will be determined at baseline and after four months of treatment. The CHD risk factors include serum lipids and lipoproteins; lipoprotein(a); subfractions of HDL and of low density tipoproteins; tissue plasminogen activator and plasminogen activator inhibitor-1; and blood pressure. Triglyceride kinetics will be determined by bolus injection of 2H/5-glycerol, and FFA kinetics by isotope dilution using a constant infusion of 3H-palmitate in the fasting state, after a standard mixed meal and during the hyperinsulinemic-euglycemic clamp procedure used to evaluate glucose disposal rates. At the completion of these studies, we expect to have detailed information on the potential therapeutic efficacy and the kinetic mechanisms of action of these two nutritional agents. This should lead to more effective therapy for the dyslipidemia of insulin resistance and ultimately to reduced risk for CHD in this burgeoning patient population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NOVEL MELANOCORTINS
REGULATION
OF
ADIPOGENESIS:
AGOUTI
&
Principal Investigator & Institution: Mynatt, Randall L.; None; Lsu Pennington Biomedical Research Ctr 6400 Perkins Rd Baton Rouge, La 70808 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Over the past 10 years the agouti/melanocortin system has become recognized as a major regulator of bodyweight homeostasis. For example, a greater number of mutations in the agouti/melanocortin signaling pathway are linked to obesity in humans than any other pathway. The basic paradigm is that melanocortins bind to a family of receptors and reduce bodyweight. Agouti and agouti related protein (AGRP) are endogenous antagonists of melanocortin receptor binding. Moreover, the chronic antagonism of melanocortin receptors by agouti/AGRP leads to obesity. Our preliminary data clearly demonstrate that humans express and regulate agouti in adipose tissue. Therefore, it is important to determine the impact of agouti/melanocortin signaling in fat on obesity and diabetes. The focus of ongoing studies in my laboratory is to understand the function of agouti/melanocortin signaling in adipose tissue and evaluate its contribution to obesity and diabetes. Data collected from transgenic mice that overexpress agouti in adipose tissue and studies in cultured adipocytes have led us to propose that agouti/melanocortins are part of a communication circuit between the brain and adipose tissue which conveys centrallymediated signals (ACTH and alpha-MSH) and modulates adipocytes responsiveness to these signals (agouti). The overall hypothesis is that Agouti/melanocortins regulate adipogenesis and adipocyte metabolism at several levels. First, we hypothesize that agouti increases the proliferation of preadipocytes. Our second hypothesis is that agouti promotes the differentiation of preadipocytes into mature adipocytes. Third, we predict that agouti alters cAMP-dependent signaling pathways in the mature adipocyte such that it is more resistant to lipolysis and more efficient at storing triglycerides. The focus of this proposal is to understand both the mechanisms of agouti/melanocortin action on preadipocytes and adipocytes and the basis for how these effects on adipocyte function contribute to obesity. The preliminary data in this proposal demonstrate that the agouti/melanocortin system is potentially one of the major regulators of adipocyte function, just as it is a major regulator of bodyweight homeostasis, This makes a strong case for studying agouti/melanocortin signaling in adipose tissue and its relevance in understanding the underlying mechanisms of obesity.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NURSE MODEL IN BLACK FAMILIES AT RISK FOR HEART DISEASE Principal Investigator & Institution: Becker, Diane M.; Professor, Department of Medicine and Di; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-MAY-2006 Summary: (provided by applicant) The family heart study will have tested the shortterm impact of a culturally-sensitive community model of one-year of risk factor care by a nurse practitioner/health educator team (NURS TEAM) and usual primary provider care (UC) in 366 apparently healthy 30-59 year old African American siblings of index patients with known premature coronary disease (<60 years of age). One-year results show a significant benefit of the NURS TEAM model when compared with usual care. We do not know whether these effects will be sustained. Maintaining long-term risk factor control is of critical importance in reducing the notably high incidence of CHD in African Americans with a strong family history of CHD. We propose a five-year followup to determine the long-term impact of the NURS TEAM model. The aims are to: (1) compare the five year impact of the NURS TEAM intervention with UC, on levels of LDL-cholesterol, systolic blood pressure, and diastolic blood pressure, (2) determine the independent contribution of (a) biological factors (obesity and comorbidity) and (b) demographic and psychosocial factors (age, sex, education, general well-being scores) on levels of LDL-C and blood pressure, and (3) describe the incidence of premature CHD events and progression of occult CHD. Secondary outcomes include levels of HDL-C, triglycerides, body mass index, and smoking cessation rates. Diet and physical activity scores at five years will be compared by group. We hypothesize that the NURS TEAM will yield significantly better long-term levels of LDL-C and blood pressure compared with UC. We propose a MANCOVA analysis for a group-randomized trial, nested cohort design, with a single baseline, a one-year posttest and a five-year followup assessment. The effect of the treatment group contingency will be the difference between the two conditions at the last follow-up, with adjustment for differences in risk factor levels at baseline. Family-adjusted survival analyses will be used to examine the patterns of clinical and occult CHD over time in high-risk African American siblings. We also use standard qualitative techniques to gain a better understanding of barriers and enhancers to successful control of their risk factors over five years in African American families. The study provides an unparalleled virtually first opportunity to describe CHD incidence in African Americans and to determine the impact of NURS TEAM interventions in a seriously understudied high-risk population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NUTRITION INTERVENTION: METABOLIC COMPLICATIONS OF HIV+ Principal Investigator & Institution: Woods, Margo N.; Associate Professor; Family Medicine & Cmty Health; Tufts University Boston Boston, Ma 02111 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): As the HIV population survives and ages, a new syndrome is being observed that appears to be affected by PI medications but is also seen independent of PI use. This syndrome is characterized by hyperlipidemia, lipodystrophy and insulin resistance. Elevated triglycerides are a common observation
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Triglycerides
with or without hypercholesterolemia. Since statin do not reduce serum triglycerides and may be counter-indicated to lower serum cholesterol because of potential liver damage in the HIV+ population that are on PI, dietary interventions have been getting more attention. Literature suggests that a diet lower in fat with reduced levels of saturated fat relative to polyunsaturated fat, increased omega 3-fatty acids intake, high fiber, and use of carbohydrates lower in glycemic index may be beneficial when they were studied individually. We propose to use a nutrition intervention in a HIV+ population that has elevated triglycerides (>220 mg/dl) to test whether a diet that combines all of these factors can have a significant effect on reducing serum triglycerides. The nutrition intervention will be a low fat diet (25% of calories from fat) with a 1:1:1 ratio of Saturated:Monounsat: Polyunsaturated fat, high in fiber (40 g/day) with carbohydrates of lower glycemic index (< 70 whenever possible). This diet will contain 3 g/day of omega 3-fatty acids which will be supplemented with 3.0 g of omega 3-fatty acids from capsules to give a total of 6 g/day of omega 3-fatty acids and a ratio of n-6/n-3 of 4:1. In addition to measuring triglycerides, serum cholesterol and its subfractions will be determined as well as insulin area under the curve (AUC) and body composition using CT scan. HIV+ participants eligible for the study (N=100) would be randomized into a control or nutrition intervention group and be tested for changes after 3 weeks, 13 weeks and 6 months of intervention. During the first 3 weeks the intervention group will be given all their meals at the hospital General Clinical Research Center, followed by an additional 10 weeks in which some food products are supplied to them along with the continued use of omega 3-fatty acids supplements at 3 gms/day (in 10 capsules). After 13 weeks the participants will be asked to continue to take the omega 3-fatty acid capsules but food products high in n-3 fatty acids will not be supplied. A 6-month follow-up will then remeasure all the study parameters to determine if the nutrition intervention group had experienced an improvement of the listed risk factors compared to the control group. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OVERPRODUCTION OF APOC III IN HYPERTRIGLYCERIDEMIA Principal Investigator & Institution: Brown, W Virgil.; Chair; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2001; Project Start 01-OCT-1974; Project End 30-NOV-2004 Summary: Our working hypothesis is that there are at least four different forms of hypertriglyceridemia: (1) mutations in the lipoprotein lipase (LPL) gene; (2) overproduction of apoB and triglycerides (TG), familial combined hyperlipidemia; (3) overproduction of TG and normal apoB production, type IV primary hypertriglyceridemia; and (4) overproduction of apoC-III, mutation in the apo AI-CIIIAIV gene cluster. These different forms can be defined by metabolic studies designed to assess the in vivo production rate of these components. As the first phase, the present proposal will develop an efficient protocol based on non-radioactive tracers which can allow the production of apoB, apoE, apoC-III and TG to be determined simultaneously in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PET METABOLISM
QUANTIFICATION
OF
MYOCARDIAL
SUBSTRATE
Principal Investigator & Institution: Gropler, Robert J.; Associate Professor; Radiology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130
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Timing: Fiscal Year 2002; Project Start 01-FEB-2002; Project End 31-JAN-2007 Summary: (provided by applicant): Shifts in myocardial substrate utilization play a key role in normal cardiac development and physiology, as well as in variety of cardiac pathologic states. Positron emission tomography (PET) is the most widely used method to quantify myocardial substrate but has several limitations. No information is provided about the subsequent metabolic fate of the extracted substrate. The contribution of myocardial glycogen and triglyceride, to overall energy metabolism is not accounted for. Measurements are limited to the utilization of extracted glucose and fatty acids, and thus, do not take into account the contributions to energy metabolism of other extracted substrates such as lactate. The goal of this research application is to develop and validate PET approaches that will permit the assessment of the metabolic fate of extracted glucose and fatty acid, the contribution to myocardial energy metabolism of myocardial glycogen and triglycerides, and the quantification of myocardial lactate utilization. The Specific Aims are: 1. To develop and validate a compartmental modeling approach that will permit the delineation of extracted 1-11C-glucose that enters a slow turnover pool and likely reflects glycogen storage from tracer that rapidly egresses from myocardium and likely reflects the combined effects of glucose oxidation and lactate production; 2. To develop and validate a compartmental modeling approach that will permit the delineation of extracted 1-11C-palmitate that enters a slow turnover pool and thus likely reflects triglyceride formation from tracer that rapidly egresses from the myocardium and likely reflects beta-oxidation; 3. By taking advantage of the improved sensitivity of 3-D PET imaging, protocols will be developed and validated to assess the myocardial turnover of glycogen and triglyceride using 1-11C-glucose and 1-11Cpalmitate, respectively and; 4. To develop and validate a compartmental modeling approach that will permit the measurement of myocardial lactate utilization by PET and L-3-11C lactate. The various PET techniques will be developed and validated against a variety of biochemical markers in a well-controlled canine model studied under a wide range of substrate, hormonal and workload conditions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PET TRACERS FOR MYOCARDIAL FATTY ACID OXIDATION Principal Investigator & Institution: Degrado, Timothy R.; Professor; Radiology; Duke University Durham, Nc 27706 Timing: Fiscal Year 2001; Project Start 01-JAN-2001; Project End 31-DEC-2003 Summary: (Verbatim from the Applicant's Abstract): Abnormalities of beta-oxidation of long-chain fatty acids preceeds functional abnormalities and irreversible tissue injury in ischemic and nonischemic diseases of the heart. The proposed work investigates the metabolism and kinetics of the palrnitate analog, 16-[F-18]fluoro-4-thia-hexadecanoic acid (FTP), and the oleate analog, 1 8-[F- 1 8]fluoro-4-thia-9Z-octadecenoic acid (FTO), in isolated rat heart. The investigations will attempt to 1) evaluate the sensitivities of FTP and FTO to beta-oxidation and select one of the two tracers for further detailed metabolic and validation studies, 2) characterize the trapped F-18 labeled metabolites of FTP/FTO in the myocardium in order to clarify the trapping mechanism, and 3) determine the relationship of tracer metabolic trapping rate in the heart with oxidation rates of exogenous fatty acids in a broad range of conditions. Isolated buffer-perfused rat heart preparations with external radioactivity detection are utilized in these studies. The metabolism of FTP/FTO in the myocardium to F-18 labeled acyl-CoA, enoyl-CoA, acyl-carnitine, triglycerides, and complex lipids in heart will be estimated by thin-layer chromatography and high-performance liquid chromatography. Gel-electrophoresis will be utilized to analyze radioactivity bound to cellular proteins as a consequence of
44
Triglycerides
metabolic processing. Experiments on the relationship of tracer trapping rate to palmitate and oleate oxidation under various conditions will provide critical data toward the development of a technique for quantitative regional assessment of fatty acid oxidation rate in myocardium using PET. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PHYSICAL ACTIVITY, ENERGY BALANCE, AND COLON CANCER RISK Principal Investigator & Institution: Matthews, Charles E.; Assistant Professor; University of South Carolina at Columbia Byrnes Bldg., Room 501 Columbia, Sc 29208 Timing: Fiscal Year 2002; Project Start 29-SEP-2002; Project End 31-AUG-2007 Summary: There is consensus that low physical activity (PA) levels increase the risk of colon cancer in humans, particularly among individuals with elevated adiposity. However, the precise mechanism(s) of action for these associations have not been established. Although initial evidence indicates a role for inflammatory markers (e.g., prostaglandin-E2) among individuals with low PA or high levels of adiposity, simple descriptions of the patterns of cell proliferation and apoptosis, or markers of these processes, across PA levels are not available. Accordingly, the first aim of this proposal is to develop and refine hypotheses concerning the biologic mechanisms through which PA reduces risk for colon cancer by: (a) evaluating the independent and combined associations of physical activity/fitness, adiposity, and metabolic predictors (blood glucose, triglycerides) of colon cancer risk in the Aerobics Center Longitudinal Study (Dallas, TX) using a nested-case control design (N=600), and (b) evaluating the independent and combined associations of PA and adiposity on biomarkers for colon cancer associated with inflammation (cyelooxygenase-2), cell proliferation (mib 1), and apoptosis (bax, bak, bcl2) in cross-sectional analyses of the Markers of Adenomatous Polyps II Study (N=200, Columbia, SC). Results from these analyses will be used to select up to 10 biomarkers for evaluation in a longitudinal pilot study. The second aim is to quantify the effect of changes in PA levels on selected biomarkers in a randomized trial (N=50, intervention vs. usual care) among adults not meeting current PA recommendations. Intervention participants will receive a 12-month home-base walking intervention based on Social Cognitive Theory that includes monthly phone contact with a health educator. Potential mediators and moderators of behavior change will be quantified (e.g., self-efficacy, social support). PA goals for the intervention group will be to walk briskly at least 5 times per week for 40-45 minute per day (1125 kcal/wk). Outcome biomarker measures will be obtained via rectal biopsy at baseline and 12months. In summary, the series of investigations outlined in this proposal will examine the independent and combined effects of PA and energy balance (adiposity) on colon cancer and adenomatous polyp outcomes, and relate these findings to parallel analyses on tissue biomarker outcomes describing the biologic mechanisms linking PA and energy balance to colon cancer risk. This work will extend our understanding of the biological mechanisms underlying these causal relationships. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PILOT--AEROBICS AND METABOLISM IN TYPE2 DIABETICS Principal Investigator & Institution: Quinn, Lauretta T.; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2001; Project Start 15-AUG-2001; Project End 31-JUL-2004
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Summary: (from applicant's Abstract) In the US, type 2 diabetes affects 90 percent of the 15.6 million individuals with diabetes (DM) and is associated with a two to fourfold increase in cardiovascular disease (CVD). Although postprandial oxidative stress, CHO and lipid metabolism have been implicated in the pathogenesis of CVD, the ability of acute aerobic exercise to modify these variables has not been explored in type 2 DM. This study will compare the effects of an acute bout of aerobic exercise (45 minutes of treadmill walking at 60 percent V02 Max) in a group of physically untrained subjects with younger-onset type 2 DM and control subjects on: (1) parameters of postprandial CHO and lipid metabolism (glucose, insulin, C-peptides, triglycerides), following 3 meals; (2) parameters of postprandial oxidative stress (total MDA, total hydroperoxides) and LDL susceptibility to oxidation, following 3 meals. In addition, the relationship between baseline insulin sensitivity, antioxidant status, VO2Max and postprandial changes in parameters of oxidative stress CHO and lipid metabolism will be explored. The study will include 11 subjects with type 2 diabetes (age 18-40 years) with duration of diabetes (< 7 years) who will participate in a nonexercise and exercise protocols, performed in random order. On day 1 of the exercise protocol, a euglycemic, hyperinsulinemic glucose clamp will be performed. On day 2 at 0800 hours. baseline parameters of oxidative stress, LDL susceptibility to oxidation, CHO and lipid metabolism will be obtained prior to an acute bout of aerobic exercise and periodically throughout the postexercise period, during which three meals will be consumed. The diet will follow American Heart Association (AHA) National Cholesterol Education Program (NCEP1) guidelines with 30 percent fat as energy, with 10: 10: 10 percent from saturated, monounsaturated and polyunsaturated fat, respectively with 113 of energy requirements to be consumed at each meal. On nonexercise experimental day, the same protocol will be followed without the acute exercise bout. The use of aerobic exercise to influence CHO and lipid represents a new approach to using aerobic exercise as a treatment for type 2 diabetes with a long-term goal of impacting complications, such as CVD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: POLYMORPHISMS OF B1 AND B2 RECEPTOR GENES AND OBESITY Principal Investigator & Institution: Lima, John J.; Professor; Nemours Children's Clinic 807 Children's Way Jacksonville, Fl 322078482 Timing: Fiscal Year 2001; Project Start 15-JUN-2001; Project End 31-MAY-2003 Summary: Obesity has been associated with insulin resistance, hyperinsulinemia, noninsulin-dependent diabetes mellitus, hypertension and a higher risk of cardiovascular disease and death. Genetic, metabolic and environmental factors are known to contribute to obesity. Genes that are involved in the regulation of catecholamine function may be important because of the role catecholamines play in energy expenditure and lipolysis. Ninety percent of fat in the body is stored in white adipose tissue as triglycerides, which are broken to free fatty acids and glycerol through the action of hormone-sensitive lipase. Lipolysis is stimulated by beta1, beta2 and beta3 adrenergic receptors in human adipocytes, with the beta1 and beta2 adrenergic receptors (beta1 and beta2 AR) being the most dominant subtypes. Catecholaminestimulated lipolysis is reduced in obesity, which is thought to be due to defects in the beta2 AR-signaling pathway. Mis-sense mutations in the beta1 AR gene results in polymorphisms at nucleic acid 145 (A->G), which results in a substitution of Ser for Gly at position 49, and at nucleic acid 1165 (G- >C, which results in a substitution of Gly for Arg and position 389. Beta1 AR polymorphisms have functional significance; whether or
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Triglycerides
not they associate with obesity is unknown. Mutations in the 5' leader and coding regions of the human beta2 AR gene give rise to several polymorphisms, which can after receptor density and function. The working hypotheses of this submission are that polymorphisms at position 389 and haplotypes of beta2 AR polymorphisms in the 5' leader and coding regions associate with obesity. Specific Aim #1: to compare the beta1 AR allele frequencies and genotypes in healthy obese and non- obese subjects. The hypothesis driving this specific aim is that obesity associates with the Gly 389 beta1 AR allele. Specific Aims #2: to compare the distribution of beta2 AR haplotypes in healthy obese (Body Mass Indexes > 30) and non-obese (BMI < 25) subjects. Beta2 AR haplotypes will be determined by PCR and direct sequencing. The thesis driving this specific aim is that obesity associates with the Arg19-Gly16- Glu27 beta2 AR haplotype. The distribution of beta2 AR haplotypes in 118 non-obese and 118 otherwise healthy obese subjects will be compared. The results of this study will determine whether polymorphisms in beta1 and beta2 AR allels associate with obesity. The information obtained from our studies are important in designing clinical trials of interventions designed to reduce body weight. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: POST ABDOMINAL FAT
MENOPAUSAL
HORMONE
THERAPY
AND
INTRA
Principal Investigator & Institution: Gower, Barbara A.; Associate Professor; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 01-DEC-2000; Project End 30-NOV-2001 Summary: Background: Hormonal and metabolic changes associated with the menopause may confer increased risk for cardiovascular disease (CVD). Data indicate that the postmenopausal period is associated with increases in total and central ("android") body fat; increases in the atherogenic components of the blood lipid profile; and deterioration of glucose tolerance - all risk factors for CVD. Changes in lipid and glucose metabolism may be secondary to accumulation of central fat, particularly intraabdominal fat (IAF), the compartment associated with dyslipidemia and insulin resistance. Hormone replacement therapy has positive effects on the lipid profile in postmenopausal women, and may affect regional fat deposition. However, the extent to which the beneficial effects of hormone therapy on disease risk factors are mediated by changes in fat distribution is not known. Few studies have examined the effects of hormone replacement therapy on body composition and fat distribution, and non have examined the effect of exogenous hormones on IAF, the adipose compartment most closely associated with disease risk. Objective: To test the hypothesis that hormone replacement therapy (HRT, combined estrogen-progestin) in postmenopausal women decreases risk by limiting IAF deposition. The proposed research will examine the effect of HRT on total, regional, and intra-abdominal fat deposition, and on the relationships between adiposity, the plasma lipid profile, and glucose metabolism. Design: Longitudinal cohort study of 140 early postmenopausal women using or not using HRT. A baseline assessment (within the first year of hormone use) and one 2-year follow-up assessment will be conducted. Total body fat will be assessed with dual-energy X-ray absorptiometry, hydrodensitometry, and deuterium dilution; and regional adiposity (thigh, abdominal, intra-abdominal) will be quantified with computed tomography. Circulating levels of total cholesterol, high- and low-density lipoprotein cholesterol, and triglycerides will be determined. Insulin sensitivity and glucose tolerance will be assessed with the tolbutaminde-modified, frequently-sampled, intravenous glucose tolerance test and minimal modeling. Significance: HRT reduces risk and incidence of
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CVD in postmenopausal women. This study will determine if HRT reduces disease risk by influencing fat distribution and decreasing IAF. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROTEASE INHIBITOR RELATED DYSLIPIDEMIA Principal Investigator & Institution: Wanke, Christine A.; Associate Professor; Family Medicine & Cmty Health; Tufts University Boston Boston, Ma 02111 Timing: Fiscal Year 2001; Project Start 12-JUL-2000; Project End 30-JUN-2005 Summary: Protease inhibitors are used as therapy in HIV patients and have been reported to cause elevations in plasma triglycerides, cholesterol, and glucose, and rarely to induce severe hypertriglyceridemia, pancreatitis, and diabetes mellitus with insulin resistance, excess fat deposition, and lipodystrophy. Our aims are to measure fasting Serum cholesterol (C), triglyceride (TG), remnant lipoprotein (RLP) C and TG, low density lipoprotein (LDL) C, high density lipoprotein C, lipoprotein(a), apolipoproteins A-I and B, apo E genotype, homocysteine, free fatty acids, glucose, insulin, and blood pressure. We will also assess smoking status, carotid artery wall thickness by ultrasound, and coronary artery calcification by computerized tomography in our prospective cohort of 400 HIV patients whose nutritional status is being evaluated and who are taking a variety of antiviral agents including protease inhibitors. Comparisons will be made on and off inhibitors and also longitudinally, and with controls. Our comparison group are participants in the Framingham Offspring Study who have had all the same parameters measured (n=3250). HIV patients who become hyperlipidemic on protease inhibitors will be treated with either gemfibrozil or atorvastatin. We will also examine the effects of protease inhibition in Hep G2 and CaCo2 cells with or without supplementation with fatty acids and cholesterol on lipoprotein assembly and secretion and apolipoprotein, LDL receptor, and microsomal transfer protein (MTP) gene expression. The effects of protease inhibition on lipoprotein metabolism and aortic foam cell formation will also be assessed in F1B hamsters on chow and on diets high in cholesterol and saturated fat. In addition, using a primed constant infusion in the constantly fed state and deuterated leucine, the secretion and catabolism of apoB-48 and apoB-100 within lipoproteins will be determined by GC/MS analysis and multicompartmental modeling in the presence or absence of protease inhibition with ritonavir in 10 males and 10 female HIV patients. We will test the following hypothesis: 1) protease inhibitors increase triglyceride and cholesterol by increasing RLP; 2) elevated RLP leads to increased carotid wall thickness and coronary calcification; 3) these increases can be ameliorated with diet, gemfibrozil and/or atorvastatin treatment; 4) in cell culture these RLP increases are elated to enhanced secretion of apo B-100 due to less intracellular degradation, and excess cellular lipid content; 5) in hamsters there are increased RLP in serum in animals on the atherogenic diet, especially with protease inhibition, and this leads to increased aortic foam cell formation; 6) in humans protease inhibition causes increased triglyceride-rich lipoprotein apo B-100 secretion. This research should define the nature of the problem, its mechanism, and methods for treatment wit regard to the hyperlipidemia induced by protease inhibitors in HIV patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: REDUCTION OF TRIGLYCERIDES IN WOMEN ON HRT Principal Investigator & Institution: Kuller, Lewis H.; Professor and Chair; Epidemiology; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260
48
Triglycerides
Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-AUG-2006 Summary: (provided by applicant): The risk and benefits of hormone replacement therapy (HRT) have come under increased concern in recent years because of the results of the HERS and WHI trials, the increased risk of breast cancer, new therapies, i.e., SERMs and lipid lowering drugs, bisphosphorates, and better understanding of hormone metabolism and disease. We have shown in several studies that the potential benefits of HRT are limited by lifestyle, cofactors, specifically weight gain, obesity and increased visceral abdominal fat associated metabolic changes in lipoproteins, inflammatory markers and estrogen metabolites. We are proposing a randomized trial of 500 women, on HRT for at least two years, aged 52-60 years, and three or more years postmenopausal to test whether reduction in waist circumference, triglycerides, dense LDLc, number of LDL particles, CPR, PAI-I by aggressive diet exercise, versus a health education control will decrease progression or result in regression of measures of subclinical vascular disease. The intervention is designed to reduce total fat intake to 17 percent of calories, 1300 kilo calories, and increase moderate activity to 150-240 minutes per week to obtain a 10 percent reduction in weight. The primary endpoint will be a 20 percent or at least a 20 mg decrease in triglyceride levels, a 5 cm decrease in waist circumference, and a 10 percent decrease in LDLc. This will result in changes in subclinical measurements including carotid ultrasound, electron beam computer tomography of the coronary and aorta, pulse wave velocity, endothelial function, and tonometry of the radial artery. NMR spectroscopy of lipoproteins, inflammatory markers, and estrogen metabolites will also be evaluated. Therefore, the primary goal of this trial is the modification of measures of subclinical disease among HRT users. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGIONAL ADIPOSITY AND SYNDROME X IN SPINAL CORD INJURY Principal Investigator & Institution: Braunschweig, Carol; Human Nutrition and Dietetics; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2004 Summary: (provided by applicant): Total and abdominal obesity frequently occur following SCI. Excessive total body adiposity, particularly excessive visceral abdominal adipose tissue (VAAT), and thigh skeletal muscle adiposity (TSKMAT), measured by magnetic resonance imaging (MRI), have been associated with a low-grade systemic inflammation and the metabolic syndrome (MS) (also called syndrome X) which has been defined as the presence of three or more of the following features: waist circumference (WC) greater than 40 inches, fasting triglycerides of at least 150 mg/dl, glucose equal or greater than 110 mg/dl, HDL cholesterol equal or less than 40 mg/dl and/or blood pressure of at least 130/85 mmHg. People with the MS are predisposed to developing insulin resistance and increased risks for diabetes mellitus, hypertension, and cardiovascular disease. Individuals with SCI have higher prevalence rates for these diseases than able-bodied individuals, however, measures of VAAT or TSKMAT volumes and their relation to a measure for inflammation, features of the MS or insulin resistance have not been reported for this population. This is unfortunate given that body fat distribution and inflammatory status are both modifiable risk factors. The purpose of this pilot investigation is to explore the association between measures of adiposity (total, abdominal, VAAT and TSKMAT), a sensitive marker of inflammation (CRP), features of the MS, and insulin resistance in paraplegic men compared to similar able-bodied men. The investigators propose a cross sectional investigation of community dwelling males (N = 60) recruited from urban SCI rehabilitation and trauma
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centers to determine whether the volume of VAAT, its anthropometric surrogates (WC and/or sagittal diameter), and/or the volume of TSKMAT predict concentrations of CRP, levels and numbers of features of the MS, and insulin resistance in paraplegic men and whether these variables are similar in direction, magnitude and association to those observed in able-bodied men. Four groups of men more than one year post SCI or trauma, frequency matched for age and ethnicity (15/group; 30 paraplegic SCI and 30 able-bodied men with a history of trauma resulting in a hospital stay over 5 days), will be recruited as follows: group 1 lean SCI (WC 40 inches), group 3 lean able-bodied (WC 40 inches). Correlation analysis, multiple regression, and analysis of variance will be used to determine the association between CRP, the MS, insulin sensitivity, and various measures of regional adiposity between these groups. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION AND ACTIVATION OF STATS IN ADIPOCYTES Principal Investigator & Institution: Stephens, Jacqueline M.; Associate Professor; Biological Sciences; Louisiana State Univ A&M Col Baton Rouge Office of Sponsored Programs Baton Rouge, La 70803 Timing: Fiscal Year 2001; Project Start 01-SEP-1999; Project End 31-AUG-2003 Summary: Adipocytes are highly specialized cells which play a central role in lipid homeostasis and the maintenance of energy balance in vertebrate organisms. These cells store energy in the form of triglycerides during periods of nutritional abundance and release it in the form of free fatty acids at times of nutritional deprivation. Pathological conditions associated with altered adipocyte cell number or function include obesity and several lipodystrophy syndromes. Obesity, an excessive accumulation of adipose tissue, is a common disorder which affects over 30 percent of Americans. In humans, obesity is an independent risk factor for non-insulin dependent diabetes mellitus (NIDDM), hypertension, and coronary artery disease and is a major contributor to morbidity and mortality. Recent studies suggest that obesity and its related disorders may be linked to a breakdown in the regulatory mechanisms which control the expression of metabolic genes in adipocytes. Significant advances toward an understanding of these regulatory processes have been made by the identification of transcription factors which regulate adipocyte differentiation and gene expression. To date, members of two transcription factor families, C/EBP (C/AAAT Enhancer Binding Proteins) and PPAR (Peroxisome Proliferator Activated Receptors) have been shown to be induced during adipocyte differentiation and play a critical role in the regulation of fat-specific genes. Our recent investigations have demonstrated that an additional family of transcription factors are induced during adipocyte differentiation. The STATs (Signal Transducers and Activators of Transcription) comprise a family of transcription factors which reside in the cytoplasm of resting cells. Unlike either C/EBPs or PPARs, STATs can be rapidly activated to control gene expression. In a manner equivalent to both C/EBPalpha and PPARgamma, expression of three STAT family members correlates with lipid accumulation. Since STAT family members have unique tissue distributions and are highly expressed in adipocytes, we hypothesize that STATs play a key role in the regulation of adipocyte gene expression. To test this hypothesis, we will examine the regulation and activation of STATs in adipocytes. We have also designed a set of experiments to elucidate the function of these proteins in adipocytes. These studies may lead to insights into the molecular mechanisms regulating energy homeostasis and may have a profound impact on the defects underlying obesity and NIDDM. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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•
Project Title: REGULATION OF TRIACYLGLYCEROL METABOLISM IN OBESITY Principal Investigator & Institution: Sidossis, Labros S.; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 18-DEC-1996; Project End 30-NOV-2002 Summary: This application focuses on the hypertriglyceridemia associated with upper body obesity. The investigator hypothesizes that increased triglycerides in upper body obesity result from increased availability of free fatty acids to the liver due to resistance to insulin mediated inhibition of peripheral lipolysis. Furthermore, hyperglycemiainduced inhibiton of hepatic fatty acid oxidation results in diversion of hepatic free fatty acids into esterification for triglycerides. The investigator further proposes that the relative importance of either increased hepatic free fatty acid availability or reduced hepatic fatty acid oxidation in abnormal triglyceride production depends on feeding. To investigate these hypotheses, the investigator proposes quantification of whole body and regional (leg and splanchnic) free fatty acid kinetics and oxidation and VLDL triglycerides secretion and clearance rates in both upper body and lower body obese individuals. These measures are to be made both fasting and fed. The investigator will also manipulate free fatty acid concentrations by adjustments with nicotinic acid, lipid and, heparin infusions. The studies employ stable and radioactive isotopes for kinetic measurements and involve detailed physiologic and kinetic mathematical modeling. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RISK OF CHD IN WOMEN WITH POLYCYSTIC OVARY SYNDROME Principal Investigator & Institution: Talbott, Evelyn O.; Faculty; Epidemiology; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2001; Project Start 30-SEP-2000; Project End 31-AUG-2004 Summary: (Adapted from the Investigator's Abstract) Polycystic ovary syndrome (PCOS), characterized by chronic anovulation, hyperandrogenism, and insulin resistance, is estimated to affect four percent to eight percent of all women. In 1992, the investigators initiated the first large-scale study of cardiovascular risk factors in women with PCOS (1992-1994). They recruited 244 women with PCOS and 244 age-, race- and neighborhood-matched controls age (19-50 years of age) and determined that PCOS cases had a profile that conferred increased cardiovascular risk (increased LDLc, triglycerides, and waist/hip ratio, obesity, decreased HDLc, hyperinsulinemia, and increased diastolic and systolic blood pressure). During phase II, (1996-99) they investigated the prevalence of subclinical atherosclerosis (SCA) of the carotid arteries in women 30+ years of age from the original cohort. In preliminary analyses, PCOS cases 45+ years had significantly higher mean intima-media wall thickness (IMT) than controls (0.75mm vs. 0.70mm, p=40 years from the original cohort to determine if PCOS cases have greater initial coronary or aortic calcification and/or greater progression during years 4 and 5, 2) evaluate the progression of carotid atherosclerosis over a 5-year period of PCOS cases and controls >=40 years who participated in Phase II of the study, 3) evaluate whether CHD risk factors can be linked to the extent of coronary and aortic calcification within cases and controls, 4) evaluate vascular stiffness in PCOS cases and controls and determine CHD risk factors for aortic stiffness, and 5) evaluate endothelial function in PCOS cases and controls and changes over five years. CHD risk factors will include: HDLt, LDLc, triglycerides, glucose, insulin, Lp(a), PAI-1, blood pressure, and anthropometric measures. Information will be obtained on medical, reproductive and physical activity history. The investigators state that this study has the potential to
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identify the determinants of early SCA in this high-risk group of women and has important implications for primary as well as secondary prevention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF FREE FATTY ACIDS IN HUMAN INSULIN METABOLISM Principal Investigator & Institution: Stein, Daniel T.; Associate Professor of Medicine; Medicine; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2006 Summary: Increased availability of lipid substrates, particularly plasma non-esterified free fatty acids and intracellular triglyceride stores have been linked to many aspects of the insulin resistance syndrome including obesity, dyslipidemia and Type 2 diabetes. Epidemiologic and animal data suggest that saturated fats have differential effects on the induction of insulin resistance as well as their effects (both stimulatory and inhibitory) on beta cell function compared to unsaturated fats. Current medical guidelines suggest limiting fat, particularly saturated fat intake. Surprisingly, considering the potential public health implications of dietary fat intake, little direct experimental data exists for human subjects in this area, and available data is contradictory. The goal of these studies, therefore, is to explore the effect of lipids on normal beta cell physiology and then to directly test the hypothesis that dietary saturated fatty acids time dependently stimulate insulin secretion more and then induce greater degrees of insulin secretory dysfunction with prolonged exposure as compared to unsaturated fats using the novel method of in vivo stable isotope peptide pharmacokinetics. As beta cell function deteriorates with prolonged NEFA exposure, hyperinsulinemia matching the degree of insulin resistance will be maintained by decreases in systemic and hepatic insulin clearance. We will also test the proposition that subjects at risk for Type 2 diabetes will be more sensitive to the effects of saturates compared to normal controls. Lastly we hypothesize that for the group as a whole, defects in insulin action, insulin clearance and finally beta cell secretory function will be exactly paralleled by accumulations of intracellular triglycerides in multiple tissues including within hepatocytes and skeletal myocytes as monitored non-invasively by magnetic resonance proton spectroscopy and that this provides the unifying link to systemic organ dysfunction with abnormal lipid metabolism in the insulin resistance syndromes. Preliminary data support the feasibility of our approach as well as our hypothesis. An improved understanding of beta cell - lipid interactions should provide evidence for future dietary recommendations to prevent type 2 diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF STEAROYL-COA DESATURASE IN METABOLISM Principal Investigator & Institution: Ntambi, James M.; Professor; Biochemistry; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 30-JUN-2006 Summary: (provided by applicant): Stearoyl-CoA desaturase is a central lipogenic enzyme catalyzing all reactions in the synthesis of monounsaturated fatty acids mainly oleate (C18:1) and palmitoleate (C16:1) which are the major monounsaturated fatty acids of membrane phospholipids, triglycerides, wax esters and cholesterol esters. Several SCD gene isoforms (SCD1, SCD2, SCD3) exist in the mouse. We have found that mice with a targeted disruption of the SCD1 isoform (SCD1-/-) have reduced body fat, plasma leptin and insulin levels and a reduced rate of triglyceride synthesis in liver. Compared to wild type mice, SCD1-/- mice are lean and resistant to high fat diet-
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induced obesity. The expression of lipogenic genes is reduced in the SCD1-/- mice. It is well known that fatty acid and triglyceride synthesis is regulated by the insulindependent gene expression and maturation of the sterol regulatory element binding protein-ic (SREBP-1c). What we found instead is that while the SREBP-1c gene expression was not altered in the SCD1-/- mice, the maturation of the SREBP-1 protein into its transcriptionally active form is blocked. The levels of ketone bodies and the mRNA levels of the peroxisome proliferator activated receptor alpha (PPAR-alpha) target genes are increased suggesting increased fatty acid Beta-oxidation in the SCD1-/mice. We hypothesize that SCD1 deficiency induces a signal that down regulates lipogenesis by modulating the SREBP-1 protein maturation and activates the PPARa pathway to partition fatty acids towards fatty acid Beta-oxidation. We shall design experiments to address this hypothesis using wild type (SCD1 +/+), heterozygotes (SCD1+/-) and homozygotes (SCD1-/-) mice as well as primary hepatocytes derived from these animals. The specific aims of this proposal are: 1. To determine whether SCD1 deficiency causes a blockage in the processing of the liver SREBP-1 protein to its mature form and down-regulates lipogenesis. 2. To elucidate how SCD1 deficiency upregulates fatty acid Beta-oxidation. Overall, our studies wil provide physiologically relevant information on the role of stearoyl-CoA desaturase gene expression in lipid and carbohydrate metabolism and will enhance our understanding of metabolic control of lipogenesis and dysregulation in diabetes and obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SLEEP METABOLISM
DISORDERED
BREATHING,
APOE
AND
LIPID
Principal Investigator & Institution: Mignot, Emmanuel J.; Director; Psychiatry and Behavioral Sci; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 21-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Recent findings suggest interrelationships between obstructive sleep apnea, lipid metabolism, and neurodegeneration. Apolipoprotein E epsilon4 (APOE e4), a genetic marker linked to increased cardiovascular disease (CVD) risk and Alzheimer's disease (AD), is associated with a two fold increased risk of sleep disordered breathing (SDB), and an increase in severity of apnea symptoms. Preliminary data suggest that this association is stronger between the ages of 50 and 65. Other experiments suggest dysregulated leptin levels in obstructive sleep apnea (OSA). Taken together, these findings suggest common pathophysiological mechanisms involving dysregulated lipid metabolism in OSA. An understanding of these mechanisms is essential for the prevention and treatment of SDB. In this project, we will: 1) extend our finding that APOE e4 increases the risk of sleep apnea in the general population using case/control and family designs; 2) examine if polymorphisms in other genes regulating lipid levels are associated with sleep apnea; 3) study the relationship between lipid regulatory gene polymorphisms, lipid profile (LDL- cholesterol, HDL-cholesterol, triglycerides), plasma leptin (and other lipid regulatory hormones), and sleep apnea levels. These studies will be critical to extend our understanding of the association between sleep apnea and the metabolic syndrome. This application will focus on one arm of this complex equation, the relationship between lipid metabolism and SDB. With lipid metabolism being critical to cardiovascular risk, this application will also trigger further studies focusing on cardiovascular impact with adequate control of SDB. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SOY AND LIPOPROTEINS IN POSTMENOPASUAL WOMEN Principal Investigator & Institution: Allen, Jerilyn K.; Associate Professor; None; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2004 Summary: (provided by applicant) Cardiovascular disease (CVD) remains the leading cause of mortality and disability in postmenopausal women. Menopause alters serum lipids and lipoproteins to produce a more atherogenic lipid profile that may contribute significantly to the increased risk for the development of CVD over the lifetime of women. Clinical trials have demonstrated a beneficial effect of soy protein containing isoflavones (soy) on plasma lipids and lipoproteins; however, these studies included small numbers of postmenopausal women and virtually none included sufficient African-American women. In addition, no published data exist on the impact of soy on atherogenic lipoprotein subclasses in postmenopausal women. Therefore, the primary aim of this study is to determine the effects of soy on lipids, lipoproteins and lipoprotein subclass in a sample of African-American and white postmenopausal women with lowdensity lipoprotein (LDL) cholesterol elevations that may increase their lifetime risk for CVD but would not qualify for definite pharmacotherapy under current guidelines. The secondary aims are to assess the impact of soy on menopausal quality of life, including menopausal symptoms, and to examine racial/ethnic differences in quality of life, acceptability, adherence to, and lipoprotein response to the soy supplementation. The proposed study is a double blind, parallel group, randomized clinical trial. A total of 160 healthy postmenopausal women (50 percent African-American) with LDL cholesterol between 130 mg/dL and 190 mg/dL will be enrolled. Following a pre-randomization run-in period on a NCEP Step I diet, women will be randomized to receive soy containing isoflavones or casein dietary supplements for 3 months. Major outcome variables will be assessed in both groups at baseline and again at 3 months. It is hypothesized that soy supplementation will result in significantly greater reduction in LDL cholesterol, LDL particle concentration, and prevalence of dense LDL particles and improvement in menopausal quality of life compared with placebo and that these effects will be comparable in African-Americans and whites. This will be the first study to determine whether a natural plant product can ameliorate the unfavorable changes in known and novel lipid risk factors that are a consequence of menopause in both African-American and white women. The unique transitional outcomes explored in this study will add substantially to the limited body of knowledge of the effects of soy. Evaluation of this nutritional alternative to hormone replacement therapy (HRT) that may provide a beneficial effect on lipid risk factors and menopausal symptoms but would be free of the adverse effects on triglycerides, the breast and uterus, and thrombotic events associated with HRT could have significant public health implications for postmenopausal women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: STRUCTURE/FUNCTION OF PROTEINS AT MOLECULAR LEVEL Principal Investigator & Institution: Stroud, Robert M.; Professor; Biochemistry and Biophysics; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001; Project Start 01-APR-1979; Project End 31-DEC-2002 Summary: The proposal seeks to uncover fundamental mechanisms of transmembrane processes at the level of atomic structure. Specific objectives are to understand the mechanisms of transmembrane signaling in the acetylcholine receptor superfamily of
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Triglycerides
pentameric, ion channel neuroreceptors by structural analysis of components, fragments of the AcCh Receptor alpha chain in complex with neurotoxins to which they bind tightly, the extracellular portion of a subunit, and portions of a whole receptor. These are to provide a three dimensional road map of interactions and will have broad impact on the understanding of fundamental elements in neurochemistry, and structure assisted development of selective psychoactive drugs. The structure of a bacterial, monomeric ion channel-forming protein colicin Ia (Col Ia), with similar conductance properties to neuronal receptors, is being extended in resolution from 3.0 Angstrom units to 2.3 Angstrom units. Mutations will be used to define the impact of charge and polar arrangements in regulating conductance I and selectivity of ion channels. Interpretation of the unique structural features, and their role in determining receptor binding, translocation and channel insertion will be defined by a combination of mutational, channel, forming, bacterial targeting, thermodynamic, and structural analysis. Electron microscopic analysis is to assist in defining the membrane bound channel state. The mechanism of host immunity to this bacteriocidal protein involves high affinity intra-membrane association with a three membrane-crossing immunity protein Imm Ia. The structure of this complex will be sought to uncover basic mechanisms of intramembrane interaction, with impact on the design of modulators of transmembrane receptors. The structure of a channel forming Bacillus thuringiensis toxin (CytA) at 2.3 Angstrom units is a paradigm for interpreting the many existing mutations that alter transmembrane assembly, and channel forming properties, to understand the mechanisms of channel formation, and the membrane bound form. The initial 1.6 Angstrom units structure of apo-Cholesterol esterase, an abundant, enzyme important in regulating transmembrane transport of triglycerides and cholesterol from cholesterol esters is to understand membrane active mechanisms, and to provide a template for structure assisted drug development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SUBSTRATE CYCLING IN ENERGY METABOLISM Principal Investigator & Institution: Wolfe, Robert R.; Professor; Surgery; University of Texas Medical Br Galveston 301 University Blvd Galveston, Tx 77555 Timing: Fiscal Year 2001; Project Start 01-DEC-1984; Project End 31-MAY-2003 Summary: In this project we will extend our previous studies defining factors controlling hepatic triglyceride (TG) metabolism under normal conditions to the situation following severe burn injury. We will investigate the general hypothesis that hepatic fatty acid oxidation is inhibited following burn injury. Related to that general hypothesis, we propose to investigate the following specific hypotheses with regard to the response to burn injury: 1. Hepatic fatty acid oxidation is limited in burn injury by an inhibition of carnitine palmitoyltransferase-I (CPT-I). 2. CPT-I is inhibited by a high concentration of hepatic malonyl-CoA. Further, we propose that the high concentration of malonyl-CoA stems from accelerated glucose metabolism and production of pyruvate. 3. Hepatic uptake of plasma free fatty acids (FFA) is a direct function of delivery and thus not limited by an inhibition of oxidation. Rather, when oxidation is limited, plasma FFA are channeled preferentially into hepatic triglycerides. 4. Changes in FFA availability have a greater effect on hepatic TG synthesis in burn injury than normal because the low activity of CPT-I limits the extent to which fatty acid oxidation can respond to changes in availability. 5. Carbohydrate intake causes a greater hepatic uptake of glucose in burn injury than normal because of hyperglycemia. As a consequence, the de novo synthesis of fatty acids in the liver is stimulated to a greater extent than normal because of the activated state of acetyl-CoA carboxylase (ACC). 6.
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Maintenance of euglycemia during glucose intake by means of infusion will decrease the proportionate uptake of glucose by the liver, and thereby reduce the rate of fatty acid synthesis. Studies will be performed in patients with severe burns and in normal volunteers. Arterial and hepatic vein catheters will enable calculation of the splanchnic balance of substrates and metabolites labeled with a combination of stable and radioactive isotopes. Corresponding studies will be performed in normal and burned pigs in order to examine in greater depth the mechanisms responsible for the observed responses in human patients. Taken together, these results will help to explain the metabolic basis for abnormal hepatic fatty acid and triglyceride metabolism in stress and insulin-resistant states such as burn injury. This information will provide a physiological basis for the development of a practical approach to controlling increased triglyceride synthesis in insulin resistant states. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THROMBOSIS GENE POLYMORPHISMS AND EARLY CHD RISK IN HERS Principal Investigator & Institution: Herrington, David M.; Professor; Internal Medicine; Wake Forest University Health Sciences Winston-Salem, Nc 27157 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2004 Summary: (provided by applicant): The Heart and Estrogen/progestin Replacement Study (HERS) and several other clinical studies and clinical trials have observed a transient increase in risk for coronary heart disease (CHD) events after initiation of hormone replacement therapy (HRT). Some evidence suggests that this adverse effect of HRT may be limited to a subgroup of women who are uniquely at risk for a thrombotic complication of estrogen therapy. There are several well-described polymorphisms in genes whose products regulate coagulation or fibrinolysis that could augment thrombotic risk in the setting of estrogen therapy. These polymorphisms include Factor V Leiden, prothrombin 20210A, Factor VII R353Q. plasminogen activator inhibitor-1 (PAI-1) 4G/5G, fibrinogen B-beta-455A, and platelet GP IIIa P1-A1.A2. We propose a nested case-control study among HERS women with CHD (n = 361) or venous thrombotic events (VTEs) (n = 95) and two clinic-matched controls to assess the relation between the above listed polymorphisms, HRT, and risk for CHD or VTEs. We will estimate the absolute and relative risk of HRT among women with and without the six candidate thrombosis gene polymorphisms and test for evidence of a genotype * HRT interaction. In secondary analyses, we will focus on events that occurred in the first year, evaluate the effect of triglycerides on risk associated with the Factor VII and PAI-1 polymorphisms, and explore the impact of combinations of polymorphisms on risk. DNA for this project will be acquired from centrally stored Pap smears that were collected during the trial. If this project reveals a high-risk subgroup based on thrombosis gene polymorphisms, women could be screened for this condition and cautioned not to use HRT. Conversely, low-risk women might be able to use HRT more safely in pursuit of various health benefits, including a possible reduction in CHD risk. Thus, this project may lead to more effective strategies to prevent CHD in women, enhance the safety of HRT, and add to the expanding body of knowledge concerning drug/gene interactions as they relate to treatment and prevention of disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TISSUE SPECIFIC REGULATION OF LIPOPROTEIN LIPASE Principal Investigator & Institution: Eckel, Robert H.; Professor of Medicine,; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2001; Project Start 01-DEC-1979; Project End 30-JUN-2005 Summary: Lipoprotein lipase (LPL) is a secretory glycoprotein which contributes to the delivery of lipid fuels to tissues where they are predominantly stored (adipose tissue) or oxidized (muscle). The regulation of LPL in adipose tissue and muscle is often divergent, and alterations in LPL and its regulation by hormones and nutrients are commonly seen in metabolic disorders of insulin resistance, i.e. obesity and type II diabetes mellitus. The importance of LPL in muscle to the regulation of energy balance has recently been demonstrated by the prevention of high fat diet-induced obesity in mice with targeted muscle- specific overexpression of LPL (MCKhLPL). Of interest, despite the reduction in plasma free fatty acids and triglycerides in MCKhLPL mice, muscle triglycerides were increased and insulin sensitivity decreased. This raises important questions about the contribution of LPL to fatty acid metabolism in muscle. In the current application, a series of related studies will be implemented to pursue the mechanisms by which LPL overexpression in muscle favorably alters body composition, but results in triglyceride accumulation in muscle and reductions in insulin sensitivity. In addition, a combined in vivo and in vitro approach will be used. Investigations will focus on the following hypotheses, that: 1) deprivation of energy intake, reductions in ambient temperature and exercise will modify energy expenditure and reduce adipose tissue mass more in MCKhLPL mice than controls, and that these perturbations will also affect the phenotype of female MCKhLPL mice, previously unaffected by LPL overexpression in skeletal muscle; and 2) in mice and in cultured C2C12 myoblasts stably transfected with LPL, that LPL will partition lipoprotein fatty acids preferentially to pathways of esterification prior to oxidation. Overall, these studies should provide new and important insights into the physiology of LPL in muscle, and how enhancing LPL expression in muscle affects fatty acid and triglyceride metabolism in muscle, insulin action and body composition. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ENZYME
TNFALPHA-LIPOPROTEIN
CONTROL
OF A
SURFACTANT
Principal Investigator & Institution: Mallampalli, Rama K.; Professor; Internal Medicine; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 31-MAY-2005 Summary: Surfactant, a surface-active mixture comprised of phosphatidylcholine (PC) and key hydrophobic proteins, is deficient in acute lung injury. The cytokine tumor necrosis factor alpha (TNFalpha),-plays a key role in the pathogenesis of sepsis-induced lung injury and decreases levels of surfactant PC. The major question addressed in this proposal is how TNFalpha decreases PC content. Previous studies have shown that TNFalpha decreases PC by increasing PC degradation. This proposal will address a complementary paradigm that TNFalpha decreases PC synthesis. The synthesis of PC is tightly regulated in cells by the rate-regulatory enzyme cytidylyltransferase (CT). CT is activated by fatty acids, but inhibited by other lipids such as ceramide and sphingosine. CT activity is also inhibited by enzyme phosphorylation induced by mitogen-activated protein (MAP) kinases. One effect of TNFalpha is the generation of ceramide derived from sphingomyelin (SM) hydrolysis. TNFalpha also activates multiple MAP kinase
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pathways, including the p42/44 MAP pathway. Ceramide rapidly deacylates to sphingosine, and sphingosine can trigger p42/44 MAP kinase activation. Further, ceramide activates cell proteases, which might degrade the CT enzyme. These observations led to the overall hypothesis that TNFalpha inhibits surfactant PC synthesis, in part, by decreasing CT activity via generation of the inhibitory lipid, ceramide. In this proposal, we will determine if the negative effects of TNFalpha on CT activity are due to induction of ceramide, and/or activation of the p42/44 MAP kinase (AIM 1), or ceramide-induced alteration of CT protein stability (AIM 2). We will also determine if fatty acids can counteract TNFalpha inhibitory effects as they stimulate CT activity and surfactant production in vitro. However, because exogenous fatty acids have mixed success and are potentially toxic in vivo, we will use a new strategy to counteract TNFalpha effects by administering very low-density lipoproteins (VLDL) with lipoprotein lipase (LPL). VLDL triglycerides are hydrolyzed to fatty acids by LPL. We will determine if activation of CT by VLDL and LPL is mediated by altering specific fatty acids or sphingolipids, and if these effects of lipoprotein pretreatment oppose inhibition of CT by TNFalpha (AIM 3). Our hypothesis will be tested by in vivo administration of TNFalpha and VLDL with analysis conducted in primary adult type II alveolar epithelial cells. These in vivo studies will be supplemented with a TNFalpha and lipoprotein-responsive type II (MLE-12) cell line. The unique contributions of this proposal impacting the field of surfactant metabolism include 1) delineation of a novel effector pathway linking TNFalpha-signaling with surfactant synthesis (AIM 1) 2) studies investigating CT protein stability which represent a new regulatory mechanism for this key surfactant enzyme (AIM 2) and 3) studies with potential clinical application by which lipoproteins modulate surfactant synthesis in the setting of cytokine-induced acute lung injury (AIM 3). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSCRIPTION FACTOR FUNCTION IN CHROMATIN Principal Investigator & Institution: Imbalzano, Anthony N.; Cell Biology; Univ of Massachusetts Med Sch Worcester Office of Research Funding Worcester, Ma 01655 Timing: Fiscal Year 2002; Project Start 01-AUG-1997; Project End 31-JUL-2006 Summary: (provided by applicant): To understand normal development and differentiation, it is necessary to determine the mechanisms by which cells initiate new programs of gene expression and promote formation of specific cell lineages. Typically, this involves activation of genes that are transcriptionally silent and that may be incorporated into repressive chromatin structure. Evidence supports the idea that differentiation specific transcriptional regulators and enzymes that remodel chromatin structure cooperate to render genomic DNA more accessible to the transcriptional machinery. SWI/SNF enzymes alter nucleosome structure in an ATP dependent manner and facilitate transcription factor function in vitro and in vivo. Components of these enzymes are essential for embryonic development and some act as tumor suppressors. Additionally, SWI/SNF enzymes interact with other known tumor suppressors and are implicated in cell cycle control. Thus these enzymes are broadly required for normal cell function and their misregulation is implicated in tumor formation.We recently demonstrated a requirement for SWI/SNF enzymes in the initiation of skeletal muscle and adipocyte differentiation. Skeletal muscle differentiation has long been a model for studying fundamental principles of differentiation. Understanding skeletal muscle differentiation at a molecular level will have significant implications for investigating muscle regeneration and the formation of rhabdomyosarcomas, which are tumors of myogenic derivation. Adipocytes are a central component of the energy balance system
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in mammals. They store triglycerides during periods of nutritional abundance and release free fatty acids during periods of caloric deficiency. In humans, excessive development of adipocyte tissue, or obesity, affects 30 percent of the adults in the U.S. This population is at significantly increased risk for non-insulin dependent diabetes, coronary artery disease, and hypertension. Characterization of the molecular events that initiate and regulate adipocyte differentiation is therefore also an important medical concern. The goals of Aims 1 and 2 are to understand the mechanisms by which SWI/SNF chromatin remodeling enzymes promote development and differentiation, with emphasis on how SWI/SNF enzymes and key transcriptional regulators initiate new programs of gene expression. Aim 3 will probe the generality of the requirement for SWI/SNF enzymes in different differentiation pathways and embryogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSLOCATION, ASSEMBLY, AND DEGRADATION OF APOB Principal Investigator & Institution: Chuck, Steven L.; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-MAR-2003 Summary: Apolipoprotein (apoB) is secreted from liver and intestine only in association with cholesterol and triglycerides as lipoprotein particles (VLDL or chylomicrons). Since the secretion of cholesterol and apo B are coupled, an understanding of the regulation of the secretion of apo B might lead to new interventions that reduce plasma cholesterol levels. The balance between assembly and degradation accounts for the primary regulation of apo B secretion. Assembly of apo B-containing lipoprotein particles in hepatic and intestinal cells appears to occur in the endoplasmic reticulum and Golgi apparatus. Intracellular degradation of newly-synthesized apo B occurs in different locations depending on the species: in HepG2 cells, apoB at the ER is degraded, whereas in rat hepatocytes, degradation of apoB occurs after it has trafficked to the golgi. The molecular mechanisms by which apo B is sorted for assembly or degradation is not known. Translocation into the endoplasmic reticulum is one step at which regulation occurs: some molecules of apoB are bound by ubiquitin while in the Sec61 complex. The sequences in apoB and the cellular proteins that mediate this early regulatory step will be identified and characterized. Other proteins that participate in the assembly or degradation of apoB also will be sought. The overall goal of these studies is to develop a molecular view of the assembly and degradation of apo B and other secretory proteins. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TRIGLYCERIDE SYNTHESIS AND LIPOTOXICITY Principal Investigator & Institution: Farese, Robert V.; Associate Investigator; J. David Gladstone Institutes 365 Vermont St San Francisco, Ca 94103 Timing: Fiscal Year 2003; Project Start 15-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): The obesity epidemic is threatening world health, largely because of its associated diseases, type 2 diabetes mellitus and atherosclerosis. Although the mechanisms underlying obesity-associated diseases are unclear, the lipotoxicity hypothesis has emerged as a plausible explanation. This hypothesis states that the deposition of excess lipids in tissues other than white adipose tissue over time leads to tissue dysfunction. For example, lipid deposition in skeletal muscle is associated with insulin resistance, in pancreatic beta cells with defective insulin secretion, and in heart muscle with cardiomyopathy. Despite these strong associations from studies in
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animals and humans, the lipotoxicity hypothesis remains unproven, and its underlying mechanisms remain unclear. Whether triglycerides themselves or precursors of triglyceride synthesis (e.g., diacylglycerol and fatty acyl CoAs) are toxic to nonadipose cells is unclear. We propose to test the lipotoxicity hypothesis by directly modulating triglyceride synthesis in specific tissues of mice. Triglyceride synthesis is catalyzed by acyl CoA:diacylglycerol (DGAT) enzymes. Aim 1 describes the generation and analysis of mice that overexpress DGAT1 in skeletal muscle, pancreatic beta cells, and cardiac muscle. Aim 2 describes the generation and analysis of mice that lack DGAT1 in skeletal muscle, beta cells, and white adipose tissue. We will use these mouse models to determine whether modulating triglyceride synthesis influences tissue lipotoxicity and to explore the mechanisms, including alterations in tissue lipids, gene expression, and signaling pathways, that contribute to lipotoxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: VLDL AND LDL PARTICLE TYPES AS CHD RISK FACTORS Principal Investigator & Institution: Sacks, Frank M.; Associate Professor; Nutrition; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2003; Project Start 28-JUL-2003; Project End 30-JUN-2007 Summary: (provided by applicant): Plasma triglyceride concentration is an independent although relatively weak risk factor for coronary heart disease (CHD). The relative weakness of plasma triglycerides to predict CHD may be due to the substantial diversity of lipoprotein particles that carry the triglycerides, some being related to atherosclerosis and CHD more than others. We have shown in patients who have had a myocardial infarction that the rather weak association between triglycerides and subsequent coronary events is secondary to a stronger relationship with specific types of VLDL remnants, those in the LDL density range that contain apoCIIl. This application seeks to extend these findings to initial coronary events in patients who do not have CHD. The Primary Specific Aim will evaluate VLDL and LDL particle types as predictors of initial coronary events in men from the Health Professional Follow-up Study (HPFS) and women from the Nurses' Health Study (NHS). A prospective nested case-control design will be used with a total of 1000 CHD cases and 1000 matched controls, with equal numbers of men and women. We will specifically investigate the role of apoCIII containing VLDL and LDL particles in diabetes by over sampling so that 50% of the patients will have type 2 diabetes mellitus. Our previous work shows that LDL apoCIII particles are independent predictors of recurrent CHD in diabetic patients who survived a myocardial infarction. We hypothesize that apoCIII may have a special role in dyslipidemia and CHD in diabetes. Secondary Aims: Besides apoCIII, other small apolipoproteins, apo C1, CII, and All are components of VLDL and LDL and modulate the metabolism of apoB lipoproteins. It is likely that these apolipoproteins have a relationship with human atherosclerosis. We will measure these apolipoproteins in VLDL and LDL and evaluate their relationship to CHD. We will also investigate the associations between these new lipoprotein risk factors and intake of foods and nutrients, physical activity, and other risk factors, including smoking, BMI, age and gender. The results will provide new means to identify nondiabetic and diabetic persons who are at high risk of developing CHD and the environmental determinants, and could form the basis for new lipoprotein targets for lipid management by diet and medicines. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: WISCONSIN EPIDEMIOLOGICAL STUDY OF CARDIOVASCULAR DISEAS Principal Investigator & Institution: Klein, Ronald; Professor; Ophthalmology and Visual Sci; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2001; Project Start 01-FEB-1999; Project End 31-JAN-2003 Summary: This proposal describes a population-based cohort aimed at determining the prevalence and incidence of cardiovascular disease morbidity and mortality in people with Type 1 diabetes of long-duration. For this epidemiologic study, subjects include all insulin-taking persons who: (1) were less than 30 years of age at the time of their diagnosis, (2) had received primary medical care in an 11-county area of south-central Wisconsin, and (3) were first identified in 1979-80. Standardized protocols for examinations and interviews have been employed during the baseline, 4-, 10-, and 14year follow up examinations. Refusal rates have been low. The mean age of the cohort and the long duration of diabetes provide an opportunity to document the prevalence and incidence of coronary heart disease, myocardial infarction, angina, congestive heart failure, stroke, transient ischemic attacks, peripheral vascular disease, and cardiovascular disease mortality in a large population-based group of persons with Type 1 diabetes. Retinal photographs of each study participant were taken at the baseline examination. This will permit us to test the predictive ability of focal and generalized retinal arteriolar narrowing and arterio-venous cross changes (i.e. A/V nicking) for subsequent macrovascular events controlling for other risk factors. These factors include blood pressure, cigarette smoking, serum lipids, body mass index, duration of diabetes, and glycemia. We plan to reexamine this cohort to obtain ECGs, blood lipid fractions not previously measured, and fibrinogen, as well as upper and lower extremity blood pressures, urine specimens, and medical records. This will provide information about silent about silent infarctions and other cardiographic abnormalities as well as previously doctor-diagnosed macrovascular events in longterm survivors of Type 1 diabetes. Study examinations will be performed in a mobile van. Participants will provide two urine specimens for determination of urinary albumin excretion. Fasting blood will be obtained for determination of glycosylated hemoglobin Alc, blood sugar, serum cholesterol, triglycerides, HDL- cholesterol, LDLcholesterol, VDL-cholesterol, LDL particle size, serum creatinine, and fibrinogen. Additional study procedures include measurements of weight and height, waist and hip girth, and brachial and ankle blood pressures. Electrocardiography will also be performed. A questionnaire will be administered Participants will subsequently be interviewed yearly and clinical and hospital records and death certificates will be collected to document new cardiovascular disease events. Findings regarding the prevalence and incidence of cardiovascular disease and associated risk factors will be of great public health importance in directing further at preventing these conditions in people with Type 1 diabetes of long duration. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: XALD: ROLE OF VERY LONG CHAIN FATTY ACYL-COA SYNTHETASES Principal Investigator & Institution: Watkins, Paul A.; Associate Professor; Kennedy Krieger Research Institute, Inc. Baltimore, Md 21205 Timing: Fiscal Year 2003; Project Start 01-FEB-1999; Project End 31-JAN-2007 Summary: (provided by applicant): Acyl-CoA synthetases (ACS) occupy a central position in fatty acid metabolism. For incorporation into phospholipids, triglycerides, or
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cholesterol esters, elongation, desaturation, degradation by b-oxidation, or acylation of proteins, a fatty acid must first be activated to its CoA thioester. Despite this vital function, only recently have the precise roles in metabolism of the numerous mammalian ACSs begun to be investigated. We have grouped ACSs by amino acid sequence similarity into at least six families. Two human and mouse ACS families, the very long-chain ACS (VLACS) family and a recently discovered ACS family that includes the BG gene (mutated in the fruit fly mutant "bubblegum") contain enzymes capable of activating very long-chain fatty acids (VLCFA; containing >22 carbons). VLCFA are essential components of complex lipids, particularly in the brain, and maintenance of VLCFA homeostasis is critical to normal health. Thus, enzymes that control the fate of VLCFA by any of the pathways noted above are of central importance. VLCFA accumulate in plasma and tissues of patients with X-linked adrenoleukodystrophy (XALD), a severe, often fatal neurodegenerative disorder. Defective VLCFA degradation via peroxisomal b-oxidation and decreased VLACS activity in peroxisomes have been implicated in the biochemical pathology of XALD. However, the gene defective in XALD, ABCD1, encodes ALDP, a peroxisomal protein of the ATP-binding cassette transmembrane transporter superfamily that has no VLACS activity. The VLACS and BG families contain a total of 8 enzymes. To understand overall VLCFA homeostasis, we must therefore understand the specific function of each of these enzymes. Therefore, we propose: 1) to develop a novel and generally applicable ACS assay, 2) to investigate the specific biological roles of human VLACSs, and 3) to characterize the BG1 knockout mouse and to assess the role of BG1 in XALD. Results of these studies will have a significant impact on our understanding of how fatty acids are channeled into specific metabolic pathways. Furthermore, they will facilitate elucidation of the role of enzymes belonging to the VLACS or BG families in XALD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ZEBRAFISH ASSAY FOR CHOLESTEROL AND LIPID LOWERING DRUGS Principal Investigator & Institution: Rubinstein, Amy L.; Zygogen, Llc Kell Hall 520 Atlanta, Ga 303033003 Timing: Fiscal Year 2003; Project Start 15-JUN-2003; Project End 31-MAY-2004 Summary: (provided by applicant): High levels of low density lipoprotein (LDL), cholesterol and triglycerides have been associated with an increase in cardiovascular disease. Drugs such as cholesterol-lowering statins and triglyceride-lowering fibrates have led to a reduction in coronary heart disease. Although current drugs have enjoyed some success, a need exists for improved lipid management and reduced side effects. Zygogen is developing a novel in vivo approach to identifying potential lipid-lowering drugs using Zebrafish, called Z-Lipotrack. Lipid processing is highly conserved in the Zebrafish. Because Zebrafish larvae are essentially transparent, lipid processing can be readily observed in the whole organism, with the aid of fluorescent lipid reporters. The goal of the proposed research is to develop Z-Lipotrack technology for use in high throughput compound screening, with the ultimate aim of discovering better drugs for lowering lipid levels. The proposed work will validate Z-Lipotrack as a compound screening tool. This includes testing additional control compounds, characterizing compounds identified in a small but diverse library of marketed drugs, and quantifying the fluorescent read-out in an automated fashion. Due to the high fecundity of Zebrafish, high throughput drug screening using Zebrafish larvae is feasible and could dramatically increase the chances of finding important new drugs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “triglycerides” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for triglycerides in the PubMed Central database: •
An Inhibitor of the Microsomal Triglyceride Transfer Protein Inhibits apoB Secretion from HepG2 Cells. by Jamil H, Gordon DA, Eustice DC, Brooks CM, Dickson JK, Chen Y, Ricci B, Chu C, Harrity TW, Ciosek CP, Biller SA, Gregg RE, Wetterau JR.; 1996 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38171
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Another hormone-sensitive triglyceride lipase in fat cells? by Saltiel AR.; 2000 Jan 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33961
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Apolipoprotein C3 SstI polymorphism and triglyceride levels in Asian Indians. by Chhabra S, Narang R, Krishnan LR, Vasisht S, Agarwal DP, Srivastava LM, Manchanda SC, Das N.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=116591
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Bioconversion of Xylan to Triglycerides by Oil-Rich Yeasts. by Fall R, Phelps P, Spindler D.; 1984 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=240078
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Consistency of genetic inheritance mode and heritability patterns of triglyceride vs. high density lipoprotein cholesterol ratio in two Taiwanese family samples. by Chien KL, Hsu HC, Su TC, Yang CY, Lee YT.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=155683
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Control of triglyceride synthesis by the intracellular level of long-chain acyl coenzyme A for lipid synthesis. by Kamiryo T.; 1983 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=215106
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Correlation of Propionibacterium acnes Populations with the Presence of Triglycerides on Nonhuman Skin. by Webster GF, Ruggieri MR, McGinley KJ.; 1981 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243900
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Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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Degradation of triglycerides by a pseudomonad isolated from milk: molecular analysis of a lipase-encoding gene and its expression in Escherichia coli. by Johnson LA, Beacham IR, MacRae IC, Free ML.; 1992 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=195672
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Direct antidiabetic effect of leptin through triglyceride depletion of tissues. by Shimabukuro M, Koyama K, Chen G, Wang MY, Trieu F, Lee Y, Newgard CB, Unger RH.; 1997 Apr 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20776
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Genetic variants in Apolipoprotein AV alter triglyceride concentrations in pregnancy. by Ward KJ, Shields B, Knight B, Salzmann MB, Hattersley AT, Frayling TM.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=280668
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Genomic interval engineering of mice identifies a novel modulator of triglyceride production. by Zhu Y, Jong MC, Frazer KA, Gong E, Krauss RM, Cheng JF, Boffelli D, Rubin EM.; 2000 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15548
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Induced mutant mouse lines that express lipoprotein lipase in cardiac muscle, but not in skeletal muscle and adipose tissue, have normal plasma triglyceride and highdensity lipoprotein-cholesterol levels. by Levak-Frank S, Hofmann W, Weinstock PH, Radner H, Sattler W, Breslow JL, Zechner R.; 1999 Mar 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15913
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Lipolysis of triglyceride-rich lipoproteins generates PPAR ligands: Evidence for an antiinflammatory role for lipoprotein lipase. by Ziouzenkova O, Perrey S, Asatryan L, Hwang J, MacNaul KL, Moller DE, Rader DJ, Sevanian A, Zechner R, Hoefler G, Plutzky J.; 2003 Mar 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151409
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Managing hypertriglyceridemia. by Fung MA, Frohlich JJ.; 2003 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151985
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Managing hypertriglyceridemia. by Mercola J.; 2003 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151984
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Palmitoylation of Apolipoprotein B Is Required for Proper Intracellular Sorting and Transport of Cholesteroyl Esters and Triglycerides. by Zhao Y, McCabe JB, Vance J, Berthiaume LG.; 2000 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=14805
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Relationships Between the Responses of Triglyceride-Rich Lipoproteins in Blood Plasma Containing Apolipoproteins B-48 and B-100 to a Fat-Containing Meal in Normolipidemic Humans. by Schneeman BO, Kotite L, Todd KM, Havel RJ.; 1993 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46022
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Treatment of cardiomyopathy and rhabdomyolysis in long-chain fat oxidation disorders using an anaplerotic odd-chain triglyceride. by Roe CR, Sweetman L, Roe DS, David F, Brunengraber H.; 2002 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151060
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Triglyceride accumulation protects against fatty acid-induced lipotoxicity. by Listenberger LL, Han X, Lewis SE, Cases S, Farese RV Jr, Ory DS, Schaffer JE.; 2003 Mar 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152249
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with triglycerides, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “triglycerides” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for triglycerides (hyperlinks lead to article summaries): •
A 52-week, multicenter, randomized, parallel-group, double-blind, double-dummy study to assess the efficacy of atorvastatin and simvastatin in reaching low-density lipoprotein cholesterol and triglyceride targets: the treat-to-target (3T) study. Author(s): Olsson AG, Eriksson M, Johnson O, Kjellstrom T, Lanke J, Larsen ML, Pedersen T, Tikkanen MJ, Wiklund O; 3T Study Investigators. Source: Clinical Therapeutics. 2003 January; 25(1): 119-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637115&dopt=Abstract
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Accumulation of 3-hydroxy-fatty acids in the culture medium of long-chain L-3hydroxyacyl CoA dehydrogenase (LCHAD) and mitochondrial trifunctional proteindeficient skin fibroblasts: implications for medium chain triglyceride dietary treatment of LCHAD deficiency. Author(s): Jones PM, Butt Y, Bennett MJ. Source: Pediatric Research. 2003 May; 53(5): 783-7. Epub 2003 March 05. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12621125&dopt=Abstract
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Allergic contact dermatitis from medium-chain triglycerides in a moisturizing lotion. Author(s): Laube S, Davies MG, Prais L, Foulds IS. Source: Contact Dermatitis. 2002 September; 47(3): 171. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492556&dopt=Abstract
6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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An enteral therapy containing medium-chain triglycerides and hydrolyzed peptides reduces postprandial pain associated with chronic pancreatitis. Author(s): Shea JC, Bishop MD, Parker EM, Gelrud A, Freedman SD. Source: Pancreatology : Official Journal of the International Association of Pancreatology (Iap). [et Al.]. 2003; 3(1): 36-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649562&dopt=Abstract
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Angiopoietin-like protein 3 mediates hypertriglyceridemia induced by the liver X receptor. Author(s): Inaba T, Matsuda M, Shimamura M, Takei N, Terasaka N, Ando Y, Yasumo H, Koishi R, Makishima M, Shimomura I. Source: The Journal of Biological Chemistry. 2003 June 13; 278(24): 21344-51. Epub 2003 April 01. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672813&dopt=Abstract
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Angiotensin-converting enzyme insertion/deletion genotype is associated with the activities of plasma coagulation factor VII and X independent of triglyceride metabolism. Author(s): Okura Y, Hayashi K, Shingu T, Kuga Y, Nomura S, Kajiyama G, Nakashima Y, Saku K. Source: Coronary Artery Disease. 2003 June; 14(4): 285-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826927&dopt=Abstract
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Apolipoprotein A5, a crucial determinant of plasma triglyceride levels, is highly responsive to peroxisome proliferator-activated receptor alpha activators. Author(s): Vu-Dac N, Gervois P, Jakel H, Nowak M, Bauge E, Dehondt H, Staels B, Pennacchio LA, Rubin EM, Fruchart-Najib J, Fruchart JC. Source: The Journal of Biological Chemistry. 2003 May 16; 278(20): 17982-5. Epub 2003 March 12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637506&dopt=Abstract
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Apolipoprotein CIII and highly active antiretroviral therapy (HAART)-induced hypertriglyceridemia. Author(s): Badiou S, Dupuy AM, Baillat V, Fabre J, Tur MD, Cristol JP, Reynes J. Source: Clin Lab. 2003; 49(1-2): 11-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12593470&dopt=Abstract
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Apolipoprotein H variant modifies plasma triglyceride phenotype in familial hypercholesterolemia: a molecular study in an eight-generation hyperlipidemic family. Author(s): Takada D, Ezura Y, Ono S, Iino Y, Katayama Y, Xin Y, Wu LL, LarringaShum S, Stephenson SH, Hunt SC, Hopkins PN, Emi M. Source: J Atheroscler Thromb. 2003; 10(2): 79-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12740481&dopt=Abstract
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Ask the doctor. At age 62 I'm a bit overweight and have diabetes. I take a statin, and my LDL cholesterol is good (84 mg/dL). But my HDL is low (30 mg/dL) and my triglycerides are above 300 mg/dL. Are high triglycerides a problem? Author(s): Lee TH. Source: Harvard Heart Letter : from Harvard Medical School. 2003 March; 13(7): 8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12654588&dopt=Abstract
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Assessment of LDL particle size by triglyceride/HDL-cholesterol ratio in nondiabetic, healthy subjects without prominent hyperlipidemia. Author(s): Maruyama C, Imamura K, Teramoto T. Source: J Atheroscler Thromb. 2003; 10(3): 186-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14564088&dopt=Abstract
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Association of prothrombin and protein S with plasma triglyceride-rich lipoproteins in humans after test meals rich in milk fat or soybean oil. Author(s): Zhou L, Xu N, Nilsson A. Source: Thrombosis Research. 2002 November 25; 108(4): 209-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12617983&dopt=Abstract
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Association of the endotoxin antagonist E5564 with high-density lipoproteins in vitro: dependence on low-density and triglyceride-rich lipoprotein concentrations. Author(s): Wasan KM, Sivak O, Cote RA, MacInnes AI, Boulanger KD, Lynn M, Christ WJ, Hawkins LD, Rossignol DP. Source: Antimicrobial Agents and Chemotherapy. 2003 September; 47(9): 2796-803. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12936976&dopt=Abstract
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Atorvastatin enhances the plasma clearance of chylomicron-like emulsions in subjects with atherogenic dyslipidemia: relevance to the in vivo metabolism of triglyceride-rich lipoproteins. Author(s): Sposito AC, Santos RD, Amancio RF, Ramires JA, Chapman MJ, Maranhao RC. Source: Atherosclerosis. 2003 February; 166(2): 311-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12535744&dopt=Abstract
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Beneficial effect of icodextrin on the hypertriglyceridemia of CAPD patients. Author(s): Sisca S, Maggiore U. Source: Perit Dial Int. 2002 November-December; 22(6): 727-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12556078&dopt=Abstract
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Cholesterol lipoproteins, triglycerides, rural-urban differences and prevalence of dyslipidaemia among males in Rajasthan. Author(s): Gupta R, Prakash H, Kaul V. Source: J Assoc Physicians India. 1997 April; 45(4): 275-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12521083&dopt=Abstract
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Comparison of triglycerides and phospholipids as supplemental sources of dietary long-chain polyunsaturated fatty acids in piglets. Author(s): Mathews SA, Oliver WT, Phillips OT, Odle J, Diersen-Schade DA, Harrell RJ. Source: The Journal of Nutrition. 2002 October; 132(10): 3081-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12368399&dopt=Abstract
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Consumption of a functional oil rich in phytosterols and medium-chain triglyceride oil improves plasma lipid profiles in men. Author(s): St-Onge MP, Lamarche B, Mauger JF, Jones PJ. Source: The Journal of Nutrition. 2003 June; 133(6): 1815-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771322&dopt=Abstract
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Contribution of APOA5 gene variants to plasma triglyceride determination and to the response to both fat and glucose tolerance challenges. Author(s): Martin S, Nicaud V, Humphries SE, Talmud PJ; EARS group. Source: Biochimica Et Biophysica Acta. 2003 April 17; 1637(3): 217-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12697303&dopt=Abstract
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Coronary artery disease risk in familial combined hyperlipidemia and familial hypertriglyceridemia: a case-control comparison from the National Heart, Lung, and Blood Institute Family Heart Study. Author(s): Hopkins PN, Heiss G, Ellison RC, Province MA, Pankow JS, Eckfeldt JH, Hunt SC. Source: Circulation. 2003 August 5; 108(5): 519-23. Epub 2003 July 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847072&dopt=Abstract
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Coronary heart disease in women: triglycerides and lipoprotein biology. Author(s): Dayspring TD. Source: J Gend Specif Med. 2002 September-October; 5(5): 27-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12380198&dopt=Abstract
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Effect of atorvastatin on lipid parameters, LDL subtype distribution, hemorrheological parameters and adhesion molecule concentrations in patients with hypertriglyceridemia. Author(s): Empen K, Geiss HC, Lehrke M, Otto C, Schwandt P, Parhofer KG. Source: Nutr Metab Cardiovasc Dis. 2003 April; 13(2): 87-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12929621&dopt=Abstract
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Effect of desirable fasting triglycerides on the postprandial response to dietary fat. Author(s): Miller M, Zhan M, Georgopoulos A. Source: Journal of Investigative Medicine : the Official Publication of the American Federation for Clinical Research. 2003 February; 51(1): 50-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580321&dopt=Abstract
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Effect of medium-chain triglycerides on the postprandial triglyceride concentration in healthy men. Author(s): Kasai M, Maki H, Nosaka N, Aoyama T, Ooyama K, Uto H, Okazaki M, Igarashi O, Kondo K. Source: Bioscience, Biotechnology, and Biochemistry. 2003 January; 67(1): 46-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12619672&dopt=Abstract
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Effect of xuezhikang, a cholestin extract, on reflecting postprandial triglyceridemia after a high-fat meal in patients with coronary heart disease. Author(s): Zhao SP, Liu L, Cheng YC, Li YL. Source: Atherosclerosis. 2003 June; 168(2): 375-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801622&dopt=Abstract
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Effects of a brisk walk on lipoprotein lipase activity and plasma triglyceride concentrations in the fasted and postprandial states. Author(s): Gill JM, Herd SL, Vora V, Hardman AE. Source: European Journal of Applied Physiology. 2003 April; 89(2): 184-90. Epub 2003 February 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665983&dopt=Abstract
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Effects of a high-sucrose diet on body weight, plasma triglycerides, and stress tolerance. Author(s): Kanazawa M, Xue CY, Kageyama H, Suzuki E, Ito R, Namba Y, Osaka T, Kimura S, Inoue S. Source: Nutrition Reviews. 2003 May; 61(5 Pt 2): S27-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828189&dopt=Abstract
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Effects of atorvastatin on glucose homeostasis, postprandial triglyceride response and C-reactive protein in subjects with impaired fasting glucose. Author(s): Costa A, Casamitjana R, Casals E, Alvarez L, Morales J, Masramon X, Hernandez G, Gomis R, Conget I. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 2003 September; 20(9): 743-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925055&dopt=Abstract
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Effects of baseline level of triglycerides on changes in lipid levels from combined fluvastatin + fibrate (bezafibrate, fenofibrate, or gemfibrozil). Author(s): Farnier M, Salko T, Isaacsohn JL, Troendle AJ, Dejager S, Gonasun L. Source: The American Journal of Cardiology. 2003 October 1; 92(7): 794-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14516878&dopt=Abstract
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Effects of estrogen and medroxyprogesterone acetate on subpopulations of triglyceride-rich lipoproteins and high-density lipoproteins. Author(s): Lamon-Fava S, Posfai B, Asztalos BF, Horvath KV, Dallal GE, Schaefer EJ. Source: Metabolism: Clinical and Experimental. 2003 October; 52(10): 1330-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14564686&dopt=Abstract
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Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride. Author(s): Jurgens G, Graudal NA. Source: Cochrane Database Syst Rev. 2003; (1): Cd004022. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12535503&dopt=Abstract
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Effects of short-term detraining on postprandial metabolism, endothelial function, and inflammation in endurance-trained men: dissociation between changes in triglyceride metabolism and endothelial function.
[email protected]. Author(s): Gill JM, Caslake MJ, McAllister C, Tsofliou F, Ferrell WR, Packard CJ, Malkova D. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 September; 88(9): 4328-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970306&dopt=Abstract
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Effects of simvastatin, an HMG-CoA reductase inhibitor, in patients with hypertriglyceridemia. Author(s): Isaacsohn J, Hunninghake D, Schrott H, Dujovne CA, Knopp R, Weiss SR, Bays H, Crouse JR 3rd, Davidson MH, Keilson LM, McKenney J, Korenman SG, Dobs AS, Stein E, Krauss RM, Maccubbin D, Cho M, Plotkin DJ, Mitchel YB. Source: Clin Cardiol. 2003 January; 26(1): 18-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12539808&dopt=Abstract
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Elevated triglyceride and decreased high density lipoprotein level in carbon disulfide workers in Taiwan. Author(s): Luo JC, Chang HY, Chang SJ, Chou TC, Chen CJ, Shih TS, Huang CC. Source: Journal of Occupational and Environmental Medicine / American College of Occupational and Environmental Medicine. 2003 January; 45(1): 73-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553181&dopt=Abstract
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Elevated triglycerides and low levels of high-density lipoprotein as markers of disease activity in association with up-regulation of the tumor necrosis factor alpha/tumor necrosis factor receptor system in systemic lupus erythematosus. Author(s): Svenungsson E, Gunnarsson I, Fei GZ, Lundberg IE, Klareskog L, Frostegard J. Source: Arthritis and Rheumatism. 2003 September; 48(9): 2533-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13130473&dopt=Abstract
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Expression of human hepatic lipase in the rabbit model preferentially enhances the clearance of triglyceride-enriched versus native high-density lipoprotein apolipoprotein A-I. Author(s): Rashid S, Trinh DK, Uffelman KD, Cohn JS, Rader DJ, Lewis GF. Source: Circulation. 2003 June 24; 107(24): 3066-72. Epub 2003 Jun 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796142&dopt=Abstract
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Fasting and daylong triglycerides in obesity with and without type 2 diabetes. Author(s): van Wijk JP, Halkes CJ, Erkelens DW, Castro Cabezas M. Source: Metabolism: Clinical and Experimental. 2003 August; 52(8): 1043-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898471&dopt=Abstract
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Fatty acids composition of plasma phospholipids and triglycerides in children with cystic fibrosis. The effect of dietary supplementation with an olive and soybean oils mixture. Author(s): Caramia G, Cocchi M, Gagliardini R, Malavolta M, Mozzon M, Frega NG. Source: Pediatr Med Chir. 2003 January-February; 25(1): 42-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12920976&dopt=Abstract
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Fatty liver in familial hypobetalipoproteinemia: triglyceride assembly into VLDL particles is affected by the extent of hepatic steatosis. Author(s): Schonfeld G, Patterson BW, Yablonskiy DA, Tanoli TS, Averna M, Elias N, Yue P, Ackerman J. Source: Journal of Lipid Research. 2003 March; 44(3): 470-8. Epub 2002 December 01. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562873&dopt=Abstract
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Flow injection chemiluminescent assays for glycerol and triglycerides using a coimmobilized enzyme reactor. Author(s): Yaqoob M, Nabi A. Source: Luminescence : the Journal of Biological and Chemical Luminescence. 2003 March-April; 18(2): 67-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687625&dopt=Abstract
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Fractional esterification rate of cholesterol and ratio of triglycerides to HDLcholesterol are powerful predictors of positive findings on coronary angiography. Author(s): Frohlich J, Dobiasova M. Source: Clinical Chemistry. 2003 November; 49(11): 1873-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14578319&dopt=Abstract
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GLUT4 expression in human muscle fibres is not correlated with intracellular triglyceride (TG) content. Is TG a maker or a marker of insulin resistance? Author(s): Gaster M, Ottosen PD, Vach W, Christiansen H, Staehr P, Beck-Nielsen H, Schroder HD. Source: Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica. 2003 February; 111(2): 338-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716391&dopt=Abstract
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Glycerol metabolism and the determination of triglycerides--clinical, biochemical and molecular findings in six subjects. Author(s): Hellerud C, Burlina A, Gabelli C, Ellis JR, Nyholm PG, Lindstedt S. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2003 January; 41(1): 46-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12636049&dopt=Abstract
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Glyceroneogenesis and the triglyceride/fatty acid cycle. Author(s): Reshef L, Olswang Y, Cassuto H, Blum B, Croniger CM, Kalhan SC, Tilghman SM, Hanson RW. Source: The Journal of Biological Chemistry. 2003 August 15; 278(33): 30413-6. Epub 2003 June 04. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788931&dopt=Abstract
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HDL-C and triglyceride levels: relationship to coronary heart disease and treatment with statins. Author(s): Gaw A. Source: Cardiovascular Drugs and Therapy / Sponsored by the International Society of Cardiovascular Pharmacotherapy. 2003 January; 17(1): 53-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843687&dopt=Abstract
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Hepatocyte apoB-containing lipoprotein secretion is decreased by the grapefruit flavonoid, naringenin, via inhibition of MTP-mediated microsomal triglyceride accumulation. Author(s): Borradaile NM, de Dreu LE, Barrett PH, Behrsin CD, Huff MW. Source: Biochemistry. 2003 February 11; 42(5): 1283-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12564931&dopt=Abstract
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High triglycerides/low high-density lipoprotein cholesterol, ischemic electrocardiogram changes, and risk of ischemic heart disease. Author(s): Jeppesen J, Hein HO, Suadicani P, Gyntelberg F. Source: American Heart Journal. 2003 January; 145(1): 103-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12514661&dopt=Abstract
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High versus low medium chain triglyceride content of formula for promoting short term growth of preterm infants. Author(s): Klenoff-Brumberg HL, Genen LH. Source: Cochrane Database Syst Rev. 2003; (1): Cd002777. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12535437&dopt=Abstract
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High-density lipoprotein cholesterol and triglycerides as therapeutic targets for preventing and treating coronary artery disease. Author(s): Gotto AM Jr. Source: American Heart Journal. 2002 December; 144(6 Suppl): S33-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12486414&dopt=Abstract
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Hypertension and triglyceride catabolism: implications for the hemodynamic model of the metabolic syndrome. Author(s): Brook RD, Glazewski L, Rajagopalan S, Bard RL. Source: Journal of the American College of Nutrition. 2003 August; 22(4): 290-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12897043&dopt=Abstract
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Hypertriglyceridemia in patients with chronic renal failure: possible mechanisms. Author(s): Prinsen BH, de Sain-van der Velden MG, de Koning EJ, Koomans HA, Berger R, Rabelink TJ. Source: Kidney International. Supplement. 2003 May; (84): S121-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694325&dopt=Abstract
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Hypertriglyceridemia is associated with increased insulin resistance in subjects with normal glucose tolerance: evaluation in a large cohort of subjects assessed with the 1999 World Health Organization criteria for the classification of diabetes. Author(s): Moro E, Gallina P, Pais M, Cazzolato G, Alessandrini P, Bittolo-Bon G. Source: Metabolism: Clinical and Experimental. 2003 May; 52(5): 616-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759893&dopt=Abstract
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Hypertriglyceridemia-induced acute pancreatitis--treatment with heparin and insulin. Author(s): Monga A, Arora A, Makkar RP, Gupta AK. Source: Indian J Gastroenterol. 2003 May-June; 22(3): 102-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839385&dopt=Abstract
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Hypoadiponectinemia is associated with insulin resistance, hypertriglyceridemia, and fat redistribution in human immunodeficiency virus-infected patients treated with highly active antiretroviral therapy. Author(s): Addy CL, Gavrila A, Tsiodras S, Brodovicz K, Karchmer AW, Mantzoros CS. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 February; 88(2): 627-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574192&dopt=Abstract
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Impaired triglyceride tolerance in hemodialysis patients with different apolipoprotein E (apo E) isoforms. Author(s): Zahalkova J, Vaverkova H, Novotny D, Kosatikova Z. Source: Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2002 December; 146(2): 73-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12572901&dopt=Abstract
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Importance of high-density lipoprotein cholesterol and triglyceride levels in coronary heart disease. Author(s): Sprecher DL, Watkins TR, Behar S, Brown WV, Rubins HB, Schaefer EJ. Source: The American Journal of Cardiology. 2003 March 1; 91(5): 575-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12615263&dopt=Abstract
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Improvement of glycaemic control in type 2 diabetes: favourable changes in blood pressure, total cholesterol and triglycerides, but not in HDL cholesterol, fibrinogen, Von Willebrand factor and (pro)insulin. Author(s): Becker A, van der Does FE, van Hinsbergh VW, Heine RJ, Bouter LM, Stehouwer CD. Source: The Netherlands Journal of Medicine. 2003 April; 61(4): 129-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852722&dopt=Abstract
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In vitro and in vivo lipolysis of plasma triglycerides increases the resistance to oxidative modification of low-density lipoproteins. Author(s): Skoglund-Andersson C, Karpe F, Hellenius ML, Regnstrom J, Hamsten A, Tornvall P. Source: European Journal of Clinical Investigation. 2003 January; 33(1): 51-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492452&dopt=Abstract
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Incidence of pain after intravenous injection of a medium-/long-chain triglyceride emulsion of propofol. An observational study in 1375 patients. Author(s): Bachmann-Mennenga B, Ohlmer A, Heesen M. Source: Arzneimittel-Forschung. 2003; 53(9): 621-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14558435&dopt=Abstract
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Increased visceral fat and serum levels of triglyceride are associated with insulin resistance in Japanese metabolically obese, normal weight subjects with normal glucose tolerance. Author(s): Katsuki A, Sumida Y, Urakawa H, Gabazza EC, Murashima S, Maruyama N, Morioka K, Nakatani K, Yano Y, Adachi Y. Source: Diabetes Care. 2003 August; 26(8): 2341-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882859&dopt=Abstract
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Incremental area under response curve more accurately describes the triglyceride response to an oral fat load in both healthy and type 2 diabetic subjects. Author(s): Carstensen M, Thomsen C, Hermansen K. Source: Metabolism: Clinical and Experimental. 2003 August; 52(8): 1034-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898469&dopt=Abstract
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Indinavir did not further increase mean triglyceride levels in HIV-infected patients treated with nucleoside reverse transcriptase inhibitors: an analysis of three randomized clinical trials. Author(s): Rojas C, Coplan PM, Rhodes T, Robertson MN, DiNubile MJ, Guess HA. Source: Pharmacoepidemiology and Drug Safety. 2003 July-August; 12(5): 361-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12899109&dopt=Abstract
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Influence of prolonged endurance cycling and recovery diet on intramuscular triglyceride content in trained males. Author(s): van Loon LJ, Schrauwen-Hinderling VB, Koopman R, Wagenmakers AJ, Hesselink MK, Schaart G, Kooi ME, Saris WH. Source: American Journal of Physiology. Endocrinology and Metabolism. 2003 October; 285(4): E804-11. Epub 2003 June 03. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783774&dopt=Abstract
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Interaction effect of Serine447Stop variant of the lipoprotein lipase gene and C-514T variant of the hepatic lipase gene on serum triglyceride levels in young adults: the Bogalusa Heart Study. Author(s): Xin X, Srinivasan SR, Chen W, Boerwinkle E, Berenson GS. Source: Metabolism: Clinical and Experimental. 2003 October; 52(10): 1337-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14564687&dopt=Abstract
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Intravenous anti TNF-alpha antibody therapy leads to elevated triglyceride and reduced HDL-cholesterol levels in patients with rheumatoid and psoriatic arthritis. Author(s): Cauza E, Cauza K, Hanusch-Enserer U, Etemad M, Dunky A, Kostner K. Source: Wiener Klinische Wochenschrift. 2002 December 30; 114(23-24): 1004-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635469&dopt=Abstract
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Lipolysis of triglyceride-rich lipoproteins generates PPAR ligands: evidence for an antiinflammatory role for lipoprotein lipase. Author(s): Ziouzenkova O, Perrey S, Asatryan L, Hwang J, MacNaul KL, Moller DE, Rader DJ, Sevanian A, Zechner R, Hoefler G, Plutzky J. Source: Proceedings of the National Academy of Sciences of the United States of America. 2003 March 4; 100(5): 2730-5. Epub 2003 February 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12606719&dopt=Abstract
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Lipoprotein production by the heart: a novel pathway of triglyceride export from cardiomyocytes. Author(s): Nielsen LB. Source: Scand J Clin Lab Invest Suppl. 2002; 237: 35-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12570165&dopt=Abstract
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Low triglyceride, not low cholesterol concentration, independently predicts poor outcome following acute stroke. Author(s): Weir CJ, Sattar N, Walters MR, Lees KR. Source: Cerebrovascular Diseases (Basel, Switzerland). 2003; 16(1): 76-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12766366&dopt=Abstract
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Medium chain triglycerides as vehicle for palatable oral liquids. Author(s): Bahal SM, Romansky JM, Alvarez FJ. Source: Pharmaceutical Development and Technology. 2003; 8(1): 111-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665204&dopt=Abstract
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Medium- versus long-chain triglycerides for 27 days increases fat oxidation and energy expenditure without resulting in changes in body composition in overweight women. Author(s): St-Onge MP, Bourque C, Jones PJ, Ross R, Parsons WE. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 January; 27(1): 95-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532160&dopt=Abstract
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Medium-chain triglycerides increase energy expenditure and decrease adiposity in overweight men. Author(s): St-Onge MP, Ross R, Parsons WD, Jones PJ. Source: Obesity Research. 2003 March; 11(3): 395-402. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634436&dopt=Abstract
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Microsomal triglyceride transfer protein and its role in apoB-lipoprotein assembly. Author(s): Hussain MM, Shi J, Dreizen P. Source: Journal of Lipid Research. 2003 January; 44(1): 22-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12518019&dopt=Abstract
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Myocardial triglycerides and systolic function in humans: in vivo evaluation by localized proton spectroscopy and cardiac imaging. Author(s): Szczepaniak LS, Dobbins RL, Metzger GJ, Sartoni-D'Ambrosia G, Arbique D, Vongpatanasin W, Unger R, Victor RG. Source: Magnetic Resonance in Medicine : Official Journal of the Society of Magnetic Resonance in Medicine / Society of Magnetic Resonance in Medicine. 2003 March; 49(3): 417-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12594743&dopt=Abstract
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Newly identified apolipoprotein AV gene predisposes to high plasma triglycerides in familial combined hyperlipidemia. Author(s): Ribalta J, Figuera L, Fernandez-Ballart J, Vilella E, Castro Cabezas M, Masana L, Joven J. Source: Clinical Chemistry. 2002 September; 48(9): 1597-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12194944&dopt=Abstract
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Octanoate inhibits triglyceride synthesis in 3T3-L1 and human adipocytes. Author(s): Guo W, Lei T, Wang T, Corkey BE, Han J. Source: The Journal of Nutrition. 2003 August; 133(8): 2512-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888629&dopt=Abstract
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Omega-3 fatty acid supplementation accelerates chylomicron triglyceride clearance. Author(s): Park Y, Harris WS. Source: Journal of Lipid Research. 2003 March; 44(3): 455-63. Epub 2002 December 01. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562865&dopt=Abstract
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Postprandial hypertriglyceridemia-induced endothelial dysfunction in healthy subjects is independent of lipid oxidation. Author(s): Bae JH, Schwemmer M, Lee IK, Lee HJ, Park KR, Kim KY, Bassenge E. Source: International Journal of Cardiology. 2003 February; 87(2-3): 259-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559548&dopt=Abstract
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Postprandial triglyceride levels in familial combined hyperlipidemia. The role of apolipoprotein E and lipoprotein lipase polymorphisms. Author(s): Reiber I, Mezo I, Kalina A, Palos G, Romics L, Csaszar A. Source: The Journal of Nutritional Biochemistry. 2003 July; 14(7): 394-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915220&dopt=Abstract
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Postprandial triglycerides in response to high fat: role of dietary carbohydrate. Author(s): Kriketos AD, Sam W, Schubert T, Maclean E, Campbell LV. Source: European Journal of Clinical Investigation. 2003 May; 33(5): 383-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713451&dopt=Abstract
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Quantitative determination of faecal fatty acids and triglycerides by Fourier transform infrared analysis with a sodium chloride transmission flow cell. Author(s): Voortman G, Gerrits J, Altavilla M, Henning M, van Bergeijk L, Hessels J. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2002 August; 40(8): 795-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12392307&dopt=Abstract
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R219K polymorphism of the ABCA1 gene and its modulation of the variations in serum high-density lipoprotein cholesterol and triglycerides related to age and adiposity in white versus black young adults. The Bogalusa heart study. Author(s): Srinivasan SR, Li S, Chen W, Boerwinkle E, Berenson GS. Source: Metabolism: Clinical and Experimental. 2003 July; 52(7): 930-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870173&dopt=Abstract
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Relation of triglyceride levels, fasting and nonfasting, to fatal and nonfatal coronary heart disease. Author(s): Eberly LE, Stamler J, Neaton JD; Multiple Risk Factor Intervention Trial Research Group. Source: Archives of Internal Medicine. 2003 May 12; 163(9): 1077-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742806&dopt=Abstract
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Relationship between stearoyl-CoA desaturase activity and plasma triglycerides in human and mouse hypertriglyceridemia. Author(s): Attie AD, Krauss RM, Gray-Keller MP, Brownlie A, Miyazaki M, Kastelein JJ, Lusis AJ, Stalenhoef AF, Stoehr JP, Hayden MR, Ntambi JM. Source: Journal of Lipid Research. 2002 November; 43(11): 1899-907. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401889&dopt=Abstract
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Relative contribution of variation within the APOC3/A4/A5 gene cluster in determining plasma triglycerides. Author(s): Talmud PJ, Hawe E, Martin S, Olivier M, Miller GJ, Rubin EM, Pennacchio LA, Humphries SE. Source: Human Molecular Genetics. 2002 November 15; 11(24): 3039-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12417525&dopt=Abstract
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Safety and metabolic tolerance of a concentrated long-chain triglyceride lipid emulsion in critically ill septic and trauma patients. Author(s): Garcia-de-Lorenzo A, Lopez-Martinez J, Planas M, Chacon P, Montejo JC, Bonet A, Ortiz-Leyba C, Sanchez-Segura JM, Ordonez J, Acosta J, Grau T, Jimenez FJ. Source: Jpen. Journal of Parenteral and Enteral Nutrition. 2003 May-June; 27(3): 208-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12757115&dopt=Abstract
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Serum leptin and triglyceride levels in patients on treatment with atypical antipsychotics. Author(s): Atmaca M, Kuloglu M, Tezcan E, Ustundag B. Source: The Journal of Clinical Psychiatry. 2003 May; 64(5): 598-604. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755665&dopt=Abstract
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Short-term triglyceride lowering with fenofibrate improves vasodilator function in subjects with hypertriglyceridemia. Author(s): Capell WH, DeSouza CA, Poirier P, Bell ML, Stauffer BL, Weil KM, Hernandez TL, Eckel RH. Source: Arteriosclerosis, Thrombosis, and Vascular Biology. 2003 February 1; 23(2): 30713. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588776&dopt=Abstract
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Skeletal muscle triglyceride: marker or mediator of obesity-induced insulin resistance in type 2 diabetes mellitus? Author(s): Goodpaster BH, Kelley DE. Source: Curr Diab Rep. 2002 June; 2(3): 216-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643176&dopt=Abstract
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Skeletal muscle triglycerides lowering is associated with net improvement of insulin sensitivity, TNF-alpha reduction and GLUT4 expression enhancement. Author(s): Mingrone G, Rosa G, Di Rocco P, Manco M, Capristo E, Castagneto M, Vettor R, Gasbarrini G, Greco AV. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 September; 26(9): 1165-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12187392&dopt=Abstract
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The effect of equicaloric medium-chain and long-chain triglycerides on pancreas enzyme secretion. Author(s): Symersky T, Vu MK, Frolich M, Biemond I, Masclee AA. Source: Clinical Physiology and Functional Imaging. 2002 September; 22(5): 307-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12487002&dopt=Abstract
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The influence of maternal triglyceride levels on infant birth weight in Peruvian women with pre-eclampsia. Author(s): Sanchez SE, Zhang C, Williams MA. Source: J Matern Fetal Neonatal Med. 2003 May;13(5):328-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12916684&dopt=Abstract
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The influence of teent (Capparis decidua) on human plasma triglycerides, total lipids and phospholipids. Author(s): Goyal R, Grewal RB. Source: Nutr Health. 2003; 17(1): 71-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803284&dopt=Abstract
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The metabolic response to intravenous medium-chain triglycerides in infants after surgery. Author(s): Donnell SC, Lloyd DA, Eaton S, Pierro A. Source: The Journal of Pediatrics. 2002 November; 141(5): 689-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12410199&dopt=Abstract
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The TNF-alpha gene NcoI polymorphism at position -308 of the promoter influences insulin resistance, and increases serum triglycerides after postprandial lipaemia in familiar obesity. Author(s): Wybranska I, Malczewska-Malec M, Niedbal S, Naskalski JW, DembinskaKiec A. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2003 April; 41(4): 501-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747594&dopt=Abstract
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Triglyceride, albuminuria and blood pressure are the major associations of non-fatal cardiovascular disease in Chinese type 2 diabetes. Author(s): Ko GT, Chan JC, Chow CC, Yeung VT, Chan WB, So WY, Ma RC, Ozaki R, Cockram CS. Source: Acta Diabetologica. 2003 June; 40(2): 80-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861405&dopt=Abstract
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Triglyceride-rich lipoproteins and vascular function. Author(s): Haynes WG. Source: Arteriosclerosis, Thrombosis, and Vascular Biology. 2003 February 1; 23(2): 1535. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588751&dopt=Abstract
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Triglyceride-rich lipoproteins are associated with hypertension in preeclampsia. Author(s): Winkler K, Wetzka B, Hoffmann MM, Friedrich I, Kinner M, Baumstark MW, Zahradnik HP, Wieland H, Marz W. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 March; 88(3): 11626. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629100&dopt=Abstract
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Update on the role of triglycerides as a risk factor for coronary heart disease. Author(s): Miller M, Cosgrove B, Havas S. Source: Current Atherosclerosis Reports. 2002 November; 4(6): 414-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12361487&dopt=Abstract
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VLDL-induced triglyceride accumulation in human macrophages is mediated by modulation of LPL lipolytic activity in the absence of change in LPL mass. Author(s): Milosavljevic D, Kontush A, Griglio S, Le Naour G, Thillet J, Chapman MJ. Source: Biochimica Et Biophysica Acta. 2003 February 20; 1631(1): 51-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573449&dopt=Abstract
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Weight gain, serum leptin and triglyceride levels in patients with schizophrenia on antipsychotic treatment with quetiapine, olanzapine and haloperidol. Author(s): Atmaca M, Kuloglu M, Tezcan E, Gecici O, Ustundag B. Source: Schizophrenia Research. 2003 March 1; 60(1): 99-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12505146&dopt=Abstract
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CHAPTER 2. NUTRITION AND TRIGLYCERIDES Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and triglycerides.
Finding Nutrition Studies on Triglycerides The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “triglycerides” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7 Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following is a typical result when searching for recently indexed consumer information on triglycerides: •
A year in review from A to Z: what made nutrition news in 1997. Source: Flynn, M.E. Environmental-nutrition (USA). (December 1997). volume 20(12) page 1, 4.
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Effects on blood pressure, glucose, and lipid levels of a high-monounsatured fat diet compared with a high-carbohydrate diet in NIDDM subjects. Source: Rasmussen, O.W. Thomsen, C. Hansen, K.W. Vesterlund, M. Winther, E. Hermansen, K. Diabetes-care (USA). (December 1993). volume 16(12) page 1565-1571.
Additional consumer oriented references include: •
After I had a heart attack and two bypass operations, I was put on Lipitor to lower my cholesterol. My cholesterol was never high--about 170-180 mg/dL. But my HDL was always low and triglycerides were somewhat high. Now my total cholesterol is 124 and my HDL has gone up slightly. My triglycerides are way down. My LDL cholesterol has fallen from 110 to 68. Is there any downside to such a low cholesterol level, other than the need to check my liver function tests? Source: Lee, T H Harv-Heart-Lett. 1999 January; 9(5): 7 1051-5313
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Ask the doctor. My total cholesterol level is well below 200. My LDL is low, my HDL high, and my triglycerides and homocysteine are both in the “desirable” range. The one thing out of whack is that my lipoprotein(a) level is more than double the “normal” limit. My cardiologist wants me to take niacin to bring it down. I can't find any information on how serious a problem this is, especially in the context of otherwise good cholesterol levels and a healthy lifestyle. (I exercise 5 days a week; eat a low-fat, high-fiber diet; and am not overweight.). Source: Lee, Thomas H Harv-Heart-Lett. 2002 June; 12(10): 8 1051-5313
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Differential influence of LDL cholesterol and triglycerides on lipoprotein(a) concentrations in diabetic patients. Source: Hernandez, C. Chacon, P. Garcia Pascual, L. Simo, R. Diabetes-care. Alexandria, Va. : American Diabetes Association, Inc. February 2001. volume 24 (2) page 350-355. 0149-5992
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Heart Disease Handbook. 3. Triglycerides turn troublesome. Source: Hudnall, M. Environmental-nutrition (USA). (April 1997). volume 20(4) page 1, 4. heart diseases lipoproteins triglycerides diet lipid metabolism 0893-4452
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Low-fat diets, triglycerides and coronary heart disease risk. Source: Nestle, M. BNF-nutr-bull. London : The British Nutrition Foundation. March 2000. volume 25 (1) page 49-53. 0141-9684
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My doctor has me taking Lopid (gemfibrozil) twice a day. My cholesterol level is only 187, but my HDL cholesterol is low at 25. My LDL cholesterol is”normal” at 98 and my triglycerides are 318. These pills give me stomach cramps and they are expensive. Do I need to take them? Source: Anonymous Harv-Heart-Lett. 1998 August; 8(12): 8 1051-5313
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Ratio of triglycerides to HDL cholesterol is an indicator of LDL particle size in patients with type 2 diabetes and normal HDL cholesterol levels. Author(s): Department of Endocrinology-Diabetology-Nutrition, University Hospital, Grenoble, France.
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Source: Boizel, R Benhamou, P Y Lardy, B Laporte, F Foulon, T Halimi, S Diabetes-Care. 2000 November; 23(11): 1679-85 0149-5992 •
The HDL/triglycerides trap. Source: Liebman, B. Nutr-Action-Health-Lett. Washington, D.C. : Center for Science in the Public Interest. Sept 1990. volume 17 (7) page 1, 5-7. ill. 0199-5510
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Those troubling triglycerides. Source: Rosenbaum, S. Vegetarian-times (USA). (January 1994). (no. 197) page 28, 30, 32. lipaemia triglycerides cholesterol risk 0164-8497
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Triglycerides and heart disease. Source: Anonymous Harv-Heart-Lett. 2000 September; 11(1): 1-5 1051-5313
The following information is typical of that found when using the “Full IBIDS Database” to search for “triglycerides” (or a synonym): •
By the way, doctor. As a regular reader of your newsletter, I have a pretty good idea of what a healthy person's cholesterol and triglyceride levels should be. But last year, I had a couple of tests, and the results were completely different. According to the first, my triglycerides were 285, my HDL 31, and my LDL 109. Eight months later, the same measurements came in at 175, 44, and 109. What could cause such a big swing? Is it something I should be worried about? Source: Lee, T H Harv-Health-Lett. 2002 March; 27(5): 8 1052-1577
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Combination of gemfibrozil and orlistat for treatment of combined hyperlipidemia with predominant hypertriglyceridemia. Author(s): Division of Endocrinology and Metabolism, Beth Israel Medical Center, Albert Einstein College of Medicine, New York, New York 10003, USA. Source: Tolentino, M C Ferenczi, A Ronen, L Poretsky, L Endocr-Pract. 2002 May-June; 8(3): 208-12 1530-891X
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Effect of beta-lactoglobulin on plasma retinol and triglyceride concentrations, and fatty acid composition in calves. Author(s): Department of Animal Production, Tohoku National Agricultural Experimental Station, Morioka, Iwate, Japan.
[email protected] Source: Kushibiki, S Hodate, K Kurisaki, J Shingu, H Ueda, Y Watanabe, A Shinoda, M JDairy-Res. 2001 November; 68(4): 579-86 0022-0299
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Fatty acids, triglycerides, and glucose metabolism: recent insights from knockout mice. Author(s): Gladstone Institute of Cardiovascular Disease, San Francisco, California 94141-9100, USA. Source: Chen, H C Farese, R V Jr Curr-Opin-Clin-Nutr-Metab-Care. 2002 July; 5(4): 35963 1363-1950
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High triglycerides. A red flag. Source: Anonymous Mayo-Clin-Health-Lett. 2002 September; 20(9): 7 0741-6245
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High versus low medium chain triglyceride content of formula for promoting short term growth of preterm infants. Author(s): Division of Newborn Medicine, The Regional Neonatal Center, New York Medical College-Westchester Medical Center, Valhalla, NY 10595, USA.
[email protected] Source: Klenoff Brumberg, H L Genen, L H Cochrane-Database-Syst-Revolume 2003; (1): CD002777 1469-493X
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Impaired triglyceride tolerance in hemodialysis patients with different apolipoprotein E (apo E) isoforms. Author(s): 3rd Clinic of Internal Medicine, University Hospital Olomouc, I.P. Pavlova 6, 775 20 Olomouc, Czech Republic.
[email protected] Source: Zahalkova, J Vaverkova, H Novotny, D Kosatikova, Z Biomed-Pap-Med-FacUniv-Palacky-Olomouc-Czech-Repub. 2002 December; 146(2): 73-6 1213-8118
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Low fasting serum triglyceride and high free fatty acid levels in pulmonary fibrosis: a previously unreported finding. Author(s): Department of Medicina Interna e Patologie Sistemiche, University of Catania Medical School, Garibaldi Hospital, 95123 Catania, Italy. Source: Iannello, Silvia Cavaleri, Antonina Camuto, Massimo Pisano, Maria Grazia Milazzo, Paolina Belfiore, Francesco MedGenMed. 2002 June 14; 4(2): 5 1531-0132
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Medium chain triglycerides. Monograph. Source: Anonymous Altern-Med-Revolume 2002 October; 7(5): 418-20 1089-5159
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Plasma lipid concentrations, macronutrient digestibility and mineral absorption in dogs fed a dry food containing medium-chain triglycerides. Author(s): Department of Nutrition, Faculty of Veterinary Medicine, Utrecht University, The Netherlands.
[email protected] Source: Beynen, A C Kappert, H J Lemmens, A G Van Dongen, A M J-Anim-PhysiolAnim-Nutr-(Berl). 2002 October; 86(9-10): 306-12 0931-2439
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Possible role of ginsenoside Rb1 on regulation of rat liver triglycerides. Author(s): Department of Biomedical Pharmacology, Korea Ginseng and Tobacco Research Institute, Taejon. Source: Park, K H Shin, H J Song, Y B Hyun, H C Cho, H J Ham, H S Yoo, Y B Ko, Y C June, W T Park, H J Biol-Pharm-Bull. 2002 April; 25(4): 457-60 0918-6158
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Reduction of plasma triglyceride level and enhancement of plasma albumin concentration by Oren-gedoku-to administration. Author(s): Department of Japanese Oriental Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University.
[email protected] Source: Sekiya, N Kogure, T Kita, T Kasahara, Y Sakakibara, I Goto, H Shibahara, N Shimada, Y Terasawa, K Phytomedicine. 2002 July; 9(5): 455-60 0944-7113
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The biomimetic [Cr(3)O(O(2)CCH(2)CH(3))(6)(H(2)O)(3)](+ )decreases plasma insulin, cholesterol, and triglycerides in healthy and type II diabetic rats but not type I diabetic rats. Author(s): Department of Chemistry and Coalition for Biomolecular Products, The University of Alabama, Tuscaloosa, AL 35487-0336, USA. Source: Sun, Y Clodfelder, B J Shute, A A Irvin, T Vincent, J B J-Biol-Inorg-Chem. 2002 September; 7(7-8): 852-62 0949-8257
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The history of Trilucent implants, and a chemical analysis of the triglyceride filler in 51 consecutively removed Trilucent breast prostheses. Author(s): Department of Plastic and Reconstructive Surgery, The Wellington Hospital, London, UK. Source: Kirkpatrick, W N Jones, B M Br-J-Plast-Surg. 2002 September; 55(6): 479-89 00071226
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The independence of signaling pathways mediating increased expression of plasminogen activator inhibitor type 1 in HepG2 cells exposed to free fatty acids or triglycerides. Author(s): Department of Medicine, The University of Vermont, Burlington 05405, USA.
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Source: Chen, Y Schneider, D J Int-J-Exp-Diabetes-Res. 2002 Apr-June; 3(2): 109-18 15604284
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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The following is a specific Web list relating to triglycerides; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Ascorbic Acid Source: Integrative Medicine Communications; www.drkoop.com Niacin Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,892,00.html Pantothenic Acid Source: Healthnotes, Inc.; www.healthnotes.com Pantothenic Acid Source: Integrative Medicine Communications; www.drkoop.com Pantothenic Acid and Pantethine Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin A Source: Healthnotes, Inc.; www.healthnotes.com Vitamin B3 Source: Healthnotes, Inc.; www.healthnotes.com Vitamin B3 Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin B5 (Pantothenic Acid) Source: Integrative Medicine Communications; www.drkoop.com Vitamin C (Ascorbic Acid) Source: Integrative Medicine Communications; www.drkoop.com
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Minerals Calcium Source: Healthnotes, Inc.; www.healthnotes.com Carnitine Source: Prima Communications, Inc.www.personalhealthzone.com Carnitine (l-carnitine) Source: Integrative Medicine Communications; www.drkoop.com Cerivastatin Source: Healthnotes, Inc.; www.healthnotes.com
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Chromium Source: Healthnotes, Inc.; www.healthnotes.com Chromium Source: Integrative Medicine Communications; www.drkoop.com Chromium Source: Prima Communications, Inc.www.personalhealthzone.com Chromium Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10018,00.html Creatine Source: Prima Communications, Inc.www.personalhealthzone.com Creatine Monohydrate Source: Healthnotes, Inc.; www.healthnotes.com L-carnitine Source: Healthnotes, Inc.; www.healthnotes.com L-carnitine Source: Integrative Medicine Communications; www.drkoop.com Lovastatin Source: Healthnotes, Inc.; www.healthnotes.com Pravastatin Source: Healthnotes, Inc.; www.healthnotes.com Simvastatin Source: Healthnotes, Inc.; www.healthnotes.com Vanadium Alternative names: Vanadate, Vanadyl Source: Integrative Medicine Communications; www.drkoop.com •
Food and Diet Artichoke Alternative names: Cynara scolymus Source: Healthnotes, Inc.; www.healthnotes.com Atkins Diet Source: Healthnotes, Inc.; www.healthnotes.com Coffee Source: Healthnotes, Inc.; www.healthnotes.com
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Diabetes Source: Healthnotes, Inc.; www.healthnotes.com Flaxseeds Source: Healthnotes, Inc.; www.healthnotes.com Garlic Alternative names: Allium sativum Source: Healthnotes, Inc.; www.healthnotes.com Garlic Source: Prima Communications, Inc.www.personalhealthzone.com Garlic Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,786,00.html High Cholesterol Source: Healthnotes, Inc.; www.healthnotes.com High-Fiber Diet Source: Healthnotes, Inc.; www.healthnotes.com Oats Alternative names: Avena sativa Source: Healthnotes, Inc.; www.healthnotes.com Omega-3 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com Omega-3 Fatty Acids Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,992,00.html Polyunsaturated Fats Source: Healthnotes, Inc.; www.healthnotes.com Salmon Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,102,00.html Soy Source: Prima Communications, Inc.www.personalhealthzone.com Soy Products Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,135,00.html
Nutrition
Tea Source: Healthnotes, Inc.; www.healthnotes.com The Pritikin Diet Program Source: Healthnotes, Inc.; www.healthnotes.com
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CHAPTER 3. TRIGLYCERIDES
ALTERNATIVE
MEDICINE
AND
Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to triglycerides. At the conclusion of this chapter, we will provide additional sources.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to triglycerides and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “triglycerides” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to triglycerides: •
A risk factor for atherosclerosis: triglyceride-rich lipoproteins. Author(s): Malloy MJ, Kane JP. Source: Adv Intern Med. 2001; 47: 111-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11795072&dopt=Abstract
•
A triglyceride-rich fat emulsion and free fatty acids but not very low density lipoproteins impair endothelium-dependent vasorelaxation. Author(s): Lundman P, Tornvall P, Nilsson L, Pernow J. Source: Atherosclerosis. 2001 November; 159(1): 35-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11689204&dopt=Abstract
•
Ask the doctor. My total cholesterol level is well below 200. My LDL is low, my HDL high, and my triglycerides and homocysteine are both in the “desirable” range. The
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one thing out of whack is that my lipoprotein(a) level is more than double the “normal” limit. My cardiologist wants me to take niacin to bring it down. I can't find any information on how serious a problem this is, especially in the context of otherwise good cholesterol levels and a healthy lifestyle. (I exercise 5 days a week; eat a low-fat, high-fiber diet; and am not overweight.). Author(s): Lee TH. Source: Harvard Heart Letter : from Harvard Medical School. 2002 June; 12(10): 8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079826&dopt=Abstract •
Association of prothrombin and protein S with plasma triglyceride-rich lipoproteins in humans after test meals rich in milk fat or soybean oil. Author(s): Zhou L, Xu N, Nilsson A. Source: Thrombosis Research. 2002 November 25; 108(4): 209-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12617983&dopt=Abstract
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Autoxidation kinetic analysis of docosahexaenoic acid ethyl ester and docosahexaenoic triglyceride with oxygen sensor. Author(s): Yoshii H, Furuta T, Siga H, Moriyama S, Baba T, Maruyama K, Misawa Y, Hata N, Linko P. Source: Bioscience, Biotechnology, and Biochemistry. 2002 April; 66(4): 749-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12036046&dopt=Abstract
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Blood glucose- and triglyceride-lowering effect of trans-dehydrocrotonin, a diterpene from Croton cajucara Benth., in rats. Author(s): Silva RM, Santos FA, Rao VS, Maciel MA, Pinto AC. Source: Diabetes, Obesity & Metabolism. 2001 December; 3(6): 452-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11903418&dopt=Abstract
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Comparison of triglycerides and phospholipids as supplemental sources of dietary long-chain polyunsaturated fatty acids in piglets. Author(s): Mathews SA, Oliver WT, Phillips OT, Odle J, Diersen-Schade DA, Harrell RJ. Source: The Journal of Nutrition. 2002 October; 132(10): 3081-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12368399&dopt=Abstract
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Consumption of a functional oil rich in phytosterols and medium-chain triglyceride oil improves plasma lipid profiles in men. Author(s): St-Onge MP, Lamarche B, Mauger JF, Jones PJ. Source: The Journal of Nutrition. 2003 June; 133(6): 1815-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771322&dopt=Abstract
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Dietary flaxseed meal is more protective than soy protein concentrate against hypertriglyceridemia and steatosis of the liver in an animal model of obesity. Author(s): Bhathena SJ, Ali AA, Haudenschild C, Latham P, Ranich T, Mohamed AI, Hansen CT, Velasquez MT.
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Source: Journal of the American College of Nutrition. 2003 April; 22(2): 157-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672712&dopt=Abstract •
Dietary fructans, but not cellulose, decrease triglyceride accumulation in the liver of obese Zucker fa/fa rats. Author(s): Daubioul C, Rousseau N, Demeure R, Gallez B, Taper H, Declerck B, Delzenne N. Source: The Journal of Nutrition. 2002 May; 132(5): 967-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11983823&dopt=Abstract
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Effect of xuezhikang, a cholestin extract, on reflecting postprandial triglyceridemia after a high-fat meal in patients with coronary heart disease. Author(s): Zhao SP, Liu L, Cheng YC, Li YL. Source: Atherosclerosis. 2003 June; 168(2): 375-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801622&dopt=Abstract
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Effects of glucagon and insulin on plasma glucose, triglyceride, and triglyceride-rich lipoprotein concentrations in laying hens fed diets containing different types of fats. Author(s): Pal L, Grossmann R, Dublecz K, Husveth F, Wagner L, Bartos A, Kovacs G. Source: Poultry Science. 2002 November; 81(11): 1694-702. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12455597&dopt=Abstract
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Effects of intravenous supplementation with alpha-tocopherol in patients receiving total parenteral nutrition containing medium- and long-chain triglycerides. Author(s): Manuel-y-Keenoy B, Nonneman L, De Bosscher H, Vertommen J, Schrans S, Klutsch K, De Leeuw I. Source: European Journal of Clinical Nutrition. 2002 February; 56(2): 121-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11857045&dopt=Abstract
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Eicosapentaenoic acid improves endothelial function in hypertriglyceridemic subjects despite increased lipid oxidizability. Author(s): Okumura T, Fujioka Y, Morimoto S, Tsuboi S, Masai M, Tsujino T, Ohyanagi M, Iwasaki T. Source: The American Journal of the Medical Sciences. 2002 November; 324(5): 247-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12449445&dopt=Abstract
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Fatty acids composition of plasma phospholipids and triglycerides in children with cystic fibrosis. The effect of dietary supplementation with an olive and soybean oils mixture. Author(s): Caramia G, Cocchi M, Gagliardini R, Malavolta M, Mozzon M, Frega NG. Source: Pediatr Med Chir. 2003 January-February; 25(1): 42-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12920976&dopt=Abstract
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Grape polyphenols decrease plasma triglycerides and cholesterol accumulation in the aorta of ovariectomized guinea pigs. Author(s): Zern TL, West KL, Fernandez ML. Source: The Journal of Nutrition. 2003 July; 133(7): 2268-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840191&dopt=Abstract
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HDL-C and triglyceride levels: relationship to coronary heart disease and treatment with statins. Author(s): Gaw A. Source: Cardiovascular Drugs and Therapy / Sponsored by the International Society of Cardiovascular Pharmacotherapy. 2003 January; 17(1): 53-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843687&dopt=Abstract
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Hepatocyte apoB-containing lipoprotein secretion is decreased by the grapefruit flavonoid, naringenin, via inhibition of MTP-mediated microsomal triglyceride accumulation. Author(s): Borradaile NM, de Dreu LE, Barrett PH, Behrsin CD, Huff MW. Source: Biochemistry. 2003 February 11; 42(5): 1283-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12564931&dopt=Abstract
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Intestinal apolipoprotein B secretion is inhibited by the flavonoid quercetin: potential role of microsomal triglyceride transfer protein and diacylglycerol acyltransferase. Author(s): Casaschi A, Wang Q, Dang K, Richards A, Theriault A. Source: Lipids. 2002 July; 37(7): 647-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12216835&dopt=Abstract
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Omega-3 fatty acid supplementation accelerates chylomicron triglyceride clearance. Author(s): Park Y, Harris WS. Source: Journal of Lipid Research. 2003 March; 44(3): 455-63. Epub 2002 December 01. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562865&dopt=Abstract
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Pharmacological management of high triglycerides and low high-density lipoprotein cholesterol. Author(s): Szapary PO, Rader DJ. Source: Current Opinion in Pharmacology. 2001 April; 1(2): 113-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11714084&dopt=Abstract
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Possible role of ginsenoside Rb1 on regulation of rat liver triglycerides. Author(s): Park KH, Shin HJ, Song YB, Hyun HC, Cho HJ, Ham HS, Yoo YB, Ko YC, Jun WT, Park HJ.
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Source: Biological & Pharmaceutical Bulletin. 2002 April; 25(4): 457-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11995924&dopt=Abstract •
Propofol in a medium- and long-chain triglyceride emulsion: pharmacological characteristics and potential beneficial effects. Author(s): Theilen HJ, Adam S, Albrecht MD, Ragaller M. Source: Anesthesia and Analgesia. 2002 October; 95(4): 923-9, Table of Contents. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12351269&dopt=Abstract
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Protective effects of flax meal against hypercholesterolemia and hypertriglyceridemia in rats. Author(s): Ratnayake WM, Gilani GS. Source: Journal of the American College of Nutrition. 2003 August; 22(4): 326-7; Author Reply 327-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12897048&dopt=Abstract
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Reduction of plasma triglyceride level and enhancement of plasma albumin concentration by Oren-gedoku-to administration. Author(s): Sekiya N, Kogure T, Kita T, Kasahara Y, Sakakibara I, Goto H, Shibahara N, Shimada Y, Terasawa K. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2002 July; 9(5): 455-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12222668&dopt=Abstract
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Role of soy isoflavones in the hypotriglyceridemic effect of soy protein in the rat. Author(s): Demonty I, Lamarche B, Deshaies Y, Jacques H. Source: The Journal of Nutritional Biochemistry. 2002 November; 13(11): 671-677. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12550064&dopt=Abstract
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Short-term administration of conjugated linoleic acid reduces liver triglyceride concentration and phosphatidate phosphohydrolase activity in OLETF rats. Author(s): Rahman SM, Huda MN, Uddin MN, Akhteruzzaman S. Source: J Biochem Mol Biol. 2002 September 30; 35(5): 494-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359092&dopt=Abstract
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The influence of teent (Capparis decidua) on human plasma triglycerides, total lipids and phospholipids. Author(s): Goyal R, Grewal RB. Source: Nutr Health. 2003; 17(1): 71-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803284&dopt=Abstract
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Value of VLCD supplementation with medium chain triglycerides. Author(s): Krotkiewski M.
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Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2001 September; 25(9): 1393-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11571605&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to triglycerides; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Atherosclerosis Source: Healthnotes, Inc.; www.healthnotes.com Atherosclerosis and Heart Disease Prevention Source: Prima Communications, Inc.www.personalhealthzone.com Athletic Performance Source: Healthnotes, Inc.; www.healthnotes.com Cardiovascular Disease Overview Source: Healthnotes, Inc.; www.healthnotes.com
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Cystic Fibrosis Source: Healthnotes, Inc.; www.healthnotes.com Diabetes Mellitus Source: Integrative Medicine Communications; www.drkoop.com Gallstones Source: Healthnotes, Inc.; www.healthnotes.com Gout Source: Integrative Medicine Communications; www.drkoop.com Heart Attack Source: Healthnotes, Inc.; www.healthnotes.com High Cholesterol Source: Integrative Medicine Communications; www.drkoop.com High Cholesterol Source: Prima Communications, Inc.www.personalhealthzone.com High Triglycerides Source: Healthnotes, Inc.; www.healthnotes.com Hypercholesterolemia Source: Integrative Medicine Communications; www.drkoop.com Hypertension Alternative names: High Blood Pressure Source: Prima Communications, Inc.www.personalhealthzone.com Hypoglycemia Source: Healthnotes, Inc.; www.healthnotes.com Hypothyroidism Source: Healthnotes, Inc.; www.healthnotes.com Insulin Resistance Syndrome Source: Healthnotes, Inc.; www.healthnotes.com Menopause Source: Integrative Medicine Communications; www.drkoop.com Obesity Source: Integrative Medicine Communications; www.drkoop.com Pancreatic Insufficiency Source: Healthnotes, Inc.; www.healthnotes.com Pancreatitis Source: Integrative Medicine Communications; www.drkoop.com
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Peripheral Vascular Disease Source: Healthnotes, Inc.; www.healthnotes.com Psoriasis Source: Healthnotes, Inc.; www.healthnotes.com Shock Source: Integrative Medicine Communications; www.drkoop.com Tinnitus Source: Healthnotes, Inc.; www.healthnotes.com Vertigo Source: Healthnotes, Inc.; www.healthnotes.com •
Alternative Therapy Fasting Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,694,00.html
•
Herbs and Supplements Acorus Alternative names: Sweet Flag; Acorus calamus L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org ALA Source: Integrative Medicine Communications; www.drkoop.com Allium Compounds Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,1024,00.html Aloe Alternative names: Aloe vera L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Aloe Alternative names: Aloe Vera Source: Integrative Medicine Communications; www.drkoop.com Aloe Vera Alternative names: Aloe Source: Integrative Medicine Communications; www.drkoop.com Alpha-Linolenic Acid (ALA) Source: Integrative Medicine Communications; www.drkoop.com
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Amino Acid K Source: Integrative Medicine Communications; www.drkoop.com Amino Acids Overview Source: Healthnotes, Inc.; www.healthnotes.com Angkak Source: Integrative Medicine Communications; www.drkoop.com Astragalus MEM Alternative names: Huang-Qi; Astragalus membranaceus Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Astragalus Sp Alternative names: Vetch, Rattlepod, Locoweed; Astragalus sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Beni-Koji Source: Integrative Medicine Communications; www.drkoop.com Bilberry Source: Prima Communications, Inc.www.personalhealthzone.com Blue-Green Algae Source: Healthnotes, Inc.; www.healthnotes.com Chinese Scullcap Alternative names: Scutellaria baicalensis Source: Healthnotes, Inc.; www.healthnotes.com Crataegus Alternative names: Hawthorn; Crataegus oxyacantha L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Curcuma Alternative names: Turmeric; Curcuma longa L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org DHA Source: Integrative Medicine Communications; www.drkoop.com Docosahexaenoic Acid Source: Healthnotes, Inc.; www.healthnotes.com Docosahexaenoic Acid (DHA) Source: Integrative Medicine Communications; www.drkoop.com Eicosapentaenoic Acid (EPA) Source: Integrative Medicine Communications; www.drkoop.com
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Equisetum Alternative names: Horsetail; Equisetum arvense L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Fenofibrate Source: Healthnotes, Inc.; www.healthnotes.com Fenugreek Alternative names: Trigonella foenum-graecum Source: Healthnotes, Inc.; www.healthnotes.com Fiber Source: Healthnotes, Inc.; www.healthnotes.com Fructo-Oligosaccharides (FOS) and Other Oligosaccharides Source: Healthnotes, Inc.; www.healthnotes.com Gemfibrozil Source: Healthnotes, Inc.; www.healthnotes.com Glipizide Source: Healthnotes, Inc.; www.healthnotes.com Glucomannan Source: Healthnotes, Inc.; www.healthnotes.com Glycyrrhiza Alternative names: Licorice; Glycyrrhiza glabra L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Grape Seed Extract Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,793,00.html Green Tea Alternative names: Camellia sinensis Source: Healthnotes, Inc.; www.healthnotes.com Guatteria Alternative names: Guatteria gaumeri Greenman Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Guggul Alternative names: Commiphora mukul Source: Healthnotes, Inc.; www.healthnotes.com Guggul Source: Prima Communications, Inc.www.personalhealthzone.com Gugulipid Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com
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Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10033,00.html Gymnema Alternative names: Gurmar; Gymnema sylvestre Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Gymnema Alternative names: Gymnema sylvestre Source: Healthnotes, Inc.; www.healthnotes.com Gymnema Sylvestre Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10034,00.html Hong Qu Source: Integrative Medicine Communications; www.drkoop.com Hung-Chu Source: Integrative Medicine Communications; www.drkoop.com Insulin Source: Healthnotes, Inc.; www.healthnotes.com Isoflavones Source: Prima Communications, Inc.www.personalhealthzone.com Lecithin Source: Prima Communications, Inc.www.personalhealthzone.com Lipase Source: Integrative Medicine Communications; www.drkoop.com L-lysine Source: Integrative Medicine Communications; www.drkoop.com Lysine Alternative names: Amino Acid K, L-Lysine Source: Integrative Medicine Communications; www.drkoop.com Maitake Alternative names: Grifola frondosa Source: Healthnotes, Inc.; www.healthnotes.com Medium Chain Triglycerides Source: Healthnotes, Inc.; www.healthnotes.com Medium-Chain Triglycerides Source: Prima Communications, Inc.www.personalhealthzone.com
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Momordica Alternative names: Bitter Gourd, Karela; Momordica charantia Linn. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Monascus Source: Integrative Medicine Communications; www.drkoop.com Ocimum Alternative names: Basil, Albahaca; Ocimum basilicum Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Panax Alternative names: Ginseng; Panax ginseng Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Plantago Psyllium Alternative names: Psyllium, Ispaghula; Plantago psyllium/ovata Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Psyllium Alternative names: Plantago ovata, Plantago ispaghula Source: Healthnotes, Inc.; www.healthnotes.com Red Koji Source: Integrative Medicine Communications; www.drkoop.com Red Leaven Source: Integrative Medicine Communications; www.drkoop.com Red Rice Source: Integrative Medicine Communications; www.drkoop.com Red Yeast Rice Alternative names: Monascus purpureus Source: Healthnotes, Inc.; www.healthnotes.com Red Yeast Rice Alternative names: Angkak, Beni-koju, Hong Qu, Hung-chu, Monascus, Red Leaven, Red Rice, Red Koji, Zhitai, Xue Zhi Kang Source: Integrative Medicine Communications; www.drkoop.com Red Yeast Rice Source: Prima Communications, Inc.www.personalhealthzone.com Red Yeast Rice Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10054,00.html Silybum Alternative names: Milk Thistle; Silybum marianum (L.) Gaertn. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Smilax Alternative names: Sarsaparilla; Smilax glabra Roxb. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Swertia Alternative names: Swertia sp Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Syzygium Clove Alternative names: Clove, Jamun; Syzygium sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Vacciniumb Alternative names: Bilberry; Vaccinium myrtillus L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Vanadate Source: Integrative Medicine Communications; www.drkoop.com Vanadyl Source: Integrative Medicine Communications; www.drkoop.com Zhitai Source: Integrative Medicine Communications; www.drkoop.com Zue Zhi Kang Source: Integrative Medicine Communications; www.drkoop.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON TRIGLYCERIDES Overview In this chapter, we will give you a bibliography on recent dissertations relating to triglycerides. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “triglycerides” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on triglycerides, we have not necessarily excluded nonmedical dissertations in this bibliography.
Dissertations on Triglycerides ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to triglycerides. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
Development of a Laser-based Infrared Detector for High-pressure Liquid Chromatography the Analysis of Cholesterol, Cholestryl Esters and Triglycerides in Serum by Stokl, Caroline; PhD from McGill University (Canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL52227
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Effects of Exercise and a Vegetarian Diet on Carcass Composition, Organ Weights, and Serum Cholesterol and Triglycerides by Klein, Daniel Allen, PhD from Michigan State University, 1971, 65 pages http://wwwlib.umi.com/dissertations/fullcit/7208722
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Physical Properties and Crystallization Kinetics of Bulk and Emulsified Triglycerides by Campbell, Shawn Douglas; MSC from University of Guelph (Canada), 2002, 88 pages http://wwwlib.umi.com/dissertations/fullcit/MQ67342
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The Combined Effects of Aerobic Exercise and Dietary Omega-3 Fatty Acids on Plasma Lipids, Platelets and Physiological Parameters in Hyperlipidemic Subjects (Triglycerides, Eicosapentaenoic Acid, Cholesterol, Oxygen Consumption, Blood
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Pressure) by Warner, James Grant, Jr., EDD from West Virginia University, 1986, 250 pages http://wwwlib.umi.com/dissertations/fullcit/8627737 •
The Effects of Exercise Training And/or Lecithin Supplement upon Serum Cholesterol Triglycerides and Beta-lipoproteins. by Krebs, Paul Samuel, EDD from University of Arkansas, 1978, 119 pages http://wwwlib.umi.com/dissertations/fullcit/7823235
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The Effects of Triglyceride Structure on the Properties of Plant Oil-based Resins by LaScala, John Joseph; PhD from University of Delaware, 2002, 408 pages http://wwwlib.umi.com/dissertations/fullcit/3062034
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The High Performance Liquid Chromatography and Detection of Phospholipids and Triglycerides by Compton, Bruce Jon; PhD from McGill University (Canada), 1981 http://wwwlib.umi.com/dissertations/fullcit/NK51915
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Triglycerides of Milk Fat by Shehata, A. Adel Y; AdvDeg from University of Guelph (Canada), 1970 http://wwwlib.umi.com/dissertations/fullcit/NK07628
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND TRIGLYCERIDES Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning triglycerides.
Recent Trials on Triglycerides The following is a list of recent trials dedicated to triglycerides.8 Further information on a trial is available at the Web site indicated. •
Niacin for Treatment of Elevated Cholesterol and Triglycerides in HIV-Infected Patients Condition(s): HIV Infections; Hypercholesterolemia; Hypertriglyceridemia; Diabetes Mellitus Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Allergy and Infectious Diseases (NIAID) Purpose - Excerpt: The purpose of this study is to evaluate the safety, efficacy, and tolerability of extended-release niacin (Niaspan) in improving the level of fats in the blood of HIV-infected patients. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00046267
•
Reduction of Triglycerides in Women on HRT Condition(s): Cardiovascular Diseases; Atherosclerosis; Postmenopause; Heart Diseases Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI)
8
These are listed at www.ClinicalTrials.gov.
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Purpose - Excerpt: To test the effect of lifestyle intervention on subclinical cardiovascular disease measures in women taking HRT. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00023543 •
Genetic Determinants:Low HDL, High Triglycerides, Obesity Condition(s): Cardiovascular Diseases; Atherosclerosis; Hypertriglyceridemia; Obesity; Heart Diseases Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To conduct genetic studies of the metabolic syndrome which is characterized by very low levels of high density lipoprotein cholesterol (HDL-C), hypertriglyceridemia, and obesity. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049881
•
Genetic Epidemiology of Hypertriglyceridemia Condition(s): Cardiovascular Diseases; Coronary Disease; Hyperlipidemia, Familial Combined; Hyperlipoproteinemia Type IV Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine prospectively the role of elevated plasma triglyceride (TG) as a risk factor for 20-year coronary heart disease (CHD) mortality in familial combined hyperlipidemia (FCHL) and familial hypertriglyceridemia (FHTG), the familial forms of hypertriglyceridemia. Also, to perform genetic epidemiologic studies of recently identified lipoprotein risk factors for CHD, including Atherogenic Lipoprotein Phenotypes (ALP) based on subclasses of low-density lipoproteins (LDL), Lipoprotein(a) (Lp(a)) and apolipoprotein (apo) B plasma levels, and apo E isoforms. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005368
•
Regulation of Sterol Homeostasis Condition(s): Hypertriglyceridemia Study Status: This study is no longer recruiting patients. Sponsor(s): Department of Veterans Affairs Medical Research Service Purpose - Excerpt: The purpose of this study is to determine how people with high triglycerides metabolize and absorb bile acids, compounds made in the body from cholesterol. This project has two objectives: A) To define the mechanism of impaired bile acid absorption in hypertriglyceridemia (specifically we will determine if the active or passive component of absorption is abnormal) and B) to determine the contribution of
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an alternative pathway of bile acid synthesis which begins with 27-hydroxylation of cholesterol. Because 27-hydroxylase is present in endothelial cells as well as liver, this pathway may play a role in removal of cholesterol from incipient atherosclerotic plaque. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00018720 •
Garlic in hyperlipidemia caused by HAART Condition(s): HIV Hyperglycemia
Infections;
Hypercholesterolemia;
Hypertriglyceridemia;
Study Status: This study is not yet open for patient recruitment. Sponsor(s): National Center for Complementary and Alternative Medicine (NCCAM) Purpose - Excerpt: This is a double-blind randomized placebo controlled trial to test the use of garlic to lower cholesterol and triglycerides in hyperlipidemic HIV-infected individuals who are being treated with highly active antiretroviral therapy (HAART). The garlic will be administered as enteric-coated tablets and in two escalating dosages. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029250 •
Re-evaluating Triglycerides in Coronary Heart Disease Condition(s): Cardiovascular Hypertriglyceridemia
Diseases;
Heart
Diseases;
Coronary
Disease;
Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To conduct a comprehensive epidemiologic investigation into the relationship between serum triglyceride (TG) levels and coronary heart disease (CHD). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005442
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “triglycerides” (or synonyms).
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While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON TRIGLYCERIDES Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “triglycerides” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on triglycerides, we have not necessarily excluded nonmedical patents in this bibliography.
Patents on Triglycerides By performing a patent search focusing on triglycerides, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an 9Adapted from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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example of the type of information that you can expect to obtain from a patent search on triglycerides: •
4-amino substituted-2-substituted-1,2,3,4-tetrahydroquinolines Inventor(s): DeNinno; Michael P. (Gales Ferry, CT), Magnus-Aryitey; George T. (Ledyard, CT), Ruggeri; Roger B. (Waterford, CT), Wester; Ronald T. (Ledyard, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,489,478 Date filed: September 27, 2000 Abstract: Cholesteryl ester transfer protein inhibitors, pharmaceutical compositions containing such inhibitors and the use of such inhibitors to elevate certain plasma lipid levels, including high density lipoprotein-cholesterol and to lower certain other plasma lipid levels, such as LDL-cholesterol and triglycerides and accordingly to treat diseases which are exacerbated by low levels of HDL cholesterol and/or high levels of LDLcholesterol and triglycerides, such as atherosclerosis and cardiovascular diseases in some mammals, including humans. Excerpt(s): This invention relates to cholesteryl ester transfer protein (CETP) inhibitors, pharmaceutical compositions containing such inhibitors and the use of such inhibitors to elevate certain plasma lipid levels, including high density lipoprotein (HDL)-cholesterol and to lower certain other plasma lipid levels, such as low density lipoprotein (LDL)cholesterol and triglycerides and accordingly to treat diseases which are affected by low levels of HDL cholesterol and/or high levels of LDL-cholesterol and triglycerides, such as atherosclerosis and cardiovascular diseases in certain mammals (i.e., those which have CETP in their plasma), including humans. Atherosclerosis and its associated coronary artery disease (CAD) is the leading cause of mortality in the industrialized world. Despite attempts to modify secondary risk factors (smoking, obesity, lack of exercise) and treatment of dyslipidemia with dietary modification and drug therapy, coronary heart disease (CHD) remains the most common cause of death in the U.S., where cardiovascular disease accounts for 44% of all deaths, with 53% of these associated with atherosclerotic coronary heart disease. Risk for development of this condition has been shown to be strongly correlated with certain plasma lipid levels. While elevated LDL-C may be the most recognized form of dyslipidemia, it is by no means the only significant lipid associated contributor to CHD. Low HDL-C is also a known risk factor for CHD (Gordon, D. J., et al.,: "High-density Lipoprotein Cholesterol and Cardiovascular Disease", Circulation, (1989), 79: 8-15). Web site: http://www.delphion.com/details?pn=US06489478__
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Blends for barrier layers for food products Inventor(s): Cain; Frederick William (Wormerveer, NL), Dekker; Willem (Wormerveer, NL), Smith; Kevin Warren (Sharnbrook, GB), Talbot; Geoffrey (Purfleet, GB) Assignee(s): Unilever Patent Holdings BV (NL) Patent Number: 6,461,654 Date filed: August 31, 2000
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Abstract: Blends of a natural wax, such as sunflower wax and glyceride materials, substantially being triglycerides and having an N20>20 display excellent properties when applied in barrier layers for compound food products. Excerpt(s): it should have a low water permeability. it should stick well to the surfaces of the layers that it is supposed to protect against the water migration. it should not be too brittle, so that the formation of cracks in this layer is avoided as much as possible. Web site: http://www.delphion.com/details?pn=US06461654__ •
Blood-pool selective carrier for lipophilic imaging agents Inventor(s): Counsell; Raymond E. (Ann Arbor, MI), Longino; Marc A. (Ann Arbor, MI), Weichert; Jamey P. (Ann Arbor, MI) Assignee(s): The Board of Regents of the University of Michigan (Ann Arbor, MI) Patent Number: 6,645,463 Date filed: April 10, 1998 Abstract: A surface-modified lipoprotein-like oil-in-water emulsion useful as a bloodpool selective delivery vehicle for lipophilic imaging agents or lipophilic derivatives of water-soluble imaging agents. The blood-pool selective delivery vehicle remains in the blood for several hours, shows very little early hepatic sequestration, and is cleared from the blood within 24 hours. The mean diameter of the oil phase is less than 150 nm which minimizes sequestration by the reticuloendothelial system. The surface of the oil phase is modified with a polyethyl glycol-modified phospholipid to prevent normal interactions with the receptor sites of the hepatocytes. In radiographic imaging, radioactive or stable, synthetic or semi-synthetic polyhalogenated triglycerides, such as 2-oleoylglycerol-1,3-bis[7-(3-amino-2,4,6-triiodophenyl)heptanoate], or lipid soluble derivatives of traditional water-soluble contrast agents, such as aliphatic esters of iopanoic, diatrizoic, and acetrizoic acid, may be incorporated into the lipophilic core of a lipoprotein-like emulsion particle. Excerpt(s): This invention relates generally to an oil-in-water emulsion, and more particularly, to an oil-in-water emulsion that functions as a blood-pool selective carrier or delivery vehicle for lipophilic imaging agents, or lipid-soluble derivatives of watersoluble, imaging agents incorporated therein. Conventional water-soluble contrast media for x-ray computed tomography (CT) and magnetic resonance imaging (MRI) rapidly diffuse out of the blood following injection. Vascular imaging, for example, therefore depends on invasive intra-arterial infusion of large amounts of contrast media at or near the suspected site of disease. Despite administration of a bolus dose of contrast media, enhancement lasts for only a few seconds. In CT angiography, as a specific example, a large amount (<200 ml) of a conventional water-soluble urographic agent is administered directly into the artery at a rate approaching 5 ml/sec. Such rapid administration can cause nausea and vomiting. Because conventional urographic agents are rapidly distributed throughout the vascular space before rapid renal elimination, CT scanning must be accomplished within 30 seconds of administration while the agent is still in the circulation phase. Intravascular contrast is rapidly lost as the agent diffuses into the extravascular space and distributes nonspecifically throughout the body. There is, therefore, a need for a delivery vehicle for CT scanning that can be administered less invasively and that will prolong the presence of the agent in the blood. Several experimental CT agents have been developed to provide extended circulation time in the blood, including high molecular weight carboxymethyl dextrans and nanocrystalline
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particulates. Iodinated versions of the dextrans have opacified blood for up to 20 minutes, however, significantly delayed clearance (greater than a day) from the liver poses a concern. The nanocrystalline particulates comprising, in one example, solid ethyl diatrizoate having a particle size ranging from 200-400 nm, are also very slowly cleared by the reticuloendothelial system (RES) of the liver and spleen. There is, thus, a need for a delivery vehicle that will circulate in the blood for a prolonged period of time, but which will be metabolized and cleared from the system within an acceptable time period. Web site: http://www.delphion.com/details?pn=US06645463__ •
Bone graft material incorporating demineralized bone matrix and lipids Inventor(s): Nimni; Marcel E. (Santa Monica, CA) Assignee(s): Interpore Cross International (Irvine, CA) Patent Number: 6,565,884 Date filed: September 10, 2001 Abstract: A demineralized bone putty composition comprises: (1) demineralized bone matrix (DBM); and (2) a lipid fraction selected from the group consisting of lecithin and a mixture of lecithin and triglycerides containing unsaturated fatty acids. The putty composition is moldable, biocompatible, slowly resorbable, and soluble in tissue fluids, and non-extrudable. The composition delivers a biologically active product to animals and humans that will enhance bone formation at sites where bone is lost, deficient, or present in suboptimal amounts. The composition can further comprise calcium, an antioxidant such as Vitamin E or Vitamin C, or a hydrophilic polymer such as methylcellulose or hydroxypropyl methylcellulose. Excerpt(s): This invention is directed to a bone graft material incorporating demineralized bone matrix and lipids for particular use in enhancing bone formation. One of the few tissues that regenerates in mammals is bone. To a great extent, this is due to the ability of specific growth factors to stimulate stem cells along the chondrogenic and osteogenic pathways and the role of mechanical forces that encourage bone remodeling. Significant efforts have been made to enhance bone healing using decalcified bone matrix as an inducer. Decalcified bone matrix, which is mostly collagen with small amounts of growth- and differentiation-inducing molecules, is able to stimulate bone formation, even after implantation (subcutaneously or intramuscularly) at ectopic sites where there is no bone. The chondro-osteogenic response induced by implants of demineralized rabbit (M. R. Urist & T. A. Dowell, "The Inductive Substratum for Osteogenesis in Pellets of Particulate Bone Matrix," Clin. Orthoped. Rel. Res. 61:61-68 (1969); M. R. Urist & B. S. Strates, "Bone Morphogenetic Protein," J. Dent. Res. 50:1392-1406 (1971)) and rat bone matrix (C. B. Huggins et al., "Transformation of Fibroblasts by Allogeneic and Xenogeneic Transplants of Demineralized Tooth arid Bone," J. Exp. Med. 132:1250-1258 (1970); A. H. Reddi & C. B. Huggins, "Influence of Transplanted Tooth and Bone on Transformation of Fibroblasts," Proc. Soc. Exp. Biol. Med. 143:634-637 (1973); G. D. Syftestad & M. R. Urist, "Degradation of Bone Matrix Morphogenetic Activity by Pulverization," Clin. Orthoped. Rel. Res. 141:281-286 (1979)). Web site: http://www.delphion.com/details?pn=US06565884__
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Cholesterol lowering structured lipids containing omega 3 polyunsaturated fatty acids and their process thereof Inventor(s): Lokesh; Belur Ramaswamy (Mysore, IN), Rao; Reena (Mysore, IN), Sambaiah; Kari (Mysore, IN) Assignee(s): Council of Scientific and Industrial Research (New Delhi, IN) Patent Number: 6,608,223 Date filed: October 22, 2001 Abstract: Unique structured lipids obtained from interestifying coconut oil with free fatty acids obtained from hydrolysis of triglycerides of an animal source, said structured lipids rich in omega-3-poly unsaturated fatty acid and medium chain fatty acid and a process for the production of said structured lipids. Excerpt(s): The present invention relates to cholesterol lowering structured lipids containing omega 3 polyunsaturated fatty acids and a process thereof. Coconut oil is a kernel oil which is a natural source of medium chain fatty acids (MCFA) (53% of C8:0C12:0). Its lauric acid content is very high (48%). The lauric fats provide high nutritional value because of their unique position in intercellular transport mechanisms; that is, either the portal or lymphatic systems can absorb them. They provide excellent nutrition for critically ill patients and do not cause any undue coronary difficulties despite their saturation. In fact, the lauric fats provide unexpected usefulness in protein catabolism, yielding positive nitrogen balance and enhanced protein formation. But coconut oil does not contain any omega 3 polyunsaturated fatty acids (PUFA). In addition to this, myristic and palmitic acids that contribute to around 33% of the total fatty acids of coconut oil have been shown to be hypercholesterolemic which is a risk factor for cardiovascular disease. Medium chain fatty acids comprise fatty acids with 6 to 12 carbon chain lengths. MCFA offer numerous health benefits. They are easily absorbed, transported via the portal system and rapidly metabolized to yield quick energy and is not deposited in the body as fat. Medium chain triglycerides (MCT) have clinical applications in the treatment of fat malabsorption disorders, gall bladder disease, hyperlipidemia, obesity and deficiency of the carnitine system. But MCT alone cannot function as an ideal fat source for humans as they do not provide PUFA. Web site: http://www.delphion.com/details?pn=US06608223__
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Coenzyme Q10 formulation and process methodology for soft gel capsules manufacturing Inventor(s): Udel; Ronald G. (Beverly Hills, CA) Assignee(s): Soft Gel Technologies, Inc. (Los Angeles, CA) Patent Number: 6,616,942 Date filed: March 28, 2000 Abstract: A formulation of Coenzyme Q.sub.10, beta-carotenes, Vitamin E, and medium chain triglycerides in rice bran oil and an optional thickener, such as bee's wax, is provided in a soft gel capsule so that a maximum of the Coenzyme Q.sub.10 is absorbed by the human body. Generally, about 60 mg of Coenzyme Q.sub.10 is the normal amount provided daily to a healthy sedentary adult. Excerpt(s): This invention relates to an improved formulation and process methodology of Coenzyme Q.sub.10 in producing soft gel capsules of this formulation. Coenzyme
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Q.sub.10 (CoQ.sub.10 or Ubiquinone) is a large molecular weight (863.63 grams) lipid compound that is produced in the liver and perhaps other body organs. The total body content is estimated to be 1.4 to 1.8 grams, depending on the age and the physical fitness of the individual. Although CoQ.sub.10 is found in the mitochondria and other organelles of every living cell, it appears to be most abundant in tissues with a high number of mitochondria and a high level of metabolic activity. For example, in the metabolically inactive blood there is approximately 4 mg, in the heart, and in the skeletal muscle 1000 mg. The blood acts as a CoQ.sub.10 reservoir and transport media between endogenous CoQ.sub.10 synthesis in the liver, exogenous CoQ.sub.10 absorption from digested food substances in the intestinal tract, and the body cells. Endogenous synthesis appears to be responsible for 56 percent and exogenous sources for 44 percent of the body's CoQ.sub.10 requirements. These numbers are currently being studied and endogenous CoQ.sub.10 synthesis may be significantly deficient in the elderly. These deficiencies are not related to the total caloric intake, but rather to the vitamin content of ingested foods. The body requires multiple vitamins for the synthesis of CoQ.sub.10. CoQ.sub.10 requirements of the body are also variable between individuals and are dependent on age, physical activity, and disease. It is estimated that the body CoQ.sub.10 utilization is between 5 and 9 mg per day. Intercellular CoQ.sub.10 is required for the synthesis of energy and therefore essential for life. Energy synthesis occurs in the mitochondria, where CoQ.sub.10 provides an electron for the electron transport chain in the cytochrome system, in which adenosine tripohosphate (ATP) is synthesized. As CoQ.sub.10 gives up an electron for ATP synthesis, it gets oxidized. If CoQ.sub.10 is used as an antioxidant, it gets oxidized and is no longer available to provide electrons and function in the synthesis of ATP. Under conditions of high metabolic stress, endogenous sources may become inadequate to meet the body's CoQ.sub.10 requirement for ATP synthesis. Under such conditions, dietary CoQ.sub.10 supplementation has been shown to be an effective source. An improved soft gel formulation and process of CoQ.sub.10 soft gel capsule manufacturing has uses to treat heart failure, chronic fatigue and patients with psoriasis and planter warts. In all cases, it has been found that the improved soft gel formulation at ingestion rates of 30-100 mg/day of CoQ.sub.10 have been proven to be superior to commercially available 60 mg dry powder capsules, and existing 100 mg/day CoQ.sub.10 soft gel formulations. An appropriate CoQ.sub.10 dosage for a normal individual compared to the dosage necessary for a diseased individual has been difficult to ascertain. Recommended doses of 10 to 30 mg/day were found to be ineffective for patients with significant CoQ.sub.10 deficiencies. In the past 15 years, it has become generally accepted that poor intestinal absorption of certain CoQ.sub.10 formulations limits their effective use. For this reason, 50 and 150 mg CoQ.sub.10 containing tablets or capsules are commercially available to the consumer, at a considerably higher cost. Web site: http://www.delphion.com/details?pn=US06616942__ •
Combinations of psyllium and chitosan for synergistic adsorption of triglyceride Inventor(s): Babish; John G. (Brooktondale, NY) Assignee(s): MetaProteomics, LLC (San Clemente, CA) Patent Number: 6,506,420 Date filed: March 29, 2002 Abstract: A composition and method for minimizing the absorption of triglycerides and fats in the gastrointestinal tract is described. The composition comprises psyllium and
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chitosan in a ratio range of 2:1 to 11:1 by weight, preferably 2:1 to 9:1, and most preferably 2:1 to 4:1 to provide a synergistic fat-binding effect. Excerpt(s): The present invention relates generally to a composition and a method for weight loss, reduction of serum cholesterol, and normalization of insulin response without requiring added caloric restriction. More specifically, the present invention relates to combinations of psyllium and chitosan, in a proper ratio, which synergistically adsorb dietary fats and inhibit their gastrointestinal absorption. In recent years, people have tended to become less physically active and consume food that has a high fat content. Such sedentary life styles and excessive lipid ingestion cause obesity and along with it a variety complications, for instance, heart and circulatory diseases, respiratory disease, diabetes and the like. It is known that the fat content of foods is a major factor in the problem of obesity. It is also understood that the body tends to store fat for future use rather than utilize it immediately, which leads to weight-gain. Furthermore, it has been shown that there is a connection between the amount of fat stored in the body and the level of serum cholesterol, with a diet high in fat being likely to lead to high serum cholesterol levels. As cholesterol has been implicated as a factor in arteriosclerosis or hardening of the arteries, the risk for heart disease and/or a heart attack is increased when a diet high in fat is followed. Web site: http://www.delphion.com/details?pn=US06506420__ •
Compositions and methods for reducing or controlling blood cholesterol, lipoproteins, triglycerides and atherosclerosis Inventor(s): Yegorova; Inna (Northridge, CA) Assignee(s): Braswell; A. Glenn (Miami, FL) Patent Number: 6,436,406 Date filed: June 15, 2000 Abstract: This invention provides compositions and methods related to the administration of red yeast rice, coenzyme Q.sub.10, and chromium, with or without inositol hexanicotinate, selenium, and mixed tocopherols to reduce or control blood cholesterol, triglycerides, low density lipoproteins, or increasing or controlling high density lipoproteins in a manunal, to reduce arterial plaque build-up, atherosclerosis, in a mammal which may be associated with cardiovascular, cerebrovascular, peripheral vascular, or intestinal vascular disorders. Excerpt(s): This invention relates to compounds and methods that reduce or control levels of cholesterol and triglycerides and their oxidation to lipid peroxidases, thus preferably inhibiting or arresting the development of atherosclerosis and restenosis when administered to mammals, including humans. The present invention relates generally to compositions and methods for treating atherosclerosis; more particularly, it relates to methods and compositions for treating or preventing atherosclerosis whereby the many and varied problems associated with the disease can be prevented, arrested, substantially alleviated or cured. In the United States and Western Europe, cardiovascular disease and its associated maladies, dysfunctions and complications are a principal cause of disability and the chief cause of death. One specific entity significantly contributing to this pathophysiologic process is atherosclerosis, which has been generally recognized as the leading health care problem both with respect to mortality and health care costs. The American Heart Association estimates that 953,110 persons died of cardiovascular diseases in 1997 (41.2 percent of all deaths), more than the
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number of mortality for cancer (539,377), accidents (95,644) and HIV (16,516) combined. Furthermore, by association calculations, close to a quarter of the US population suffers from one or more forms of cardiovascular disease. AMERICAN HEART Assoc., 2000, http://www.americanheart.org/Heart_and_Stroke_A_Z_Guide/cvds.html. The medical costs associated with coronary heart disease are estimated at $95 billion dollars a year. Gonzalez & Kannewurf, 55 (19) AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY S4-7 (Supp. 1, 1998). Web site: http://www.delphion.com/details?pn=US06436406__ •
Cosmetic product systems comprising a transfer resistant, flexible film-forming cosmetic product and an oil-containing composition Inventor(s): Dohmae; Terutomo (Shiga, JP), Drechsler; Lee Ellen (Cincinnati, OH), Hines; Christina M. (Houston, TX), Rabe; Thomas Elliot (Baltimore, MD), Smith, III; Edward Dewey (Mason, OH) Assignee(s): The Procter & Gamble Company (Cincinnati, OH) Patent Number: 6,555,097 Date filed: May 28, 1999 Abstract: Cosmetic product systems comprise a transfer resistant, flexible film forming cosmetic product having a solubility parameter on the Hildebrand scale of less than or equal to 8.5 (calories/cm.sup.3).sup.1/2, and a second composition comprising an oil having a C log P value greater than or equal to 13. The oil is selected from the group consisting of polyol fatty acid polyesters, triglycerides, glycerin/diethylene glycol/adipate cross polymers and mixtures thereof. Excerpt(s): The invention is for compositions and method for using said compositions to improve the performance of long-wearing cosmetic products. These compositions and methods for using such compositions enable the user to significantly enhance the attributes of long-wearing cosmetic products without compromising their primary advantages. Compositions used to enhance cosmetic products are known in the art. Such compositions include those that are applied over top compositions such as lipstick to provide attributes such as gloss, lubricity and transfer-resistance of the cosmetic product they are applied over. These enhancement products utilize a variety of polymeric fluids and film forming technologies. For example, acrylic film-formers that are incorporated in lipstick overcoat products such as CSI Incorporated's "Sealed with a Kiss" are delivered in a volatile vehicle, alcohol, which is spread over the lipstick surface. wherein R.sup.1 though R.sup.5 are independent fluorine atoms, perfluoroalkyl groups, or oxyperfluoroalkyl groups; the value of p, q, and r is at least zero; wherein the perfluoropolyether molecular weight is from about 500 to about 10,000, wherein P, Q and R may be equal, but, not zero. The preferred perfluoropolyether disclosed therein is a commercially available product known as Fomblin HC-04, HC-25, and HC-R available from Montefluosu of Milano, Italy. Web site: http://www.delphion.com/details?pn=US06555097__
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Crisp filled pastry after microwave baking Inventor(s): Ferrari-Philippe; Fabiana (Beauvais, FR), Tharrault; Jean-Francois (Coincourt, FR) Assignee(s): Nestec S.A. (Vevey, CH) Patent Number: 6,503,546 Date filed: July 26, 2000 Abstract: A filled pastry that can be baked in a microwave to achieve a baked pastry-like taste and a crisp final texture is described. The pastry mixture includes flour, a first fat, water, yeast, emulsifier, pentosanase, and amino acids. A liquid filling with a high water content is trapped in the pastry by a moisture barrier placed in contact therewith. The moisture barrier contains from about 80 to about 98 percent fat, from about 7 percent to about 13 percent of a film-forming protein, and from about 0.7 to about 1.3 percent of a hydrocolloid. The fat may includes medium-chain triglycerides whose melting point is between 20.degree. C. and 35.degree. C. The film-forming protein may be calcium or sodium caseinate. The hydrocolloid may be an iota-type carrageenan. This moisture barrier mixture is disposed between the filling and the pastry in an amount of about 1 to about 15 g/100 cm.sup.2. Excerpt(s): The subject of the present invention is a deep-frozen filled pastry which becomes crisp after microwave baking. The crisp products which are currently on the market are based on prebaked pastries. These prebaked pastries are normally heated in a microwave. The crispness of these products is entirely due to the presence of susceptors which create temperatures of about 200.degree. C. in contact with the product and thus allow drying of the surface. The baking of raw filled pastries in a microwave is delicate because the baking time is short and the filling rapidly arrives at high temperatures. In addition, the distribution of the microwaves is heterogeneous. Maillard reactions are very weak and therefore pastries cooked with microwaves have a raw flour-like taste and do not brown. Web site: http://www.delphion.com/details?pn=US06503546__
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Electrical apparatus with dielectric fluid blend of polyalphaolefins and polyol esters or triglycerides Inventor(s): Gauger; Gary A. (Franklin, WI), Goedde; Gary L. (Racine, WI), Lapp; John (Franklin, WI), Yerges; Alan Paul (Muskego, WI) Assignee(s): Cooper Industries, Inc. (Houston, TX) Patent Number: 6,485,659 Date filed: June 16, 1998 Abstract: The present invention comprises a mixture of hydrocarbons having a welldefined chemical composition that is suitable for use as a dielectric coolant in electrical equipment in general, and specifically in transformers. The dielectric coolants of the present invention are particularly suited for use in sealed, non-vented transformers, and have improved performance characteristics, including decreased degradation of the paper insulating layers, as well as a greater degree of safety and environmental acceptability. The present dielectric coolants comprise relatively pure blends of compounds selected from the group consisting of aromatic hydrocarbons,
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polyalphaolefins, polyol esters, and natural vegetable oils, along with additives to improve pour point, increase stability and reduce oxidation rate. Excerpt(s): Not applicable. This invention relates generally to equipment utilized in the transmission and distribution of electrical power. More specifically, the invention relates to transformers and other apparatus containing dielectric fluids, particularly dielectric fluids comprising relatively pure blends of compounds selected from the group consisting of aromatic hydrocarbons, polyalphaolefins, polyol esters, and natural vegetable oils. The invention further relates to the methods for preparing and processing such fluids and filling and sealing electrical apparatus with such fluids. Many types of conventional electrical equipment contain a dielectric fluid for dissipating the heat that is generated by energized components, and for insulating those components from the equipment enclosure and from other internal parts and devices. Examples of such equipment include transformers, capacitors, switches, regulators, circuit breakers and reclosers. A transformer is a device that transfers electric power from one circuit to another by electrical magnetic means. Transformers are used extensively in the transmission of electrical power, both at the generating end and the user's end of the power distribution system. A distribution transformer is one that receives electrical power at a first voltage and delivers it at a second, lower voltage. Web site: http://www.delphion.com/details?pn=US06485659__ •
Engines lubricated with vegetable oil lubricants Inventor(s): Johnson; Duane L. (113 OBrien Ter., Big Fork, MT 59911), Lambert; James W. (1127 W. Colorado Ave., Colorado Springs, CO 80904) Assignee(s): none reported Patent Number: 6,531,430 Date filed: August 23, 2001 Abstract: An internal or an external combustion engine which has at least one surface coated with a lubricant made up of vegetable-based products. The products preferably include a base oil containing primarily mono, di and triglycerides and free fatty acids, 530% by volume hydroxy fatty acids and 5-10% of the oil additives by volume of animal or vegetable waxes. Excerpt(s): This invention relates to internal and external combustion engines of all types lubricated with vegetable-based lubricants. The engines utilize the lubricants to prevent metal-to-metal contact between multiple moving parts and/or moving and nonmoving parts. Traditionally, internal combustion engines have utilized petroleum-based lubricants. These lubricants are increasingly becoming an environmental problem because bacteria which metabolize these materials are not widely distributed in the environment. Previously, animal and/or vegetable oils and waxes have been added to petroleum-based lubricants to enhance one or more properties of the lubricant. The lubricants of this invention, however, utilize vegetable-based oils and waxes as the primary lubricant with any coal or petroleum-based materials being present in small amounts as an additive(s). The new lubricants can also include commonly used, nonhydrocarbon additives, e.g., alkaline earth phenates, micronized nylon and silicones. Web site: http://www.delphion.com/details?pn=US06531430__
Patents 121
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Enzymatic methods for polyunsaturated fatty acid enrichment Inventor(s): Breton; Gildas (Penanguer, Concarneau, FR F-29900) Assignee(s): none reported Patent Number: 6,537,787 Date filed: March 13, 1998 Abstract: A process for obtaining polyunsaturated fatty acid concentrates comprising subjecting a fish oil containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), to a selective enzymatic hydrolysis in position 1, 3 or 2, to obtain a mixture of free fatty acids, monoglycerides and diglycerides, separating the constituents of this mixture, collecting the free fatty acids which are purified by crystallization from urea, to increase the EPA and DHA content, decomplexing the isolated fatty acids by an interesterification between the free fatty acids concentrated into polyunsaturated fatty acids and the crude oil, in the presence of a lipase specific for position or steric hindrance, to obtain a mixture enriched with polyunsaturated fatty acid triglycerides which is separated and freed from the free fatty acids and a process for enrichment with polyunsaturated fatty acids (EPA, DHA) of phospholipids by an enzymatic route, as well as in the synthesis of monoacylglycerols of polyunsaturated fatty acids of the n3 series, by enzymatic synthesis starting with a 1,2-dialkylene glycerol which are useful in the domain of foodstuffs, cosmetics and pharmacology. Excerpt(s): A subject of the present invention is new processes for the production of polyunsaturated fatty acid esters in a pure or concentrated form. A more particular subject of the invention is processes for the production of esters of polyunsaturated fatty acids of the.omega.-3 series starting with glycerides of fatty acids extracted from fish oils, phospholipids, or 1,2-dialkyene glycerols, using an enzymatic treatment. A specific subject of the invention is a process for the production of glycerides of polyunsaturated fatty acids in a pure or concentrated form from fish oil or other sources, characterized in that it allows, by enzymatic treatment, a mixture to be obtained containing a high content of docosahexaenoic acid (DHA) and/or of eicosapentaenoic acid (EPA), which can reach, in the case of fish oils, 60%. Web site: http://www.delphion.com/details?pn=US06537787__
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Fatty-acid thermal storage devices, cycle, and chemicals Inventor(s): Suppes; Galen J. (4009 Day Flower Ct., Columbia, MO 65203) Assignee(s): none reported Patent Number: 6,574,971 Date filed: September 5, 2001 Abstract: This invention is a method for producing phase change material (PCM) chemicals containing fatty acids or fatty-acid derivatives. These derivatives (1) are renewable, being produced by biomass or livestock such as cattle, (2) can be manufactured at low to moderate prices, and (3) can be manufactured in a variety of ways to produce PCM chemicals effective at several temperatures of interest in climate control and food maintenance.Unlike paraffin PCM chemicals that are largely limited to fractions available in either crude oil or irreversible chemical synthesis processes, the ester bond chemistry of triglycerides (fats and oils) is reversible allowing repeated reaction until the desired PCM chemicals combinations are synthesized and isolated.
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This method in a process based on contacting of reactants, reversible ester bond chemistry, separation of fractions with the desired latent heat properties, and recycle of those fractions that do not have the desired latent heat properties. Excerpt(s): This invention is on phase change material (PCM) chemicals used in PCM devices to store or remove thermal energy. Applications include (1) walls, flooring, and tank devices used to moderate climates in buildings (2) food storage coolers or other types of coolers, (3) devices used to keep food warm, and (4) essentially any device used to keep a substance at a relatively constant temperature between -20.degree. C. and 150.degree. C. More specifically, this invention is on a composition of PCM chemicals largely comprised of fatty acid derivatives, a method for producing these PCM chemicals, and a method for using these PCM chemicals. The term "phase change material" or PCM is known in the science as that class of materials that uses phase changes to absorb or release heat at a relatively constant temperature. Typically the phase changes are fusion (or melting) with an associated latent heat. 1. Eliminating need of air conditioner or heater requirements during substantial portions of the year. Web site: http://www.delphion.com/details?pn=US06574971__ •
Food emulsion containing an emulsifier from sorbitan Inventor(s): Fisch; Tanja (Burgkirchen, DE), Scherl; Franz Xaver (Burgkirchen, DE), Turowski-Wanke; Angelika (Kelkheim, DE) Assignee(s): Clariant GmbH (Frankfurt, DE) Patent Number: 6,465,036 Date filed: November 27, 2000 Abstract: This type of foods, in particular margarine, comprises, as emulsifier, reaction products of sorbitol with triglycerides. Excerpt(s): The invention relates to the use of sorbitol esters of fatty acids, in particular sorbitol esters based on rapeseed oil, in foods as flavor-neutral emulsifier having a very effective action on the reduction of surface tension of both polar and nonpolar liquids and high stability even under temperature stress and at low concentrations in use. The inventive low-melting emulsifiers based on renewable raw materials exhibit outstanding hydrophilic and hydrophobic properties which cause good emulsifying action in water-in-oil emulsions. The present invention relates to foods in the form of oil-in-water or water-in-oil emulsions which comprise, as emulsifiers, a reaction product of sorbitol and triglycerides. The reaction of sorbitol with the fatty acid triglycerides or methyl esters of fatty acids takes place in a one-pot process without solvent at temperatures of approximately 120-140.degree. C. in the presence of an alkaline catalyst. The reaction time is generally 12 to 13 hours. Since sorbitol is customarily commercially available as an aqueous solution, the water must firstly be removed. This is performed by distillation under reduced pressure at a maximum of 120.degree. C. The molar ratio of sorbitol to fatty acid triglycerides is generally 1:4.5, preferably 1:3.5 to 1:4.5. Web site: http://www.delphion.com/details?pn=US06465036__
Patents 123
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Infant formula with free amino acids and nucleotides Inventor(s): Gohman; Sharon (New Brighton, MN), Lowry; Carol Jo (Minneapolis, MN) Assignee(s): Novartis Nutrition AG (Berne, CH) Patent Number: 6,511,696 Date filed: December 13, 2000 Abstract: A fat-rich powder provides the complete nutritional needs of an at-risk infant no more than one year old, who has acquired a milk allergy, such as cow's milk allergy ("CMA"), and/or an allergy to protein in "soy milk", as well as digestive or absorption problems resulting in a damaged gut. Because such an infant must derive all its protein from amino acids it is not fed any ingredient derived from mammalian milk, but a combination of amino acids with nucleotides in specified amounts along with free Lglutamine, maintaining specified ratios of their relative amounts, which ratios in the ranges stated are found to be beneficial for healing of the infant's damaged gut, and for promoting cell division to assure its normal growth. A typical feeding of 32.6 gm of the powder delivers 160 cals; the powder, including triglycerides of relatively long chain fatty acids which contribute about 50% of the total caloric content of the powder, is nevertheless solubilized when the powder is manually shaken at 35.degree. C. in a bottle containing 240 ml (8 fl oz) of water. Excerpt(s): This invention relates to a non-milk based hypoallergenic infant-formula for "at-risk" infants no more than one year old, who have a documented milk allergy, such as cow's milk allergy ("CMA"), and/or an allergy to protein in "soy milk". By "non-milk based" is meant that no ingredient of the formula is derived from mammalian milk. Because typically, such infants have acquired digestive or absorption problems, the only source of protein in the formula is to be from free amino acids, and the formula is to be storable in powder form but have specified deliverability. By "specified deliverability" is meant that the powder is solubilized in an essentially homogeneous liquid form within less than 30 secs when a unit dosage amount of 32.6 gm of the powder is manually shaken with water at 35.degree. C. in a bottle containing 240 ml (8 fl oz) of water. By "solubilized" is meant that the powder is either soluble in water or forms an emulsion in water forming a liquid having physical characteristics analogous to those of human milk. Still more particularly, the novel formula of the invention does not otherwise mimic human milk in that nutrient powder contains no intact or antigenic proteins; when the powder is solubilized as a ready-to-feed liquid, it is required to have a viscosity less than 10 cp at 25.degree. C. to allow flow through a tube if the formula is delivered enterally rather than taken orally. By "intact protein" is meant a tripeptide or larger molecule having a molecular weight greater than about 500 Daltons; protein hydrolysates of whey or casein contain a major proportion by weight of tripeptides or larger molecules. Hereafter the term "enterally" specifically refers to feeding through a tube such as is typically inserted into the stomach of an infant who cannot easily be fed orally; and the term "at-risk infant" is used to specify one which is no more than one year old. The age limit is critical because a child more than one year old is not seriously "at-risk" since a one-year old is typically fed other food along with formula, and is relatively tolerant to an unbalanced formula for long enough a time to allow a competent nutritionist to alleviate the effects of the misdirected or misapplied diet. A typical infant, not a prematurely born infant, who is to be fed the novel formula weighs in the range from about 2.3 kg (5 lb) to 5.5 kg (12 lb) at birth, and weighs in the range from about 4.5 kg (10 lb) to 11.5 kg (25 lb) after one year. The problem is to provide a storable powder formula which (i) provides the entire nutrition requirement of an atrisk infant needing an energy content in the range from about 200-250 Kcal/g nitrogen,
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without including any intact protein, (ii) is "gut-healing", that is, effective to heal damage already inflicted on the infant's digestive system, and (iii) yet meets the deliverability requirements specified. The problem is solved with a formula having a tailored distribution of amino acids and nucleotides which in combination with a source of unsaturated fats and relatively short chain carbohydrates and other ingredients, provide all the vitamin and mineral needs of the infant, yet prevent GI problems. A nucleotide consists of a nucleoside combined with phosphoric acid; a nucleoside is a compound made of a sugar and a purine or pyrimidine base, especially one obtained by hydrolysis of a nucleic acid, such as adenosine. The term "nucleotide" is used herein as an equivalent of "nucleoside" in that the form in which the compound is present is not critical so long as the specified number of "nucleotide equivalents" are used. A "nucleotide equivalent" refers to the nucleotide content present in any one or more of the following forms: ribo-nucleosides, ribo-nucleotides, RNA, phosphate esters and d-ribose adducts of one with another; the various forms of nucleotides are determined, calculated and expressed as the monophosphate esters. Web site: http://www.delphion.com/details?pn=US06511696__ •
Injectable formulations of avermectins and milbemycins Inventor(s): Grosse-Bley; Michael (Koln, DE), Kujanek; Richard (Koln, DE) Assignee(s): Bayer Aktiengesellschaft (Leverkusen, DE) Patent Number: 6,617,314 Date filed: March 10, 1999 Abstract: The present application relates to injection formulations of avermectins and milbemycins based on a solvent mixture comprising sesame oil, medium-chain triglycerides, glycol esters or fatty acid esters and a further solvent from the group consisting of mono- or polyhydric aliphatic or aromatic alcohols and their derivatives (e.g. cyclic carbonates; acetates; acetals; ketals) or castor oil. Excerpt(s): The invention relates to new injection formulations of avermectins and milbemycins based on solvent mixtures which contain sesame oil. Injection formulations of ivermectin are disclosed in EP-A 146 414. The formulations contain a solvent mixture of propylene glycol and glycerol formal in the ratio 60:40 v/v. It is known of propylene glycol that in certain concentrations it can cause local intolerabilities (see review: B. Kruss, Acta Pharm. Technol. 35(4) (1989) 187-196). The precipitation of the waterinsoluble active compound ivermectin can also occur in the tissue around the administration site. Thus when using corresponding formulations marked swellings and tissue incompatibilities were observed at the injection sites, some of which only receded after several weeks. Injection formulations of specific avermectins are disclosed in EP-A 393 890. They are oil formulations based on sesame oil and ethyl oleate in the ratio 90:10 v/v. These formulations are tolerable, but have the disadvantage that the solubility for avermectin/milbemycins is often inadequate to achieve a concentration of 1% m/v or higher which is desirable for use. As a rule, under elevated temperature conditions (T.gtoreq.80.degree. C.) supersaturated 1% n/v solutions are obtained, which permanently crystallize out again at lower temperatures. Web site: http://www.delphion.com/details?pn=US06617314__
Patents 125
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Linseed oil and method for preparation thereof Inventor(s): Selder; Mikkel (Huddungeby, SE) Assignee(s): Linotech AB (Jarl.ang.sa, SE) Patent Number: 6,610,870 Date filed: May 28, 2002 Abstract: Processed linseed oil essentially consisting of linolenic, linolic and oleic acids, mainly in the form of triglycerides, its content of free tocoferol being less than about 100 ppm; and a process for the manufacture of linseed oil comprising the following steps: a) heating crude linseed oil to an increased temperature lower than the boiling point of water, b) adding a heated inorganic acid to the oil and mixing the oil, c) separation of precipitated materials, d) adding a heated aqueous solution of alkali to the oil and mixing the oil, e) discharge of the soap formed, and f) rinsing the oil with hot water until a clear rinsing water is obtained. Excerpt(s): The present invention relates to linseed oil which has been processed for the purpose of improving the properties of the oil in connection with the use in for example impregnation of products based on cellulose, such as wood. The invention also relates to a process for the manufacture of such linseed oil. Even if the present invention is applicable in relation to other cellulose-based products than wood the invention will in the following be described in connection with wood in the form of different types of lumber. Decomposition of wood when used outdoors is almost exclusively caused by fungi and bacteria. The requirement for growth of such micro-organisms is the presence of water. Furthermore, a suitable temperature and access to nutrition and oxygen are required. Prevention of decomposition can be based on the elimination of one or more of these conditions necessary for the growth of the micro-organisms. As an example there can be mentioned that if the moisture content is brought down to a value lower than about 20% biological decomposition is substantially prevented. A number of different impregnation processes for the protection of wood are known, and these methods can in principle be divided up into techniques based on the supply of a substance poisonous to the growth of the micro-organisms, and techniques whereby the wood is given hydrofobic properties, for example by impregnation with some kind or oil. In the latter case an impregnation agent is crude linseed which can be of hot- or cold-pressed type, both of which by suitable heat treatment are concerted into boiled linseed oils. The use of such linseed oils is, however, associated with certain drawbacks for example a viscosity which is unfavourably high for ease of handling, a contents of components constituting substrate for the relevant micro-organisms, unfavourable drying properties, etc. One method used for lowering the viscosity is dilution with a solvent something which, however, is environmentally unacceptable. The use of chemical poisons is presently frequently used but should for the future be mainly prohibited for environmental reasons. Also impregnation with a combination of hydrofobation and toxic treatment is used, for example treatment with creosote. Web site: http://www.delphion.com/details?pn=US06610870__
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Method for producing a non-fatty softener based on wax-esters Inventor(s): Cecchi; Georges (Marseille, FR) Assignee(s): Sophim (Peyrius, FR) Patent Number: 6,596,886 Date filed: February 15, 2002 Abstract: The invention relates to a process for manufacturing non-oily emollients with a molecular weight below about 600 Dalton, preferably below 550 Dalton, and still more preferably below about 450 Dalton, based on alcohol and fatty acid esters (wax-esters), which consists of the following steps:a) interesterification of the triglycerides contained in a fatty material by a primary alcohol, in the presence of a catalyst;b) elimination of the catalyst;c) distillation of the residual alcohol preferably in the presence of a bleaching agent followed by elimination of the bleaching agent;d1) either frigelisation of the preferably bleached residue such that residual glycerides are at least partially crystallized, followed by elimination of said crystallized residual glycerides,d2) or hydrogenation of the residue, preferably bleached. Excerpt(s): The invention relates to the field of fine chemicals. More precisely, the invention relates to a process for the manufacture of a non-oily emollient. Emollients are widely used in the cosmetic and pharmaceutical industries to render dry skin soft and to improve its elasticity. The term emollient generally refers to the set of perceptions conveyed by the senses of touch and sight. Perceptions evoked by touch are softness, elasticity and smoothness. Perceptions evoked by sight are shininess and dullness. A considerable number of emollients are offered by suppliers of cosmetic starting materials. These emollients differ from each other in terms of their chemistry, as well as in terms of the result of two factors: emollience on application and residual emollience. There are therefore emollients with a protective effect, others with a highly oily effect, while some give the impression of dryness and others still have an astringent effect. Web site: http://www.delphion.com/details?pn=US06596886__
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Method for the prediction of preeclampsia and other diseases Inventor(s): Arbogast; Bradley W. (Johnson City, TN) Assignee(s): Arbogast Pharmaceuticals, Inc. (Johnson City, TN) Patent Number: 6,642,055 Date filed: March 31, 2000 Abstract: The invention disclosed is a process for determining the cytoprotective activity of plasma that prevents the destruction of endothelial cells and forestalls the development of a number of diseases such as atherosclerosis, preeclampsia, edema, nephrotic syndrome, and stroke. The present invention includes a method of diagnosing a patient's proclivity to develop a disease having a correlation to a reduction in the concentration of pI 5.6 albumin in the plasma by determining a value indicative of the concentration of the pI 5.6 albumin that is not bound to VLDL ("free pI 5.6 albumin") in the patient's blood serum. The preferred embodiment of the process utilizes in vitro methods to obtain an indicator of the free pI 5.6 albumin instead of directly measuring the concentration of the free pI 5.6 albumin. The preferred method comprises the steps of:(a) providing a plasma sample containing free albumin, triglycerides, very low density lipoproteins, low density lipoproteins, and non-esterified fatty acids bound to
Patents 127
the free albumin;(b) determining the concentration of the free albumin;(c) determining the concentration of the non-esterified fatty acids bound to the free albumin; and(d) calculating a value indicative of the toxicity preventing ability of the plasma by comparing the concentration of the free albumin to the concentration of the nonesterified fatty acids bound to the free albumin. The present process does not provide direct measurement of the cytoprotective activity of plasma, but rather, an empirical value which has clinical relevance in identifying patients with a high chance of developing diseases inhibited by pI 5.6 albumin. Excerpt(s): The present invention relates to methods for predicting and following illnesses. More particularly, the present invention relates to the diagnosis of preeclampsia and other diseases. Vascular disease is often related to the composition of blood flowing therethrough. In particular, high concentrations of very low density lipoproteins (VLDL) in blood have a deleterious effect on vascular integrity. Very low density lipoproteins in blood tend to break down the inner vascular walls causing vascular diseases including preeclampsia, atherosclerosis, stroke, peripheral vascular disease, diabetic vascular disease, and such. Methods providing earlier detection of vascular diseases, and methods for diagnosing a patient's proclivity toward developing a vascular disease at a later point in his life are desirable so that such disease may be better controlled, or even avoided. The early detection of preeclampsia is particularly important. Web site: http://www.delphion.com/details?pn=US06642055__ •
Oat lipid based surfactants and derivatives and process for preparing same Inventor(s): Syed; Samad A. (Paramus, NJ), Walele; Ismail I. (Saddle Brook, NJ) Assignee(s): Finetex, Inc. (Elmwood Park, NJ) Patent Number: 6,464,991 Date filed: April 21, 2000 Abstract: Novel oat-lipid based derivatives, surfactants and emollients are disclosed, as well as their use in the production of surface active derivatives or non-surface active esters, and ester emollients. The surfactants and fatty derivatives are useful as emollients, dispersants, emulsifiers, and conditioners for hair care and skin care products. For example, derivatives such as amides of oat fatty triglycerides ("OFTG")/Monoethanolamine; Acyl Amidopropyl Dimethyl Amines of OFTG as Cationic Surfactants; Betaines based on OFTG; Esters of OFTG based Fatty Acids and Isostearyl Alcohol; Quaternaries based on OFTG based Amido-propyl Dimethyl Amine; Sulfosuccinamates based on OFTG--MEA Amides; and Sulfosuccinamates based on OFTG--Iso Propanolamines have been prepared. Derivatives may also include those involving other reactive groups known to those skilled in the art. Excerpt(s): The present invention relates to novel oat-lipid based surfactants and derivatives, and emollients, their process of manufacture, their use in the production of surface active derivatives, non-surface active esters, and ester emollients, and skin and hair care preparations containing the surfactants, derivatives, and emollients. The surfactants and fatty ester derivatives are useful as emollients, dispersants, emulsifiers, and conditioners for hair care and skin care products. Surfactants and derivatives are known for a variety of different applications for cosmetic, pharmaceutical, and medicinal purposes. Numerous references describe the production and use of surface active derivatives or non-surface active esters, and ester emollients. For example, it is
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known to use oats and oat extract in cosmetic preparations to obtain the benefits of mildness, antioxidant properties, etc. Surfactants and fatty derivatives useful as emollients, dispersants, emulsifiers and conditioners for hair and skin care products are commonly produced from a wide variety of fatty acids, fatty alcohols and amines, polyamines, dialkyl propylamines, alkanolamines, etc. However, none of these references teach or suggest the specific novel oat-based surfactants made from the fatty oil triglyceride obtained from oats, or OFTG, of this invention or the use of OFTG to produce surface active derivatives or non-surface active esters, and ester emollients for cosmetics and personal care products. Web site: http://www.delphion.com/details?pn=US06464991__ •
Oil-and-fat feedstock for production of cream and low-oil cream composition Inventor(s): Ebihara; Yoshitaka (Sakai, JP), Hidaka; Hiroshi (Sakai, JP), Iwai; Naomi (Sakai, JP), Izumi; Tugio (Sennan-gun, JP), Miyabe; Masaaki (Hannan, JP) Assignee(s): Fuji Oil Co., Ltd. (Osaka, JP) Patent Number: 6,497,914 Date filed: February 3, 1994 Abstract: There is provided a low oil cream composition which does not require a large amount of any particular emulsifying agent but has good physical properties after the whipping as well as good flavor and melting property in the mouth, even a low oily ingredient content such as not greater than 40%, and also provides is an oil-and-fat feedstock for production of the cream composition.The oil-and-fat feedstock for production of the cream composition is obtained by formulating not less than 30% of SUS-type triglycerides and 5 to 60% of a lauric-type oil-and-fat ingredient. A low-oil cream composition can be produced by the feedstock alone or, by further adding a cream containing milk fat to the cream. Then, it is possible to provide a low-oil cream composition having flavor and body comparable with fresh cream and to provide a process for production thereof. Excerpt(s): The present invention relates to an oil-and-fat feedstock for production of cream by a specific formulation with particular physical properties. It also relates to a low-oil cream composition produced from such an oil-and-fat feedstock. In recent years, there has been a demand in the field of food industry on the development of low-caloric, light and soft food with varying the habit of eating and with increasing the intention of health. Although fresh cream obtained from fresh milk is excellent in view of its flavor, body and the like, it has a very high fat content and is not necessarily suitable in veiw of the recent demand for the development of low-caloric food. In addition, fresh cream has unstable physical properties and is expensive. Web site: http://www.delphion.com/details?pn=US06497914__
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Oral pharmaceutical compositions liphophilic surfactants
containing
long-chain
triglycerides
and
Inventor(s): Aylwin; Elizabeth Anne (Swindon, GB), Banbury; Susan (Cheltenham, GB), de Nijs; Henrik (Oss, NL), Ferdinando; Josephine Joan Christine (Tadley, GB) Assignee(s): R.P. Scherer Technologies, Inc. (Paradise Valley, NV) Patent Number: 6,652,880 Date filed: December 21, 2001 Abstract: This invention is directed to pharmaceutical compositions for oral administration, wherein the drug or active ingredient is known to have stability problems associated with the use of free fatty acids. The compositions of the invention enhance the solubility of such compounds and improve the storage stability thereof and can be advantageously used in soft-gel and hard-shell capsular formulations. The liquid pharmaceutical compositions, according to the present invention, have a drug dissolved in a liquid vehicle. The liquid vehicle comprising a glyceride of a long chain fatty acid and a lypophilic surfactant having an HLB of less than ten. The composition, according to the invention, is also substantially free of free fatty acids. Excerpt(s): The invention relates to pharmaceutical compositions for oral administration. In particular, the invention relates to liquid pharmaceutical compositions suitable for softgel encapsulation. A number of drugs are known to require formulation in the presence of fatty acids, such as oleic acid, to provide optimum conditions for bioavailability. For example, long-chain fatty acids can be predisposed for lymphatic absorption, and therefore, are useful in pharmaceutical formulations in which the lymphatic system is the desired target site for the active ingredient. One of the problems associated with the formulations containing fatty acids is that chemical instability can arise due to their acidic nature and the presence of reactive carboxyl groups. Esterification can occur with drug molecules containing alcohol groups or transesterification of ester molecules. In the past, this problem has been solved by continuing to use free fatty acids in formulations which are encapsulated in softgel capsules and storing the capsules under refrigerated conditions to reduce the rate of reaction between the drug and fatty acids. However, where the drug is not sufficiently soluble in the formulation, cold storage methods result in crystallization which in turn necessitates equilibrating the capsules at room temperature to ensure crystal dissolution prior to consumption. Accordingly, complex storage regimens are required throughout the supply chain for the use of such formulations. Web site: http://www.delphion.com/details?pn=US06652880__ •
Plant growth regulating formulations Inventor(s): King; Roderick Whitfield (Deakin, AU), Kober; Reiner (Fussgonheim, DE), Mander; Lewis Norman (Aranda, AU), Pharis; Richard Persons (Cochrane, CA), Rademacher; Wilhelm (Limburgerhof, DE), Schneider; Karl-Heinrich (Kleinkarlbach, DE) Assignee(s): BASF Aktiengesellschaft (Ludwigshafen, DE) Patent Number: 6,458,746 Date filed: January 2, 2001
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Abstract: Plant growth regulating preparations comprising:(a) 0.1-20 wt. % of a 16,17dihydro gibberellin of formula (Ia) or (Ib);(b) up to 99.9 wt. % of a formulation additive selected from:(b1) the reaction products of triglycerides based on carboxylic acids having 2-30C and ethylene oxide and/or propylene oxide in the presence of a base, and/or(b2) fatty acid alcohol polyethoxylates;(c) up to 50 wt. % of an organic solvent;(d) 0.1-50 wt. % of a formulation auxiliary different from (b1) and (b2);(e) up to 50 wt. % of additional plant growth regulating compounds can be used in agriculture and horticulture to induce the desired effects on, for example, seed germination and seedling growth, rooting, dormancy, juvenility, maturity and senescence, flowering, abscission of leaves, flowers and fruit, fruit set and development, tuber formation, growth of shoot and root, photoassimilation, control of unwanted plants and senescence of whole plants or single organs. The 16,17-dihydroGA's are used to synergize the biological activity of exogenously supplied gibberellins. Particularly in graminaceous species, the compounds synergize the action of exogenous GA's and can, thus, be used to increase the yield of malt and decrease the amount of time required for the malting process, increase the yield of sugar cane and stimulate germination and seedling development in rice, wheat, barley, oats, rye, maize, sorghum, turf grasses and other plant species. Excerpt(s): e) up to 50% by weight of additional plant growth regulating compounds. Furthermore, the present invention relates to the use of the said preparations for the regulation of plant growth. Gibberellins (GAs) represent one group of plant growth substances. GAs occur naturally in higher plants where they function as phytohormones being involved in the regulation of growth and flowering and numerous other developmental processes. Certain GAs, particularly gibberellic acid or GA.sub.3 (ent3.alpha.,10,13-trihydroxy-20-norgiberrell-1,16-diene-7,19-dioic acid 19,10-lactone), are commercially available as fermentation products of the fungus Gibberella fujikuroi. Web site: http://www.delphion.com/details?pn=US06458746__ •
Podophyllotoxin preparation containing triglycerides Inventor(s): Gunzinger; Jan (Couvet, CH), Leander; Kurt (Peseux, CH), Rosen; Borje (Vallentuna, SE) Assignee(s): Analytecon SA (Couvet, CH) Patent Number: 6,440,428 Date filed: September 27, 1993 Abstract: The invention refers to new pharmaceutical preparations for the treatment of psoriasis and condyloma acuminata, and containing podophyllotoxin in combination with a liquid triglyceride. Excerpt(s): The present invention relates to new pharmaceutical preparations, primarily in the form av creams, which contain podophyllotoxin as the active ingredient, for the treatment of psoriasis and condyloma acuminata. The invention also refers to the use of such preparations for the manufacture of creams for the treatment of psoriasis and condyloma acuminata. From EP-B1-119 852, preparations of podophyllotoxin for the treatment of condyloma acuminata are known. These preparations comprise podophyllotoxin and at least one glycol selected from alkylene glycols and polyalkylene glycols. Furthermore, U.S. Pat. No. 4,788,216 describes a method of treating psoriasis, wherein podophyllotoxin is administered. It is mentioned that a cream can be used, but no specific pharmaceutical preparation is described. Web site: http://www.delphion.com/details?pn=US06440428__
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Preparation of a blend of triglycerides Inventor(s): Bons; Johannes Robert (Vlaardingen, NL), Floeter; Eckhard (Vlaardingen, NL), Stellema; Cornelis Sjouke (Vlaardingen, NL) Assignee(s): Lipton, division of Conopco, Inc. (Englewood Cliffs, NJ) Patent Number: 6,475,548 Date filed: June 13, 2001 Abstract: Triglyceride fat comprising a stearin fraction of a high stearic, high oleic sunflower oil and a margarine fat phase comprising said stearin in admixture with a liquid vegetable oil in a weight ratio of 20:80 to 80:20. Excerpt(s): The present invention refers to a process for the preparation of a blend of triglycerides and to food products containing such blends. Vegetable oils are the major constituents for the manufacture of margarine and similar fat continuous emulsion spreads. However, natural vegetable oils either do not have the triglyceride composition for imparting a proper plastic consistency to the final product or the obtained spreads show various product defects and/or nutritional drawbacks. Additional processing is necessary for a vegetable fat to become a suitable fat phase for spread manufacture. Usually a relative large amount of unprocessed liquid oil is blended with a relatively small amount of fat which is selected because of its liquid oil structuring ability. Such fat usually is a solid fat which has been subjected to one or more processing treatments. Current developments in food production aim at reducing artificial treatments of food in general and of fat in particular. Particularly, chemical processing such as hydrogenation is expected to be largely abandoned. When developing new margarine fats one of the aims is to find and grow plants which produce fat which after harvesting and purification is suited for margarine manufacture without additional fat processing. Present margarine fats have a high nutritional value because of a high unsaturated fatty acids acid content, but lack the relatively high stearic acid content and particularly the SUS triglycerides which are needed for structuring the liquid part of the fat blend. On the other side too much stearic acid has to be avoided for nutritional reasons. Breeding novel sunflower plants is a promising route for obtaining improved oils. Web site: http://www.delphion.com/details?pn=US06475548__
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Process for making soap bar comprising about 6% and greater triglycerides Inventor(s): Lanza; William (Towaco, NJ), Massaro; Michael (Congers, NY), Shafer; Georgia (Garfield, NJ), Yarovoy; Yury (Berkeley Heights, NJ) Assignee(s): Unilever Home & Personeal Care USA division of Conopco, Inc. (Greenwich, CT) Patent Number: 6,423,672 Date filed: April 26, 2001 Abstract: The invention relates to soap bars comprising 6% to 13% triglyceride oils wherein said bars simultaneously have post processing properties and maintain good lather. In a second embodiment, the invention relates to a process of making predominantly soap bars having noted properties comprising adding 6 to about 13% by wt. triglyceride oil(s) at finishing stage post crystallization.
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Excerpt(s): The present invention relates to a process for making predominantly soap based bars having about 6% by wt. or more (up to about 13% by wt.) of specific oils (i.e., triglyceride oils) which both process well (e.g., as measured by bar integrity, yield/++stress) and retain desirable users properties (e.g., lather) as per specifically defined tests. Traditionally, emollient oils (e.g., mineral oils, silicones, emollients esters) have been incorporated into soap bars at relatively low levels, or, less that 5.0% by wt. Higher levels are generally avoided to avoid problems in processability and/or in user properties (e.g., mineral oils lather poorly). At such levels, however, there is little discernible sensory effect. Typical of such bars having emollient levels of up to 5% is U.S. Pat. No. 5,952,276 to de Ferran et al. One reason why higher oils levels have not been used is because it has been traditionally difficult to add such high levels during soap milling step (i.e., the point in processing when other additives, such as colorants or odorants, have been added) or any time after cooling and when, accordingly, solidification has begun. Web site: http://www.delphion.com/details?pn=US06423672__ •
Process for separating a triglyceride comprising a docosahexaenoic acid residue from a mixture of triglycerides Inventor(s): Corley; David G. (Pranginf, CH), Doom; James P. (St. Peters, MO), Duffin; Kevin L. (Manchester, MO), Zeller; Samuel G. (San Diego, CA) Assignee(s): Omegatech, Inc. (Boulder, CO) Patent Number: 6,399,803 Date filed: February 17, 2000 Abstract: This invention is directed to a process for separating a first triglyceride comprising a docosahexaenoic acid residue from a second triglyceride. The process comprises introducing a feed mixture comprising the first triglyceride and the second triglyceride into a chromatographic separation zone, and then isolating a fraction of the feed mixture in the separation zone that has a mass ratio of the first triglyceride to the second triglyceride that is greater than in the feed mixture. The separation zone comprises a stationary phase which comprises metal ions that are capable of coordinating with a double bond of a fatty acid residue of the first triglyceride to form a metal complex with the fatty acid residue. Excerpt(s): This invention relates generally to adsorptive separation of triglycerides. More specifically, this invention relates to a novel process for separating a first triglyceride comprising a docosahexaenoic acid residue from at least one other triglyceride using a chromatographic separation zone having a stationary phase which comprises metal ions that are capable of coordinating with a double bond of a fatty acid residue of the first triglyceride to form a metal complex with the fatty acid residue. Docosahexaenoic acids ("DHA") are 22-carbon, naturally-occurring, unbranched fatty acids containing 6 carbon--carbon double bonds. It is well known that many triglycerides comprising a DHA residue (and particularly triglycerides comprising two DHA residues) have beneficial nutritional and pharmaceutical properties. For example, such compounds may be used to treat cardiovascular and inflammatory diseases. They also may be added to infant formula to promote the development of brain and retina functions. Unsaturated fatty acid residues of triglycerides are sometimes identified in the literature by an omega (".omega.") number. This nomenclature is used herein. The omega number denominates the position of the first double bond, when counting from the terminal methyl group of the fatty acid residue. For example, in Formula (II), the
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DHA residue is an.omega.-3 fatty acid residue, and the DPA residue is an.omega.-6 fatty acid residue. Often, fatty acid residues (and particularly the DHA residues) having the most beneficial cardiovascular effects are.omega.-3 fatty acid residues, although other fatty acid residues (such as arachidonic acid and.gamma.-linolenic acid, which are both.omega.-6 fatty acid residues) also have proven to be beneficial as well. Web site: http://www.delphion.com/details?pn=US06399803__ •
Process for the preparation of materials with a high content of long chain polyunsaturated fatty acids Inventor(s): Cain; Frederick William (Wormerveer, NL), McNeill; Gerald Patrick (Sharnbrook, GB), Moore; Stephen Raymond (Sharnbrook, GB), Zwemmer; Olga Cornelia (Wormerveer, NL) Assignee(s): Loders Croklaan B. V. (Wormerveer, NL) Patent Number: 6,534,110 Date filed: June 27, 2002 Abstract: Organic materials, comprising a mixture of at least two products (I) and (II), both containing isomers of conjugated long chain polyunsaturated fatty acids moieties (L.sub.1) and (L.sub.2) can be obtained by subjecting an organic material, selected from free fatty acids, mono-, di- or triglycerides, phospholipids, alkylesters or wax-esters, containing at least 5 wt. % of these conjugated polyunsaturated fatty acids, to an enzymic conversion (acidolysis, alcoholysis, esterification, hydrolysis) using an enzyme that can be discriminated between (L.sub.1) and (L.sub.2), so that original ratio L.sub.1 /L.sub.2 =X.sub.A in starting material is increased to X.sub.B, wherein X.sub.B.gtoreq.1.1 X.sub.A. Excerpt(s): The beneficial effects of conjugated long chain polyunsaturated fatty acids in food products for animals or humans have been recognised in the prior art. According to EP 440.325 CLA's can be applied as "metal chelator" in natural foods. The CLA's contain 9.11 and 10.12-octadecadienoic acid, salts or other derivatives thereof. The free acids can be prepared by e.g. an enzymic treatment, using.DELTA.sup.12 cis.DELTA.sup.11 trans isomerase, of linoleic acid. In U.S. Pat. No. 5,430,066 it is disclosed, that CLA's can be applied in foods for preventing weight loss, reduction in weight gain or anorexia in animals or humans. Also disclosed is, that these CLA's can alleviate the adverse catabolic effects of a product from the immune-system, in particular from interleukin-1. Web site: http://www.delphion.com/details?pn=US06534110__
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Protective coating compositions containing natural-origin materials, and method of use thereof Inventor(s): Kinnaird; Michael Gates (Durham, NC) Assignee(s): Chemtek, Incorporated (Yanceyville, NC) Patent Number: 6,623,554 Date filed: December 20, 2000 Abstract: A useful composition for protecting metal equipment from corrosion and/or other damage comprises 1) gilsonite, which is a mined asphalt; and/or some other
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natural-origin or naturally-derived resin, 2) a naturally-derived solvent such as dlimonene and/or other terpenes, and 3) a naturally-derived non-drying plasticizer such as fatty acid triglycerides. 4) Optionally, additives for controlling rheology, viscosity, lubricity, corrosion rates etc. can be added to obtain specific properties which may be desirable. The invention also relates to a method of preventing corrosion or other damage to metal equipment by applying the above-mentioned coating to the equipment by spraying, rolling and/or brushing. Excerpt(s): 3) a naturally-derived non-drying plasticizer exemplified by many fatty acid triglycerides. Optionally, additives for controlling rheology, viscosity, lubricity, etc. can be added to obtain specific properties which may be desirable. What makes the instant invention particularly useful is that the material is either mined directly from the ground as an inert solid, or contains naturally-derived, biodegradable, renewable materials. This makes it more "environmentally friendly" than many of the current coatings on the market, which contain petroleum solvents and/or petroleum asphalt. Another object of the instant invention is to provide an alternative to more expensive coatings that may be used, such as epoxy coatings. The compositions are useful as protective coatings for painted or unpainted metal surfaces, such as heavy equipment, bridges, piping, tanks, etc. Web site: http://www.delphion.com/details?pn=US06623554__ •
Skin cleansing bar comprising a fatty alcohol with low mush Inventor(s): Abbas; Syed Husain (Symour, CT), Coyle; Laurie Ann (Park Ridge, NJ), Hui; Ray (College Point, NY) Assignee(s): Unilever Home & Personal Care USA (Greenwich, CT) Patent Number: 6,458,751 Date filed: July 23, 2001 Abstract: A cleansing bar composition is described comprising an anionic surfactant, a C6 to C18 free fatty acid, and a fatty alcohol having a melting point under about 35.degree.C. and optionally a hydrophobic emollient. Useful emolients include triglycerides, hydrocarbons, silicones, fatty esters, and mixtures thereof. Useful anionic surfactants include C8 to C18 alkali metal acyl isethionates. Suitable low melting fatty alcohols include lauryl alcohol, oleyl alcohol, and a mixture thereof. The inventive bars have excellent mush, lather and wear properties. Excerpt(s): This invention relates generally to cleansing bars, and more particularly to cleansing bars having low mush. Synthetic detergent or syndet toilet bars have found considerable use as mild cleansing bars but such bars have the potential to exhibit unacceptable mush levels. Furthermore, syndet melt cast formulations require a higher level of solubilizers and suspending or dispersing agents than extruded formulations to dissolve all the components of the formulation. These solubilizers, such as fatty alcohols disadvantageously increase the mush level of the bar. U.S. Pat. No. 5,691,287 issued to Villars et al. on Nov. 25, 1997 discloses a sodium cocoyl isethionate cleansing bar containing cetyl and stearyl alcohol in a total concentration range of about 6 to 11 wt percent. U.S. Pat. No. 5,372,751 issued to Rys-Cucciari et al. on Dec. 13, 1994 discloses an acyl isethionate cleansing bar containing free fatty alcohols of 8-22 carbon atoms in an amount of 0-10 wt. percent. Web site: http://www.delphion.com/details?pn=US06458751__
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Soap bar comprising high levels of specific alkoxylated triglycerides which provide enhanced sensory properties and process well Inventor(s): Massaro; Michael (Congers, NY), Patel; Rajesh (Lyndhurst, NJ), Yarovoy; Yury (Berkeley Heights, NJ) Assignee(s): Unilever Home & Personal Care USA, Division of Conopco, Inc. (Greenwich, CT) Patent Number: 6,544,938 Date filed: October 2, 2001 Abstract: The present invention relates to the composition comprising soap and alkoxylated triglyceride wherein said bars have improved sensory properties (e.g., reduced drag and stickiness; and enhanced slipperiness) relative to identical bar with non-alkoxylated triglyceride. Excerpt(s): The present invention relates to predominately soap based bars (e.g., about 50% to 85% by wt. soap) comprising high levels (e.g., 7% to 15%, preferably 8% to 14%) of alkoxylated triglycerides. The alkoxylated triglycerides used at these levels provide excellent sensory properties (e.g., wet skin feel associated with moisturization and skin care, less "draggy" feel, creamy lather). In addition, the alkoxylated triglycerides provide acceptable to superior hardness and yield stress and thus are "readily" processable. In this regard, the alkoxylated triglycerides provide a single, inexpensive method of providing skin care benefits into simple soap base. Traditionally, emollient oils such as mineral oils, silicone oils, emollient esters and triglycerides have been incorporated into soap bars at relatively low levels, i.e., less than 5.0%. Higher levels have been avoided because they have been believed to cause problems in processing and in user properties (e.g., poor lather). At the low levels used, however, there is little discernible sensory effect. In U.S. Pat. Nos. 3,814,698 and 3,941,712, both to Ferrara, compositions having much higher levels of "bath oil" are added at bar saponification step (when ingredients are liquid) rather than milling steps. Web site: http://www.delphion.com/details?pn=US06544938__
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Solvent and method for extraction of triglyceride rich oil Inventor(s): Flanigan; Virgil J. (Rolla, MO), Kapila; Shubhen (Rolla, MO), Nam; Paul K. S. (Rolla, MO) Assignee(s): University of Missouri Board of Curators (Columbia, MO) Patent Number: 6,547,987 Date filed: January 25, 2000 Abstract: The present invention relates to a solvent for use in extracting oil from an oil bearing material, such as soybeans, with the solvent resulting in the selective extraction of a triglyceride rich oil, which contains 95% or greater triglycerides and non-polar constituents, with the solvent comprised of a hydrocarbon, preferably hexane, and a fluorocarbon, so that the solvent has a viscosity less than 2.6 centipoise and a polarity of less than 0.1. The present invention also relates to a method of using the solvent to extract the triglyceride rich oil, with the method including preferably extracting the oil at a temperature ranging between 35.degree. C. and 55.degree. C., and then preferably cooling resulting miscella to a temperature ranging between 15.degree. C. and 25.degree. C.
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Excerpt(s): The present invention relates to a method and solvent for use in extracting oil from oil bearing materials, preferably a triglyceride rich oil is selectively extracted from the oil bearing material. More preferably, the present invention relates to a solvent, comprised of a hydrocarbon and a fluorocarbon, and a method that will preferably remove an amount of oil comprised of greater than 95% by weight triglycerides and other non-polar constituents from an oil bearing material, such as a soybean material. Oils, especially oils comprised primarily of triglycerides and other non-polar constituents, are used in a variety of applications including uses as edible and nonedible oils. Edible oils that are high in triglycerides are especially desired and are typically used as food ingredients or as a medium for frying or cooking foods. Triglyceride rich edible oils are preferred for use because they have a high smoke temperature, meaning they do not readily smoke or burn when heated, making them ideal for frying or cooking, and have a desirable flavor. It should be pointed out that most edible oils sold in grocery stores are primarily comprised of triglycerides. Nonedible oils include technical oils such as lubricating oils and hydraulic fluids and fuel. There are a variety of sources available for use in extracting oils which are high in triglycerides. Some of the available raw material sources include: soybeans, corn, sunflower, palm, cotton seed, olives, peanuts, linseed, and coconut. Additionally, there are other types of vegetable and animal matter which can be used to extract oil that is high in triglycerides. Regardless of the source of the oil, it is generally preferred that the extracted oil be devoid of unsaponifiable matter, pigments, phospholipids or phosphatides, and odoriferous components. This is especially true if the oil is going to be used for cooking or edible oil purposes. Unfortunately, most known methods for extracting oil from oil bearing materials initially result in an oil which contains these unwanted components. As such, it is often necessary to pass the extracted oil through a number of refining steps to ensure adequate removal of the odoriferous components, phospholipids, and pigments. Additional refining steps, however, are undesirable because additional steps generally raise the cost associated with producing both edible and non-edible oils. Increased energy inputs are required and often more equipment is necessary. For these reasons, it is desired to have a more cost efficient and less energy intensive method which most likely requires fewer steps for removing oils rich in triglycerides from oil bearing materials. Web site: http://www.delphion.com/details?pn=US06547987__ •
Specific pancreatic lipase inhibitors and their applications Inventor(s): Chapus; Catherine (Marseilles, FR) Assignee(s): Laboratoire Laphal (Laboratoire de Pharmacologie Appliquee) (Allauch, FR) Patent Number: 6,432,400 Date filed: September 27, 1999 Abstract: The invention concerns specific pancreatic lipase inhibitors and their applications in the treatment and prevention of cardiovascular diseases, of lyperlipemia and of obesity, as well as diagnostic reagent and as regulating agent in a process of controlled lipolysis of triglycerides. Said inhibitors correspond in particular to a peptide consisting of a C-terminal fragment of pancreatic lipase including the recognition site of a colipase. Excerpt(s): The present invention relates to specific pancreatic lipase inhibitors and to their applications in the treatment and prevention of cardiovascular diseases, of
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hyperlipemia and of obesity, and also as diagnostic reagent and as regulating agent in a method of controlled lipolysis of triglycerides. Dietary fats represent an efficient source of energy for the body. Indeed, the quantity of energy metabolized from lipids is significantly greater than that metabolized from carbohydrates or proteins. However, given that practically all the lipids ingested are assimilated by the body, a dietary excess of lipids can cause substantial health disorders: cardiovascular disorders, hyperlipemias and obesity. These disorders are frequently encountered in industrialized countries where the populations often have diets which are too high in saturated fats. Web site: http://www.delphion.com/details?pn=US06432400__ •
Super absorption coenzyme Q10 Inventor(s): Udell; Ronald G. (Beverly Hills, CA), Hari; Siva P. (Riverside, CA) Assignee(s): Soft Gel Technologies, Inc. (Los Angeles, CA) Patent Number: 6,623,734 Date filed: June 22, 2001 Abstract: A new soft gelatine formulation and process methodology is disclosed herein that increases single Coenzyme Q10 molecules presented to the absorption channels of the small intestines by providing medium chain triglycerides, Vitamin E, and natural beta carotene to Coenzyme Q10 in a soft gel capsule to increase the absorption thereof. Excerpt(s): This invention relates to a new soft gelatine formulation and process methodology that increases single Coenzyme Q10 molecules presented to the absorption channel of the small intestines. Coenzyme Q.sub.10 (CoQ.sub.10) is a large molecular weight lipid compound that is produced in the liver and other organs. The total human body content is 1.4 to 1.8 grams depending on the individual's age and fitness level. CoQ.sub.10 is found in all tissues of the body. It is mostly concentrated in the mitochondria and other organelles that help the body metabolize nutrients into energy. These include organs with high levels of metabolic activity. Organs, whose primary purpose is energy production, tend to store and use CoQ.sub.10 in large amounts. Such organs include the heart, liver, and skeletal muscle tissue. The heart and skeletal muscle of an aaverage human contain about 1000 mg of CoQ.sub.10. This is in contrast to metabolically inactive body components such as the blood, which only contains about 4 mg of CoQ.sub.10. However, blood plays an important role in as a CoQ.sub.10 reservoir. Blood helps to transport CoQ.sub.10 from endogenous CoQ.sub.10 made in the liver and exogenous CoQ.sub.10 absorbed from digested food in the intestinal tract. Endogenous CoQ.sub.10 accounts for approximately 56 percent of the body's supply. The remaining 44 percent must be provided through diet and supplementation. These numbers are currently being studied but the latest studies indicate lower endogenous production of CoQ.sub.10, which indicates a significant deficiency, in correlation with increased age. Furthermore, certain disease states such as cardio myopathy and high cholesterol levels, which are treated with Statin drugs, seem to deplete endogenous CoQ.sub.10 production thereby indicating a need for supplementation. These deficiencies in the nutrient have no relation to daily caloric intake but are indicative of poor vitamin absorption from ingested foods. The body requires the addition of vitamins to aid in the endogenous production of CoQ.sub.10; in particular, the B Vitamins play a crucial role in this synthesis. The human body's need for CoQ.sub.10 varies between individuals. Factors that affect this are age, physical activity, and health. The body uses an estimated 5 to 9 mg per day of CoQ.sub.10. This nutrient is essential for life because it is important in the synthesis of energy. The vast majority of energy
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synthesis occurs in the mitochondria of cells. Here CoQ.sub.10 primarily functions as an electron carrier in the Electron Transport Chain where Adenosine Triphosphate (ATP) is synthesized. CoQ.sub.10 donates an electron during ATP synthesis and is subsequently oxidized. CoQ.sub.10 also can function as an antioxidant during synthesis where oxidation removes its electron making it non-functional for use in ATP synthesis. Web site: http://www.delphion.com/details?pn=US06623734__ •
Triglycerides, rich in polyunsaturated fatty acids Inventor(s): Cain; Frederick William (Voorburg, NL), McNeill; Gerald Patrick (Rushden, GB), Moore; Stephen Raymond (Thrapston, GB) Assignee(s): Loders-Croklaan B.V. (Wormerveer, NL) Patent Number: 6,410,078 Date filed: December 3, 2001 Abstract: Triglycerides, that have at least two long chain polyunsaturated fatty acids L.sub.1 and L.sub.2, from which at least one is present for more than 20 wt %, while the weight ratio L.sub.1 :L.sub.2 is at least 2 and which triglycerides also contain at least 2 wt % of saturated fatty acids with 2-12 and/or 20-24 C-atoms, but not more than 10 wt % of saturated fatty acids with 16-18 C-atoms, while at least 5 wt % of the saturated C.sub.2 -C.sub.12 or C.sub.20 -C.sub.24 fatty acid residues is bonded on a triglyceride molecule, wherein at least L.sub.1 and/or L.sub.2 is present, display a number of advantageous properties (e.g. higher oxidative stability, healthier, lower caloric, structuring properties, digestibility). Excerpt(s): According to EP 265 699 fats with a superior digestibility and absorptivity are obtained, when these fats are composed of triglycerides having a specific amount of C.sub.8 to C.sub.14 fatty acid residues at the 2-position, while residues with C.sub.18 or higher fatty acids are bonded at the 1.3-positions. Typical examples of the C.sub.18 and higher fatty acids are polyunsaturated fatty acids, such as arachidonic acid, eicosapentenoic acid and dodecahexenoic acid. However nothing is disclosed about fat compositions that combine in the fat saturated fatty acid residues and at least two different long chain polyunsaturated fatty acid residues. In WO 90/04012 it is disclosed that triglycerides that contain saturated C.sub.8 /C.sub.10 fatty acid residues in 1.3 and simultaneously a polyunsaturated fatty acid residue (in particular DHA) in the 2position, have beneficial nutritional properties, in particular for enteral or parenteral purposes. However again, nothing is disclosed about fat compositions that contain in the fat specific amounts of saturated and two different polyunsaturated fatty acid residues. From WO 94/00044 it is known that fatblends that contain unhardened fish oil have significant health benefits. Fish oil often contains appreciable amounts of two different polyunsaturated fatty acids, e.g. DHA and EPA. However it is also known that fish oil has a number of draw backs, such as a low oxidative stability (e.g. noticed as off taste during storage at ambient temperature). Further fish oils do not have structuring properties, which makes it difficult to apply them in fat compositions wherein a structuring agent is required in order to give the fat composition a performance, that is desired to make the fat applicable in foodproducts. From Endo c.s in Bioscience Biotechn. Biochem. 57 (12) 1993 pages 2202-2024 it is known, that incorporation of myristic acid groups into sardine oil leads to a product with a slightly improved oxidation rate, whereas incorporation of stearic acid in the sardine oil hardly had any effect on the oxidation rate. This incorporation of saturated fatty acid is performed by an enzymic process, applying Candida cylindracea or lypozyme as an enzyme. It is taught
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that starting from sardine oil with about 8% DHA and 12% EPA, products are obtained with a decreased amount of total long chain polyunsaturated fatty acids (about 11% if C.sub.14:0 was incorporated and about 17.5% if stearic acid was incorporated). Web site: http://www.delphion.com/details?pn=US06410078__ •
Use of estrogens and delta-gonadien-21-Ol-3,20-diones for treating insulin dependent and non-insulin dependent diabetes Inventor(s): Wassermann; Karsten (Gentofte, DK) Assignee(s): Novo Nordisk A/S (Bagsvaerd, DK) Patent Number: 6,555,530 Date filed: January 31, 2000 Abstract: Analysis of full-blood glucose, serum insulin, serum triglycerides and total serum cholesterol were performed. Glucose levels in blood samples from the oral glucose tolerance test were used for calculation of the incremental Area Under the Curve (AUC.sub.0-120 min-baseline). All data are expressed as percentage change of vehicle treated animals (cf. FIGS. 1 and 2). Excerpt(s): The present invention relates to the use of a combination of estrogens or SERMs with delta-gonadien-21-ol-3,20-diones for treating diabetes, particularly type II diabetes. The present invention also embraces pharmaceutical compositions and kits comprising these compounds and methods of using the compounds and their pharmaceutical compositions. Diabetes mellitus is a systemic disease characterized by disorders in the actions of insulin and other regulatory hormones in the metabolism of carbohydrates, fats and proteins, and in the structure and function of blood vessels. The primary symptom of diabetes is hyperglycemia, often accompanied by glucosuria, the presence in urine of large amounts of glucose, and polyuria, the excretion of large volumes of urine. Additional symptoms arise in chronic or long standing diabetes. These symptoms include degeneration of the walls of blood vessels. Although many different organs are affected by these vascular changes, the nerves, eyes and kidneys appear to be the most susceptible. As such, long-standing diabetes mellitus, even when treated with insulin, is a leading cause of blindness. There are two recognized types of diabetes. Type I diabetes is of juvenile onset, ketosisprone, develops early in life with much more severe symptoms and has a near-certain prospect of later vascular involvement. Control of this type of diabetes is difficult and requires exogenous insulin administration. Type II diabetes mellitus is of adult onset, ketosis-resistant, develops later in life, is milder and has a more gradual onset. Web site: http://www.delphion.com/details?pn=US06555530__
Patent Applications on Triglycerides As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to triglycerides: 10
This has been a common practice outside the United States prior to December 2000.
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Antisense modulation of microsomal triglyceride transfer protein expression Inventor(s): Crooke, Rosanne M.; (Carlsbad, CA), Graham, Mark J.; (San Clemente, CA) Correspondence: Licata & Tyrrell P.C.; 66 E. Main Street; Marlton; NJ; 08053; US Patent Application Number: 20030086912 Date filed: July 30, 2001 Abstract: Antisense compounds, compositions and methods are provided for modulating the expression of microsomal triglyceride transfer protein. The compositions comprise antisense compounds, particularly antisense oligonucleotides, targeted to nucleic acids encoding microsomal triglyceride transfer protein. Methods of using these compounds for modulation of microsomal triglyceride transfer protein expression and for treatment of diseases associated with expression of microsomal triglyceride transfer protein are provided. Excerpt(s): The present invention provides compositions and methods for modulating the expression of microsomal triglyceride transfer protein. In particular, this invention relates to compounds, particularly oligonucleotides, specifically hybridizable with nucleic acids encoding microsomal triglyceride transfer protein. Such compounds have been shown to modulate the expression of microsomal triglyceride transfer protein. Triglycerides are one of the most efficient storage forms of free energy. Because of their insolubility in biological fluids, their transport between cells and tissues requires that they be assembled into lipoprotein particles. Genetic disruption of the lipoprotein assembly/secretion pathway leads to several human disorders associated with malnutrition and developmental abnormalities. In contrast, patients displaying inappropriately high rates of lipoprotein production display increased risk for the development of atherosclerotic cardiovascular disease (Davis, Biochim. Biophys. Acta, 1999, 1440, 1-31). The mammalian lipoprotein assembly/secretion pathway requires 2 components: apolipoprotein B (ApoB, an amphipathic protein) and a lipid transfer protein (microsomal triglyceride transfer protein, MTP). In the endoplasmic reticulum, ApoB has two possible metabolic fates: entrance into the lipoprotein assembly pathway within the lumen of the endoplasmic reticulum (ER), or degradation in the cytoplasm by the ubiquitin-dependent proteasome. The destiny of ApoB is determined by the relative availability of individual lipids and the level of expression of microsomal triglyceride transfer protein (Davis, Biochim. Biophys. Acta, 1999, 1440, 1-31). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Blends comprising a substituted fatty acid or a derivative thereof Inventor(s): Barclay, Scott Sinclair; (Sharnbrook, GB), Bosley, John Anthony; (Sharnbrook, GB), Cain, Frederick William; (Wormerveer, NL), Koenen, Claudia; (Wormerveer, NL), Rogers, Julia Sarah; (Sharnbrook, GB), Schmid, Ulrike; (Wormerveer, NL) Correspondence: Morgan Lewis & Bockius Llp; 1111 Pennsylvania Avenue NW; Washington; DC; 20004; US Patent Application Number: 20030129294 Date filed: August 29, 2002 Abstract: The inventon concerns blends of a hydroquinone substituted poly unsaturated fatty acid (as present in Kombo nut oil) or a derivative thereof, which blends
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comprised:(i) 0.1-99.9 wt % of the substituted acid(ii) 0-99.8 wt % of Kombo butter glycerides(iii) 0.1-99.9 wt % of other triglyceridesFood products and food supplements comprising such hydroquinone substituted acids are also part of the invention.The substituted acids display many useful health benefits. Excerpt(s): Kombo nut seed fat is a known product that can be obtained from the seeds of Pycnanthus angolensis (cf WO 96/39130) The components present in this fat were analysed by different groups and a number of terpenoid acid type ingredients were identified. One of these ingredients was identified as a novel polyprenylated hydroquinone substituted carboxylic acid named kombic acid which was identified as having a structure mentioned in Lok c.s. Phytochemistry 22, p. 1973 from 1983. (i.e. 16(2.sup.1, 5.sup.1-dihydroxy-3.sup.1 methylphenyl)-2,6,10,14 tetramethyl-2,6,10,14 hexadecatetraenoic acid). Although kombo nut oil, containing its terpenoid acid type ingredient is disclosed as useful and having a number of health benefits such as hypoglycemic activity, activity against fungal skin infections; activity for the treatment of shingles; or against leprosy; headaches, body aches; chest pains; or as an anti sterility agent for women; or as an antihelmintic; or poison antidote; or as an anti toothache agent; or as an anti bleeding agent; etc (cf WO 96/39130) no relation is given between the presence of a specific component and the occurrence of a specific health effect. U.S. Pat. No. 3,615,588 discloses blends made from oils, rich in trimyristin and other oils. The trimyristin used can be obtained from Kombo nut oil. We analysed the kombo nut fat further and found that this fat contains an ingredient which was identified by mass spectroscopy and.sup.13C-NMR as sargahydroquinoic acid (=SHQA)[(CA name: 12(2.sup.1,5.sup.1-dihydroxy-3.sup.1-methylphenyl)-6,10 dimethyl-2-(4.sup.1-methyl3.sup.1-pentenyl)-2E, 6E, 10E dodecatrienoic acid)] and that this compound and a number of its derivatives displays useful health benefits. This compound SHQA is normally applied in combination with glycerides. These glycerides can be the triglycerides present in kombo nut oil but also other glycerides can be used in combination with SHQA. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Carbonate catalyzed alcoholysis of triglycerides Inventor(s): Suppes, Galen J.; (Lawrence, KS) Correspondence: Hovey Williams Llp; Suite 400; 2405 Grand BLVD.; Kansas City; MO; 64108; US Patent Application Number: 20030149289 Date filed: February 26, 2003 Abstract: A process for the carbonate-catalyzed alcoholysis of fatty acid glycerides is disclosed, wherein an alcohol (e.g., a C1-C6 mono-, di- or trialcohol) is reacted with a fatty acid glyceride (e.g., a plant or animal derived triglyceride) at elevated temperatures and superatmospheric pressures to give high yields of the corresponding ester. The preferred catalysts are the alkali metal, alkaline earth metal or zinc carbonates, with calcium carbonate being especially preferred because of its ready availability and physical integrity under reaction conditions. The alcoholysis reaction may be carried out in a single reactor, or on a continuous basis using a plug flow reactor. Excerpt(s): This application is a continuation of application Ser. No. 09/798,197 filed Mar. 2, 2001 and claims the benefit of provisional applications Serial No. 60/265,601 filed Feb. 2, 2001, Serial No. 60/260,201 filed Jan. 9, 2001, Serial No. 60/197,613 filed
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Apr. 19, 2000 and Serial No. 60/187,102 filed Mar. 6, 2000. The present invention is concerned with carbonate-catalyzed processes for the alcoholysis of glycerides to produce biodiesel or other useful products. More particularly, the invention pertains to such methods wherein an alkali metal, alkaline earth metal or zinc carbonate is used to catalyze the reaction between a glyceride and an alcohol at elevated temperatures (e.g., from about 160-300 C) and superatmospheric pressures to give very high alcoholysis yields. Ester formation constitutes one of the most important classes of reactions in value-added processing of animal fats and vegetable oils. Typical schemes for ester formation include reactions of 1) an alcohol with an acid (esterification), 2) an ester with an alcohol (alcoholysis), 3) two different esters (transesterification), and 4) an ester with an acid (acidolysis). Of these reaction schemes, esterification and alcoholysis are by far the most important to the fat and oil industry since these make use of the fatty acid components that comprise most of fats and oils. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Carboxamides useful as inhinitors of microsomal triglyceride transfer protein and of apolipoprotein b secretion Inventor(s): Ksander, Gary Michael; (Milford, NJ) Correspondence: Thomas Hoxie; Novartis Corporation; Patent And Trademark Dept; 564 Morris Avenue; Summit; NJ; 079011027 Patent Application Number: 20030109700 Date filed: July 11, 2002 Abstract: 1Compounds of formula (1) wherein R.sub.2--C, R.sub.3--C, R.sub.4--C or R.sub.5--C may be replaced by N; and wherein n is 1, 2 or 3; R.sub.1 is aryl, heteroaryl or (aryl or heteroaryl)-lower alkoxy; R.sub.2, R.sub.3, R.sub.4 and R.sub.5 are independently hydrogen, lower alkyl, lower alkoxy, halo, trifluoromethyl or cyano; R.sub.6 is (i) or (ii) m is 1, 2 or 3; R.sub.7 is hydrogen, lower alkyl (aryl or heteroaryl)lower alkyl, lower alkoxy, (aryl or heteroaryl)-lower alkoxy, hydroxy, oxo, lower alkylenedioxy or lower alkanoyloxy; W is O, S or NR.sub.8; R.sub.8 is --COR.sub.a, (iii), --COOR.sub.d, --SO.sub.2R.sub.e, hydrogen, optionally substituted lower alkyl, aryl, heteroaryl or (aryl or heteroaryl)-lower alkyl; R.sub.a, R.sub.d and R.sub.e, are independently optionally substituted lower alkyl, cycloalkyl, adamantyl, aryl, heteroaryl or (aryl or heteroaryl)-lower alkyl; R.sub.b and R.sub.c are independently hydrogen, cycloalkyl, optionally substituted lower alkyl, aryl, heteroaryl or (aryl or heteroaryl) lower alkyl; or R.sub.b and R.sub.c together represent lower alkylene; and pharmaceutically acceptable salts thereof; and enantiomers thereof; which are useful as inhibitors of microsomal triglyceride transfer protein (MTP) and of apolipoprotein B (apoB) secretion. Excerpt(s): and pharmaceutically acceptable salts thereof; and enantiomers thereof. Compounds of formula I are useful as inhibitors of microsomal triglyceride transfer protein (MTP) and of apolipoprotein B (apoB) secretion and accordingly for the treatment of MTP and apo B dependent conditions. wherein R.sub.2--C, R.sub.3--C, R.sub.4--C or R.sub.5--C may be replaced by N; and wherein n, and R.sub.1-R.sub.6 have meaning as defined above; pharmaceutically acceptable salts thereof; and enantiomers thereof. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Cholesterol lowering structured lipids containing omega 6 polyunsaturated fatty acids and the process thereof Inventor(s): Lokesh, Belur Ramaswamy; (Mysore, IN), Rao, Reena; (Mysore, IN), Sambaiah, Kari; (Mysore, IN) Correspondence: Merchant & Gould PC; P.O. Box 2903; Minneapolis; MN; 55402-0903; US Patent Application Number: 20030077340 Date filed: December 10, 2001 Abstract: Unique structured lipids obtained from interesterifying coconut oil with free fatty acids obtained from hydrolysis of triglycerides of vegetable source, said structured lipids rich in omega 6 polyunsaturated fatty acids and medium chain fatty acids and a process for the production of said structural lipids. Excerpt(s): The present invention relates to cholesterol lowering structured lipids containing omega 6 polyunsaturated fatty acids and a process thereof. Coconut oil is a kernel oil which is a natural source of MCFA (53% of C 8:0-C 12:0). Its lauric acid content is very high (48%). The lauric fats provide high nutritional value because either the portal or lymphatic systems can absorb them. They provide excellent nutrition for critically ill patients and do not cause any undue coronary difficulties despite their saturation. In fact, the lauric fats provide unexpected usefulness in protein catabolism, yielding positive nitrogen balance and enhanced protein formation. But coconut oil contains very low levels of polyunsaturated fatty acids (PUFA) (1.8% of linoleic acid). Long term feeding of coconut oil as the sole source of fat in the diet of experimental rats has shown EFA deficiency symptoms characterized by scaly dermatitis, excessive water loss through the skin, impaired growth and reproduction and poor wound healing. In addition to this, myristic and palmitic acids that contribute to around 33% of the total fatty acids of coconut oil have been shown to be hypercholesterolemic which is a risk factor for cardiovascular disease. Medium chain fatty acids (MCFA) comprise fatty acids with 6 to 12 carbon chain length. MCFA offer numerous health benefits. They are easily absorbed, transported via the portal system and rapidly metabolized to yield quick energy and is not deposited in the body as fat. Medium chain triglycerides (MCT) have clinical applications in the treatment of fat malabsorption disorders, gall bladder disease, hyperlipidemia, obesity and deficiency of the carnitine system. But MCT alone cannot function as an ideal fat source for humans as they do not provide essential fatty acids (EFA) (EFA cannot be synthesized by the body and must be therefore ingested in the diet). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Compositions, screening systems and methods for modulating HDL cholesterol and triglyceride levels Inventor(s): Hayden, Michael R.; (Vancouver, CA), Singaraja, Roshni R.; (Vancouver, CA) Correspondence: Alan J. Grant, ESQ.; C/o Carella, Byrne, Bain, Gilfillan Cecchi,; Stewart & Olstein; 6 Becker Farm Road; Roseland; NJ; 07068; US Patent Application Number: 20030092157 Date filed: March 15, 2002
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Abstract: The invention features novel ABC1 splice variants and transgenic mice expressing human ABC1 which are useful for studying ABC1 expression, localization, and activity in vivo. Additionally, these ABC1 splice variants and transgenic mice are useful in screening for compounds that modulate cholesterol and triglyceride levels. Excerpt(s): This application claims priority of U.S. Provisional Application Serial No. 60/276,387, filed Mar. 16, 2001, the disclosure of which is hereby incorporated by reference in its entirety. The present invention relates to the field of transgenic animals incorporating selected sequences, such as mutated exons of human genes, and the use of such animals in assays for chemical agents that elevate plasma HDL levels. Low HDL cholesterol (HDL-C), or hypoalphalipoproteinemia, is a blood lipid abnormality which correlates with a high risk of cardiovascular disease (CVD), in particular coronary artery disease (CAD), but also cerebrovascular disease, coronary restenosis, and peripheral vascular disease. HDL-C levels are influenced by both environmental and genetic factors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Conjugated linoleic acid powder Inventor(s): Fimreite, Duane; (Chicago, IL) Correspondence: Medlen & Carroll, Llp; 101 Howard Street, Suite 350; San Francisco; CA; 94105; US Patent Application Number: 20030149288 Date filed: July 23, 2002 Abstract: A powder containing a high amount of conjugated linoleic acid or other oil is provided. The powder contains either triglycerides containing CLA, free fatty acids of CLA, or alkylesters of CLA, or another desired oil. The powder is free flowing and has good organoleptic properties. The powder may be used as a dietary supplement or combined with foodstuffs to form a food product suitable for consumption by animals or humans. Excerpt(s): This application is a Continuation in Part of U.S. patent application Ser. No. 09/836,788, filed Apr. 17, 2001, which claims priority to U.S. Provisional Application No. 60/198,487, filed Apr. 18, 2000. The present invention relates to the field of human and animal nutrition, and in particular to a novel composition of conjugated linoleic acid (CLA) powder. In 1978, researchers at the University of Wisconsin discovered the identity of a substance contained in cooked beef that appeared to inhibit mutagenesis. The substance was found to be a mixture of positional isomers of linoleic acid (C18:2) having conjugated double bonds. The c9,t11 and t10,c12 isomers are present in greatest abundance, but it is uncertain which isomers are responsible for the biological activity observed. It has been noted from labeled uptake studies that the 9, 11 isomer appears to be somewhat preferentially taken up and incorporated into the phospholipid fraction of animal tissues, and to a lesser extent the 10, 12 isomer (Ha, et al., Cancer Res., 50: 1097 [1990]). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Fat based food products Inventor(s): Lievense, Lourus Cornelis; (Vlaardingen, NL) Correspondence: Unilever; Patent Department; 45 River Road; Edgewater; NJ; 07020; US Patent Application Number: 20030134028 Date filed: February 24, 2003 Abstract: The invention concers a fat based food product comprising natural fat components which have a blood cholesterol lowering effect in amounts sufficient to obtain a blood cholesterol lowering effect if the food product is used accroding to the common needs and customs of the consumer, wherein at least one of toctrienol, oryzanol and phytosterol is present, and preferably at least two and in a further preferred embodiment at least 0.1 wt % of tocotrienol, 0.1 wt % of oryzanol and 0.4 wt % of phytosterol. In a further preferred embodiment the fat in the product comprises at least 30 wt %, preferably at least 45 wt % of pufa-triglycerides. By the regular consumption of the now found fat based food products a positive contribution to health in general, and in particular to the lowering of the blood cholesterol level can be found. Excerpt(s): The present invention concerns a fat based food product comprising natural fat components which have a blood cholesterol lowering effect in amounts sufficient to obtain a blood cholesterol lowering effect if the food product is used according to the common needs of the consumer. Such fat based food products are available on the market for quite some time, and are to a large extend based on the use of fat which comprises a particular amount of triacylglycerides with poly-unsaturated fatty acid chains. In particular, the use of butter like spreads comprising a significant amount of these triacylglycerides having polyunsaturated fatty acid chains (hereinafter called pufatriglycerides) is well known in the western world to reduce high blood cholesterol levels. The variation in the mean plasma total cholesterol concentration among populations is highly correlated with the variation in the extent of atherosclerosis and in the incidence of Coronary Heart Disease (CHD), which is one of the major causes of death in the Western society. Populations with a low cholesterol level (less than 180 mg/dl (4.7 mmol/L) are found to be largely free of atherosclerosis and coronary heart disease, whereas those with mean cholesterol levels above 220 mg/dl (5.7 mmol/L; hypercholesterolaemia) have increased rates of death due to CHD. Thus, a clear need for a method by which the cholesterol level can be lowered exists. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Fats and oils composition for reducing lipids in blood Inventor(s): Aoyama, Toshiaki; (Yokosuka, JP) Correspondence: Armstrong,westerman & Hattori, Llp; 1725 K Street, NW; Suite 1000; Washington; DC; 20006; US Patent Application Number: 20030170368 Date filed: January 27, 2003 Abstract: The present invention relates to fats and oils composition for reducing lipids in blood, comprising a triglyceride in which specified fatty acids are artificially combined at the first portion, the second portion and third portion of the triglyceride molecule. The present composition is preferably useful for foods. Such fats and oils composition for reducing lipids in blood, comprising triglycerides containing a
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R.sub.MR.sub.LR.sub.M triglyceride as an effective component, having Formula I. In formula I, wherein R.sub.M is an acyl group of a saturated medium chain fatty acid having 8 to 10 carbon atoms, R.sub.L is an acyl group of a monounsaturated long chain fatty acid having 16 to 18 carbon atoms, C.sup.1 is the first carbon of the triglyceride, C.sup.2 is the second carbon of the triglyceride, and C.sup.3 is the third carbon of the triglyceride. 1 Excerpt(s): This application is a continuation-in-part of application Ser. No. 10/028,315, filed Dec. 28, 2001. The present invention relates to a fats and oils composition for reducing lipids in blood, and in particular, the present invention relates to a fats and oils composition for reducing lipids in blood (blood fat), comprising a triglyceride as an effective compound in which specified fatty acids are combined at the first carbon, second carbon and third carbon of the triglyceride. The present composition is preferably useful for cooking or foods. Recently and in particular in Japan, the number of persons who suffer from ischemic heart disease or brain infarction has increased, and the average of age of the persons who suffer from such diseases has been getting younger and younger. These diseases are generally caused by arteriosclerosis, which mainly results from deposition of cholesterol and otherwise lipids in the blood vessel. It is considered that hypercholesterolemia or hyperlipidemia is one of the dangerous factors that causes arteriosclerosis. Although Japanese people used to have a cholesterol value in plasma lower than that of Europeans or Americans, it is reported that recently, there is no significant difference in the cholesterol value in plasma, in particular between Japanese teenagers and European or American teenagers. It is considered to be due to the recent change in Japanese eating habit. Therefore, it has been said that it is required to take necessary and prompt measures related to diet in order to prevent arteriosclerosis from the period of childhood (Current internal Medicine 3, Hiperlipidemia edited by Haruo Nakamura, pages 44 to 52, published by Kanahara & Co., Ltd., 1995). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Functional proteins and therapeutic and diagnostic methods for use thereof Inventor(s): Murphy, Andrew J.; (Croton-On-Hudson, NY) Correspondence: Regeneron Pharmaceuticals, Inc; 777 Old Saw Mill River Road; Tarrytown; NY; 10591; US Patent Application Number: 20030211549 Date filed: February 25, 2003 Abstract: This invention relates to OGH BETA 14 proteins as well as methods of producing and using such proteins. The present invention provides a functional Oghbeta14 protein. The proteins of the invention are useful for decreasing body weight, decreasing body fat, decreasing serum cholesterol, decreasing triglycerides, decreasing blood glucose, and increasing adrenal medullary mass in a subject Excerpt(s): The application claims priority to U.S. application Ser. No. 09/684,197, filed on Oct. 6, 2000. The disclosure of this application is hereby incorporated by reference into this application. This invention relates to OGH BETA 14 proteins as well as methods of producing and using such proteins. Hormones that signal via GPCRs include, but are not limited to, the tropic adenohypophyseal hormones follicle stimulating hormone (FSH), luteinizing hormone (LH), and thyroid stimulating hormone (TSH). In addition, chorionic gonadotropin (CG), which is secreted by a
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developing embryo following endometrial implantation, also signals through a GPCR. In fact, LH and CG signal through the same GPCR. All four hormones are glycoproteins and belong to the glycoprotein hormone-beta family. Each hormone is a heterodimer comprised of a common glycoprotein hormone alpha (a) subunit and a beta (b) subunit. All four family members share the same a subunit, but each has its own unique b subunit. The b subunit provides for binding specificity to each hormone's cognate GPCR. This family of polypeptide hormones represents an important class of molecules with functions ranging from reproduction, cellular metabolism, and growth and development to blood calcium and bone homeostasis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Lipophilic drug compositions Inventor(s): Sung, Michael T.; (Raleigh, NC) Correspondence: Alston & Bird Llp; Bank OF America Plaza; 101 South Tryon Street, Suite 4000; Charlotte; NC; 28280-4000; US Patent Application Number: 20030108596 Date filed: April 29, 2002 Abstract: The invention is directed to biologically active lipophilic compositions comprising a biologically active covalently attached to, or encapsulated within, a lipid. Preferably, a biologically active agent is both covalently attached to a lipid and encapsulated within a lipid composition. Preferred lipid components include triglycerides and fatty acids. The resulting composition is preferably adapted for oral administration. Excerpt(s): This application claims the benefit of Provisional Application Serial No. 60/314,092, filed Aug. 23, 2001, which is incorporated herein by reference in its entirety. The invention relates to lipophilic drug compositions comprising biologically active agents in association with lipid components, methods of making such compositions, and methods of using such compositions in drug delivery. The small intestine is the primary site for the absorption of drugs administered orally. The most important element in the small intestine controlling absorption is the brush border membrane. It consists of a phospholipid bilayer into which polysaccharides and proteins are incorporated. This membrane creates absorption barriers to many polar drugs. A successful approach in the pharmaceutical industry has been to synthesize prodrugs with increasing membrane permeability by esterifying the charge functionalities. For example, the prodrug of 6azauridine for the treatment of psoriasis and neoplastic disease is acetylated to form 2',3',5'-triacetyl-6-azauridine in order to enhance bioavailability (Bloch, A., "The Design of Biologically Active Nucleoside", Drug Design, Vol. IV, Chapter 8, Ariens, EJ (Ed.), Academic Press, New York, 1973) (see also, Sinkula, AA, "Application of the Prodrug Approach to Antibiotics", Pro-drug as Novel Drug Delivery Systems, pp116-153, Higuchi, T. and Stella, V. (Eds.), ACS Symposium Series 14, American Cancer Society, Washington DC, 1975; Yalkowski, SH and Morozowich, W., Drug Design, Vol.9, pp 121, Ariens, EJ (Ed.), Academic Press, New York, 1980). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for production of radically post-cured polymers by addition of reactive anhydrides Inventor(s): Bemmann, Ralf; (Neuss, DE), Hoefer, Rainer; (Duesseldorf, DE), Skwiercz, Michael; (Langenfeld, DE), Sulzbach, Horst; (Duesseldorf, DE) Correspondence: Cognis Corporation; 2500 Renaissance BLVD., Suite 200; Gulph Mills; PA; 19406 Patent Application Number: 20030134927 Date filed: November 26, 2002 Abstract: The invention relates to a method for production of radically post-cured polymers. In a first stage, at least one, or several compounds (a), which are the reaction products of epoxidised fatty acid esters and/or epoxidised triglycerides with acrylic acid and/or methacrylic acid, are converted into the corresponding polyurethane (a*) and said polyurethane (a*) is subsequently radically post-cured, in a second stage, in the presence of at least one radical initiator (b), with the additional proviso that, in the second stage, a combination of compounds (a*) with one or several compounds (c) are used, where the compounds (c) are chosen from the group of the reactive anhydrides. The polymers thus obtained are excellent matrix agents for composite materials. Excerpt(s): This invention relates to a process for the production of radically postcrosslinked polymers. In a first stage of the process according to the invention, one or more special acrylic or methacrylic acid derivatives based on naturally occurring oils is/are reacted with aromatic and/or aliphatic isocyanates and, in a second stage, the polyurethanes (a*) thus obtained are subsequently subjected to radical post-crosslinking in the presence of a radical initiator (b), with the proviso that a combination of the compounds (a*) with one or more compounds (c) selected from the group of reactive anhydrides is used in the second stage. The use of radiation curing in the coating industry for producing high-quality coating materials is known from the prior art. In radiation curing, olefinically unsaturated compounds (monomers, oligomers, polymers, prepolymers), i.e. compounds containing C.dbd.C double bonds as structural elements, are cured by exposure to high-energy radiation, for example UV light or electron beams. The actual radiation curing process is sometimes preceded by physical drying. It is also known that particularly high-quality coatings are obtained in radiation curing when the olefinically unsaturated starting compounds used contain polyurethane groups as further structural elements. Unsaturated radiation-curable urethane acrylates are known from Manfred Bock (Ed. Ulrich Zorll), "Polyurethane fur Lacke und Beschichtungen", Hannover 1999, pages 73-74. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for reducing cholesterol and triglycerides Inventor(s): Harrison, Stanley F. JR.; (Alexandria, VA) Correspondence: Donald C. Casey; Suite 100; 311 North Washington Street; Alexandria; VA; 22314; US Patent Application Number: 20030166614 Date filed: March 1, 2002 Abstract: A method of treating excessive blood lipid levels in humans is described. The treatment includes a daily dosage of food supplements available over-the-counter
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without a prescription. The supplements are fish oil concentrate, niacin (flush free), and lecithin. In the preferred embodiment two 500 mg tablets of niacin, 2 1200 mg soft gels of lecithin, and two 1250 mg soft gels of fish oil concentrate are administered orally once to twice per day. Excerpt(s): This invention relates to a method for treating humans with high levels of cholesterol and/or triglycerides using a combination of over-the-counter dietary supplements. As is well known, increased levels of cholesterol, and in particular low density lipoproteins (LDL) is associated with circulation problems which often lead to heart attack and stroke. The increased level of cholesterol often is also accompanied by an increased level of triglycerides in the circulatory system. Increased plasma lipid levels have been associated with the build up of plaque within blood vessels, and there are a variety of treatments known to reduce these levels. Some treatments are more effective than others, and most are associated with undesirable side effects in many patients. The total cholesterol level includes both the beneficial high density lipoproteins (HDL) and the troublesome low density lipoproteins, (LDL). Measurement of the total cholesterol level then can be misleading because if the LDL concentration is low and the HDL is also low this can be an undesirable situation. It is necessary to have the HDL concentration above a preset value, and the LDL concentration below a preset value, and both must be measured to provide an accurate picture. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of reducing serum glucose and triglyceride levels and for inhibiting angiogenesis using substitute indolealkanoic acids Inventor(s): Jacot, Jorge; (Branford, CT), Sredy, Janet; (Milford, CT) Correspondence: Steven J. Sarussi; Mcdonnell Boehnen Hulbert & Berghoff; 32nd Floor; 300 S. Wacker Drive; Chicago; IL; 60606; US Patent Application Number: 20030216452 Date filed: March 26, 2003 Abstract: Disclosed are methods of reducing serum glucose and triglyceride levels and for inhibiting angiogenesis, the methods comprising administration of substituted indolealkanoic acids to patients in need of such treatment. Also disclosed are such compounds useful in the treatment of angiogenesis, hyperglycemia, hyperlipidemia and chronic complications arising from diabetes mellitus. Also disclosed are pharmaceutical compositions containing the compounds. Excerpt(s): The use of aldose reductase inhibitors (ARIs) for the treatment of diabetic complications is well known. The complications arise from elevated levels of glucose in tissues such as the nerve, kidney, retina and lens that enters the polyol pathway and is converted to sorbitol via aldose reductase. Because sorbitol does not easily cross cell membranes, it accumulates inside certain cells resulting in changes in osmotic pressure, alterations in the redox state of pyridine nucleotides (i.e. increased NADH/NAD.sup.+ ratio) and depleted intracellular levels of myomositol. These biochemical changes, which have been linked to diabetic complications, can be controlled by inhibitors of aldose reductase. The use of aldose reductase inhibitors for the treatment of diabetic complications has been extensively reviewed, see: (a) Textbook of Diabetes, 2nd ed.; Pickup, J. C. and Williams, G. (Eds.); Blackwell Science, Boston, Mass. 1997.; (b) Larson, E. R.; Lipinski, C. A. and Sarges, R., Medicinal Research Reviews, 1988, 8 (2), 159-198; (c) Dvornik, D. Aldose Reductase Inhibition. Porte, D. (ed), Biomedical Information Corp.,
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New York, N.Y. Mc Graw Hill 1987; (d) Petrash, J. M., Tarle, I., Wilson, D. K. Quiocho. F. A. Perspectives in Diabetes, Aldose Reductase Catalysis and Crystalography: Insights From Recent Advances in Enzyme Structure and Function, Diabetes, 1994, 43, 955; (e) Aotsuka, T.; Abe, N.; Fukushima, K.; Ashizawa, N.and Yoshida, M., Bioorg. & Med. Chem. Letters, 1997, 7, 1677, (f), T., Nagaki, Y.; Ishii, A.; Konishi, Y.; Yago, H; Seishi, S.; Okukado, N.; Okamoto, K., J. Med. Chem., 1997, 40, 684; (g) Ashizawa, N.; Yoshida, M.; Sugiyama, Y.; Akaike, N.; Ohbayashi, S.; Aotsuka, T.; Abe, N.; Fukushima, K.; Matsuura, A, Jpn. J. Pharmacol. 1997, 73, 133; (h) Kador, P. F.; Sharpless, N. E., Molecular Pharmacology, 1983, 24, 521; (I) Kador, P. F.; Kinoshita, J. H.; Sharpless, N. E., J. Med. Chem. 1985, 28 (7), 841; (j) Hotta, N., Biomed. & Pharmacother. 1995, 5, 232; (k) Mylar, B.; Larson, E. R.; Beyer, T. A.; Zembrowski, W. J.; Aldinger, C. E.; Dee, F. D.; Siegel, T. W.; Singleton, D. H., J. Med. Chem. 1991, 34, 108; (1) Dvornik, D. Croatica Chemica Acta 1996, 69 (2), 613. Previously described aldose reductase inhibitors most closely related to the present invention include those sighted in: (a) U.S. Pat. No. 5,700,819: 2-Substituted benzothiazole derivatives useful in the treatment of diabetic complications, (b) U.S. Pat. No. 4,868,301: Processes and intermediates for the preparation of oxophthalazinyl acetic acids having benzothiazole or other heterocyclic side chains, (c) U.S. Pat. No. 5,330,997: 1H-indazole-3-acetic acids as aldose reductase inhibitors, and (d) U.S. Pat. No. 5,236,945: 1H-indazole-3-acetic acids as aldose reductase inhibitors. Although many aldose reductase inhibitors have been extensively developed, none have demonstrated sufficient efficacy in human clinical trials without significant undesirable side effects. Thus no aldose reductase inhibitors are currently available as approved therapeutic agents in the United States; and consequently, there is still a significant need for new, efficacious and safe medications for the treatment of diabetic complications. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method to counter oxidation of LDL, decrease triglyceride or cholesterol and inhibit atherosclerosis using hibiscus sabdariffa extract Inventor(s): Wang, Chau-Jong; (Taichung, TW) Correspondence: Birch Stewart Kolasch & Birch; PO Box 747; Falls Church; VA; 220400747; US Patent Application Number: 20030096021 Date filed: November 21, 2001 Abstract: A method for countering oxidization of low density lipoproteins, reducing cholesterol or triglyceride in plasma or inhibiting atherosclerosis comprising administering an effective amount of a Hibiscus sabdariffa extract. Excerpt(s): The present invention relates to the novel applications of the Hibiscus sabdariffa extract in countering oxidization of low density lipoproteins, reducing cholesterol or triglyceride in plasma or inhibiting atherosclerosis. Conventionally, Hibiscus sabdariffa is a local soft drink material and medical herb demonstrating analgesic and antipyretic effects and can be used to cure liver-complaint. The past studies showed that Hibiscus sabdariffa possesses analgesic activity as well as antipyretic and anti-inflammatory action American Journal of Chinese Medicine, Vol. XXIV, Nos. 3-4, pp. 263-269, antispasmodic potential Journal of Ethnopharmacology, 31 (1991) 249-257 Elsevier Scientific Publishers Ireland Ltd., antimutagenic and chemopreventive activity Food and Chemical Toxicology 37 (1999) 591-601, antioxidant activity Food and Chemical Toxicology 35 (1997) 1159-1164 and is able to quench the free radicals of 1,1-diphenyl-2-picrylhydrazyl Food and Chemical Toxicology 38 (2000)
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411-416 and lower high blood pressure Journal of Ethnopharmacology v.65(3) JUNE 1999 P. 231-236. The vessel-related diseases such as apoplexy and heart attack have been the major causes of death in many countries. Though vessel-related diseases are caused by interactions of many factors, atherosclerosis has been the major factor contributing to vessel-related diseases according to the previously published literature. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods and compositions using stearoyl-CoA desaturase to identify triglyceride reducing therapeutic agents Inventor(s): Attie, Alan D.; (Madison, WI), Brownlie, Alison J.; (Vancouver, CA), GrayKeller, Mark P.; (Middleton, WI), Hayden, Michael R.; (Vancouver, CA), Miyazaki, Makoto; (Madison, WI), Ntambi, James M.; (Madison, WI) Correspondence: Alan J. Grant, ESQ.; C/o Carella, Byrne, Bain, Gilfillan,; Cecchi, Stewart & Olstein; 6 Becker Farm Road; Roseland; NJ; 07068; US Patent Application Number: 20030157552 Date filed: February 23, 2001 Abstract: The use of screening assays based on the role of human stearoyl-CoA desaturase-1 ("hSCD1") in human diseases, disorders or conditions relating to serum levels of triglyceride, VLDL, HDL, LDL, total cholesterol, or production of secretions from mucous membranes, monounsaturated fatty acids, wax esters, and the like, is disclosed. Also disclosed are conventions useful in the prevention and/or treatment of such diseases. Excerpt(s): This application claims priority of U.S. Provisional Application No. 60/184,526, filed Feb. 24, 2000, U.S. Provisional Application No. 60/221,697, filed Jul. 31, 2000, and U.S. Provisional Application No. 60/255,771, filed Dec. 15, 2000, the disclosures of which are hereby incorporated by reference in their entirety. The present invention relates generally to the field of stearoyl-CoA desaturase and its involvement in various human diseases. Stearoyl-CoA desaturase, and the gene encoding it, are useful for identification and development of therapeutic agents for the treatment of such diseases. Acyl desaturase enzymes catalyze the formation of double bonds in fatty acids derived from either dietary sources or de novo synthesis in the liver. Mammals synthesize four desaturases of differing chain length specificity that catalyze the addition of double bonds at the.DELTA.9,.DELTA.6,.DELTA.5 and.DELTA.4 positions. Stearoyl-CoA desaturases (SCDs) introduce a double bond in the.DELTA.9-position of saturated fatty acids. The preferred substrates are palmitoyl-CoA (16:0) and stearoylCoA (18:0), which are converted to palmitoleoyl-CoA (16:1) and oleoyl-CoA (18:1), respectively. The resulting mono-unsaturated fatty acids are substrates for incorporation into phospholipids, triglycerides, and cholesterol esters. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods for activating lipid catabolism and improving lipid metabolism in small intestinal epithelium Inventor(s): Hase, Tadashi; (Haga-gun, JP), Kondo, Hidehiko; (Haga-gun, JP), Murase, Takatoshi; (Haga-gun, JP), Watanabe, Hiroyuki; (Haga-gun, JP) Correspondence: Oblon Spivak Mcclelland Maier & Neustadt PC; Fourth Floor; 1755 Jefferson Davis Highway; Arlington; VA; 22202; US Patent Application Number: 20030096866 Date filed: April 25, 2002 Abstract: Disclosed are a method for activating lipid metabolism in the small intestine epithelium and also a method for promoting accumulation of fatty acids into the small intestine epithelium, each of which features administering an effective amount of a diglyceride. Ingestion of the diglyceride leads to accumulation of the fatty acids in the small intestine. The fatty acids so accumulated promote induction of.beta.-oxidation, thereby not only activating lipid catabolism but also making it difficult to allow lipids to accumulate as triglycerides. This series of actions eventually results in development of lowering action for blood remnant-like lipoprotein level and also lowering action for blood leptin level, and hence, lipid metabolism is improved. Further, energy consumption is enhanced by promoting the induction of.beta.-oxidation and activating lipid catabolism. Excerpt(s): This invention relates to a method for promoting accumulation of fatty acids into the small intestinal epithelium, and also to a method for improving lipid metabolism in the small intestine epithelium for the suppression of triglyceride synthesis, the enhancement of.beta.-oxidation, the enhancement of uncoupling protein (UCP) expression, the promotion of energy consumption, the lowering of blood leptin level, the lowering of blood remnant level and/or the like purpose. From research in recent years, elucidations have been made increasingly as to a connection between lipid metabolism disorders, such as an increase in blood leptin level and an increase in blood remnant level, and diseases such as angina pectoris, myocardial infarction, cerebral thrombosis, cerebral infarction and aortic aneurysm. It is, therefore, desired to lower the remnant and leptin levels by improving lipid metabolism (Fertil Steril March 2002; 77(3), 433-44). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods for affecting various diseases utilizing LXR compounds Inventor(s): Bischoff, Eric D.; (San Diego, CA), Schulman, Ira G.; (San Diego, CA), Tangirala, Rajendra K.; (San Diego, CA) Correspondence: Morrison & Foerster Llp; 3811 Valley Centre Drive; Suite 500; San Diego; CA; 92130-2332; US Patent Application Number: 20030073614 Date filed: October 17, 2001 Abstract: The present invention relates to methods for elevating high density lipoprotein (HDL) plasma levels, decreasing the absorption of dietary cholesterol in the intestine, decreasing the plasma level of low density lipoprotein (LDL), and increasing the conversion of cholesterol to bile acids, utilizing LXR.beta. selective agonists, usually without elevating the plasma levels of triglycerides. Also provided are methods of
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using such agonists to treat metabolic diseases alone or in combination with other active agents. Also provided are methods for decreasing hyperglycemia and insulin resistance methods for treating type II diabetes, and methods for treating type II diabetes and reducing the cardiovascular complications of type II diabetes, utilizing an LXR agonist. Further provided are methods for treating obesity and methods for treating the complications of obesity including type II diabetes, cardiovascular disease, hyperlipidemia, and hypertension, administering an LXR.alpha.-selective antagonist. Excerpt(s): The present invention relates to LXR.beta.-selective agonists and their use in increasing reverse cholesterol transport, elevating the plasma level of high density lipoprotein (HDL) in a mammal, and in treating metabolic disorders including, but not restricted to, cardiovascular disease, diabetes, obesity, gallstone disease, syndrome X, hypertension, hypercholesterolemia, cholesterol absorption or transport disease, HDL deficiencies, and hyperlipidemia. Also provided by the present invention are methods for decreasing hyperglycemia and insulin resistance, and methods for treating type II diabetes and reducing the cardiovascular complications of type II diabetes, said methods comprising administering to said mammal, a therapeutically-effective amount of an LXR agonist. Further provided are methods for treating obesity, and methods for treating the complications of obesity including type II diabetes, cardiovascular disease, hyperlipidemia, and hypertension, said methods comprising administering a therapeutically-effective amount of an LXR.alpha.-selective antagonist. Also included in the present invention are methods of identifying said agonists and antagonists. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods for increasing stearate content in soybean oil Inventor(s): Kridl, Jean; (Davis, CA) Correspondence: Arnold & Porter; IP Docketing Department; RM 1126(b); 555 12th Street, N.W.; Washington; DC; 20004-1206; US Patent Application Number: 20030070190 Date filed: February 4, 2002 Abstract: This invention relates to a method for increasing stearate as a component of total triglycerides found in soybean seed. The method generally comprises growing a soybean plant having integrated into its genome a DNA construct comprising, in the 5' to 3' direction of transcription, a promoter functional in a soybean plant seed cell, a DNA sequence encoding an acyl-ACP thioesterase protein having substantial activity on C18:0 acyl-ACP substrates, and a transcription termination region functional in a plant cell. The present invention also provides a soybean seed with about 33 weight percent or greater stearate as a component of total fatty acids found in seed triglycerides. Excerpt(s): This application is a continuation-in-part of Application U.S. Ser. No. 09/134,26 filed Aug. 14, 1998. The invention relates to genetic modification of plants, plant cells and seeds, particularly altering fatty acid composition. Soybean (Glycine max) is one of the highest value crops currently grown in the United States (.apprxeq.$16 billion in 1996). Ranking close to corn (25%) and wheat (22%), soybean accounted for 19% of the United States crop acres planted in 1994. Often referred to as a "miracle crop", soybean offers tremendous value through the oil, protein and whole soybean products. Agronomic traits, food quality traits related to oils and protein quality are all important for the soybean industry. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Microsomal triglyceride transfer protein Inventor(s): Biller, Scott A.; (Ewing, NJ), Dickson, John K.; (Mount Holly, NJ), Gregg, Richard E.; (Pennington, NJ), Holava, Henry M.; (Meriden, CT), Lawrence, R. Michael; (Yardley, PA), Lawson, John E.; (Wallingford, CT), Partyka, Richard A.; (Neshanic, NJ), Sharp, Daru Young; (Perrineville, NJ), Wetterau, John R. II; (Langhorne, PA) Correspondence: Stephen B. Davis; Bristol-myers Squibb Company; Patent Department; P O Box 4000; Princeton; NJ; 08543-4000; US Patent Application Number: 20030166590 Date filed: August 21, 2001 Abstract: Nucleic acid sequences, particularly DNA sequences, coding for all or part of the high molecular weight subunit of microsomal triglyceride transfer protein, expression vectors containing the DNA sequences, host cells containing the expression vectors, and methods utilizing these materials. The invention also concerns polypeptide molecules comprising all or part of the high molecular weight subunit of microsomal triglyceride transfer protein, and methods for producing these polypeptide molecules. The invention additionally concerns novel methods for preventing, stabilizing or causing regression of atherosclerosis and therapeutic agents having such activity. The invention concerns further novel methods for lowering serum liquid levels and therapeutic agents having such activity. Excerpt(s): This is a continuation-in-part of U.S. patent application Ser. No. 015,449, which is a continuation-in-part of U.S. patent application Ser. No. 847, 503, filed Mar. 6, 1992, now abandoned, each of which is hereby incorporated by reference. This invention relates to microsomal triglyceride transfer protein, genes for the protein, expression vectors comprising the genes, host cells comprising the vectors, methods for producing the protein, methods for detecting inhibitors of the protein, and methods of using the protein and/or its inhibitors. The microsomal triglyceride transfer protein (MTP) catalyzes the transport of triglyceride (TG), cholesteryl ester (CE), and phosphatidylcholine (PC) between small unilamellar vesicles (SUV). Wetterau & Zilversmit, Chem. Phys. Lipids 3, 205-22 (1985). When transfer rates are expressed as the percent of the donor lipid transferred per time, MTP expresses a distinct preference for neutral lipid transport (TG and CE), relative to phospholipid transport. The protein from bovine liver has been isolated and characterized. Wetterau & Zilversmit, Chem. Phys. Lipids38, 205-22 (1985). Polyacrylamide gel electrophoresis (PAGE) analysis of the purified protein suggests that the transfer protein is a complex of two subunits of apparent molecular weights 58,000 and 88,000, since a single band was present when purified MTP was electrophoresed under nondenaturing condition, while two bands of apparent molecular weights 58,000 and 88,000 were identified when electrophoresis was performed in the presence of sodium dodecyl sulfate (SDS). These two polypeptides are hereinafter referred to as 58 kDa and 88 kDa, respectively, or the 58 kDa and the 88 kDa component of MTP, respectively, or the low molecular weight subunit and the high molecular weight subunit of MTP, respectively. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Moisture resistant, repulpable paper products and method of making same Inventor(s): Seydel, Scott O.; (Atlanta, GA) Correspondence: Mcnair Law Firm; P.O. Box 10827; Greenville; SC; 29603-0827; US Patent Application Number: 20030198826 Date filed: April 8, 2003 Abstract: Hydrogenated triglycerides having melting points above 50.degree. C. are substituted for paraffin as a coating material for the surface of paper products and the resulting paper products have improved wet strength and moisture resistance in addition to being repulpable thereby providing a distinct environmental advantage over paraffin coated products. Excerpt(s): This application claims priority from provisional application Serial No. 60/373,952 filed Apr. 19, 2002, having the same title and inventor. This invention relates to moisture resistant and water proof paper products including linerboard and corrugated board. Particularly, this invention relates to moisture resistant paper products that can be repulped and recycled to be part of the feedstock for new paper products. Even more particularly, this invention relates to the use of a moistureproofing, treating material that minimizes environmental concerns. In the manufacture of paper and paperboard, and of products made from paper and paperboard, petroleum derived paraffin waxes and synthetic polymers have been used for many years as moisture retardants, water repellents, oil repellents, stiffeners, strengtheners, and release agents. Besides paraffin, material used most often is probably polyethylene, but other widely used polymers include polymerized acrylics, vinyls, styrenes, ethylenes and copolymers or hetero-polymers of these monomers. The paper and paperboard to which these traditional materials are applied becomes difficult and often impossible to repulp and recycle in standard paper mill processes because the petroleum derived polymers and, particularly, the petroleum waxes are non-biodegradable in mill white waters (circulated process waters) and discharge effluents, and the residue of the petroleum waxes that is not removed from pulp fibers during the repulping and recycling processes cause severe problems due to buildup that occurs on the screens and felts used during the process of forming and making the paper or paperboard sheet. In addition, paper and paperboard coated or impregnated with petroleum waxes resist biodegradation and composting when disposed of in landfills and other waste disposal systems. Paper and paperboard coated or impregnated with traditional synthetic polymers and hetero-polymers are also difficult and often impossible to repulp and recycle owing to their resistance to separation from the fiber in the standard repulping processes resulting in significant fiber losses in efforts to repulp and recycle them, and these are also non-biodegradable and therefore resist composting. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Mono-and diacylglycerol acyltransferases and methods of use thereof Inventor(s): Cases, Sylvaine; (Belmont, CA), Farese, Robert V. JR.; (San Francisco, CA), Stone, Scot J.; (Fairfield, CA), Yen, Chi-Liang Eric; (San Francisco, CA), Zhou, Ping; (Walnut Creek, CA) Correspondence: Bozicevic, Field & Francis Llp; 200 Middlefield RD; Suite 200; Menlo Park; CA; 94025; US Patent Application Number: 20030124126 Date filed: January 14, 2002 Abstract: Nucleic acid compositions encoding polypeptide products with diglyceride acyltransferase and/or monoacylglycerol acyltransferase activity, as well as the polypeptide products encoded thereby, i.e., mammalian DGAT2.alpha. and MGAT1 polypeptide products, and methods for producing the same, are provided. Also provided are: methods and compositions for modulating DGAT2.alpha. and MGAT1 activity; DGAT2.alpha. and MGAT1 transgenic cells, animals and plants, as well as methods for their preparation; and methods for making diglyceride, diglyceride compositions, triglycerides and triglyceride compositions, as well as the compositions produced by these methods. The subject methods and compositions find use in a variety of different applications, including research, medicine, agriculture and industry applications. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 09/794,715, filed Feb. 26, 2001, which application claims priority to the filing date of the U.S. Provisional Patent Application Serial No. 60/271,307, filed Feb. 23, 2001, the disclosures of which are herein incorporated by reference in their entirety. The field of the invention is enzymes, particularly acyltransferases. Diacylglycerol O-Acyltransferase (EC 2.3.1.20), also known as diglyceride acyltransferase or DGAT, is a critical enzyme in triacylglycerol synthesis. Triacylglycerols are quantitatively the most important storage form of energy for eukaryotic cells. DGAT catalyzes the rate-limiting and terminal step in triacylglycerol synthesis using diacylglycerol and fatty acyl CoA as substrates. As such, DGAT plays a fundamental role in the metabolism of cellular diacylglycerol and is important in higher eukaryotes for intestinal fat absorption, lipoprotein assembly, fat storage in adipocytes, milk production and possibly egg production and sperm maturation. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Novel apolipoprotein gene involved in lipid metabolism Inventor(s): Pennacchio, Len A.; (Sebastopol, CA), Rubin, Edward; (Berkeley, CA) Correspondence: Lawrence Berkeley National Laboratory; One Cyclotron Road, Mail Stop 90b; University OF California; Berkeley; CA; 94720; US Patent Application Number: 20030150003 Date filed: August 27, 2002 Abstract: Methods and materials for studying the effects of a newly identified human gene, APOAV, and the corresponding mouse gene apoAV. The sequences of the genes are given, and transgenic animals which either contain the gene or have the endogenous gene knocked out are described. In addition, single nucleotide polymorphisms (SNPs) in the gene are described and characterized. It is demonstrated that certain SNPs are
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associated with diseases involving lipids and triglycerides and other metabolic diseases. These SNPs may be used alone or with SNPs from other genes to study individual risk factors. Methods for intervention in lipid diseases, including the screening of drugs to treat lipid-related or diabetic diseases are also disclosed. Excerpt(s): This application claims priority to Application No. 60/318,219, which was filed on Aug. 27, 2001, hereby incorporated by reference. Applicants assert that the paper copy of the Sequence Listing is identical to the Sequence Listing in computer readable form found on the accompanying computer disk. Applicants incorporate the contents of the sequence listing by reference in its entirety. This invention generally relates to human lipid metabolism, particularly to apolipoproteins, genes encoding these apolipoproteins, related proteins, and their mutations and polymorphisms as they relate to cardiovascular, coronary and other diseases. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Novel oat lipid based surfactants and derivatives and process for preparing same Inventor(s): Syed, Samad A.; (Paramus, NJ), Walele, Ismail I.; (Saddle Brook, NJ) Correspondence: Weingram & Associates P.C.; P.O. Box 927; Maywood; NJ; 07607; US Patent Application Number: 20030198653 Date filed: June 21, 2002 Abstract: Novel oat-lipid based derivatives, surfactants and emollients are disclosed, as well as their use in the production of surface active derivatives or non-surface active esters, and ester emollients. The surfactants and fatty derivatives are useful as emollients, dispersants, emulsifiers, and conditioners for hair care and skin care products. For example, derivatives such as amides of oat fatty triglycerides ("OFTG")/Monoethanolamine; Acyl Amidopropyl Dimethyl Amines of OFTG as Cationic Surfactants; Betaines based on OFTG; Esters of OFTG based Fatty Acids and Isostearyl Alcohol; Quaternaries based on OFTG based Amido-propyl Dimethyl Amine; Sulfosuccinamates based on OFTG--MEA Amides; and Sulfosuccinamates based on OFTG--Iso Propanolamines have been prepared. Derivatives may also include those involving other reactive groups known to those skilled in the art. Excerpt(s): The present invention relates to novel oat-lipid based surfactants and derivatives, and emollients, their process of manufacture, their use in the production of surface active derivatives, non-surface active esters, and ester emollients, and skin and hair care preparations containing the surfactants, derivatives, and emollients. The surfactants and fatty ester derivatives are useful as emollients, dispersants, emulsifiers, and conditioners for hair care and skin care products. Surfactants and derivatives are known for a variety of different applications for cosmetic, pharmaceutical, and medicinal purposes. Numerous references describe the production and use of surface active derivatives or non-surface active esters, and ester emollients. For example, it is known to use oats and oat extract in cosmetic preparations to obtain the benefits of mildness, antioxidant properties, etc. Surfactants and fatty derivatives useful as emollients, dispersants, emulsifiers and conditioners for hair and skin care products are commonly produced from a wide variety of fatty acids, fatty alcohols and amines, polyamines, dialkyl propylamines, alkanolamines, etc. However, none of these references teach or suggest the specific novel oat-based surfactants made from the fatty oil triglyceride obtained from oats, or OFTG, of this invention or the use of OFTG to
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produce surface active derivatives or non-surface active esters, and ester emollients for cosmetics and personal care products. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Oral capsule formulation with increased physical stability Inventor(s): Burnside, Beth A.; (Bethesda, MD), Ibrahim, Scott A.; (Burtonville, MD), Shojaei, Amir H.; (Gaithersburg, MD) Correspondence: Gregory P. Lapointe; Bachman & Lapointe, P.C.; 900 Chapel Street, Suite 1201; New Haven; CT; 06510-2802; US Patent Application Number: 20030124182 Date filed: December 20, 2002 Abstract: A formulation for a stabilized capsule for oral administration of a hydrophobic pharmaceutically active agent; comprising a non-aqueous solubilizer selected from 2pyrrolidone, N-alkylpyrrolidones and combinations thereof; and a capsule stabilizing agent selected from mono-,di-and triglycerides, mono-and di-fatty esters of polyethylene glycol, fatty acids and combinations thereof wherein capsule integrity is maintained for at least 24 hours is disclosed. Excerpt(s): The present invention relates to an oral capsule formulation with increased physical stability. It is generally accepted that many of the new pharmaceutically active molecules are insoluble or poorly soluble in water. In order to improve the bioavailability of drugs that exhibit dissolution rate limited oral absorption profiles or to simplify the formulation process, it often becomes necessary to administer the drug in form of a solution or a suspension. Such an approach would then mandate the use of suitable solubilizers in which the pharmaceutical active agent can be fully or partially dissolved. The liquid formulation would then have to be encapsulated in a suitable capsule shell (i.e., hard gelatin, soft gelatin, HPMC hard shell, etc.) to be administered as a solid dosage form. There is often the problem of lack of capsule shell integrity in presence of effective non-aqueous solubilizers such as N-methyl-2-pyrrolidone (NMP) and pyrrolidone derivatives. The capsule shell is either completely dissolved in the solubilizer or it softens as a result of the strong solubilizing properties of the nonaqueous solubilizers. Such deformities would lead to product failures and would limit further dosage formulation development. The problem of gelatin capsule stability has been addressed by many (see U.S. Pat. Nos. 2,780,355, 4,497,157, 4,777,048, 4,780,316, 5,037,698 and 5,376,381), these innovations have generated different solutions tailored to specific wall destabilizing agents such as hygroscopic and deliquescent components, ethanol, lubricants, salts, etc. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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PAPER SIZING COMPOSITIONS AND METHODS Inventor(s): Dauplaise, David L.; (Stamford, CT), Dilts, Kimberly C.; (Beacon Falls, CT), Proverb, Robert J.; (Danbury, CT) Correspondence: Bayer Chemicals Corporation; 100 Bayer Road; Pittsburgh; PA; 15205; US Patent Application Number: 20030205167 Date filed: May 6, 2003 Abstract: This invention relates to paper sizing compositions comprised of at least one sizing agent selected from ASA, AKD and rosin where the at least one sizing agent is emulsified in water, at least one emulsion stabilizer, and from about 0.01% to about 15% by weight of at least one hydrophobic substance, based on the total weight of sizing agent present, provided that the hydrophobic substance is not highly alkoxylated. The sizing promotion efficiency of the paper sizing compositions, as determined by at least one method selected from the Cytec size testing method, the Hercules size testing method, and the Cobb size testing method, is greater than or equal to about 4. Exemplary hydrophobic substances include fatty acid esters, triglycerides, hydrocarbons, esters and/or amides derived from ASA, silicone oils, alcohols, and stearic anhydride. The invention also relates to methods for sizing paper products with these paper sizing compositions and paper or paperboard treated with these sizing compositions. Excerpt(s): The present invention relates to sizing compositions and methods of sizing paper. The sizing compositions of this invention comprise at least one hydrophobic substance which is not a sizing agent, at least one sizing agent selected from ASA, AKD and rosin where the sizing agent is emulsified in water, and at least one emulsion stabilizer. This invention relates to paper sizing, i.e., rendering paper more resistant to penetration by liquids, such as inks. The control of the penetration of liquids, such as aqueous inks, into paper and the water-resistance of paper are important properties of many grades of paper and for many applications. Control of ink penetration is important in writing and printing grades and, especially, for ink-jet printing. For example, good printing performance may require a limited amount of wetting by the ink but the rate of penetration of the ink into the sheet should be low. Paper and paperboard are often sized with various sizing agents, such as alkyl and alkenyl succinic anhydride (hereafter "ASA"), alkyl and alkylene ketene dimers (hereafter "AKD"), rosin and rosin derivatives such as rosin soap, starch, sodium silicate, fluorocarbons, certain styrene-maleic anhydride copolymers and cyclic dicarboxylic acid anhydrides. Sizing can be accomplished by either internal sizing processes, which usually involve wet end addition, or surface sizing processes, which usually involve addition at the size press. For effective sizing of paper pulp, it is desirable that the sizing agent be uniformly distributed throughout the fibrous slurry of pulp. Therefore, sizing agents may be emulsified to a small particle size using an emulsion stabilizer and the aqueous sizing emulsion is then added to the pulp at the wet end of the papermaking process. Emulsion stabilizers commonly used to prepare sizing emulsions include, for example, cationic starches and cationic polymers. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Plant diacylglycerol O-acyltransferase and uses thereof Inventor(s): Cases, Sylvaine; (Belmont, CA), Farese, Robert V. JR.; (San Francisco, CA) Correspondence: Bozicevic, Field & Francis Llp; 200 Middlefield RD; Suite 200; Menlo Park; CA; 94025; US Patent Application Number: 20030074695 Date filed: August 15, 2002 Abstract: Plant nucleic acid compositions encoding polypeptide products with diacylglyceride acyltransferase (DGAT) activity, as well as the polypeptide products encoded thereby and methods for producing the same, are provided. Methods and compositions for modulating DGAT activity in a plant, particularly DGAT activity in plant seeds, and transgenic plants with altered DGAT activity are provided. Such plants and seeds are useful in the production of human food and animal feedstuff, and have several other industrial applications. Also provided are methods for making triglycerides and triglyceride compositions, as well as the compositions produced by these methods. The subject methods and compositions find use in a variety of different applications, including research, medicine, agriculture and industry. Excerpt(s): This application is a continuation-in-part of application Ser. No. 10/040,315 filed Oct. 29, 2001; which application is: (a) a continuation-in-part of application Ser. No. 09/339,472 filed on Jun. 23, 1999, which application claims priority to the filing date of United States Provisional Patent Application Serial No. 60/107,771 filed Nov. 9, 1998; and (b) a continuation-in-part of PCT application serial no. PCT/US98/17883, filed Aug. 28, 1998, which application is a continuation in part of application Ser. No. 09/103,754, now U.S. Pat. No. 6,344,548, filed Jun. 24, 1998; the disclosures of which applications are herein incorporated by reference. The field of the invention is plant enzymes, particularly plant acyltransferases. Triacylglycerol is synthesized by the sequential transfer of acyl chains to a glycerol backbone by a series of enzymes in the Kennedy pathway. These enzymes are glycerol-3-phosphate acyltransferase (which adds a first acyl chain to a glycerol backbone to form a glycerol-3-phosphate), lysophosphatidic acid acyltransferase (which adds a second acyl chain to glycerol-3-phosphate to form diacylglycerol) and diacylglycerol acyltransferase (DGAT), which transfers a third acyl chain to diacylglycerol to form triacylglycerol (TAG) (see Topfer el al. Science 1995 268: 681-686). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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POLYSTYRENE BINDERS Inventor(s): BOEGE, KAI; (DUESSELDORF, DE), DZIALLAS, MICHAEL; (HAAN, DE), HELPENSTEIN, KLAUS; (MOENCHENGLADBACH, DE), KLAUCK, WOLFGANG; (MEERBUSCH, DE), KLEIN, JOHANN; (DUSSELDORF, DE), LOTH, HELMUT; (ESSEN, DE), URBATH, HARTMUT; (WUPPERTAL, DE), WINDHOEVEL, UDO; (MONHEIM, DE) Correspondence: Henkel Corporation; 2500 Renaissance Blvd; Ste 200; Gulph Mills; PA; 19406; US Patent Application Number: 20030188828 Date filed: February 11, 1998
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Abstract: The invention relates to polystyrene binders modified by fatty compounds. The fatty compounds used are, in particular, esters of fatty acids or fatty alcohols, more especially triglycerides of higher fatty acids, preferably natural fats and oils. They may be added to the binder in high concentrations without adversely affecting the properties of the binder. However, their addition is of advantage in regard to the wetting properties, resistance to water and, above all, hardness. Dispersion adhesives, hotmelt adhesives and sealing compounds in particular can be improved with the binders according to the invention. Excerpt(s): This invention relates to binders based on homopolymers or copolymers of styrene, to their production and to their use for bonding, coating and sealing. Binders in the context of the invention are substances which are capable of bonding or firmly adhering to substrates of the same or different types. They are generally based on substances, especially polymers, which set chemically or physically. Physical setting consists in solidification from the melt or in the drying of an aqueous or organic solution or dispersion. The substances or rather polymers are generally modified by additives in such a way that they are more suitable for bonding, adhesive sealing and coating. Corresponding additives are, for example, resins, plasticizers, solvents, fillers, pigments, accelerators, stabilizers and dispersants. Accordingly, the adhesives, sealing compounds and coating compounds are based on correspondingly modified binders. Plasticizers are added to improve the plasticity or to reduce the hardness of adhesives, sealing compounds and coating compositions. Plasticizers are liquid or solid, generally inert organic substances of low vapor pressure. According to general expert knowledge (see Habenicht, Gerd: "Kleben: Grundlagen, Technologie-Anwendungen", 2nd Edition,1990, page 100), the disadvantage of plasticizer-containing adhesive layers lies in their impaired ageing and adhesion properties and in the reduced strengths of the adhesive layer and in its tendency to creep and migrate. Accordingly, well-balanced consideration has to be given to the priorities between plasticity on the one hand and strength of the other hand. In "Ullmanns Encyclopidie der technischen Chemie", the use of plasticizers is also described under the keyword "Weichmacher (Plasticizer)" (see pages 371 to 377, Vol. 24, 4th Edition, 1983). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Pourable fatty dispersions Inventor(s): Floter, Eckhard; (Vlaardingen, NL), Gude, Michael; (Vlaardingen, NL), Laan, Johannes Arie; (Vlaardingen, NL) Correspondence: Unilever; Patent Department; 45 River Road; Edgewater; NJ; 07020; US Patent Application Number: 20030134029 Date filed: December 19, 2002 Abstract: Liquid margarines and other pourable dispersions which contain a hardstock fat derived from plant waxes. The fat consists of a mixture of triglycerides, which fat is non-hydrogenated and contains less than 10 wt. % of fatty acid residues with a chain length of 6-10 carbon atoms, of which less than 50 wt. % of the triglycerides consist of monoacyl triglycerides and which fat is characterized in that its content of fatty acid residues which are saturated and contain at least 20 carbon atoms is at least 30 wt. %, preferably at least 40 wt. % and more preferably at least 50 wt. % calculated on total fatty acid residues. Such fat can be obtained by a process comprising the steps:selecting a plant wax,reacting the wax esters from the wax or a reactive derivative of those wax esters with glycerol or with a reactive glycerol derivative,purifying and recovering the
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obtained triglycerides,optionally admixing the product with a triglyceride fat such that the mixture complies with the above fat definition. Excerpt(s): The present invention relates to a novel triglyceride fat and to pourable fatty dispersions consisting of a triglyceride oil in which a non-fat phase is dispersed and which dispersion further contains a stabilising amount of the novel fat. Liquid margarine is an example of such dispersion. Margarine consists of a continuous fat phase and an aqueous phase which is dispersed as fine droplets in the fat phase. At ambient temperature liquid margarine has a pourable consistency which is realized by a proper selection of the fat phase ingredients. Generally, margarine fat consists of a mixture of a fat which at ambient temperature is fully liquid (an oil) and the so-called hardstock fat which contains solid fat and which is included for its stabilising functionality. The ratio of liquid and solid fat is chosen such that after proper processing together with an aqueous phase the crystals of the solid fat form a lattice throughout the liquid oil resulting into a structured fat phase. The aqueous phase droplets are fixed within the spaces of the lattice of solid fat crystals. In this way coalescence of the droplets and separation of the heavier aqueous phase from the fat phase is prevented and a stable W/O-emulsion results. A liquid margarine needs a special hardstock fat which not only structures the liquid oil, but in the same time ensures pourability of the product. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
PREPARED FOODS CONTAINING TRIGLYCERIDE-RECRYSTALLIZED NONESTERIFIED PHYTOSTEROLS Inventor(s): Hayes, Kenneth; (Wellesley, MA), Perlman, Daniel; (Arlington, MA), Pronczuk, Andrzej; (Milton, MA) Correspondence: Foley & Lardner; P.O. Box 80278; San Diego; CA; 92138-0278; US Patent Application Number: 20030096035 Date filed: November 14, 2002 Abstract: A prepared food product for ingestion by mammals is described and methods for preparing such products. The food product includes an oxidation-resistant fat-based composition substantially free of exogenous solubilizing and dispersing agents for phytosterols. The fat-based composition includes between 75% and 98% by weight of at least one triglyceride-based edible oil or fat, and between 2% and 25% by weight of nonesterified phytosterols. Typically, approximately 1.5% by weight of phytosterols remain soluble at room temperature, and between 0.5% and 23.5% by weight are converted to triglyceride-recrystallized phytosterols (TRPs). The fat-based composition which has been partially oxidized in the prepared food by exposure to air (and typically heat), contains a reduced amount of oxidative by-products compared to a similar fat-based composition lacking these non-esterified phytosterols. Excerpt(s): The present invention relates to prepared foods, such as fried snack foods, fortified with non-esterified phytosterols delivered in fats or oils that are essentially free of emulsifiers and the like, and to the utility of such phytosterols for stabilizing heated fats and oils against oxidation, as well as to the surprising bioavailability of triglyceriderecrystallized phytosterols in such foods, for decreasing plasma cholesterol levels in mammals. It has been a widely held belief that to obtain appreciable benefit from phytosterols, i.e., either plant sterols, stanols, or combinations thereof [including betasitosterol, beta-sitostanol, campesterol, campestanol, stigmasterol, stigmastanol,
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brassicasterol, brassicastanol, clionasterol and clionastanol (collectively termed phytosterol or phytosterols)] for lowering plasma cholesterol, the phytosterol should be dissolved in an edible oil or other solvent so that it can enter micelles in the small intestine to inhibit the absorption of cholesterol. This belief has been supported by early research carried out in the 1950s through the 1970s showing that large doses of phytosterols in their solid form, i.e., coarse powders, were required to achieve meaningful decreases in plasma cholesterol levels. For example, in 1956, Faquhar et al., (Circulation, 14, 77-82, 1956) showed that doses of 12-18 g per day of beta sitosterol (provided in divided doses) were required to achieve a 15-20% lowering of serum cholesterol in males with atherosclerosis. In another study, 9 g per day (3 g t.i.d.) of soybean-derived phytosterols were required to lower plasma cholesterol approximately 9% (Kucchodkar et al., Atherosclerosis, 23 239-248, 1976). In yet another study, 3-9 g per day of tall oil-derived phytosterols were required to lower plasma cholesterol approximately 12% (Lees et al., Atherosclerosis, 28: 325-333, 1977). In a recent study, 1.7 g per day of finely powdered tall oil-derived phytosterols were sufficient to lower total plasma cholesterol by 9% and LDL-cholesterol by about 15% (Jones et al., Am J Clin Nutr, 69: 1144-1150, 1999). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Procedure to obtain biodiesel fuel with improved properties at low temperature Inventor(s): Delgado Puche, Juan; (Madrid, ES) Correspondence: Ladas & Parry; 26 West 61st Street; New York; NY; 10023; US Patent Application Number: 20030167681 Date filed: December 23, 2002 Abstract: Procedure to generate biodiesel fuels with improved properties at low temperature by the transesterification of triglycerides with alcohols such as methanol or ethanol, optionally in the presence of methyl or ethyl acetates of fatty acids and an inert solvent, to produce methyl or ethyl esters of fatty acids, glycerine and, where appropriate, glycerine triacetate, followed by the separation of crude glycerine that is reacted with aldehydes, ketones and/or acetic acid or methyl or ethyl acetates to produce acetals, glycerine cetals and/or glycerine acetates. The acetals, glycerine cetals and/or glycerine acetates are mixed with methyl or ethyl esters of fatty acids in concentrations of approximately 0.5-20% by weight to obtain a biodiesel with improved properties at low temperatures. Excerpt(s): It is known that methyl and/or ethyl esters obtained by transesterification of triglycerides with methanol and/or ethanol are used as biodiesel fuels to substitute petroleum-derived diesels. It is also known that this reaction is relatively slow and that the reaction rate can be substantially increased in the presence of inert solvents. Simple ethers such as tetrahydrofuran (THF) and methyl tert-butyl ether (MTB) are particularly effective solvents according to the Canadian patent 2.131.654 published in March, 1996. During the transesterification, which is usually conducted in the presence of basic catalysts, relatively important amounts of crude glycerine are produced. Hence, for example, in the transesterification of soya oil with methanol approximately 20% of crude glycerine is generated for which applications must be found. The purification of this glycerine for its commercial application is a difficult and expensive procedure, even to obtain a poor quality product of doubtful value. Therefore, a procedure to transform this glycerine, via an inexpensive process, into compounds that can be mixed with biodiesel to improve its properties, especially its behavior at low temperature and
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improve its combustion, is a long sought after objective that would have great technical and commercial value and would solve the problem of finding an interesting application for crude glycerine. This objective can be achieved within the scope of this invention. Currently, the relatively high price of biodiesel compared to diesel oils derived from petroleum is the main obstacle to their complete commercial acceptance. One way to make these procedures more economically viable would be to find new applications for crude glycerine. The procedures proposed to date for the use of crude glycerine are unsatisfactory and include mixing it with animal manure to produce fertilizers or incorporating it into animal feed. These applications are described, for example, in the article titled "Technical Uses of Fatty Acid Esters", Meffert, JAOCS, vol. 61, February 1984. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Process for the production of CLA triglycerides Inventor(s): Cain, Frederick William; (Wormerveer, NL), Harris, John Bernard; (Bedford, GB), Schmid, Ulrike; (Wormerveer, NL), Yan, Youchun; (Wormerveer, NL) Correspondence: Morgan Lewis & Bockius Llp; 1111 Pennsylvania Avenue NW; Washington; DC; 20004; US Patent Application Number: 20030225295 Date filed: April 10, 2003 Abstract: The invention concerns a novel process for the production of glycerol esters of polyunsaturated fatty acids, in particular of C18:2 conjugated fatty acids, by converting the polyunsaturated fatty acids with glycerol in the presence of a mixed catalyst comprising a combination of a food grade salt of a strong base and a weak acid and a soap of an organic acid with 2-26 C-atoms, preferably 10-20 C-atoms. Excerpt(s): Glycerol esters of polyunsaturated fatty acids are known materials. Examples thereof can be found in nature e.g. in fish oils these esters are often present in limited amounts. However it also disclosed in the prior art that these esters can be made from glycerol and free fatty acids. In this processing enzymes are applied as catalysts. Although enzymes have a number of advantages over chemical compounds as a catalyst they also have a number of disadvantages such as the use of enzymes require a careful control of the water content of the reaction system because too high water content will prevent an esterification. This control of water content however is not always easy and complicates the enzymic conversion. Moreover the products of the enzymic conversion often contain polymeric isomers of the polyunsaturated products while also unwanted geometric isomers (i.e. cis/trans isomers) are formed in undesirable too high amounts. Therefore we studied whether we could find another route for the production of glycerol esters from conjugated polyunsaturated fatty acids. We found this route, which avoids all the disadvantages mentioned above and which is based on the use of a chemical catalytic system in the form of a combination of a salt of a weak acid and a strong base and a soap. Although trans esterification reactions of glycerol with saturated fatty acid alkyl esters using e.g. sodium carbonate as catalyst are known (cf U.S. Pat. No. 5,254,722) while also esterification of glycerol with fatty acids are known using a soap as catalyst (cf Szelag c.s in Fett Lipid 100 (7) 302-307 July 1998) we found that when applying these systems to polyunsaturated fatty acid a problem occurred i.e. since polyunsaturated fatty acids are very heat-sensitive, the reaction temperatures used were so high that the polyunsaturated fatty acids were already destroyed during the esterification. Moreover when the reaction was carried out at low temperature
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(.ltoreq.140.degree. C.), the initial reaction rate was so slow that the reaction could not be started in the beginning. Unexpectedly we found that this problem could be overcome when a combination of a salt of a weak acid and a strong base and a soap was applied. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Reduced calorie fat compositions Inventor(s): Adams, Stacey Lynne; (Ft Collins, CO), Kester, Jeffrey John; (West Chester, OH), McRorie Jr, Johnson Watson; (Lebanon, OH), Naber, Russell Bruce; (Cincinnati, OH), Schafermeyer, Richard Gerard; (Cincinnati, OH) Correspondence: The Procter & Gamble Company; Intellectual Property Division; Winton Hill Technical Center - Box 161; 6110 Center Hill Avenue; Cincinnati; OH; 45224; US Patent Application Number: 20030215556 Date filed: October 11, 2002 Abstract: Reduced calorie fat compositions which contain combinations of substantially non-absorbable, substantially nondigestible polyol polyesters and certain reduced calorie triglycerides that function as anti-anal leakage agents and provide textural/taste benefits are disclosed. These reduced calorie fat compositions are useful in a variety of food applications, including frying oils for salted snacks, chocolate-flavored candy bars and cooking/salad oils. Excerpt(s): The present application relates to reduced calorie fat compositions which contain combinations of non-absorbable, nondigestible polyol polyesters and reduced calorie triglycerides that function as anti-anal leakage agents and provide textural/taste benefits, e.g., less waxiness/greasiness, improved mouthmelt. The present application further relates to food products, such as frying oils for salted snacks, firm chocolateflavored products and cooking/salad oils, containing combinations of these polyesters and triglycerides. Polyol fatty acid polyesters are known in the art for use as low calorie substitutes for normal triglyceride fats. For example, U.S. Pat. No. 3,600,186 to Mattson et al., issued Aug. 17, 1971, discloses low calorie food compositions in which at least a portion of the fat content of a conventional food is provided by a non-absorbable, nondigestible sugar fatty acid polyester with each fatty acid having from 8 to 22 carbon atoms. Foods in which these polyol polyesters are particularly useful include salad and cooking oils, mayonnaise, margarine, dairy products, and plastic shortenings for use in frying, cake making, breadmaking or the like. Unfortunately, regular ingestion of moderate to high levels of liquid forms of these polyol polyesters can produce an undesirable laxative side effect, namely, leakage of the polyesters through the anal sphincter. U.S. Pat. No. 4,005,195 to Jandacek, issued Jan. 25, 1977 discloses a means for preventing these undesirable laxative effects through the addition of anti-anal leakage agents. These anti-anal leakage agents include solid fatty acids (melting point 37.degree. C. or higher) and their digestible triglyceride and ester sources, as well as edible solid, nondigestible, non-absorbable polyol fatty acid polyesters. Solid fatty acids, solid triglycerides and solid polyol polyesters have drawbacks when used as anti-anal leakage agents in low calorie food compositions. For example, a fatty acid, triglyceride or polyester providing a high solids content at body temperature tastes waxy in the mouth when ingested. Additionally, cooking and salad oils containing solid fatty acids, solid triglycerides or solid polyol polyesters can be cloudy or opaque at room temperature, i.e., at about 70.degree. F. (21.1.degree. C.), or below, instead of clear. Accordingly, it would be desirable to provide anti-anal leakage agents for liquid polyol
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polyesters which do not impart a waxy mouthfeel and can be used in formulating clear cooking oils. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Sebum-like preparation to be used as lipidic component in cosmetics Inventor(s): Passi, Siro; (Rome, IT) Correspondence: Young & Thompson; 745 South 23rd Street 2nd Floor; Arlington; VA; 22202 Patent Application Number: 20030185920 Date filed: May 19, 2003 Abstract: A preparation similar to sebum to be used as lipidic component in formulations to be administered topically is characterized in that it consits of active principale of only natural origin capable of fulfilling the requirement of meeting the average qualitative-quantitative composition of the human dermal surface lipides. In particular, it consits of substances of natural origin capable of providing triglycerides which are rich in saturated, monounsaturated and diunsaturated acids, squalene, waxes, free and esterified cholesterol in quantities which are equivalent to those present in the human sebum. Excerpt(s): The present invention relates to formulations to be administered topically and intended to re-establish the equilibrium of lipids functional to the dermal homeostasis and altered by ageing and different dermatosis. Such formulations are characterized in that they include active principles of only natural origin capable of fulfilling the requirement of meeting the average qualitative-quantitative composition of the human dermal surface lipids. Human dermal surface lipids have the peculiarity of being the sole lipid in the animal and vegetal kingdoms both as far as plenty of fraction and the complexity and the peculiarity of their intimate structure is concerned. The following Table 1 shows the average percentage and weight composition of dermal surface lipids (DSL) calculated on the forehead of 30 normal subjects aged between 20 and 35: the DSL are formed by 90% sebum. In the other dermal areas rich in oil glands (cheeks, chest, back) the percentage of the lipidic fraction is similar to that of Table 1 relating to the forehead. As it can be easily inferred, the quantity (.mu.g/cm.sup.2) of extracted lipids varies in a proportional way as the density of the oil glands. For example, it is 122.5.+-.21.2.mu.g/cm.sup.2 in the chest (at the clavicula). It is known that fat represents one of the primary components of cosmetics and its function is to protect and to re-establish the equilibrium of lipids in the skin. It should be pointed out, however, that the fats used in cosmetics are almost of synthetic origin and do not fulfil at all the qualitative-quantitative composition shown in Table 1. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Single-phase process for production of fatty acid methyl esters from mixtures of triglycerides and fatty acids Inventor(s): Boocock, David Gavin Brooke; (Ajax, CA) Correspondence: Russell D. Orkin; Webb Ziesenheim Logsdon Orkin & Hanson; 700 Koppers Building; 436 Seventh Avenue; Pittsburgh; PA; 15219; US Patent Application Number: 20030083514 Date filed: July 22, 2002 Abstract: A process for the esterification of a mixture of fatty acids and triglycerides. The process comprises forming a single phase solution of fatty acids and triglyceride in an alcohol selected from methanol and ethanol, the ratio of said alcohol to triglyceride being 15:1 to 35:1. The solution further comprises a co-solvent in an amount to form the single phase. In a first step, an acid catalyst for the esterification of the fatty acids is added. After a period of time, the acid catalyst is neutralised and a base catalyst for the transesterification of triglycerides is added. After a further period of time, esters are separated from the solution. Excerpt(s): The present invention relates to the production of fatty acid methyl esters from mixtures of triglycerides and fatty acids. In particular, the invention relates to a single-phase process, which may be referred to as a two-step process, for production of fatty acid methyl esters from mixtures of triglycerides and fatty acids. The process does not require separation of any phases in intermediate steps in the process. The transesterification of vegetable oils to form esters, and in particular, methyl esters, has received considerable attention, primarily because the esters may be used as "biofuels" or "biodiesel". Biofuels are fuels derived from renewable resources such as naturally occurring fats and oils. Such fats and oils may be obtained from a variety of plant and animals. Biodiesel relates to the specific application to diesel fuel. The major components of an oil or fat are fatty acid triglycerides, in which three long chain fatty acid moieties are joined to one glycerol moiety by ester linkages, particularly when the fats and oils are in the form of vegetable oils. Other sources of fats and oils contain a significant proportion of fatty acids. Such fatty acids may include lauric acid, palmitic acid, stearic acid, oleic acid and linoleic acid. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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SOLID CARRIERS FOR IMPROVED DELIVERY OF HYDROPHOBIC ACTIVE INGREDIENTS IN PHARMACEUTICAL COMPOSITIONS Inventor(s): Chen, Feng-Jing; (Salt Lake City, UT), Patel, Mahesh V.; (Salt Lake City, UT) Correspondence: Reed & Eberle Llp; 800 Menlo Avenue, Suite 210; Menlo Park; CA; 94025; US Patent Application Number: 20030064097 Date filed: March 6, 2001 Abstract: The present invention provides solid pharmaceutical compositions for improved delivery of a wide variety of pharmaceutical active ingredients contained therein or separately administered. In one embodiment, the solid pharmaceutical composition includes a solid carrier, the solid carrier including a substrate and an encapsulation coat on the substrate. The encapsulation coat can include different combinations of pharmaceutical active ingredients, hydrophilic surfactant, lipophilic
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surfactants and triglycerides. In another embodiment, the solid pharmaceutical composition includes a solid carrier, the solid carrier being formed of different combinations of pharmaceutical active ingredients, hydrophilic surfactants, lipophilic surfactants and triglycerides. The compositions of the present invention can be used for improved delivery of hydrophilic or hydrophobic pharmaceutical active ingredients, such as drugs, nutrionals, cosmeceuticals and diagnostic agents. Excerpt(s): The present invention relates to pharmaceutical delivery systems for pharmaceutical active ingredients, such as drugs, nutritionals, cosmeceuticals, and diagnostic agents. In particular, the present invention provides compositions and dosage forms including solid carriers for improved delivery of pharmaceutical active ingredients. Hydrophobic active ingredients, such as progesterone, cyclosporine, itraconazole and glyburide present delivery challenges due to their poor aqueous solubility and slow dissolution rate. Several commercial products of these hydrophobic drugs are available, the various products using different methods to try to enhance in vivo performance. One approach is size reduction by micronization, such as in Prometrium (micronized progesterone) and Micronase (micronized glyburide). Other approaches include size reduction in emulsion formulations, such as in Sandimmune (cyclosporine emulsion) and NeOral (cyclosporine microemulsion). These approaches suffer from several disadvantages. Micronization/nanonization presents processing and stability challenges, as well as dissolution limitations, since the micronized/nanosized drug still possesses a high degree of crystallinity. Liquid formulations present drug precipitation and packaging challenges, due to solvent evaporation. Moreover, nonsolid formulations are more prone to chemical instability and capsule-shell incompatibility, leading to the possibility of leakage upon storage. For hydrophilic active ingredients, the formulation challenges are different. Although these compounds are readily soluble in the aqueous gastrointestinal environment, they are poorly absorbed, due to poor membrane permeability and/or enzymatic degradation. Surfactants and lipophilic additives have been reported to improve membrane permeability; see, e.g., LeCluyse and Sutton, "In vitro models for selection of development candidates. Permeability studies to define mechanisms of absorption enhancement", Advanced Drug Delivery Reviews, 23, 163-183 (1997). However, these compositions fail to maintain effective levels and type of enhancers for bioacceptable absorption enhancement. Most solid dosage forms of hydrophilic active ingredients exhibit poor or no absorption of the active. Moreover, these non-solid formulations suffer from the disadvantages of chemical instability, leakage and capsule shell incompatibility as discussed above. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Statin-carboxyalkylether combinations Inventor(s): Bisgaier, Charles Larry; (Ann Arbor, MI), Newton, Roger Schofield; (Ann Arbor, MI) Correspondence: Francis J. Tinney; Warner-lambert Company; 2800 Plymouth Road; Ann Arbor; MI; 48105; US Patent Application Number: 20030105154 Date filed: September 17, 2002 Abstract: The invention is a pharmaceutical composition comprising a carboxyalkylether which lowers triglycerides and elevated HDL, and a statin which inhibits HMG-CoA
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reductase, thereby reducing LDL, said composition being useful for treating vascular diseases. Excerpt(s): This invention concerns a combination of a statin compound, which is known to cause a reduction in plasma levels of low-density lipoprotein (LDL) cholesterol, and a carboxyalkylether, a compound which causes a rise in high-density lipoprotein (HDL) cholesterol. The combination is useful for treating vascular disorders and diabetes mellitus. Several clinical studies have established that lowering certain forms of cholesterol in a mammal is an effective way to treat and prevent heart attacks, sudden death, and angina, both in subjects having higher than normal levels of circulating cholesterol, as well as those having normal levels of cholesterol. Lowering LDL, the bad form of cholesterol, is now one of the primary objectives of physicians treating patients who have, or who have a high risk of developing, cardiovascular diseases such as coronary heart disease, atherosclerosis, myocardial infarction, stroke, cerebral infarction, and even restenosis following balloon angioplasty. Many physicians are now utilizing cholesterol lowering agents purely as a prophylactic treatment in healthy subjects whose cholesterol levels are normal, thereby guarding against development of cardiovascular diseases. The most commonly used cholesterol lowering agents are the statins, which are compounds which inhibit the enzyme 3-hydroxy-3methylglutaryl-c- oenzyme A (HMG-CoA) reductase, the enzyme responsible for catalyzing the conversion of HMG-CoA to mevalonate, which is an early and ratelimiting step in the cholesterol biosynthetic pathway. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Test strip for determining concentration of triglycerides Inventor(s): Anaokar, Sunil G.; (Indianapolis, IN), Antonopoulos, Gena Lynn; (Indianapolis, IN), Cunningham, Patrick; (Indianapolis, IN) Correspondence: Michael C. Bartol; 111 Monument Circle, Suite 4600; P.O. Box 44924; Indianapolis; IN; 46244; US Patent Application Number: 20030170768 Date filed: December 30, 2002 Abstract: A dry-phase triglycerides test strip that can be stored at room or elevated temperatures for several months without significant degradation in its effectiveness. The test strip includes a test membrane which receives plasma and forms a colored response in proportion to concentration of triglycerides in the plasma. The test membrane is impregnated with an aqueous solution containing lipoprotein lipase (LPL) and 4aminoantipyrine (4AAP). The inventors have found that by reducing the pH of the impregnating solution to less than that of the recommended pH range for one of the key components (viz., less than pH 6.0), overall stability of the test strips was dramatically improved. The improvement in storage capability of these triglycerides test strips represents not just a difference in degree, but a difference in kind. Excerpt(s): This application claims priority to U.S. Provisional Patent Application Serial No. 60/344,300, filed Dec. 28, 2001. This application incorporates by reference herein in its entirety another application entitled Test Strip for Determining Concentration of Multiple Analytes, which is commonly owned with the present application and has been filed on even date herewith. The present invention relates generally to testing of body fluids for concentration of analytes and more particularly to methods and apparatus for dry-phase testing of analytes. The level of certain analytes in blood and
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other body fluids can predict disease or risk thereof. For example, the amounts of cholesterol and triglycerides in blood are a significant indicator of risk of coronary heart disease ("CHD"). Excess triglycerides in plasma is called "hypertriglyceridemia," and is linked to the occurrence of atherosclerosis and CHD in some people. Elevated triglycerides may be a consequence of other disease, such as untreated diabetes mellitus. Like cholesterol, increases in triglyceride levels can be detected by plasma measurements. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Treatment of hair by addition of exogenous enzymes, alcohols and acids or triglycerides Inventor(s): Duvault, Yolanda; (Aulnay s/Bois, FR), Kaba, Genevieve; (Ivry s/Seine, FR), Semeiria, Didier; (Livry-Gargan, FR) Correspondence: Nixon & Vanderhye, PC; 1100 N Glebe Road; 8th Floor; Arlington; VA; 22201-4714; US Patent Application Number: 20030091526 Date filed: October 8, 2002 Abstract: The present invention relates to compositions for treating keratin materials by adding at least one exogenous enzyme, long-chain alcohols, and long-chain acids or triglycerides, which gives rise to an enzymatic reaction directly on the hair, and to methods of treating hair which employ these compositions. Excerpt(s): The hair is subject to continual aggressive influences, which may make it brittle, difficult to disentangle or dull. It is therefore important to find products capable of conditioning the hair and so leaving it easy to style, supple, soft to the touch, and lustrous. It would also be advantageous for the properties of softness and sheen of these products to persist over a number of shampooings. It has been observed that the soft and shiny appearance of the treated fibre is particularly great if long-chain esters are applied to the hair. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Treatment of vegetable oils or animal fats with sulfur or nitrogen donor compounds for animal food flavorings Inventor(s): Nelles, Lynn P.; (O'Fallon, MO), Sucan, Mathias; (Schaumburg, IL), Trivedi, Nayankumar B.; (O'Fallon, MO) Correspondence: Patrick D. Kelly; 11939 Manchester #403; ST. Louis; MO; 63131; US Patent Application Number: 20030104102 Date filed: November 13, 2001 Abstract: Oils or fats from plants and/or animals are chemically treated to create flavor/palatability enhancer (FPE) products for use with animal foods, such as dog or cat food. This method involves mixing triglycerides (from the oil or fat) with sulfur and/or nitrogen donor compounds, such as sodium sulfide. The mixture is cooked at a temperature close to boiling, or higher if pressure-cooking is used, for a period of time sufficient to break down large numbers of triglyceride molecules into their constituent fatty acids and other fragments. Under suitable cooking conditions, the organic
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fragments will react with sulfur and/or nitrogen atoms from the donor compound(s), to form relatively small organic molecules containing sulfur and/or nitrogen. These cooked products can be used as FPE's for pet foods for dry kibbles or biscuits, either alone, or mixed with a standard base compound such as a hydrolyzed liver digest. Twobowl comparison tests indicate that these FPE's are effective, and they do not suffer from unpleasant odors that would disturb pet owners. This method can be used to process various types of fatty or oily wastes created by food-service or manufacturing operations, and because the cooking process will totally sterilize the ingredients, it can be used with contaminated, adulterated, or partially-spoiled food substances that are not adequately safe for human consumption. Excerpt(s): This invention is in the field of pet foods and pet food chemistry, and relates to methods of chemically treating animal fats and vegetable oils, to create products that can enhance the flavor and palatability of food products intended for companion animals such as dogs or cats. This invention is in the field of foods for "companion animals," such as dogs or cats. All references herein to food of any sort are intended to refer only to food that is manufactured and marketed for companion animals, such as dogs or cats. Although testing to date has focused on dogs, this invention can also be adapted for use with cats, pot-bellied pigs, ferrets, and similar classes of companion animals which generally are carnivorous or omnivorous. If desired, the invention disclosed herein also can be tested to evaluated its suitability for use with still other classes of animals, including rodents (hamsters, guinea pigs, rabbits, etc.), birds, and reptiles, as well as for horses and any type of livestock. However, since dogs and cats show higher levels of sensitivity to taste and aroma than rodents, livestock, and most other classes of animals, and since dogs and cats form the largest categories (by far) of animals which receive flavor-enhanced animal foods, this text uses the term "pets", for convenience, to refer to any and all animals that are likely to receive the types of flavorenhanced foods that are described herein. For convenience, a food product which is manufactured and marketed for animals, and which is likely to benefit from a flavor and/or palatability enhancer as disclosed herein, is referred to herein simply as a pet food, animal food, etc. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Triglyceride emulsion for deinking process Inventor(s): Li, Chin; (Huntington, WV), Segelstrom, Rodger; (Appleton, WI) Correspondence: Basf Corporation; Anne Gerry Sabourin; 26701 Telegraph Road; Southfield; MI; 48034-2442; US Patent Application Number: 20030106654 Date filed: November 28, 2001 Abstract: A method is provided for deinking paper. Repulped paper is treated with a deinking agent. The deinking agent comprises a triglyceride. A preferred triglyceride is beef tallow. Excerpt(s): The present invention is directed to the addition of a triglyceride in a deinking process. Paper is a renewable resource and can be recycled to make new paper. Papers that can be recycled include, but are not limited to, newspaper, mixed office waste, and magazine paper. In order to be recycled, the paper is repulped into cellulose fibers. The fibers are swelled with alkaline water to form an aqueous slurry to assist in detaching the ink particles from the fibers. In order to remove these detached ink
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particles from the slurry, many deinking processes are available. One method of deinking is washing. In wash deinking, at least one surfactant is added to make the ink hydrophilic, and to allow the ink to be washed away. The particle size of the ink is generally about 2-20.mu.m in order to allow the ink particles to flow through a fiber mat. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Triglyceride fat suitable for spread manufacture Inventor(s): Floter, Eckhard; (Vlaardingen, NL) Correspondence: Unilever; Patent Department; 45 River Road; Edgewater; NJ; 07020; US Patent Application Number: 20030161934 Date filed: February 27, 2003 Abstract: Triglyceride fat which comprises HUU triglycerides and at least 18 wt. % of HOH and HLH triglycerides, while the ratio HOH:HLH is in the range 30/70 to 85/15, which fat is characterized in that the fat contains at least 20 wt. % of HUU and 8-30 wt. % of SOO triglycerides,where O denotes the residue of oleic acid, S of stearic acid, L of linoleic acid, U of oleic acid or linoleic acid and H denotes the residue of a saturated fatty acid with more than 15 carbon atoms with the proviso that at least 50 wt. % of the saturated fatty acids in HOH, HLH and HUU are stearic acid. The fat is obtained preferably by blending two natural high stearic fats. Excerpt(s): The present invention deals with a fat suitable for the manufacture of fat continuous emulsion spreads, with a process for the preparation of such fat and with emulsion spreads containing such fat. Butter is an edible emulsion spread consisting of a continuous fat phase and an aqueous phase which is dispersed as fine droplets in the fat phase. The fat phase consists of dairy fat, a 100% natural fat. Margarine too is a fat continuous emulsion, but margarine fat is not natural, since it has been processed so that margarine obtains properties which are desirable for a spread. Generally, the fat phase of margarine and of similar fat continuous emulsion spreads is a mixture of a fat which is fully liquid (the oil part of the fat phase) and a fat which is solid at ambient temperature. The solid fat, further denoted as hardstock fat, serves to structure the fat phase and helps to stabilize the emulsion. For imparting to common margarine a semisolid, plastic, spreadable consistency this stabilizing and structuring functionality plays an important role. The crystals of the solid fat form a network throughout the liquid oil resulting into a structured fat phase. The aqueous phase droplets are fixed within the spaces of the lattice of solid fat crystals. In this way coalescence of the droplets and separation of the heavier aqueous phase from the fat phase is prevented. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Use of amylin agonists to modulate triglycerides Inventor(s): Fineman, Mark; (San Diego, CA), Kolterman, Orville G.; (Poway, CA), Maggs, David G.; (Del Mar, CA), Weyer, Christian; (San Diego, CA) Correspondence: Arnold & Porter; IP Docketing Department; RM 1126(b); 555 12th Street, N.W.; Washington; DC; 20004-1206; US Patent Application Number: 20030130177 Date filed: January 8, 2003 Abstract: Methods of improving lipid profile, including methods for lowering fasting triglyceride levels and post-prandial triglyceride excursions are disclosed comprising administering an effective amount of an amylin or amylin agonist. Excerpt(s): This application claims the benefit of and priority to U.S. Provisional Application No. 60/347,128, filed Jan. 8, 2002, which is incorporated herein by reference in its entirety. The field of the invention is modulation of circulating lipid levels, especially triglyceride levels. Amylin is a 37-amino acid polypeptide hormone normally co-secreted with insulin by pancreatic beta cells in response to nutrient intake (see, e.g., Koda et al., Lancet 339:1179-1180, 1992). Preclinical studies indicate that amylin acts as a neuroendocrine hormone that complements the actions of insulin in post-prandial glucose control via several effects that collectively reduce the influx of glucose into the circulation to a rate that better matches the rate of insulin-mediated glucose efflux (Weyer et al., Curr Pharm Des 7:1353-73, 2001; Young, Curr Opin Endocrinol Diab 4:282290, 1997). These effects include a slowing of the rate at which nutrients are delivered from the stomach to the small intestine for absorption (Young et al., Diabetologia 38:642648, 1995), and a suppression of nutrient-stimulated glucagon secretion (Gedulin et al., Metabolism 46:67-70, 1997). Pramlintide (.sup.25, 28, 29Pro-h-amylin) is a synthetic, soluble, non-aggregating analog of human amylin under development as an adjunct to insulin therapy in both type-1 and type-2 diabetes (Weyer et al., Curr Pharm Des 7:135373, 2001; Buse et al Clin Diabetes 20: 137-144, 2002; Edelman and Weyer, Diabetes Technology and Therapeutics 4: 175-189, 2002). Short-term clinical studies in patients with type-1 diabetes have shown that mealtime amylin replacement with subcutaneous (s.c.) injections of pramlintide, in addition to mealtime insulin, slows the rate of gastric emptying (Kong et al., Diabetologia 41:577-583, 1998), suppresses mealtime glucagon secretion (Nyholm et al, Metabolism 48:935-941, 1999; Fineman et al., Metabolism,51:636641, 2002) and, consequently, improves post-prandial glucose excursions (Nyholm et al., Metabolism 48:935-941, 1999; Thompson et al., Diabetes 46:632-636, 1997). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Use of conjugated acid derivatives Inventor(s): Cain, Frederick William; (Wormerveer, NL), Mohede, Ingrid Celestina Maria; (Wormerveer, NL), O'Shea, Marianne; (Channahon, IL), Schmid, Ulrike; (Wormerveer, NL) Correspondence: Morgan Lewis & Bockius Llp; 1111 Pennsylvania Avenue NW; Washington; DC; 20004; US Patent Application Number: 20030215465 Date filed: April 17, 2003
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Abstract: The invention concerns the use of conjugated linoleic acid (=CLA) or derivatives thereof, such as partial glycerides or triglycerides, alkyl esters or salts for the production of a food, a food supplement or a pharmaceutical preparation with the property to prevent or to cure influenza, to boost the effects of an influenza vaccination and/or to alleviate the effects of an influenza vaccination in humans and/or animals. Excerpt(s): the nature of the illness caused by the different viruses is different. Thogoto viruses leading to a more severe illness than influenza viruses such as optic neuritis and fatal meningitis. Because of these basic differences in mechanism a man skilled in the art never would have expected that CLA could have a positive effect on all the family members of the whole Orthomyxovirus family. U.S. Pat. No. 5,827,885 being the mother patent of above U.S. Pat. No. 376 has a similar teaching although the claims now are limited to the anti viral effects of CLA. Again influenza is not disclosed in this document. Here the same argument as above will account. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Use of medium-chain triglycerides for the prevention and therapy of adiposity Inventor(s): Feldheim, Walter; (Kronshagen, DE), Kuzela, Lubomir; (Praha, CZ) Correspondence: Birch Stewart Kolasch & Birch; PO Box 747; Falls Church; VA; 220400747; US Patent Application Number: 20030130346 Date filed: June 25, 2002 Abstract: Use of medium-chain triglycerides for the prevention and therapy of adiposity The use of medium-chain triglycerides or of a composition containing said mediumchain triglycerides for the prevention or therapy of overweight or adiposity is described. Said composition preferably also contains long-chain essential triglycerides, preferably.alpha.-linoleic acid and/or linolenic acid as well as, optionally, further components and/or additives. Excerpt(s): This nonprovisional application claims priority under 35 U.S.C.sctn.119(a) on Patent Application No. DE 101 30 491.9 filed in Germany on Jun. 25, 2001, which is herein incorporated by reference. The present invention relates to the use of mediumchain triglycerides (MCT) or a composition containing medium-chain triglycerides, for example a dietetic foodstuff for the prevention or therapy of overweight or adiposity. This composition preferably also contains long-chain essential triglycerides, preferably a-linoleic acid and/or.alpha.-linolenic acid, as well as optionally further components and/or additives. In the affluent industrial nations, the biggest problem concerning nutrition is overnutrition. The constantly rising number of persons suffering from overweight or adiposity, a considerable share of which are children or adolescents, is problematic due to its consequence, namely the increase in nutrition-related diseases. Overweight is a risk factor for diseases of the skeletal and musculoskeletal system, hypertension (4-fold risk), type 2 diabetes mellitus (6-fold risk), heart attack (4-fold risk), breast cancer (3-fold risk), biliary stones (10-fold risk), gout etc. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Vegetable oil candle Inventor(s): Mathews, Heather; (Reynoldsburg, OH), Pesu, Maxine; (Gahanna, OH) Correspondence: Notaro & Michalos P.C.; Suite 110; 100 Dutch Hill Road; Orangeburg; NY; 10962-2100; US Patent Application Number: 20030091949 Date filed: November 14, 2001 Abstract: A candle composition has a paraffin wax mixture of a high melting point paraffin wax and a low melting point paraffin wax, and a hydrogenated vegetable oil that is present in a greater amount than the mixture of the varying grades of paraffin wax, and the vegetable oil contains no more than 0.15% free fatty acid, with the remainder being triglycerides. Candles of the composition have good burn characteristics, particularly good fragrance intensity and produce a unique crystallization effect after the first burn. Excerpt(s): The present invention relates generally to the field of candlemaking and in particular to a candle that has a greater concentration of hydrogenated vegetable oil than paraffin wax, where the hydrogenated vegetable oil contains no more than 0.15% free fatty acid and a remaining portion of trigylcerides, while the paraffin wax may be a combination of more than one type of wax with varying melting points. Many prior patents disclose candle compositions intended to burn more cleanly or longer having various components. Some patents teach using vegetable oils in the candle composition. U.S. Pat. No. 1,954,659 discloses a homogenous, solid, and self-sustaining candle formed of 50% or more of a hydrogenated vegetable oil, preferably rape-seed oil, and a wax including paraffin wax, stearic acid and beeswax. One embodiment disclosed in the patent has 49% wax and 51% hydrogenated vegetable oil. The U.S. Pat. No. 1,954,659 patent teaches that the candle may be made of other types of hydrogenated vegetable oils besides rape-seed oil, provided the oil comprises 50% or more of the composition. But, the use of vegetable oils with less than naturally occurring amounts of free fatty acids is not disclosed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with triglycerides, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “triglycerides” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on triglycerides. You can also use this procedure to view pending patent applications concerning triglycerides. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON TRIGLYCERIDES Overview This chapter provides bibliographic book references relating to triglycerides. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on triglycerides include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “triglycerides” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on triglycerides: •
Dietary Guidelines for Peritoneal Dialysis Source: Birmingham, AL: Department of Food and Nutrition Services, University Hospital. 1992. 11 p. Contact: Available from Department of Food and Nutrition Services, University Hospital. 619 South 19th Street, Birmingham, AL 35233. (205) 934-8055. Fax (205) 9342987. PRICE: $2.50 per copy; bulk copies available; plus shipping and handling. Summary: This booklet provides guidelines for a diet for patients using peritoneal dialysis to treat their decreased kidney function. Normally the kidneys act as filters, helping the body get rid of waste products, excess water, and sodium. When the kidneys begin to fail, these substances build up to dangerous levels in the blood. It then becomes necessary to utilize dialysis, a special diet, and prescribed medications. The booklet includes space for the dietitian to record the patient's individual recommendations or prescription for protein (low phosphorus), sodium, and fluid. The
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booklet reviews each of five categories of nutrients and the foods that are high in each nutrient. The categories are protein, potassium, sodium and fluid, phosphorus, and cholesterol and triglycerides. After a summary of the general guidelines for this type of diet, the booklet offers extensive charts of food choices, from which readers can create breakfast, lunch, dinner, and snack menus. The booklet emphasizes the importance of replacing the protein and potassium often lost in dialysis therapy and of following all prescribed medication guidelines.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “triglycerides” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “triglycerides” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “triglycerides” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Analysis of triglycerides by Carter Litchfield; ISBN: 0124519504; http://www.amazon.com/exec/obidos/ASIN/0124519504/icongroupinterna
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Cholesterol & Triglycerides: Questions You Have.Answers You Need by Ellen Moyer (1995); ISBN: 1882606515; http://www.amazon.com/exec/obidos/ASIN/1882606515/icongroupinterna
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Cure Indigestion, Heartburn, Cholesterol, Triglyceride & Liver Problems with Artichoke Extract by Gary Ross, et al; ISBN: 1893910016; http://www.amazon.com/exec/obidos/ASIN/1893910016/icongroupinterna
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Infrared spectra of monoacid triglycerides With some applications to fat analysis by W. C. de Ruig; ISBN: 9022003507; http://www.amazon.com/exec/obidos/ASIN/9022003507/icongroupinterna
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Kidney Patients' Wellness Diet--Tasty Recipes: Low Protein, Low Potassium, Low Sodium, and Low Fat Diet: Combined Renal and Triglyceride Diet, V. 2 by Emma W. Keenan; ISBN: 0915133113; http://www.amazon.com/exec/obidos/ASIN/0915133113/icongroupinterna
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Medium Chain Triglycerides by J. Senior (1968); ISBN: 0812275640; http://www.amazon.com/exec/obidos/ASIN/0812275640/icongroupinterna
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Triglyceride, high density lipoprotein, and coronary heart disease : January 1989 through February 1992 plus selected earlier literature : 1636 citations (SuDoc HE 20.3615/2:91-16) by Naomi Miller; ISBN: B000109KM8; http://www.amazon.com/exec/obidos/ASIN/B000109KM8/icongroupinterna
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Triglycerides: The Role of Diabetes and Atherosclerosis (Atherosclerosis Reviews, Vol 22) by Antonio M. Gotto, Rodolfo Paoletti (Editor); ISBN: 0881678139; http://www.amazon.com/exec/obidos/ASIN/0881678139/icongroupinterna
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What You Should Know About Triglycerides: The Missing Link in Heart Disease by Dennis, Md. Sprecher; ISBN: 0380809400; http://www.amazon.com/exec/obidos/ASIN/0380809400/icongroupinterna
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “triglycerides” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •
Effect of free fatty acids and exogenous triglycerides upon the action and secretion of insulin Author: Taskinen, Marja-Riitta.; Year: 1992; Helsinki: [s.n.], 1969
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Fatty acids and triglycerides: biosynthesis and transport in normal and pathological conditions: proceedings of the 3rd Meeting of Italian Society for Inborn Error Diseases, Milan, October 1978 Author: Italian Society for Inborn Error Diseases. Meeting; Year: 1980; Milan, Italy: Ermes, 1979, c1980
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Global perspectives in lipid management: regulating LDL-cholesterol, HDLcholesterol, and triglycerides: their role in the primary prevention of CHD: proceedings of a symposium sponsored by Parke-Davis Pharmaceuticals, held in London, UK, 9-10 October 1997 Author: Got¯o, Y¯uichir¯o,; Year: 1963; London; New York: Royal Society of Medicine Press, c1998; ISBN: 1853153516
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Hypertriglyceridemia: January 1980 through September 1983: 144 citations in English Author: Segal, Pesach.; Year: 1983; [Bethesda, Md.]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1983
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Interrelationships of triglycerides and apolipoproteins in the fasting and postprandial states Author: Barr, Susan Irene.; Year: 1982; [Minneapolis?: s.n.], 1982
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Medium chain triglycerides. John R. Senior, editor; consulting editors: Theodore B. van Itallie [and] Norton J. Greenberger. Author: Greenberger, Norton J.; Year: 1968; [Philadelphia, Distributed by Univ. of Pennsylvania Press c1968]
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Mittelkettige Triglyceride (MCT) in der Diät. MCT in dietetics. Vorträge aus dem II. Internationalen Symposium. Hrsg. von Hans Kaunitz, Konrad Lang [und] W. Fekl. Author: Fekl, W. (Werner); Year: 1970; Darmstadt, Steinkopff, 1974; ISBN: 3798504067 http://www.amazon.com/exec/obidos/ASIN/3798504067/icongroupinterna
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Studies of human gastric lipolysis of medium and long chain triglycerides. Author: Cohen, Manley.; Year: 1972; [Minneapolis] 1970
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Studies on the metabolism of chyle triglycerides in the rat. Author: Belfrage, Per.; Year: 1992; Lund, Studentlitteratur, 1966
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In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
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Triglyceride, high density lipoprotein, and coronary heart disease: January 1989 through February 1992 plus selected earlier literature: 1636 citations Author: Miller, Naomi,; Year: 1998; Bethesda, Md.: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Library of Medicine, Reference Section; Washington, D.C.: Sold by the Supt. of Docs., U.S. G.P.O., [1992]
Chapters on Triglycerides In order to find chapters that specifically relate to triglycerides, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and triglycerides using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “triglycerides” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on triglycerides: •
Fatty Liver (Macrosteatosis and Microsteatosis) Source: in Okuda, K., ed.,et al. Hepatobiliary Diseases: Pathophysiology and Imaging. Malden, MA: Blackwell Science, Inc. 2001. p. 152-168. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail:
[email protected]. Website: www.blackwell-science.com. PRICE: $275.00. ISBN: 0632055421. Summary: Lipids (fats) make up about 20 percent of the liver mass, mostly in the form of phospholipids in membranes; neutral fat or triglycerides constitute less than 5 percent of the liver mass. This chapter on fatty liver is from a textbook that familiarizes the reader with various imaging modalities, the information they provide, and the merits of each, in order to facilitate the combined use of different imaging techniques in the diagnosis and management of hepatobiliary (liver and bile tract) diseases. Hepatocellular (liver cells) accumulation of fat results from increased delivery to the liver of dietary fat or fatty acids released from fat tissue, increased synthesis of fatty acids, reduced oxidation of fat, impaired export of triglycerides out of the liver, and excessive conversion of carbohydrate to fatty acids. The predominant contributing factor may be apparent with certain lifestyle and eating conditions, but in most cases it is difficult to determine. Steatosis (fatty liver) is easily diagnosed using ultrasound, CT scan, and MRI. The authors discuss classification, etiology and pathophysiology; macrosteatosis (nonalcoholic), including that due to obesity, diabetes mellitus, and hyperlipoprotinemias; microsteatosis, including acute fatty liver of pregnancy, Reye's syndrome, and that attributed to tetracycline; imaging strategies; the pathophysiology of focal sparing and focal fat deposits; distinguishing miscellaneous steatosis from liver tumor; and treatment, complications, and prognosis. 20 figures. 31 references.
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Possible Causes Source: in Haybach, P.J. Meniere's Disease: What You Need to Know. Portland, OR: Vestibular Disorders Association. 1998. p. 53-60.
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Contact: Available from Vestibular Disorders Association. P.O. Box 4467, Portland, OR 97208-4467. (800) 837-8428. E-mail:
[email protected]. Website: www.vestibular.org. PRICE: $24.95 plus shipping and handling. ISBN: 0963261118. Summary: The cause of Meniere's disease is unknown, however many theories have been proposed to explain the symptoms of Meniere's or the factors that may aggravate those symptoms. This chapter is from a book that provides information for people who have or suspect they have Meniere's disease want to know more about its diagnosis and treatment, as well as strategies for coping with its effects. Written in nontechnical language, this chapter discusses the possible causes of Meniere's disease. Listed in alphabetical order, they include: abnormal circulation, adrenal-pituitary insufficiency, allergy, autoimmune disease, autonomic nervous system malfunction, bacterial infection, blockage of endolymph, estrogen insufficiency, head injury, heredity, hormonal imbalance, malformed or small endolymphatic sac, malfunction in the use of foods by the body (high cholesterol, triglycerides, or lipids), meningitis, menstrual or premenstrual problems, noise pollution (noise trauma or acoustic trauma), otosclerosis, stress, and viral infection. The author discusses the most widely accepted theories of the causes of Meniere's disease and then briefly considers specific conditions that are known or thought to sometimes cause symptoms like those of Meniere's disease. 24 references. •
Medications Used To Treat Complications of Diabetes Source: in Carlisle, B.A.; Kroon, L.A.; Koda-Kimble, M.A. 101 Medication Tips for People with Diabetes. Alexandria, VA: American Diabetes Association. 1999. p. 66-75. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $14.95 plus shipping and handling. ISBN: 1580400329. Order number 483301. Summary: This chapter answers questions about the meditations used to treat diabetes complications, including nonprescription analgesics, tricyclic antidepressants, capsaicin cream, angiotensin converting enzyme (ACE) inhibitors, laxatives, and calcium channel blockers. Nonprescription analgesics, antidepressants, and narcotic analgesics can be used to treat the pain associated with diabetic neuropathy. Capsaicin cream, a chemical found in hot chili peppers, can be applied to the feet to relieve pain. ACE inhibitors can be used to treat microalbuminuria, an early sign of kidney damage. The symptoms of gastroparesis, a condition that affects the nerves of the stomach, can be treated with metoclopramide, cisapride, and erythromycin. These medications increase the stomach's ability to contract and aid in digestion. Constipation can be treated by increasing the amount of fluid and fiber in a person's diet. Laxatives may also be useful in treating constipation. Men who have diabetes and experience impotence can use the medications alprostadil and sildenafil to maintain an erection. People who have diabetes and high blood pressure can be treated with ACE inhibitors, diuretics, and calcium channel blockers. Angiotensin receptor II antagonists and calcium channel blockers can be used to treat kidney disease. People who have diabetes should take any medications their doctor prescribes for other conditions, such as high blood pressure, heart disease, high cholesterol or triglycerides, obesity, and insulin resistance.
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Laboratory Tests Source: in Lockhart, P.B. Oral Medicine and Hospital Practice. Chicago, IL: Special Care Dentistry. 1997. p. 10.3-10.12.
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Contact: Available from Special Care Dentistry. 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2660. Fax (312) 440-2824. PRICE: $27.00 (member) or $30.00 (nonmember), plus shipping and handling; institutional prices and bulk orders available. ISBN: 0965719103. Summary: This chapter is from a manual designed to help dental residents, students and practitioners engaged in the care of patients in the hospital setting. This chapter presents information on common laboratory tests. The chapter describes hematology, including complete blood count (CBC), sickle cell tests, and coagulation tests; blood chemistry, including total protein, calcium, phosphorus, cholesterol, glucose, uric acid, creatinine, phosphatase, and transaminases; other blood determinations, including blood urea nitrogen (BUN), bilirubin, creatine phosphokinase (CPK or CK), serum iron, total iron binding capacity (TIBC), serum osmolality, glucose tolerance test (GTT), triglycerides, and electrolytes; thyroid testing, including hormones and radioactive iodine (RAI) uptake test; urinalysis, including color, odor, specific gravity, chemical examination, and microscopic examination; cerebrospinal fluid, including glucose, protein, white blood cells, and red blood cells; and arterial blood gases. For each test, the author notes the expected normal value, the significance of high or low values, and the relevant oral findings. Most information is presented in outline format, for ease of access. 1 table. •
Pancreatitis in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 329-332. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on pancreatitis is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and Ulcerative Colitis (UC), together known as inflammatory bowel disease (IBD). There is a higher incidence and prevalence of pancreatitis in patients with inflammatory bowel disease (IBD) than in the general population. The pancreatitis can be acute or chronic, or subclinical or overt, and has many causes. The most common cause is medications used to treat IBD, especially azathioprine and 6 mercaptopurine. Other causes of pancreatitis include duodenal involvement from Crohn's disease (CD), gallstones (cholelithiasis), and primary sclerosing cholangitis (PSC). Pancreatitis also can be caused by high serum concentrations of triglycerides during total parenteral nutritional (TPN) therapy for CD, and may also be a primary extra-intestinal manifestation of IBD. Treatment is different for each cause. For drug-induced pancreatitis, discontinuation of the drug should improvethe pancreatitis. For TPNinduced pancreatitis, oral medium-chain triglycerides should be substituted for the lipid emulsion. For pancreatitis that has developed from gallstones, the usual treatment is laparoscopic cholecystectomy (removal of the gallbladder). Idiopathic (of unknown cause) pancreatitis is often successfully treated by treating the underlying IBD. 1 table. 10 references.
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Physical and Metabolic Characteristics of Persons with Diabetes Source: in Harris, M.I., et al., eds., for the National Diabetes Data Group (NDDG). Diabetes in America. 2nd ed. Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. 1995. p. 117-164.
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Contact: Available from National Diabetes Information Clearinghouse (NDIC). 1 Information Way, Bethesda, MD 20892-3560. (800) 860-8747 or (301) 654-3327. Fax (301) 634-0716. E-mail:
[email protected]. Also available at http://www.niddk.nih.gov/. PRICE: Full-text book and chapter available online at no charge; book may be purchased for $20.00. Order number: DM-96 (book). Summary: This chapter on the physical and metabolic characteristics of persons with diabetes is from a compilation and assessment of data on diabetes and its complications in the United States. The primary data sources used by the authors are the 1989 National Health Interview Survey (NHIS), a household interview survey of a representative sample of the U.S. civilian, noninstitutionalized population older than 18 years of age; the 1976-1980 Second National Health and Nutrition Examination Survey (NHANES II), which included a representative sample of the U.S. population age 20 to 74 years who were administered a household interview, a physical examination with certain clinical and laboratory tests, and an oral glucose tolerance test (OGTT) to detect undiagnosed diabetes; and the 1982-1984 Hispanic Health and Nutrition Examination Survey (HHANES), which included Mexican Americans, Puerto Ricans, and Cuban Americans age 20 to 74 years from certain regions of the United States and employed methods similar to those used in the NHANES II. By definition, persons with NIDDM have much higher fasting plasma glucose levels than persons with impaired glucose tolerance (IGT). A family history of diabetes is more frequent in NIDDM than in other groups. Mean body mass index (BMI) is highest in persons with NIDDM, followed by those with IGT, and persons with normal glucose tolerance. In general, mean blood pressure is as high in persons with undiagnosed NIDDM and IGT as in persons with a medical history of NIDDM, but lower in persons with normal glucose tolerance. Compared with nondiabetic persons, persons with NIDDM have higher mean total cholesterol, low density lipoprotein (LDL) cholesterol, and triglycerides, and lower mean high-density lipoprotein (HDL) cholesterol. Parity (number of children) is greater in persons with NIDDM than in nondiabetic persons. Except at youngest ages, a slightly higher percent of nondiabetic persons smoke (26.1 percent) than do persons with diabetes (20.1 percent). Excellent or very good health status was reported in 64.9 percent of nondiabetic adults, but only in 19.5 percent of persons with NIDDM. 50 appendices. 28 figures. 19 references. (AA-M). •
What You Need to Know About Lipids and Exercise Source: in Hirsch, I.B. 12 Things You Must Know About Diabetes Care Right Now!. Alexandria, VA: American Diabetes Association. 2000. p. 115-130. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $14.95 plus shipping and handling. ISBN: 1580400612. Summary: This chapter provides information on blood lipids and exercise to treat lipid problems. Lipids, which are body fats, include triglycerides and cholesterol. Neither triglycerides nor cholesterol can be dissolved in blood, so they travel in the blood by joining with proteins called lipoproteins. Low density lipoprotein (LDL) is the major carrier for cholesterol in the blood. An excess of LDL causes atherosclerosis. High density lipoprotein (HDL), however, takes cholesterol away from the blood vessel walls and into the liver. Problems occur when levels of triglycerides and LDL and HDL cholesterol are out of balance. The most common problems in people who have type 2 diabetes have to do with triglycerides and HDL cholesterol. People who have type 1 diabetes and poor glucose control will have high triglyceride and LDL cholesterol levels.
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Adults who have high or out of balance lipids should be tested each year for total cholesterol, fasting triglycerides, and HDL and LDL cholesterol. The first approach to balancing lipid levels should be to improve blood glucose control with weight loss, exercise, and better meal planning. When lipid levels do not improve with meal planning, exercise, and glucose control, treatment with lipid lowering drugs is recommended. Drugs used to treat lipid problems include bile acid binding resins, fibric acid derivatives, HMG-CoA reductase inhibitors, nicotinic acid, estrogen, and aspirin. The chapter discusses the effects of these drugs and presents guidelines on coronary disease screening. In addition, the chapter includes a list of questions a patient may ask a doctor and questions a doctor may ask a patient. 3 tables. •
Blood Fats Source: in American Diabetes Association. Diabetes A to Z: What You Need to Know About Diabetes, Simply Put. 4th ed. Alexandria, VA: American Diabetes Association. 2000. p. 6-8. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $12.95 for members; $14.95 for nonmembers; plus shipping and handling. ISBN: 1580400353. Summary: This chapter provides people who have diabetes with information on blood fats. People with diabetes often have high blood fat levels. This increases their risk for cardiovascular problems. Fats in the body include cholesterol and triglycerides. They are carried by lipoproteins, including very low density lipoproteins, low density lipoproteins, and high density lipoproteins. The chapter presents the healthiest blood fat levels and suggests ways to improve blood fat levels if they exceed healthy levels. Tips include controlling one's diabetes, losing weight, cutting back on all fats, replacing saturated fats with unsaturated fats, eating fewer high cholesterol foods and more high fiber foods, exercising, and quitting smoking.
•
Nutrition Management of the Adult Peritoneal Dialysis Patient Source: in American Dietetic Association. Clinical Guide to Nutrition Care in End-Stage Renal Disease. Chicago, IL: American Dietetic Association. 1994. p. 37-55. Contact: Available from American Dietetic Association. 216 West Jackson Boulevard Chicago, IL 60606-6995. (312) 899-0040. PRICE: $24 for members; $28 for non-members; plus shipping and handling. ISBN: 0880911247. Summary: This chapter, from a manual that provides guidelines for the clinical nutrition care of patients with end-stage renal disease (ESRD), discusses the nutrition management of the adult peritoneal dialysis (PD) patient. Topics include the regimen of peritoneal dialysis care; measuring dialysis adequacy; specific nutritional considerations, including for protein, caloric intake, sodium and fluid, potassium, phosphorus, calcium, fiber, vitamins and minerals, and cholesterol and triglycerides; PD therapy for patients with diabetes; the role of exercise; and preventing and managing peritonitis. 5 tables. 94 references.
•
Nutrition Management of Chronic Renal Failure Source: in American Dietetic Association. Manual of Clinical Dietetics. Chicago, IL: American Dietetic Association. 1996. p. 535-553.
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Contact: Available from American Dietetic Association. 216 West Jackson Boulevard, Chicago, IL 60606. (800) 877-1600 or (312) 899-0040. Fax (312) 899-4899. PRICE: $59.95 for members, $70.00 for nonmembers. ISBN: 0880911530. Summary: This section providing guidelines for the nutritional management of chronic renal failure (CRF) is from a manual that serves as a nutrition care guide for dietetics professionals, physicians, nurses, and other health professionals. The manual integrates current knowledge of nutrition, medical science, and food to set forth recommendations for healthy individuals and those for whom medical nutrition therapy (MNT) is indicated. The diet for CRF is designed to meet nutritional requirements, prevent malnutrition, and maintain acceptable blood chemistries, blood pressure, and fluid status in patients with impaired renal (kidney) function. The text notes the purpose, use, modifications, and adequacy of the diet. The diet is used for patients with CRF requiring hemodialysis or peritoneal dialysis treatments. Generally, the diet controls intake of protein, potassium, sodium, phosphorus, and fluids. Additional modifications of fat, cholesterol, triglycerides, and fiber may be necessary based on individual requirements. The section also outlines the related physiology. Charts provide a brief sample menu, food lists, and calculation figures for planning the CRF diet. 5 tables. 25 references. (AAM).
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CHAPTER 8. MULTIMEDIA ON TRIGLYCERIDES Overview In this chapter, we show you how to keep current on multimedia sources of information on triglycerides. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Bibliography: Multimedia on Triglycerides The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in triglycerides (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on triglycerides: •
Characterization of transgenic animal models for human dyslipoproteinemias [videorecording]: new insights into the role of enzymes involved in triglyceride & HDL medabolism [i.e. metabolism] Source: Medical Arts and Photography Branch; Year: 1995; Format: Videorecording; [Bethesda, Md.: The Branch, 1995]
•
Hypertriglyceridemia and the atherogenic lipoprotein profile [videorecording]: new risk factors for CAD? Source: Marshfield Clinic, Saint Joseph's Hospital; a presentation of the Marshfield Video Network; Year: 1998; Format: Videorecording; Marshfield, WI: The Network, c1998
•
The usefulness of medium chain triglycerides [slide] Source: American Gastroenterological Association; Year: 1969; Format: Slide; [Thorofare, N. J.]: The Association, 1969
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CHAPTER 9. PERIODICALS AND NEWS ON TRIGLYCERIDES Overview In this chapter, we suggest a number of news sources and present various periodicals that cover triglycerides.
News Services and Press Releases One of the simplest ways of tracking press releases on triglycerides is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “triglycerides” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to triglycerides. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “triglycerides” (or synonyms). The following was recently listed in this archive for triglycerides: •
PPAR-gamma important in triglyceride and glucose regulation Source: Reuters Medical News Date: March 11, 2003
•
Triglyceride lowering improves vascular function in hypertriglyceridemia Source: Reuters Industry Breifing Date: February 26, 2003
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•
Triglycerides decrease effectiveness of elemental diet for Crohn's disease Source: Reuters Medical News Date: February 03, 2003
•
Gemfibrozil only modestly effective for HIV protease inhibitor-related hypertriglyceridemia Source: Reuters Industry Breifing Date: December 06, 2002
•
"Hypertriglyceridemic waist" predicts presence of insulin resistance syndrome Source: Reuters Medical News Date: October 30, 2002 The NIH
Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “triglycerides” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “triglycerides” (or synonyms). If you know the name of a company that is relevant to triglycerides, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/.
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BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “triglycerides” (or synonyms).
Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “triglycerides” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on triglycerides: •
Heart Disease Handbook, Part 3: Triglycerides Turn Troublesome Source: Environmental Nutrition. 20(4): 1, 6. April 1997. Contact: Available from Environmental Nutrition. P.O. Box 420451, Palm Coast, FL 32142-0451. (800) 829-5384. Summary: This newsletter article describes triglycerides, or fat (lipids). Triglycerides from food travel through the bloodstream by way of chylomicrons, the largest of the lipid carriers (needed because fat and blood do not mix). Other triglycerides come from the liver, which manufactures them from excess carbohydrates and alcohol as a way to store energy. These triglycerides travel through blood via carriers called very lowdensity lipoproteins (VLDLs). The author discusses the problems occurring with high triglyceride levels, notably risk for heart disease. A recent study of 201 men and women found that high triglycerides increase heart disease risk independently. Treatment should include ways to control levels of triglycerides. Diet is the first line of treatment; drugs are used only when patients already have heart disease or when triglyceride levels exceed 500. For people who are overweight, simply losing weight can lower triglycerides. Other dietary suggestions include getting or staying physically active, cutting back on saturated fats, limiting carbohydrates to 55 percent of calories or less, avoiding alcohol, and discussing fish oil supplements with a physician. (AA-M).
Academic Periodicals covering Triglycerides Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to triglycerides. In addition to these sources, you can search for articles covering triglycerides that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the
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name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for triglycerides. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with triglycerides. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to triglycerides: Atorvastatin •
Systemic - U.S. Brands: Lipitor http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203635.html
Cerivastatin •
Systemic - U.S. Brands: Baycol http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203060.html
Clofibrate •
Systemic - U.S. Brands: Abitrate; Atromid-S http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202150.html
Fenofibrate •
Systemic - U.S. Brands: Tricor http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203516.html
Gemfibrozil •
Systemic - U.S. Brands: Lopid http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202256.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html.
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Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
•
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
•
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
•
National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
•
National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
•
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
12
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
•
National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
•
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
•
National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
•
National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
•
National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
•
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
•
National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
•
National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
•
National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
•
National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
•
National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
•
National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
•
Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
•
National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
•
National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
•
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
•
Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
•
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
13 Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.
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•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “triglycerides” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 52397 200 310 314 1 53222
HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “triglycerides” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
15
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
16
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 17 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 18 19
The HSTAT URL is http://hstat.nlm.nih.gov/.
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.
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Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
The Genome Project and Triglycerides In the following section, we will discuss databases and references which relate to the Genome Project and triglycerides. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).23 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. 20 Adapted 21
from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process. 23 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “triglycerides” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for triglycerides: •
Hypertriglyceridemia, Familial Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?145750
•
Microsomal Triglyceride Transfer Protein, 88-kd Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?157147
•
Triglyceride Storage Disease with Impaired Long-chain Fatty Acid Oxidation Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?275630 Genes and Disease (NCBI - Map)
The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
•
Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
•
Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
•
Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
•
Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome,
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Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html •
Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html
•
Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez
Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: •
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
•
Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
•
Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
•
NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
•
Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
•
OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
•
PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
•
ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
•
Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
•
PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
•
Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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•
Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “triglycerides” (or synonyms) into the search box and click “Go.” Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database24
This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database25 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “triglycerides” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
24 Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 25 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on triglycerides can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to triglycerides. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to triglycerides. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “triglycerides”:
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•
Other guides Diabetes http://www.nlm.nih.gov/medlineplus/diabetes.html Dietary Fats http://www.nlm.nih.gov/medlineplus/dietaryfats.html Heart Diseases http://www.nlm.nih.gov/medlineplus/heartdiseases.html
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. Healthfinder™ Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •
Triglyceride Summary: Triglycerides (tri-GLIS'er-ídz) are the chemical form in which most fat exists in food as well as in the body. Source: American Heart Association http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7104
•
Triglycerides Test Summary: Why get tested? To assess the risk of developing heart disease When to get tested? As part of a lipid profile during a regular medical exam or if you are being treated for high triglycerides Source: American Association for Clinical Chemistry http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7105 The NIH Search Utility
The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to triglycerides. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or
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specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMDHealth: http://my.webmd.com/health_topics
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to triglycerides. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with triglycerides. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about triglycerides. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “triglycerides” (or a synonym), and you will receive information on all relevant organizations listed in the database.
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Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “triglycerides”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “triglycerides” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “triglycerides” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.26
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
26
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)27: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
•
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
•
Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
•
California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
•
California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
•
California: Gateway Health Library (Sutter Gould Medical Foundation)
•
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
•
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
•
California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
•
California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
•
California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
•
California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
•
California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
•
California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
•
Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
•
Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
•
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
27
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
•
Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
•
Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
•
Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
•
Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
•
Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
•
Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
•
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
•
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
•
Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
•
Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
•
Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
•
Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
•
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
•
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
•
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
•
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
•
Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
•
Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
•
Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
•
Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
•
Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
•
Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
•
Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
•
Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
•
Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
•
Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
•
Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
•
Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
•
Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
•
Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
•
Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
•
National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
•
National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
•
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
•
New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
•
New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
•
New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
•
New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
•
New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
•
New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
•
New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
•
Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
•
Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
•
Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
•
Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
•
Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
•
Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
•
Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
•
Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
•
Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
•
Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
•
Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
•
Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
•
Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
•
Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
•
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on triglycerides: •
Basic Guidelines for Triglycerides Triglyceride level Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003493.htm
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Signs & Symptoms for Triglycerides Fainting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003092.htm Muscle Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003193.htm
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Diagnostics and Tests for Triglycerides Blood pressure Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003398.htm Venipuncture Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003423.htm
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•
Nutrition for Triglycerides Ascorbic acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002404.htm Carbohydrates Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002469.htm Fat Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002468.htm Fats Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002468.htm Lipids Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002468.htm Protein in diet Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002467.htm
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Background Topics for Triglycerides Adolescent test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002054.htm Bleeding Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000045.htm Infant test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002055.htm Metabolism Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002257.htm Preschooler test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002057.htm Schoolage test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002058.htm Toddler test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002056.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
Online Glossaries 219
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MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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TRIGLYCERIDES DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal fat: Fat (adipose tissue) that is centrally distributed between the thorax and pelvis and that induces greater health risk. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetic Acids: Acetic acid and its derivatives which may be formed by substitution reactions. Mono- and di-substituted, as well as halogenated compounds have been synthesized. [NIH] Acetone: A colorless liquid used as a solvent and an antiseptic. It is one of the ketone bodies produced during ketoacidosis. [NIH] Acetrizoic Acid: An iodinated radiographic contrast medium used as acetrizoate sodium in hysterosalpingography. [NIH] Acetylcarnitine: An acetic acid ester of carnitine that facilitates movement of acetyl CoA into the matrices of mammalian mitochondria during the oxidation of fatty acids. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acoustic: Having to do with sound or hearing. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acyl: Chemical signal used by bacteria to communicate. [NIH] Acylation: The addition of an organic acid radical into a molecule. [NIH] Acyltransferases: Enzymes from the transferase class that catalyze the transfer of acyl groups from donor to acceptor, forming either esters or amides. (From Enzyme Nomenclature 1992) EC 2.3. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH]
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Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adhesives: Substances that cause the adherence of two surfaces. They include glues (properly collagen-derived adhesives), mucilages, sticky pastes, gums, resins, or latex. [NIH] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adrenergic beta-Antagonists: Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic betaantagonists are used for treatment of hypertension, cardiac arrythmias, angina pectoris, glaucoma, migraine headaches, and anxiety. [NIH] Adrenoleukodystrophy: A chromosome X-linked disease. [NIH] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerobic Exercise: A type of physical activity that includes walking, jogging, running, and dancing. Aerobic training improves the efficiency of the aerobic energy-producing systems that can improve cardiorespiratory endurance. [NIH] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the
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tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Ageing: A physiological or morphological change in the life of an organism or its parts, generally irreversible and typically associated with a decline in growth and reproductive vigor. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Akathisia: 1. A condition of motor restlessness in which there is a feeling of muscular quivering, an urge to move about constantly, and an inability to sit still, a common extrapyramidal side effect of neuroleptic drugs. 2. An inability to sit down because of intense anxiety at the thought of doing so. [EU] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Albuminuria: More than normal amounts of a protein called albumin in the urine. Albuminuria may be a sign of kidney disease. [NIH] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] Aldose Reductase Inhibitor: A class of drugs being studied as a way to prevent eye and nerve damage in people with diabetes. Aldose reductase is an enzyme that is normally present in the eye and in many other parts of the body. It helps change glucose (sugar) into a sugar alcohol called sorbitol. Too much sorbitol trapped in eye and nerve cells can damage these cells, leading to retinopathy and neuropathy. Drugs that prevent or slow (inhibit) the action of aldose reductase are being studied as a way to prevent or delay these complications of diabetes. [NIH] Aldosterone: (11 beta)-11,21-Dihydroxy-3,20-dioxopregn-4-en-18-al. A hormone secreted by the adrenal cortex that functions in the regulation of electrolyte and water balance by
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increasing the renal retention of sodium and the excretion of potassium. [NIH] Alfalfa: A deep-rooted European leguminous plant (Medicago sativa) widely grown for hay and forage. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-helix: One of the secondary element of protein. [NIH] Alpha-Linolenic Acid: A fatty acid that is found in plants and involved in the formation of prostaglandins. [NIH] Alprostadil: A potent vasodilator agent that increases peripheral blood flow. It inhibits platelet aggregation and has many other biological effects such as bronchodilation, mediation of inflammation, etc. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Ameliorated: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amniotic Fluid: Amniotic cavity fluid which is produced by the amnion and fetal lungs and kidneys. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU]
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Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable. [NIH] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgenic: Producing masculine characteristics. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angina Pectoris: The symptom of paroxysmal pain consequent to myocardial ischemia usually of distinctive character, location and radiation, and provoked by a transient stressful situation during which the oxygen requirements of the myocardium exceed the capacity of the coronary circulation to supply it. [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiography: Radiography of blood vessels after injection of a contrast medium. [NIH] Angioplasty: Endovascular reconstruction of an artery, which may include the removal of atheromatous plaque and/or the endothelial lining as well as simple dilatation. These are procedures performed by catheterization. When reconstruction of an artery is performed surgically, it is called endarterectomy. [NIH] Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild
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natriuresis without affecting heart rate and contractility. [NIH] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [NIH] Anhydrides: Chemical compounds derived from acids by the elimination of a molecule of water. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anionic: Pertaining to or containing an anion. [EU] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Ankle: That part of the lower limb directly above the foot. [NIH] Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Anovulation: Suspension or cessation of ovulation in animals and humans. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Anterior Cerebral Artery: Artery formed by the bifurcation of the internal carotid artery. Branches of the anterior cerebral artery supply the caudate nucleus, internal capsule, putamen, septal nuclei, gyrus cinguli, and surfaces of the frontal lobe and parietal lobe. [NIH] Anthropometric measurements: Measurements of human body height, weight, and size of component parts, including skinfold measurement. Used to study and compare the relative proportions under normal and abnormal conditions. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody therapy: Treatment with an antibody, a substance that can directly kill specific tumor cells or stimulate the immune system to kill tumor cells. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidepressant: A drug used to treat depression. [NIH] Antidiabetic: An agent that prevents or alleviates diabetes. [EU]
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Antidote: A remedy for counteracting a poison. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]
Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antihypertensive: An agent that reduces high blood pressure. [EU] Antihypertensive Agents: Drugs used in the treatment of acute or chronic hypertension regardless of pharmacological mechanism. Among the antihypertensive agents are diuretics (especially diuretics, thiazide), adrenergic beta-antagonists, adrenergic alpha-antagonists, angiotensin-converting enzyme inhibitors, calcium channel blockers, ganglionic blockers, and vasodilator agents. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiproliferative: Counteracting a process of proliferation. [EU] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are
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caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Antispasmodic: An agent that relieves spasm. [EU] Antiviral: Destroying viruses or suppressing their replication. [EU] Antiviral Agents: Agents used in the prophylaxis or therapy of virus diseases. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Aortic Aneurysm: Aneurysm of the aorta. [NIH] Apnea: A transient absence of spontaneous respiration. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Aqueous: Having to do with water. [NIH] Arachidonate 12-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in platelets. EC 1.13.11.31. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH]
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Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriolosclerosis: Sclerosis and thickening of the walls of the smaller arteries (arterioles). Hyaline arteriolosclerosis, in which there is homogeneous pink hyaline thickening of the arteriolar walls, is associated with benign nephrosclerosis. Hyperplastic arteriolosclerosis, in which there is a concentric thickening with progressive narrowing of the lumina may be associated with malignant hypertension, nephrosclerosis, and scleroderma. [EU] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Aspartame: Flavoring agent sweeter than sugar, metabolized as phenylalanine and aspartic acid. [NIH] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-amino-acids is obtained by the hydrolysis of proteins. [NIH] Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. [NIH] Aspartic Endopeptidases: A sub-subclass of endopeptidases that depend on an aspartic acid residue for their activity. EC 3.4.23. [NIH] Aspergillosis: Infections with fungi of the genus Aspergillus. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astringent: Causing contraction, usually locally after topical application. [EU] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atherogenic: Causing the formation of plaque in the lining of the arteries. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition,
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or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Axillary: Pertaining to the armpit area, including the lymph nodes that are located there. [NIH]
Axillary Artery: The continuation of the subclavian artery; it distributes over the upper limb, axilla, chest and shoulder. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Azauridine: A triazine nucleoside used as an antineoplastic antimetabolite. It interferes with pyrimidine biosynthesis thereby preventing formation of cellular nucleic acids. As the triacetate, it is also effective as an antipsoriatic. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Bacteriuria: The presence of bacteria in the urine with or without consequent urinary tract infection. Since bacteriuria is a clinical entity, the term does not preclude the use of urine/microbiology for technical discussions on the isolation and segregation of bacteria in the urine. [NIH]
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Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Benzene: Toxic, volatile, flammable liquid hydrocarbon biproduct of coal distillation. It is used as an industrial solvent in paints, varnishes, lacquer thinners, gasoline, etc. Benzene causes central nervous system damage acutely and bone marrow damage chronically and is carcinogenic. It was formerly used as parasiticide. [NIH] Beta carotene: A vitamin A precursor. Beta carotene belongs to the family of fat-soluble vitamins called carotenoids. [NIH] Beta Rays: A stream of positive or negative electrons ejected with high energy from a disintegrating atomic nucleus; most biomedically used isotopes emit negative particles (electrons or negatrons, rather than positrons). Cathode rays are low-energy negative electrons produced in cathode ray tubes, also called television tubes or oscilloscopes. [NIH] Bezafibrate: Antilipemic agent that lowers cholesterol and triglycerides. It decreases low density lipoproteins and increases high density lipoproteins. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile Ducts: Tubes that carry bile from the liver to the gallbladder for storage and to the small intestine for use in digestion. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU]
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Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biodegradation: The series of processes by which living organisms degrade pollutant chemicals, organic wastes, pesticides, and implantable materials. [NIH] Biological Factors: Compounds made by living organisms that contribute to or influence a phenomenon or process. They have biological or physiological activities. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biomass: Total mass of all the organisms of a given type and/or in a given area. (From Concise Dictionary of Biology, 1990) It includes the yield of vegetative mass produced from any given crop. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bladder: The organ that stores urine. [NIH] Blastomycosis: A fungal infection that may appear in two forms: 1) a primary lesion characterized by the formation of a small cutaneous nodule and small nodules along the lymphatics that may heal within several months; and 2) chronic granulomatous lesions characterized by thick crusts, warty growths, and unusual vascularity and infection in the middle or upper lobes of the lung. [NIH] Bloating: Fullness or swelling in the abdomen that often occurs after meals. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH]
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Blood urea: A waste product in the blood that comes from the breakdown of food protein. The kidneys filter blood to remove urea. As kidney function decreases, the BUN level increases. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Body Composition: The relative amounts of various components in the body, such as percent body fat. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Bolus: A single dose of drug usually injected into a blood vessel over a short period of time. Also called bolus infusion. [NIH] Bolus infusion: A single dose of drug usually injected into a blood vessel over a short period of time. Also called bolus. [NIH] Bolus injection: The injection of a drug (or drugs) in a high quantity (called a bolus) at once, the opposite of gradual administration (as in intravenous infusion). [EU] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Remodeling: The continuous turnover of bone matrix and mineral that involves first, an increase in resorption (osteoclastic activity) and later, reactive bone formation (osteoblastic activity). The process of bone remodeling takes place in the adult skeleton at discrete foci. The process ensures the mechanical integrity of the skeleton throughout life and plays an important role in calcium homeostasis. An imbalance in the regulation of bone remodeling's two contrasting events, bone resorption and bone formation, results in many of the metabolic bone diseases, such as osteoporosis. [NIH] Bone Resorption: Bone loss due to osteoclastic activity. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachial: All the nerves from the arm are ripped from the spinal cord. [NIH] Brachial Artery: The continuation of the axillary artery; it branches into the radial and ulnar arteries. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Infarction: The formation of an area of necrosis in the brain, including the cerebral hemispheres (cerebral infarction), thalami, basal ganglia, brain stem (brain stem infarctions), or cerebellum secondary to an insufficiency of arterial or venous blood flow. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH]
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Brain Stem Infarctions: Infarctions that occur in the brain stem which is comprised of the midbrain, pons, and medulla. There are several named syndromes characterized by their distinctive clinical manifestations and specific sites of ischemic injury. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchopulmonary: Pertaining to the lungs and their air passages; both bronchial and pulmonary. [EU] Bronchopulmonary Dysplasia: A chronic lung disease appearing in certain newborn infants treated for respiratory distress syndrome with mechanical ventilation and elevated concentration of inspired oxygen. [NIH] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge of electricity. [NIH] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium Carbonate: Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement. [NIH] Calcium channel blocker: A drug used to relax the blood vessel and heart muscle, causing pressure inside blood vessels to drop. It also can regulate heart rhythm. [NIH] Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cell membranes or on the release and binding of calcium in intracellular pools. Since they are inducers of vascular and other smooth muscle relaxation, they are used in the drug therapy of hypertension and cerebrovascular spasms, as myocardial protective agents, and in the relaxation of uterine spasms. [NIH] Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH]
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Caloric intake: Refers to the number of calories (energy content) consumed. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capsaicin: Cytotoxic alkaloid from various species of Capsicum (pepper, paprika), of the Solanaceae. [NIH] Capsular: Cataract which is initiated by an opacification at the surface of the lens. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Captopril: A potent and specific inhibitor of peptidyl-dipeptidase A. It blocks the conversion of angiotensin I to angiotensin II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the renin-angiotensin system and inhibits pressure responses to exogenous angiotensin. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carboxy: Cannabinoid. [NIH] Carboxylic Acids: Organic compounds containing the carboxy group (-COOH). This group of compounds includes amino acids and fatty acids. Carboxylic acids can be saturated, unsaturated, or aromatic. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Cardiac: Having to do with the heart. [NIH] Cardiomyopathy: A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [NIH] Carnitine: Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carotenoids: Substance found in yellow and orange fruits and vegetables and in dark green,
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leafy vegetables. May reduce the risk of developing cancer. [NIH] Carotid Arteries: Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Castor Oil: Oil obtained from seeds of Ricinus communis that is used as a cathartic and as a plasticizer. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Catheters: A small, flexible tube that may be inserted into various parts of the body to inject or remove liquids. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Adhesion Molecules: Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH]
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Cell Division: The fission of a cell. [NIH] Cell Lineage: The developmental history of cells as traced from the first division of the original cell or cells in the embryo. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell Physiology: Characteristics and physiological processes of cells from cell division to cell death. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cellobiose: A disaccharide consisting of two glucose units in beta (1-4) glycosidic linkage. Obtained from the partial hydrolysis of cellulose. [NIH] Cellular metabolism: The sum of all chemical changes that take place in a cell through which energy and basic components are provided for essential processes, including the synthesis of new molecules and the breakdown and removal of others. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH] Ceramide: A type of fat produced in the body. It may cause some types of cells to die, and is being studied in cancer treatment. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebellum: Part of the metencephalon that lies in the posterior cranial fossa behind the brain stem. It is concerned with the coordination of movement. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebral Infarction: The formation of an area of necrosis in the cerebrum caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., infarction, anterior cerebral artery), and etiology (e.g., embolic infarction). [NIH]
Cerebrospinal: Pertaining to the brain and spinal cord. [EU]
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Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemopreventive: Natural or synthetic compound used to intervene in the early precancerous stages of carcinogenesis. [NIH] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chest Pain: Pressure, burning, or numbness in the chest. [NIH] Chlamydia: A genus of the family Chlamydiaceae whose species cause a variety of diseases in vertebrates including humans, mice, and swine. Chlamydia species are gram-negative and produce glycogen. The type species is Chlamydia trachomatis. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Cholangitis: Inflammation of a bile duct. [NIH] Cholecystectomy: Surgical removal of the gallbladder. [NIH] Cholelithiasis: Presence or formation of gallstones. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chorea: Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as choreatic disorders. Chorea is also a frequent manifestation of basal ganglia diseases. [NIH] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been
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listed as known carcinogens. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chyle: An opaque, milky-white fluid consisting mainly of emulsified fats that passes through the lacteals of the small intestines into the lymphatic system. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Citric Acid: A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability. [NIH] Citric Acid Cycle: A series of reactions involving oxidation of a two-carbon acetyl unit to carbon dioxide and water with the production of high-energy phosphate bonds by means of tricarboxylic acid intermediate. [NIH] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH] Civilization: The distinctly human attributes and attainments of a particular society. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Claviceps: A genus of ascomycetous fungi, family Clavicipitaceae, order Hypocreales, parasitic on various grasses. The sclerotia contain several toxic alkaloids. Claviceps purpurea on rye causes ergotism. [NIH] Clear cell carcinoma: A rare type of tumor of the female genital tract in which the inside of the cells looks clear when viewed under a microscope. [NIH] Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH]
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Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Coal: A natural fuel formed by partial decomposition of vegetable matter under certain environmental conditions. [NIH] Cod Liver Oil: Oil obtained from fresh livers of the cod family, Gadidae. It is a source of vitamins A and D. [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Combinatorial: A cut-and-paste process that churns out thousands of potentially valuable compounds at once. [NIH] Communis: Common tendon of the rectus group of muscles that surrounds the optic foramen and a portion of the superior orbital fissure, to the anterior margin of which it is attached at the spina recti lateralis. [NIH] Comorbidity: The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival. [NIH]
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Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH]
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Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Condyloma: C. acuminatum; a papilloma with a central core of connective tissue in a treelike structure covered with epithelium, usually occurring on the mucous membrane or skin of the external genitals or in the perianal region. [EU] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constitutional: 1. Affecting the whole constitution of the body; not local. 2. Pertaining to the constitution. [EU] Consumption: Pulmonary tuberculosis. [NIH] Contact dermatitis: Inflammation of the skin with varying degrees of erythema, edema and vesinculation resulting from cutaneous contact with a foreign substance or other exposure. [NIH]
Contraceptive: An agent that diminishes the likelihood of or prevents conception. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contrast Media: Substances used in radiography that allow visualization of certain tissues. [NIH]
Contrast Sensitivity: The ability to detect sharp boundaries (stimuli) and to detect slight changes in luminance at regions without distinct contours. Psychophysical measurements of this visual function are used to evaluate visual acuity and to detect eye disease. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH] Controlled clinical trial: A clinical study that includes a comparison (control) group. The comparison group receives a placebo, another treatment, or no treatment at all. [NIH] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments,
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etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Angiography: Radiography of the vascular system of the heart muscle after injection of a contrast medium. [NIH] Coronary Circulation: The circulation of blood through the coronary vessels of the heart. [NIH]
Coronary Disease: Disorder of cardiac function due to an imbalance between myocardial function and the capacity of the coronary vessels to supply sufficient flow for normal function. It is a form of myocardial ischemia (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Coronary Vessels: The veins and arteries of the heart. [NIH] Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that has ruptured and discharged its ovum. [NIH] Corrosion: Irreversible destruction of skin tissue. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Corticosteroids: Hormones that have antitumor activity in lymphomas and lymphoid leukemias; in addition, corticosteroids (steroids) may be used for hormone replacement and for the management of some of the complications of cancer and its treatment. [NIH] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Creatine: An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. [NIH]
Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Crystallization: The formation of crystals; conversion to a crystalline form. [EU] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH]
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Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cysteine Endopeptidases: Endopeptidases which have a cysteine involved in the catalytic process. This group of enzymes is inactivated by sulfhydryl reagents. EC 3.4.22. [NIH] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Dairy Products: Raw and processed or manufactured milk and milk-derived products. These are usually from cows (bovine) but are also from goats, sheep, reindeer, and water buffalo. [NIH] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] De novo: In cancer, the first occurrence of cancer in the body. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Death Certificates: Official records of individual deaths including the cause of death certified by a physician, and any other required identifying information. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Decompensation: Failure of compensation; cardiac decompensation is marked by dyspnea, venous engorgement, and edema. [EU] Decubitus: An act of lying down; also the position assumed in lying down. [EU] Decubitus Ulcer: An ulceration caused by prolonged pressure in patients permitted to lie too still for a long period of time. The bony prominences of the body are the most frequently affected sites. The ulcer is caused by ischemia of the underlying structures of the skin, fat,
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and muscles as a result of the sustained and constant pressure. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydroepiandrosterone: DHEA. A substance that is being studied as a cancer prevention drug. It belongs to the family of drugs called steroids. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delirium: (DSM III-R) an acute, reversible organic mental disorder characterized by reduced ability to maintain attention to external stimuli and disorganized thinking as manifested by rambling, irrelevant, or incoherent speech; there are also a reduced level of consciousness, sensory misperceptions, disturbance of the sleep-wakefulness cycle and level of psychomotor activity, disorientation to time, place, or person, and memory impairment. Delirium may be caused by a large number of conditions resulting in derangement of cerebral metabolism, including systemic infection, poisoning, drug intoxication or withdrawal, seizures or head trauma, and metabolic disturbances such as hypoxia, hypoglycaemia, fluid, electrolyte, or acid-base imbalances, or hepatic or renal failure. Called also acute confusional state and acute brain syndrome. [EU] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Dermal: Pertaining to or coming from the skin. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Dermatosis: Any skin disease, especially one not characterized by inflammation. [EU] DES: Diethylstilbestrol. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [NIH] Desmin: An intermediate filament protein found predominantly in smooth, skeletal, and cardiac muscle cells. Localized at the Z line. MW 50,000 to 55,000 is species dependent. [NIH] Detergents: Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action
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that depends on possessing both hydrophilic and hydrophobic properties. [NIH] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Dextrans: A group of glucose polymers made by certain bacteria. Dextrans are used therapeutically as plasma volume expanders and anticoagulants. They are also commonly used in biological experimentation and in industry for a wide variety of purposes. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diastole: Period of relaxation of the heart, especially the ventricles. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diastolic blood pressure: The minimum pressure that remains within the artery when the heart is at rest. [NIH] Diastolic pressure: The lowest pressure to which blood pressure falls between contractions of the ventricles. [NIH] Diathermy: The induction of local hyperthermia by either short radio waves or highfrequency sound waves. [NIH] Diatrizoate: A commonly used x-ray contrast medium. As Diatrizoate meglumine and as Diatrizoate sodium, it is used for gastrointestinal studies, angiography, and urography. [NIH] Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados. [NIH]
Dietetics: The study and regulation of the diet. [NIH] Dietitian: An expert in nutrition who helps people plan what and how much food to eat. [NIH]
Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dihydroxy: AMPA/Kainate antagonist. [NIH] Dilatation: The act of dilating. [NIH] Dilatation, Pathologic: The condition of an anatomical structure's being dilated beyond normal dimensions. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH]
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Dilution: A diluted or attenuated medicine; in homeopathy, the diffusion of a given quantity of a medicinal agent in ten or one hundred times the same quantity of water. [NIH] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Dissociative Disorders: Sudden temporary alterations in the normally integrative functions of consciousness. [NIH] Diuretic: A drug that increases the production of urine. [NIH] Diuretics, Thiazide: Diuretics characterized as analogs of 1,2,4-benzothiadiazine-1,1dioxide. All have a common mechanism of action and differ primarily in the dose required to produce a given effect. They act directly on the kidney to increase the excretion of sodium chloride and water and also increase excretion of potassium ions. [NIH] Domesticated: Species in which the evolutionary process has been influenced by humans to meet their needs. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dormancy: The period when an organism (i. e., a virus or a bacterium) is in the body but not producing any ill effects. [NIH] Dosage Forms: Completed forms of the pharmaceutical preparation in which prescribed doses of medication are included. They are designed to resist action by gastric fluids, prevent vomiting and nausea, reduce or alleviate the undesirable taste and smells associated with oral administration, achieve a high concentration of drug at target site, or produce a delayed or long-acting drug effect. They include capsules, liniments, ointments, pharmaceutical solutions, powders, tablets, etc. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH]
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Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dyslipidemia: Disorders in the lipoprotein metabolism; classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high-density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low-density lipoprotein (LDL) cholesterol and low levels of HDL cholesterol predispose to premature atherosclerosis. [NIH] Dyspareunia: Painful sexual intercourse. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Dystonia: Disordered tonicity of muscle. [EU] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. [NIH] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [NIH]
Ectopic: Pertaining to or characterized by ectopia. [EU] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elastomers: A generic term for all substances having the properties of natural, reclaimed, vulcanized, or synthetic rubber, in that they stretch under tension, have a high tensile strength, retract rapidly, and recover their original dimensions fully. [NIH] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrolysis: Destruction by passage of a galvanic electric current, as in disintegration of a chemical compound in solution. [NIH]
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Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]
Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e., radiation. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryogenesis: The process of embryo or embryoid formation, whether by sexual (zygotic) or asexual means. In asexual embryogenesis embryoids arise directly from the explant or on intermediary callus tissue. In some cases they arise from individual cells (somatic cell embryoge). [NIH] Emollient: Softening or soothing; called also malactic. [EU] Empirical: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [NIH] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endarterectomy: Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called atherectomy. [NIH] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endocrinology: A subspecialty of internal medicine concerned with the metabolism,
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physiology, and disorders of the endocrine system. [NIH] Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. Endosomes play a central role in endocytosis. [NIH] Endoderm: The inner of the three germ layers of the embryo. [NIH] Endolymph: The fluid contained in the membranous labyrinth of the ear. [NIH] Endolymphatic Duct: Duct connecting the endolymphatic sac with the membranous labyrinth. [NIH] Endolymphatic Sac: The blind pouch at the end of the endolymphatic duct. [NIH] Endometrial: Having to do with the endometrium (the layer of tissue that lines the uterus). [NIH]
Endometrium: The layer of tissue that lines the uterus. [NIH] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxic: Of, relating to, or acting as an endotoxin (= a heat-stable toxin, associated with the outer membranes of certain gram-negative bacteria. Endotoxins are not secreted and are released only when the cells are disrupted). [EU] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Energy Intake: Total number of calories taken in daily whether ingested or by parenteral routes. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Enteric-coated: A term designating a special coating applied to tablets or capsules which prevents release and absorption of their contents until they reach the intestines. [EU] Environmental Exposure: The exposure to potentially harmful chemical, physical, or
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biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Erectile: The inability to get or maintain an erection for satisfactory sexual intercourse. Also called impotence. [NIH] Erection: The condition of being made rigid and elevated; as erectile tissue when filled with blood. [EU] Ergot: Cataract due to ergot poisoning caused by eating of rye cereals contaminated by a fungus. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythromycin: A bacteriostatic antibiotic substance produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. [NIH]
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Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Esterification: The process of converting an acid into an alkyl or aryl derivative. Most frequently the process consists of the reaction of an acid with an alcohol in the presence of a trace of mineral acid as catalyst or the reaction of an acyl chloride with an alcohol. Esterification can also be accomplished by enzymatic processes. [NIH] Estradiol: The most potent mammalian estrogenic hormone. It is produced in the ovary, placenta, testis, and possibly the adrenal cortex. [NIH] Estrogen: One of the two female sex hormones. [NIH] Estrogen receptor: ER. Protein found on some cancer cells to which estrogen will attach. [NIH]
Estrogen Replacement Therapy: The use of hormonal agents with estrogen-like activity in postmenopausal or other estrogen-deficient women to alleviate effects of hormone deficiency, such as vasomotor symptoms, dyspareunia, and progressive development of osteoporosis. This may also include the use of progestational agents in combination therapy. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Ethylenes: Derivatives of ethylene, a simple organic gas of biological origin with many industrial and biological use. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evacuation: An emptying, as of the bowels. [EU] Excisional: The surgical procedure of removing a tumor by cutting it out. The biopsy is then examined under a microscope. [NIH] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exons: Coding regions of messenger RNA included in the genetic transcript which survive the processing of RNA in cell nuclei to become part of a spliced messenger of structural RNA in the cytoplasm. They include joining and diversity exons of immunoglobulin genes. [NIH]
Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture
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dishes adhere. [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extravascular: Situated or occurring outside a vessel or the vessels. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Faecal: Pertaining to or of the nature of feces. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Fatty Liver: The buildup of fat in liver cells. The most common cause is alcoholism. Other causes include obesity, diabetes, and pregnancy. Also called steatosis. [NIH] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [NIH] Ferrets: Semidomesticated variety of European polecat much used for hunting rodents and/or rabbits and as a laboratory animal. [NIH] Fertilizers: Substances or mixtures that are added to the soil to supply nutrients or to make available nutrients already present in the soil, in order to increase plant growth and productivity. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibrinolysis: The natural enzymatic dissolution of fibrin. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH]
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Filarioidea: A superfamily of nematodes of the suborder Spirurina. Its organisms possess a filiform body and a mouth surrounded by papillae. [NIH] Filler: An inactive substance used to make a product bigger or easier to handle. For example, fillers are often used to make pills or capsules because the amount of active drug is too small to be handled conveniently. [NIH] Fish Oils: Oils high in unsaturated fats extracted from the bodies of fish or fish parts, especially the livers. Those from the liver are usually high in vitamin A. The oils are used as dietary supplements, in soaps and detergents, as protective coatings, and as a base for other food products such as vegetable shortenings. [NIH] Flatus: Gas passed through the rectum. [NIH] Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride to prevent dental caries. [NIH] Flush: Transient, episodic redness of the face and neck caused by certain diseases, ingestion of certain drugs or other substances, heat, emotional factors, or physical exertion. [EU] Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Frontal Lobe: The anterior part of the cerebral hemisphere. [NIH] Fructans: Polysaccharides composed of D-fructose units. [NIH] Fructose: A type of sugar found in many fruits and vegetables and in honey. Fructose is used to sweeten some diet foods. It is considered a nutritive sweetener because it has calories. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallstones: The solid masses or stones made of cholesterol or bilirubin that form in the gallbladder or bile ducts. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglionic Blockers: Agents having as their major action the interruption of neural transmission at nicotinic receptors on postganglionic autonomic neurons. Because their actions are so broad, including blocking of sympathetic and parasympathetic systems, their therapeutic use has been largely supplanted by more specific drugs. They may still be used in the control of blood pressure in patients with acute dissecting aortic aneurysm and for the induction of hypotension in surgery. [NIH]
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Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Emptying: The evacuation of food from the stomach into the duodenum. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas). [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gastroparesis: Nerve or muscle damage in the stomach. Causes slow digestion and emptying, vomiting, nausea, or bloating. Also called delayed gastric emptying. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gels: Colloids with a solid continuous phase and liquid as the dispersed phase; gels may be unstable when, due to temperature or other cause, the solid phase liquifies; the resulting colloid is called a sol. [NIH] Gemfibrozil: A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol. These decreases occur primarily in the VLDL fraction and less frequently in the LDL fraction. Gemfibrozil increases HDL subfractions HDL2 and HDL3 as well as apolipoproteins A-I and A-II. Its mechanism of action has not been definitely established. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Germ Layers: The three layers of cells comprising the early embryo. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Gestational Age: Age of the conceptus. In humans, this may be assessed by medical history,
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physical examination, early immunologic pregnancy tests, radiography, ultrasonography, and amniotic fluid analysis. [NIH] Gibberellin: One of a class of plant hormones that promote elongation. Synthesis occurs mainly in leaves and roots. They function by stimulating cell division and the hydrolisis of sugars to glucose and fructose, and stimulate extensive growth, especially of internodes. [NIH]
Ginseng: An araliaceous genus of plants that contains a number of pharmacologically active agents used as stimulants, sedatives, and tonics, especially in traditional medicine. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Gluconeogenesis: The process by which glucose is formed from a non-carbohydrate source. [NIH]
Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucose tolerance: The power of the normal liver to absorb and store large quantities of glucose and the effectiveness of intestinal absorption of glucose. The glucose tolerance test is a metabolic test of carbohydrate tolerance that measures active insulin, a hepatic function based on the ability of the liver to absorb glucose. The test consists of ingesting 100 grams of glucose into a fasting stomach; blood sugar should return to normal in 2 to 21 hours after ingestion. [NIH] Glucose Tolerance Test: Determination of whole blood or plasma sugar in a fasting state before and at prescribed intervals (usually 1/2 hr, 1 hr, 3 hr, 4 hr) after taking a specified amount (usually 100 gm orally) of glucose. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [NIH] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]
Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of
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chlorpropamide. [NIH] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerol Kinase: An enzyme that catalyzes the formation of glycerol 3-phosphate from ATP and glycerol. Dihydroxyacetone and L-glyceraldehyde can also act as acceptors; UTP and, in the case of the yeast enzyme, ITP and GTP can act as donors. It provides a way for glycerol derived from fats or glycerides to enter the glycolytic pathway. EC 2.7.1.30. [NIH] Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycols: A generic grouping for dihydric alcohols with the hydroxy groups (-OH) located on different carbon atoms. They are viscous liquids with high boiling points for their molecular weights. [NIH] Glycolysis: The pathway by which glucose is catabolized into two molecules of pyruvic acid with the generation of ATP. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosidic: Formed by elimination of water between the anomeric hydroxyl of one sugar and a hydroxyl of another sugar molecule. [NIH] Glycosylation: The chemical or biochemical addition of carbohydrate or glycosyl groups to other chemicals, especially peptides or proteins. Glycosyl transferases are used in this biochemical reaction. [NIH] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Gonad: A sex organ, such as an ovary or a testicle, which produces the gametes in most multicellular animals. [NIH] Gonadal: Pertaining to a gonad. [EU] Gonadotropin: The water-soluble follicle stimulating substance, by some believed to originate in chorionic tissue, obtained from the serum of pregnant mares. It is used to supplement the action of estrogens. [NIH] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH]
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Grafting: The operation of transfer of tissue from one site to another. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Growth Substances: Signal molecules that are involved in the control of cell growth and differentiation. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Guinea Pigs: A common name used for the family Caviidae. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research. [NIH]
Haloperidol: Butyrophenone derivative. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Care Costs: The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from health expenditures, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost. [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Health Expenditures: The amounts spent by individuals, groups, nations, or private or public organizations for total health care and/or its various components. These amounts may or may not be equivalent to the actual costs (health care costs) and may or may not be shared among the patient, insurers, and/or employers. [NIH]
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Health Status: The level of health of the individual, group, or population as subjectively assessed by the individual or by more objective measures. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartbeat: One complete contraction of the heart. [NIH] Hematology: A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts. [NIH] Hepatic: Refers to the liver. [NIH] Hepatobiliary: Pertaining to the liver and the bile or the biliary ducts. [EU] Hepatocyte: A liver cell. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Heritability: The proportion of observed variation in a particular trait that can be attributed to inherited genetic factors in contrast to environmental ones. [NIH] Heterodimer: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterotrophic: Pertaining to organisms that are consumers and dependent on other organisms for their source of energy (food). [NIH] Heterozygotes: Having unlike alleles at one or more corresponding loci on homologous
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chromosomes. [NIH] High blood cholesterol: Cholesterol is the most abundant steroid in animal tissues, especially in bile and gallstones. The relationship between the intake of cholesterol and its manufacture by the body to its utilization, sequestration, or excretion from the body is called the cholesterol balance. When cholesterol accumulates, the balance is positive; when it declines, the balance is negative. In 1993, the NHLBI National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults issued an updated set of recommendations for monitoring and treatment of blood cholesterol levels. The NCEP guidelines recommended that total cholesterol levels and subfractions of high-density lipoprotein (HDL) cholesterol be measured beginning at age 20 in all adults, with subsequent periodic screenings as needed. Even in the group of patients at lowest risk for coronary heart disease (total cholesterol 200 mg/dL and HDL 35 mg/dL), the NCEP recommended that rescreening take place at least once every 5 years or upon physical examination. [NIH] High-density lipoproteins: Lipoproteins that contain a small amount of cholesterol and carry cholesterol away from body cells and tissues to the liver for excretion from the body. Low-level HDL increases the risk of heart disease, so the higher the HDL level, the better. The HDL component normally contains 20 to 30 percent of total cholesterol, and HDL levels are inversely correlated with coronary heart disease risk. [NIH] Hirsutism: Excess hair in females and children with an adult male pattern of distribution. The concept does not include hypertrichosis, which is localized or generalized excess hair. [NIH]
Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Homozygotes: An individual having a homozygous gene pair. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hormone Replacement Therapy: Therapeutic use of hormones to alleviate the effects of hormone deficiency. [NIH] Hormone therapy: Treatment of cancer by removing, blocking, or adding hormones. Also called endocrine therapy. [NIH] Hospital Records: Compilations of data on hospital activities and programs; excludes patient medical records. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU]
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Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophilic: Readily absorbing moisture; hygroscopic; having strongly polar groups that readily interact with water. [EU] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxylation: Hydroxylate, to introduce hydroxyl into (a compound or radical) usually by replacement of hydrogen. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hygienic: Pertaining to hygiene, or conducive to health. [EU] Hyperandrogenism: A state characterized or caused by an excessive secretion of androgens by the adrenal cortex, ovaries, or testes. The clinical significance in males is negligible, so the term is used most commonly with reference to the female. The common manifestations in women are hirsutism and virilism. It is often caused by ovarian disease (particularly the polycystic ovary syndrome) and by adrenal diseases (particularly adrenal gland hyperfunction). [NIH] Hypercholesterolemia: Abnormally high levels of cholesterol in the blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hyperlipoproteinemia: Metabolic disease characterized by elevated plasma cholesterol and/or triglyceride levels. The inherited form is attributed to a single gene mechanism. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertriglyceridemia: Condition of elevated triglyceride concentration in the blood; an inherited form occurs in familial hyperlipoproteinemia IIb and hyperlipoproteinemia type IV. It has been linked to higher risk of heart disease and arteriosclerosis. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH]
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Hypobetalipoproteinemia: A disease in which the low density lipoprotein (betalipoprotein) concentrations are far below normal. [NIH] Hypoglycemic: An orally active drug that produces a fall in blood glucose concentration. [NIH]
Hypotension: Abnormally low blood pressure. [NIH] Hypothalamic: Of or involving the hypothalamus. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hysterosalpingography: Radiography of the uterus and fallopian tubes after the injection of a contrast medium. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Ileum: The lower end of the small intestine. [NIH] Imaging procedures: Methods of producing pictures of areas inside the body. [NIH] Immaturity: The state or quality of being unripe or not fully developed. [EU] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] Impotence: The inability to perform sexual intercourse. [NIH] Impregnation: 1. The act of fecundation or of rendering pregnant. 2. The process or act of saturation; a saturated condition. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH]
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Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indinavir: A potent and specific HIV protease inhibitor that appears to have good oral bioavailability. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infantile: Pertaining to an infant or to infancy. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate a carcinogenic process. [NIH] Inlay: In dentistry, a filling first made to correspond with the form of a dental cavity and then cemented into the cavity. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own
264 Triglycerides
psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Interindividual: Occurring between two or more individuals. [EU] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intracellular: Inside a cell. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intraocular: Within the eye. [EU] Intraocular pressure: Pressure of the fluid inside the eye; normal IOP varies among individuals. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a
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positive charge are known as cations; those with a negative charge are anions. [NIH] Irritable Bowel Syndrome: A disorder that comes and goes. Nerves that control the muscles in the GI tract are too active. The GI tract becomes sensitive to food, stool, gas, and stress. Causes abdominal pain, bloating, and constipation or diarrhea. Also called spastic colon or mucous colitis. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic stroke: A condition in which the blood supply to part of the brain is cut off. Also called "plug-type" strokes. Blocked arteries starve areas of the brain controlling sight, speech, sensation, and movement so that these functions are partially or completely lost. Ischemic stroke is the most common type of stroke, accounting for 80 percent of all strokes. Most ischemic strokes are caused by a blood clot called a thrombus, which blocks blood flow in the arteries feeding the brain, usually the carotid artery in the neck, the major vessel bringing blood to the brain. When it becomes blocked, the risk of stroke is very high. [NIH] Isocyanates: Organic compounds that contain the -NCO radical. [NIH] Isoflavones: 3-Phenylchromones. Isomeric form of flavones in which the benzene group is attached to the 3 position of the benzopyran ring instead of the 2 position. [NIH] Itraconazole: An antifungal agent that has been used in the treatment of histoplasmosis, blastomycosis, cryptococcal meningitis, and aspergillosis. [NIH] Ivermectin: A mixture of ivermectin component B1a (RN 71827-03-7) and B1b (RN 70209-813), which is a semisynthetic product from Streptomyces avermitilis. A potent macrocyclic lactone disaccharide antiparasitic agent used to prevent and treat parasite infestations in animals. The compound has activity against internal and external parasites and has been found effective against arthropods, insects, nematodes, filarioidea, platyhelminths, and protozoa. [NIH] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratin: A class of fibrous proteins or scleroproteins important both as structural proteins and as keys to the study of protein conformation. The family represents the principal constituent of epidermis, hair, nails, horny tissues, and the organic matrix of tooth enamel. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms an alpha-helix, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. [NIH] Keratolytic: An agent that promotes keratolysis. [EU] Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [NIH] Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Ketosis: A condition of having ketone bodies build up in body tissues and fluids. The signs of ketosis are nausea, vomiting, and stomach pain. Ketosis can lead to ketoacidosis. [NIH]
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Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney stone: A stone that develops from crystals that form in urine and build up on the inner surfaces of the kidney, in the renal pelvis, or in the ureters. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Labyrinth: The internal ear; the essential part of the organ of hearing. It consists of an osseous and a membranous portion. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]
Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Leprosy: A chronic granulomatous infection caused by Mycobacterium leprae. The granulomatous lesions are manifested in the skin, the mucous membranes, and the peripheral nerves. Two polar or principal types are lepromatous and tuberculoid. [NIH] Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Lesion: An area of abnormal tissue change. [NIH] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Libido: The psychic drive or energy associated with sexual instinct in the broad sense (pleasure and love-object seeking). It may also connote the psychic energy associated with instincts in general that motivate behavior. [NIH] Library Services: Services offered to the library user. They include reference and circulation.
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[NIH]
Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Linkage Disequilibrium: Nonrandom association of linked genes. This is the tendency of the alleles of two separate but already linked loci to be found together more frequently than would be expected by chance alone. [NIH] Lipaemia: The presence of an excess of fats or lipids in the blood. [NIH] Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3. [NIH] Lipid: Fat. [NIH] Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipodystrophy: A collection of rare conditions resulting from defective fat metabolism and characterized by atrophy of the subcutaneous fat. They include total, congenital or acquired, partial, abdominal infantile, and localized lipodystrophy. [NIH] Lipolysis: The hydrolysis of lipids. [NIH] Lipophilic: Having an affinity for fat; pertaining to or characterized by lipophilia. [EU] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Lipoprotein Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34. [NIH] Lipoprotein(a): A family of lipoprotein particles varying in density and size depending on the protein-lipid ratio and the protein composition. These particles consist of apolipoprotein B-100 covalently linked to apolipoprotein-a by one or two disulfide bonds. There is a correlation between high plasma levels of this lipoprotein and increased risk for atherosclerotic cardiovascular disease. [NIH] Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives.
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Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Lipoxygenase Inhibitors: Compounds or agents that combine with lipoxygenase and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of the eicosanoid products hydroxyeicosatetraenoic acid and various leukotrienes. [NIH] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Long-Term Care: Care over an extended period, usually for a chronic condition or disability, requiring periodic, intermittent, or continuous care. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (hydroxymethylglutaryl CoA reductases), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] Lubricants: Oily or slippery substances. [NIH] Luciferase: Any one of several enzymes that catalyze the bioluminescent reaction in certain marine crustaceans, fish, bacteria, and insects. The enzyme is a flavoprotein; it oxidizes luciferins to an electronically excited compound that emits energy in the form of light. The color of light emitted varies with the organism. The firefly enzyme is a valuable reagent for measurement of ATP concentration. (Dorland, 27th ed) EC 1.13.12.-. [NIH] Lumen: The cavity or channel within a tube or tubular organ. [EU] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
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Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Magnetic Resonance Spectroscopy: Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (magnetic resonance imaging). [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammary: Pertaining to the mamma, or breast. [EU] Mammogram: An x-ray of the breast. [NIH] Manic: Affected with mania. [EU] Mannans: Polysaccharides consisting of mannose units. [NIH] Mean blood pressure: The average blood pressure, taking account of the rise and fall that occurs with each heartbeat. It is often estimated by multiplying the diastolic pressure by two, adding the systolic pressure, and then dividing this sum by three. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Meat Products: Articles of food which are derived by a process of manufacture from any portion of carcasses of any animal used for food (e.g., head cheese, sausage, scrapple). [NIH] Mechanical ventilation: Use of a machine called a ventilator or respirator to improve the
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exchange of air between the lungs and the atmosphere. [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medroxyprogesterone: (6 alpha)-17-Hydroxy-6-methylpregn-4-ene-3,20-dione. A synthetic progestational hormone used in veterinary practice as an estrus regulator. [NIH] Medroxyprogesterone Acetate: An injectable contraceptive, generally marketed under the name Depo-Provera. [NIH] Meglumine: 1-Deoxy-1-(methylamino)-D-glucitol. A derivative of sorbitol in which the hydroxyl group in position 1 is replaced by a methylamino group. Often used in conjunction with iodinated organic compounds as contrast medium. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Menopause: Permanent cessation of menstruation. [NIH] Menstrual Cycle: The period of the regularly recurring physiologic changes in the endometrium occurring during the reproductive period in human females and some primates and culminating in partial sloughing of the endometrium (menstruation). [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH]
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Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mercaptopurine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH] Mesoderm: The middle germ layer of the embryo. [NIH] Mesolimbic: Inner brain region governing emotion and drives. [NIH] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metalloendopeptidases: Endopeptidases which use a metal, normally zinc, in the catalytic mechanism. This group of enzymes is inactivated by metal chelators. EC 3.4.24. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Methanol: A colorless, flammable liquid used in the manufacture of formaldehyde and acetic acid, in chemical synthesis, antifreeze, and as a solvent. Ingestion of methanol is toxic and may cause blindness. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Methylcellulose: Methylester of cellulose. Methylcellulose is used as an emulsifying and suspending agent in cosmetics, pharmaceutics and the chemical industry. It is used therapeutically as a bulk laxative. [NIH] Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Micelles: Electrically charged colloidal particles or ions consisting of oriented molecules; aggregates of a number of molecules held loosely together by secondary bonds. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcalcifications: Tiny deposits of calcium in the breast that cannot be felt but can be detected on a mammogram. A cluster of these very small specks of calcium may indicate that cancer is present. [NIH] Microfilaments: The smallest of the cytoskeletal filaments. They are composed chiefly of actin. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living
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organisms, they are sometimes classified as microorganisms. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microsomal: Of or pertaining to microsomes : vesicular fragments of endoplasmic reticulum formed after disruption and centrifugation of cells. [EU] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Microwaves: That portion of the electromagnetic spectrum lying between UHF (ultrahigh frequency) radio waves and heat (infrared) waves. Microwaves are used to generate heat, especially in some types of diathermy. They may cause heat damage to tissues. [NIH] Midaxillary line: An imaginary vertical line that passes midway between the anterior and posterior axillary (armpit) folds. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Millimeter: A measure of length. A millimeter is approximately 26-times smaller than an inch. [NIH] Mineral Oil: A mixture of liquid hydrocarbons obtained from petroleum. It is used as laxative, lubricant, ointment base, and emollient. [NIH] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]
Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular Structure: The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds. [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH]
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Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Monophosphate: So called second messenger for neurotransmitters and hormones. [NIH] Monotherapy: A therapy which uses only one drug. [EU] Monounsaturated fat: An unsaturated fat that is found primarily in plant foods, including olive and canola oils. [NIH] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Movement Disorders: Syndromes which feature dyskinesias as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments. [NIH] Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Musculoskeletal System: Themuscles, bones, and cartilage of the body. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be
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induced by mutagens. [NIH] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myalgia: Pain in a muscle or muscles. [EU] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myopathy: Any disease of a muscle. [EU] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] N-acetyl: Analgesic agent. [NIH] N-acetyl cysteine: An antioxidant drug that may keep cancer cells from developing or reduce the risk of growth of existing cancer. [NIH] Naive: Used to describe an individual who has never taken a certain drug or class of drugs (e. g., AZT-naive, antiretroviral-naive), or to refer to an undifferentiated immune system cell. [NIH] Narcosis: A general and nonspecific reversible depression of neuronal excitability, produced by a number of physical and chemical aspects, usually resulting in stupor. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH]
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Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephropathy: Disease of the kidneys. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nerve Fibers: Slender processes of neurons, especially the prolonged axons that conduct nerve impulses. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neuritis: A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include pain; paresthesias; paresis; or hypesthesia. [NIH] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to stimulation of the nervous system. [NIH] Neuroleptic: A term coined to refer to the effects on cognition and behaviour of antipsychotic drugs, which produce a state of apathy, lack of initiative, and limited range of emotion and in psychotic patients cause a reduction in confusion and agitation and normalization of psychomotor activity. [EU] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropeptide: A member of a class of protein-like molecules made in the brain. Neuropeptides consist of short chains of amino acids, with some functioning as neurotransmitters and some functioning as hormones. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotoxins: Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept. [NIH] Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only
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messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Niacin: Water-soluble vitamin of the B complex occurring in various animal and plant tissues. Required by the body for the formation of coenzymes NAD and NADP. Has pellagra-curative, vasodilating, and antilipemic properties. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] Observational study: An epidemiologic study that does not involve any intervention, experimental or otherwise. Such a study may be one in which nature is allowed to take its course, with changes in one characteristic being studied in relation to changes in other characteristics. Analytical epidemiologic methods, such as case-control and cohort study designs, are properly called observational epidemiology because the investigator is observing without intervention other than to record, classify, count, and statistically analyze results. [NIH]
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Occult: Obscure; concealed from observation, difficult to understand. [EU] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Odour: A volatile emanation that is perceived by the sense of smell. [EU] Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH] Oleic Acids: A group of fatty acids that contain 16 carbon atoms and a double bond at the omega 9 carbon. [NIH] Oligosaccharides: Carbohydrates consisting of between two and ten monosaccharides connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form. [NIH] Omega-3 fatty acid: A type of fat obtained in the diet and involved in immunity. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic disc: The circular area (disc) where the optic nerve connects to the retina. [NIH] Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Optic Neuritis: Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as multiple sclerosis, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis). [NIH] Orbital: Pertaining to the orbit (= the bony cavity that contains the eyeball). [EU] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Organoleptic: Of, relating to, or involving the employment of the sense organs; used especially of subjective testing (as of flavor, odor, appearance) of food and drug products. [NIH]
Orlistat: A lipase inhibitor used for weight loss. Lipase is an enzyme found in the bowel that assists in lipid absorption by the body. Orlistat blocks this enzyme, reducing the amount of
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fat the body absorbs by about 30 percent. It is known colloquially as a "fat blocker." Because more oily fat is left in the bowel to be excreted, Orlistat can cause an oily anal leakage and fecal incontinence. Orlistat may not be suitable for people with bowel conditions such as irritable bowel syndrome or Crohn's disease. [NIH] Orthostatic: Pertaining to or caused by standing erect. [EU] Osmolality: The concentration of osmotically active particles in solution expressed in terms of osmoles of solute per kilogram of solvent. The osmolality is directly proportional to the colligative properties of solutions; osmotic pressure, boiling point elevation, freezing point depression, and vapour pressure lowering. [EU] Osmoles: The standard unit of osmotic pressure. [NIH] Osmosis: Tendency of fluids (e.g., water) to move from the less concentrated to the more concentrated side of a semipermeable membrane. [NIH] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Ossicles: The hammer, anvil and stirrup, the small bones of the middle ear, which transmit the vibrations from the tympanic membrane to the oval window. [NIH] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Otosclerosis: The formation of spongy bone in the labyrinth capsule. The ossicles can become fixed and unable to transmit sound vibrations, thereby causing deafness. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH] Ovulation: The discharge of a secondary oocyte from a ruptured graafian follicle. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH]
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Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Palmitic Acid: A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Papilloma: A benign epithelial neoplasm which may arise from the skin, mucous membranes or glandular ducts. [NIH] Paraffin: A mixture of solid hydrocarbons obtained from petroleum. It has a wide range of uses including as a stiffening agent in ointments, as a lubricant, and as a topical antiinflammatory. It is also commonly used as an embedding material in histology. [NIH] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parenteral Nutrition: The administering of nutrients for assimilation and utilization by a patient who cannot maintain adequate nutrition by enteral feeding alone. Nutrients are administered by a route other than the alimentary canal (e.g., intravenously, subcutaneously). [NIH] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Particle: A tiny mass of material. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Pelvic: Pertaining to the pelvis. [EU] Penicillin: An antibiotic drug used to treat infection. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Hydrolases: A subclass of enzymes from the hydrolase class that catalyze the
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hydrolysis of peptide bonds. Exopeptidases and endopeptidases make up the sub-subclasses for this group. EC 3.4. [NIH] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Perianal: Located around the anus. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Pericytes: Smooth muscle cell that wraps around normal blood vessels. [NIH] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Periodicity: The tendency of a phenomenon to recur at regular intervals; in biological systems, the recurrence of certain activities (including hormonal, cellular, neural) may be annual, seasonal, monthly, daily, or more frequently (ultradian). [NIH] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nerves: The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Vascular Disease: Disease in the large blood vessels of the arms, legs, and feet. People who have had diabetes for a long time may get this because major blood vessels in their arms, legs, and feet are blocked and these limbs do not receive enough blood. The signs of PVD are aching pains in the arms, legs, and feet (especially when walking) and foot sores that heal slowly. Although people with diabetes cannot always avoid PVD, doctors say they have a better chance of avoiding it if they take good care of their feet, do not smoke, and keep both their blood pressure and diabetes under good control. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneal Dialysis: Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness, constipation, vomiting, and moderate fever. [EU] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides
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(industrial fungicides), insecticides, rodenticides, etc. [NIH] Petrolatum: A colloidal system of semisolid hydrocarbons obtained from petroleum. It is used as an ointment base, topical protectant, and lubricant. [NIH] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield combustible fuels, petrochemicals, and lubricants. [NIH] Pharmaceutical Preparations: Drugs intended for human or veterinary use, presented in their finished dosage form. Included here are materials used in the preparation and/or formulation of the finished dosage form. [NIH] Pharmaceutical Solutions: Homogeneous liquid preparations that contain one or more chemical substances dissolved, i.e., molecularly dispersed, in a suitable solvent or mixture of mutually miscible solvents. For reasons of their ingredients, method of preparation, or use, they do not fall into another group of products. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenolphthalein: An acid-base indicator which is colorless in acid solution, but turns pink to red as the solution becomes alkaline. It is used medicinally as a cathartic. [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylates: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs
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of disease or abnormality. [NIH] Physical Fitness: A state of well-being in which performance is optimal, often as a result of physical conditioning which may be prescribed for disease therapy. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plant sterols: Plant-based compounds that can compete with dietary cholesterol to be absorbed by the intestines. This results in lower blood cholesterol levels. They may have some effect in cancer prevention. Also known as phytosterols. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasma Volume: Volume of plasma in the circulation. It is usually measured by indicator dilution techniques. [NIH] Plasmalogens: Any glycerophospholipid in which one of the two acyl chains is attached to glycerol with an ether alkenyl linkage instead of an ester as with the other glycerophospholipids. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH]
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Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Plasticizers: Materials incorporated mechanically in plastics (usually PVC) to increase flexibility, workability or distensibility; due to the non-chemical inclusion, plasticizers leach out from the plastic and are found in body fluids and the general environment. [NIH] Plastids: Self-replicating cytoplasmic organelles of plant and algal cells that contain pigments and may synthesize and accumulate various substances. Plastids are used in phylogenetic studies. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Platyhelminths: A phylum of acoelomate, bilaterally symmetrical flatworms, without a definite anus. It includes three classes: Cestoda, Turbellaria, and Trematoda. [NIH] Pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Podophyllotoxin: The main active constituent of the resin from the roots of may apple or mandrake (Podophyllum peltatum and P. emodi). It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [NIH] Poly U: A group of uridine ribonucleotides in which the phosphate residues of each uridine ribonucleotide act as bridges in forming diester linkages between the ribose moieties. [NIH] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polyesters: Polymers of organic acids and alcohols, with ester linkages--usually polyethylene terephthalate; can be cured into hard plastic, films or tapes, or fibers which can
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be woven into fabrics, meshes or velours. [NIH] Polyethylene: A vinyl polymer made from ethylene. It can be branched or linear. Branched or low-density polyethylene is tough and pliable but not to the same degree as linear polyethylene. Linear or high-density polyethylene has a greater hardness and tensile strength. Polyethylene is used in a variety of products, including implants and prostheses. [NIH]
Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polyp: A growth that protrudes from a mucous membrane. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Polyurethanes: A group of thermoplastic or thermosetting polymers containing polyisocyanate. They are used as elastomers, as coatings, as fibers and as foams. [NIH] Polyuria: Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes. [NIH] Portal System: A system of vessels in which blood, after passing through one capillary bed, is conveyed through a second set of capillaries before it returns to the systemic circulation. It pertains especially to the hepatic portal system. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postprandial: Occurring after dinner, or after a meal; postcibal. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH]
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Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Prealbumin: A tetrameric protein, molecular weight between 50,000 and 70,000, consisting of 4 equal chains, and migrating on electrophoresis in 3 fractions more mobile than serum albumin. Its concentration ranges from 7 to 33 per cent in the serum, but levels decrease in liver disease. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Precipitation: The act or process of precipitating. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Preeclampsia: A toxaemia of late pregnancy characterized by hypertension, edema, and proteinuria, when convulsions and coma are associated, it is called eclampsia. [EU] Pre-Eclampsia: Development of hypertension with proteinuria, edema, or both, due to pregnancy or the influence of a recent pregnancy. It occurs after the 20th week of gestation, but it may develop before this time in the presence of trophoblastic disease. [NIH] Pregnancy Tests: Tests to determine whether or not an individual is pregnant. [NIH] Premenstrual: Occurring before menstruation. [EU] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary endpoint: The main result that is measured at the end of a study to see if a given treatment worked (e.g., the number of deaths or the difference in survival between the treatment group and the control group). What the primary endpoint will be is decided before the study begins. [NIH] Primary Prevention: Prevention of disease or mental disorders in susceptible individuals or populations through promotion of health, including mental health, and specific protection, as in immunization, as distinguished from the prevention of complications or after-effects of existing disease. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare
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the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Propofol: A widely used anesthetic. [NIH] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Propylene Glycol: A clear, colorless, viscous organic solvent and diluent used in pharmaceutical preparations. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a
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protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH] Protective Agents: Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent. [NIH]
Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific proteinbinding measures are often used as assays in diagnostic assessments. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Prothrombin: A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia. [NIH]
Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychology: The science dealing with the study of mental processes and behavior in man
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and animals. [NIH] Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Psyllium: Dried, ripe seeds of Plantago psyllium, P. indica, and P. ovata (Plantaginaceae). Plantain seeds swell in water and are used as demulcents and bulk laxatives. [NIH] Puberty: The period during which the secondary sex characteristics begin to develop and the capability of sexual reproduction is attained. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Fibrosis: Chronic inflammation and progressive fibrosis of the pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from oxygen lack or right heart failure. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purgative: 1. Cathartic (def. 1); causing evacuation of the bowels. 2. A cathartic, particularly one that stimulates peristaltic action. [EU] Purifying: Respiratory equipment whose function is to remove contaminants from otherwise wholesome air. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quercetin: Aglucon of quercetrin, rutin, and other glycosides. It is widely distributed in the plant kingdom, especially in rinds and barks, clover blossoms, and ragweed pollen. [NIH] Quinones: Hydrocarbon rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH]
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Radial Artery: The direct continuation of the brachial trunk, originating at the bifurcation of the brachial artery opposite the neck of the radius. Its branches may be divided into three groups corresponding to the three regions in which the vessel is situated, the forearm, wrist, and hand. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radio Waves: That portion of the electromagnetic spectrum beyond the microwaves, with wavelengths as high as 30 KM. They are used in communications, including television. Short Wave or HF (high frequency), UHF (ultrahigh frequency) and VHF (very high frequency) waves are used in citizen's band communication. [NIH] Radioactive: Giving off radiation. [NIH] Radioactivity: The quality of emitting or the emission of corpuscular or electromagnetic radiations consequent to nuclear disintegration, a natural property of all chemical elements of atomic number above 83, and possible of induction in all other known elements. [EU] Radiography: Examination of any part of the body for diagnostic purposes by means of roentgen rays, recording the image on a sensitized surface (such as photographic film). [NIH] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radius: The lateral bone of the forearm. [NIH] Random Allocation: A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects. [NIH] Randomization: Also called random allocation. Is allocation of individuals to groups, e.g., for experimental and control regimens, by chance. Within the limits of chance variation, random allocation should make the control and experimental groups similar at the start of an investigation and ensure that personal judgment and prejudices of the investigator do not influence allocation. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Rape: Unlawful sexual intercourse without consent of the victim. [NIH] Reaction Time: The time from the onset of a stimulus until the organism responds. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU]
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Rectal: By or having to do with the rectum. The rectum is the last 8 to 10 inches of the large intestine and ends at the anus. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recur: To occur again. Recurrence is the return of cancer, at the same site as the original (primary) tumor or in another location, after the tumor had disappeared. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary,
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4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respirator: A mechanical device that helps a patient breathe; a mechanical ventilator. [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Detachment: Separation of the inner layers of the retina (neural retina) from the pigment epithelium. Retinal detachment occurs more commonly in men than in women, in eyes with degenerative myopia, in aging and in aphakia. It may occur after an uncomplicated cataract extraction, but it is seen more often if vitreous humor has been lost during surgery. (Dorland, 27th ed; Newell, Ophthalmology: Principles and Concepts, 7th ed, p310-12). [NIH] Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retinoids: Derivatives of vitamin A. Used clinically in the treatment of severe cystic acne, psoriasis, and other disorders of keratinization. Their possible use in the prophylaxis and treatment of cancer is being actively explored. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retrobulbar: Behind the pons. [EU] Reverse Transcriptase Inhibitors: Inhibitors of reverse transcriptase (RNA-directed DNA polymerase), an enzyme that synthesizes DNA on an RNA template. [NIH] Rhabdomyolysis: Necrosis or disintegration of skeletal muscle often followed by myoglobinuria. [NIH] Rheology: The study of the deformation and flow of matter, usually liquids or fluids, and of the plastic flow of solids. The concept covers consistency, dilatancy, liquefaction, resistance to flow, shearing, thixotrophy, and viscosity. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH]
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Rheumatoid: Resembling rheumatism. [EU] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Ritonavir: An HIV protease inhibitor that works by interfering with the reproductive cycle of HIV. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rutin: 3-((6-O-(6-Deoxy-alpha-L-mannopyranosyl)-beta-D-glucopyranosyl)oxy)-2-(3,4dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one. Found in many plants, including buckwheat, tobacco, forsythia, hydrangea, pansies, etc. It has been used therapeutically to decrease capillary fragility. [NIH] Ryanodine: Insecticidal alkaloid isolated from Ryania speciosa; proposed as a myocardial depressant. [NIH] Rye: A hardy grain crop, Secale cereale, grown in northern climates. It is the most frequent host to ergot (claviceps), the toxic fungus. Its hybrid with wheat is triticale, another grain. [NIH]
Sagittal: The line of direction passing through the body from back to front, or any vertical plane parallel to the medial plane of the body and inclusive of that plane; often restricted to the medial plane, the plane of the sagittal suture. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saponification: The hydrolysis of an ester into an alcohol and acid. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoplasmic Reticulum: A network of tubules and sacs in the cytoplasm of skeletal muscles that assist with muscle contraction and relaxation by releasing and storing calcium ions. [NIH] Saturated fat: A type of fat found in greatest amounts in foods from animals, such as fatty cuts of meat, poultry with the skin, whole-milk dairy products, lard, and in some vegetable oils, including coconut, palm kernel, and palm oils. Saturated fat raises blood cholesterol more than anything else eaten. On a Step I Diet, no more than 8 to 10 percent of total calories should come from saturated fat, and in the Step II Diet, less than 7 percent of the day's total calories should come from saturated fat. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Scleroproteins: Simple proteins characterized by their insolubility and fibrous structure. Within the body, they perform a supportive or protective function. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical
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structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Sebaceous gland: Gland that secretes sebum. [NIH] Sebum: The oily substance secreted by sebaceous glands. It is composed of keratin, fat, and cellular debris. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedentary: 1. Sitting habitually; of inactive habits. 2. Pertaining to a sitting posture. [EU] Sediment: A precipitate, especially one that is formed spontaneously. [EU] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senescence: The bodily and mental state associated with advancing age. [NIH] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Sequence Analysis: A multistage process that includes the determination of a sequence (protein, carbohydrate, etc.), its fragmentation and analysis, and the interpretation of the resulting sequence information. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serine Endopeptidases: Any member of the group of endopeptidases containing at the active site a serine residue involved in catalysis. EC 3.4.21. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH]
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Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sex Determination: The biological characteristics which distinguish human beings as female or male. [NIH] Sharks: A group of elongate elasmobranchs. Sharks are mostly marine fish, with certain species large and voracious. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Silicone Oils: Organic siloxanes which are polymerized to the oily stage. The oils have low surface tension and density less than 1. They are used in industrial applications and in the treatment of retinal detachment, complicated by proliferative vitreoretinopathy. [NIH] Siloxanes: Silicon polymers that contain alternate silicon and oxygen atoms in linear or cyclic molecular structures. [NIH] Simvastatin: A derivative of lovastatin and potent competitive inhibitor of 3-hydroxy-3methylglutaryl coenzyme A reductase (hydroxymethylglutaryl CoA reductases), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL receptors, it increases breakdown of LDL-cholesterol (lipoproteins, LDL cholesterol). [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH]
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Skin Care: Maintenance of the hygienic state of the skin under optimal conditions of cleanliness and comfort. Effective in skin care are proper washing, bathing, cleansing, and the use of soaps, detergents, oils, etc. In various disease states, therapeutic and protective solutions and ointments are useful. The care of the skin is particularly important in various occupations, in exposure to sunlight, in neonates, and in decubitus ulcer. [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Soaps: Sodium or potassium salts of long chain fatty acids. These detergent substances are obtained by boiling natural oils or fats with caustic alkali. Sodium soaps are harder and are used as topical anti-infectives and vehicles in pills and liniments; potassium soaps are soft, used as vehicles for ointments and also as topical antimicrobials. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] Socioeconomic Factors: Social and economic factors that characterize the individual or group within the social structure. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Dodecyl Sulfate: An anionic surfactant, usually a mixture of sodium alkyl sulfates, mainly the lauryl; lowers surface tension of aqueous solutions; used as fat emulsifier, wetting agent, detergent in cosmetics, pharmaceuticals and toothpastes; also as research tool in protein biochemistry. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solitary Nucleus: Gray matter located in the dorsomedial part of the medulla oblongata associated with the solitary tract. The solitary nucleus receives inputs from most organ systems including the terminations of the facial, glossopharyngeal, and vagus nerves. It is a major coordinator of autonomic nervous system regulation of cardiovascular, respiratory, gustatory, gastrointestinal, and chemoreceptive aspects of homeostasis. The solitary nucleus is also notable for the large number of neurotransmitters which are found therein. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall
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in contrast to the viscera. [EU] Somatotropin: A small peptide hormone released by the anterior pituitary under hypothalamic control. Somatotropin, or growth hormone, stimulates mitosis, cell growth, and, for some cell types, differentiation in many tissues of the body. It has profound effects on many aspects of gene expression and metabolism. [NIH] Sorbitol: A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications. [NIH] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrometer: An apparatus for determining spectra; measures quantities such as wavelengths and relative amplitudes of components. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Sperm Maturation: Posttesticular ripening of spermatozoa. [NIH] Spermatozoa: Mature male germ cells that develop in the seminiferous tubules of the testes. Each consists of a head, a body, and a tail that provides propulsion. The head consists mainly of chromatin. [NIH] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Stabilizer: A device for maintaining constant X-ray tube voltage or current. [NIH] Steatosis: Fatty degeneration. [EU] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and
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instrumentation. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stimulants: Any drug or agent which causes stimulation. [NIH] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stupor: Partial or nearly complete unconsciousness, manifested by the subject's responding only to vigorous stimulation. Also, in psychiatry, a disorder marked by reduced responsiveness. [EU] Styrene: A colorless, toxic liquid with a strong aromatic odor. It is used to make rubbers, polymers and copolymers, and polystyrene plastics. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Sudden death: Cardiac arrest caused by an irregular heartbeat. The term "death" is somewhat misleading, because some patients survive. [NIH] Sulfates: Inorganic salts of sulfuric acid. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and
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methionine. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Suppositories: A small cone-shaped medicament having cocoa butter or gelatin at its basis and usually intended for the treatment of local conditions in the rectum. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]
Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Systolic blood pressure: The maximum pressure in the artery produced as the heart contracts and blood begins to flow. [NIH] Systolic pressure: The highest pressure to which blood pressure rises with the contraction of the ventricles. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late in appearing. [EU] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein
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synthesis. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tissue Distribution: Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate
300 Triglycerides
organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios. [NIH] Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts plasminogen to plasmin. It has fibrin-binding activity and is immunologically different from urinary plasminogen activator. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases. EC 3.4.21.68. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tonometry: The standard to determine the fluid pressure inside the eye (intraocular pressure). [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Toothache: Pain in the adjacent areas of the teeth. [NIH] Topical: On the surface of the body. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Toxaemia: 1. The condition resulting from the spread of bacterial products (toxins) by the bloodstream. 2. A condition resulting from metabolic disturbances, e.g. toxaemia of pregnancy. [EU] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicokinetics: Study of the absorption, distribution, metabolism, and excretion of test substances. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Tracer: A substance (such as a radioisotope) used in imaging procedures. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Traction: The act of pulling. [NIH] Transaminases: A subclass of enzymes of the transferase class that catalyze the transfer of an amino group from a donor (generally an amino acid) to an acceptor (generally a 2-keto acid). Most of these enzymes are pyridoxyl phosphate proteins. (Dorland, 28th ed) EC 2.6.1. [NIH]
Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA
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molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transferases: Transferases are enzymes transferring a group, for example, the methyl group or a glycosyl group, from one compound (generally regarded as donor) to another compound (generally regarded as acceptor). The classification is based on the scheme "donor:acceptor group transferase". (Enzyme Nomenclature, 1992) EC 2. [NIH] Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]
Transient Ischemic Attacks: Focal neurologic abnormalities of sudden onset and brief duration that reflect dysfunction in the distribution of the internal carotid-middle cerebral or the vertebrobasilar arterial system. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Trauma Centers: Specialized hospital facilities which provide diagnostic and therapeutic services for trauma patients. [NIH] Triad: Trivalent. [NIH] Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] Trigger zone: Dolorogenic zone (= producing or causing pain). [EU] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Troglitazone: A drug used in diabetes treatment that is being studied for its effect on reducing the risk of cancer cell growth in fat tissue. [NIH] Truncal: The bilateral dissection of the abdominal branches of the vagus nerve. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or
302 Triglycerides
kidneys. [NIH] Tubulin: A microtubule subunit protein found in large quantities in mammalian brain. It has also been isolated from sperm flagella, cilia, and other sources. Structurally, the protein is a dimer with a molecular weight of approximately 120,000 and a sedimentation coefficient of 5.8S. It binds to colchicine, vincristine, and vinblastine. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Type 2 diabetes: Usually characterized by a gradual onset with minimal or no symptoms of metabolic disturbance and no requirement for exogenous insulin. The peak age of onset is 50 to 60 years. Obesity and possibly a genetic factor are usually present. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ubiquitin: A highly conserved 76 amino acid-protein found in all eukaryotic cells. [NIH] Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Unsaturated Fats: A type of fat. [NIH] Uraemia: 1. An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. In current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]
Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Urethane: Antineoplastic agent that is also used as a veterinary anesthetic. It has also been used as an intermediate in organic synthesis. Urethane is suspected to be a carcinogen. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH] Urinalysis: Examination of urine by chemical, physical, or microscopic means. Routine urinalysis usually includes performing chemical screening tests, determining specific gravity, observing any unusual color or odor, screening for bacteriuria, and examining the sediment microscopically. [NIH]
Dictionary 303
Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Plasminogen Activator: A proteolytic enzyme that converts plasminogen to plasmin where the preferential cleavage is between arginine and valine. It was isolated originally from human urine, but is found in most tissues of most vertebrates. EC 3.4.21.73. [NIH]
Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urography: Radiography of any part of the urinary tract. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginal: Of or having to do with the vagina, the birth canal. [NIH] Vagus Nerve: The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx). [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vasomotor: 1. Affecting the calibre of a vessel, especially of a blood vessel. 2. Any element or agent that effects the calibre of a blood vessel. [EU] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vegetative: 1. Concerned with growth and with nutrition. 2. Functioning involuntarily or unconsciously, as the vegetative nervous system. 3. Resting; denoting the portion of a cell cycle during which the cell is not involved in replication. 4. Of, pertaining to, or characteristic of plants. [EU] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator. [NIH] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide
304 Triglycerides
back for gas exchange. [NIH] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventilator: A breathing machine that is used to treat respiratory failure by promoting ventilation; also called a respirator. [NIH] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Very low-density lipoprotein: The lipoprotein particles that initially leave the liver, carrying cholesterol and lipid. VLDLs contain 10 to 15 percent of the total serum cholesterol along with most of the triglycerides in the fasting serum; VLDLs are precursors of LDL, and some forms of VLDL, particularly VLDL remnants, appear to be atherogenic. [NIH] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Vestibular: Pertaining to or toward a vestibule. In dental anatomy, used to refer to the tooth surface directed toward the vestibule of the mouth. [EU] Vestibule: A small, oval, bony chamber of the labyrinth. The vestibule contains the utricle and saccule, organs which are part of the balancing apparatus of the ear. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Vimentin: An intermediate filament protein found in most differentiating cells, in cells grown in tissue culture, and in certain fully differentiated cells. Its insolubility suggests that it serves a structural function in the cytoplasm. MW 52,000. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virilism: Development of masculine traits in the female. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Virus Diseases: A general term for diseases produced by viruses. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral Afferents: The sensory fibers innervating the viscera. [NIH]
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Visceral fat: One of the three compartments of abdominal fat. Retroperitoneal and subcutaneous are the other two compartments. [NIH] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Vitamin E: Vitamin found largely in plant materials, especially wheat germ, corn, sunflower seed, rapeseed, soybean oils, alfalfa, and lettuce. It is used as an antioxidant in vegetable oils and shortenings. [NIH] Vitamin K: A substance that promotes the clotting of blood. [NIH] Vitelline Membrane: The plasma membrane of the egg. [NIH] Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the crystalline lens of the eye and in front of the retina. It is contained in a thin hyoid membrane and forms about four fifths of the optic globe. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Waist circumference: To define the level at which the waist circumference is measured, a bony landmark is first located and marked. The subject stands, and the technician, positioned to the right of the subject, palpates the upper hip bone to locate the right ileum. Just above the uppermost lateral border of the right ileum, a horizontal mark is drawn and then crossed with a vertical mark on the midaxillary line. The measuring tape is then placed around the trunk, at the level of the mark on the right side, making sure that it is on a level horizontal plane on all sides. The tape is then tightened slightly without compressing the skin and underlying subcutaneous tissues. The measure is recorded in centimeters to the nearest millimeter. [NIH] Warts: Benign epidermal proliferations or tumors; some are viral in origin. [NIH] Weight Gain: Increase in body weight over existing weight. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] World Health: The concept pertaining to the health status of inhabitants of the world. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Yolk Sac: An embryonic membrane formed from endoderm and mesoderm. In reptiles and birds it incorporates the yolk into the digestive tract for nourishing the embryo. In placental
306 Triglycerides
mammals its nutritional function is vestigial; however, it is the source of most of the intestinal mucosa and the site of formation of the germ cells. It is sometimes called the vitelline sac, which should not be confused with the vitelline membrane of the egg. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
307
INDEX A Abdomen, 221, 232, 233, 251, 264, 268, 279, 280, 296, 297, 299, 303 Abdominal, 24, 27, 35, 46, 48, 221, 222, 265, 267, 279, 280, 301, 305 Abdominal fat, 24, 46, 48, 221, 305 Abdominal Pain, 221, 265, 280 Aberrant, 27, 221 Acceptor, 221, 267, 278, 300, 301 Acetic Acids, 150, 221 Acetone, 221, 265 Acetrizoic Acid, 113, 221 Acetylcarnitine, 30, 221 Acetylcholine, 53, 221, 238, 276 Acoustic, 181, 221 Actin, 19, 221, 271, 273 Acyl, 18, 24, 43, 59, 60, 62, 127, 134, 146, 151, 153, 156, 157, 160, 221, 252, 282 Acylation, 61, 221 Acyltransferases, 156, 160, 221 Adaptation, 30, 221, 283 Adenine, 221, 222 Adenosine, 116, 124, 138, 222, 281 Adenovirus, 8, 9, 222 Adhesives, 161, 222 Adipocytes, 12, 39, 40, 45, 49, 57, 76, 156, 222, 266 Adipose Tissue, 13, 19, 35, 39, 40, 45, 48, 49, 56, 58, 63, 221, 222, 267 Adjustment, 41, 221, 222 Adjuvant, 222, 255 Adolescence, 5, 222 Adrenal Cortex, 222, 223, 243, 252, 261, 285, 290 Adrenal Medulla, 146, 222, 236, 251, 276 Adrenergic, 45, 222, 227, 247, 251 Adrenergic beta-Antagonists, 222, 227 Adrenoleukodystrophy, 61, 222 Adsorption, 116, 222 Adsorptive, 132, 222 Adverse Effect, 53, 55, 222, 294 Aerobic, 18, 45, 105, 222, 272 Aerobic Exercise, 18, 45, 105, 222 Afferent, 222, 266, 277 Affinity, 37, 54, 222, 223, 267, 295 Agar, 223, 282 Age of Onset, 223, 302 Ageing, 161, 166, 223
Agonist, 153, 173, 223, 247 Airway, 223, 295 Akathisia, 223, 227 Albumin, 60, 84, 95, 126, 223, 282 Albuminuria, 37, 79, 223 Aldehydes, 163, 223 Aldose Reductase Inhibitor, 149, 223 Aldosterone, 69, 223 Alfalfa, 224, 305 Algorithms, 224, 232 Alimentary, 224, 279 Alkaline, 120, 122, 141, 142, 171, 224, 234, 281 Alkaloid, 224, 235, 273, 292 Alleles, 7, 224, 259, 267 Allogeneic, 114, 224, 257 Alpha Particles, 224, 289 Alpha-helix, 224, 265 Alpha-Linolenic Acid, 20, 224 Alprostadil, 181, 224 Alternative medicine, 190, 224 Ameliorated, 47, 224 Amino Acid Sequence, 61, 224, 226, 255 Ammonia, 224, 256, 302 Amniotic Fluid, 224, 256 Amplification, 14, 224 Anabolic, 14, 26, 29, 224, 246 Anaesthesia, 225, 263 Anal, 5, 165, 225, 251, 278 Analgesic, 150, 225, 273, 274 Analog, 43, 173, 225 Analogous, 123, 225, 283, 301 Analysis of Variance, 49, 225 Analytes, 169, 225 Anaphylatoxins, 225, 241 Anatomical, 225, 246, 249, 262, 292 Androgenic, 14, 225 Androgens, 222, 225, 261 Anemia, 205, 225 Aneurysm, 225, 228, 303 Angina, 60, 152, 169, 222, 225 Angina Pectoris, 152, 222, 225 Angiogenesis, 149, 225 Angiography, 113, 225, 246 Angioplasty, 169, 225 Angiotensin-Converting Enzyme Inhibitors, 225, 227 Angiotensinogen, 226, 290
308 Triglycerides
Anhydrides, 148, 159, 226 Animal model, 6, 11, 18, 33, 36, 92, 187, 226 Anionic, 134, 226, 295 Anions, 223, 226, 265, 294 Ankle, 60, 226 Anorexia, 133, 226, 302 Anovulation, 50, 226 Antagonism, 40, 226 Anterior Cerebral Artery, 226, 237 Anthropometric measurements, 16, 226 Antibacterial, 226, 296 Antibiotic, 226, 251, 279, 296, 298 Antibodies, 34, 37, 226, 230, 258, 269, 273, 282 Antibody, 74, 223, 226, 227, 241, 258, 260, 262, 263, 270, 273, 296 Antibody therapy, 74, 226 Anticoagulant, 9, 226, 287 Antidepressant, 14, 226 Antidiabetic, 63, 226, 256 Antidote, 141, 227 Antiemetic, 227, 271 Antifungal, 227, 265 Antigen, 223, 226, 227, 241, 260, 261, 262, 263, 270 Antigen-Antibody Complex, 227, 241 Antihypertensive, 17, 227 Antihypertensive Agents, 17, 227 Anti-infective, 227, 261, 264, 295 Anti-inflammatory, 150, 227, 229, 256, 279 Anti-Inflammatory Agents, 227, 229 Antimetabolite, 227, 230 Antineoplastic, 227, 230, 283, 302 Antioxidant, 45, 114, 116, 128, 138, 150, 157, 227, 229, 274, 278, 305 Antiproliferative, 38, 227 Antipsychotic, 80, 227, 275 Antipyretic, 150, 228 Antispasmodic, 150, 228 Antiviral, 47, 228 Antiviral Agents, 47, 228 Anus, 225, 228, 233, 280, 283, 290 Aorta, 11, 48, 94, 228, 304 Aortic Aneurysm, 152, 228, 254 Apnea, 52, 228 Apolipoproteins, 5, 9, 33, 34, 47, 59, 63, 157, 179, 228, 255, 267 Apoptosis, 18, 35, 44, 228 Aqueous, 122, 125, 158, 159, 161, 162, 168, 169, 171, 172, 228, 231, 244, 249, 261, 266, 295
Arachidonate 12-Lipoxygenase, 228, 268 Arachidonate 15-Lipoxygenase, 228, 268 Arachidonate Lipoxygenases, 228, 268 Arachidonic Acid, 133, 138, 228, 266, 268, 286 Arginine, 225, 228, 276, 303 Aromatic, 119, 120, 124, 148, 228, 235, 281, 297 Arterial, 11, 16, 21, 29, 55, 113, 117, 182, 228, 229, 233, 235, 237, 238, 261, 287, 298, 301 Arteries, 19, 117, 228, 229, 232, 233, 236, 243, 265, 268, 271, 274, 299 Arteriolar, 60, 229, 233, 290 Arterioles, 229, 233, 235, 274 Arteriolosclerosis, 229 Arteriosclerosis, 78, 79, 117, 146, 229, 261, 274 Ascorbic Acid, 10, 86, 229, 261 Aseptic, 229, 297 Aspartame, 229 Aspartic, 229, 250 Aspartic Acid, 229 Aspartic Endopeptidases, 229, 250 Aspergillosis, 229, 265 Aspirin, 184, 229 Assay, 19, 24, 36, 61, 229 Astringent, 126, 229 Asymptomatic, 21, 38, 229, 279 Ataxia, 205, 229, 299 Atherogenic, 5, 8, 9, 10, 16, 22, 23, 46, 47, 53, 66, 108, 187, 229, 304 Atrophy, 5, 204, 205, 229, 267 Attenuated, 230, 247 Atypical, 78, 230 Autoantibodies, 7, 230 Autoantigens, 230 Autodigestion, 230, 279 Autoimmune disease, 181, 230, 273 Autonomic, 181, 221, 227, 230, 254, 276, 280, 295, 298 Autonomic Nervous System, 181, 230, 280, 295, 298 Axillary, 230, 233, 272 Axillary Artery, 230, 233 Axons, 230, 275, 277, 280 Azauridine, 147, 230 B Bacteria, 120, 125, 221, 222, 226, 227, 230, 231, 245, 246, 249, 250, 253, 258, 268, 271, 272, 293, 296, 301, 303 Bacterial Physiology, 221, 230
Index 309
Bactericidal, 230, 252 Bacteriophage, 230, 282, 301 Bacteriostatic, 230, 251 Bacterium, 230, 247 Bacteriuria, 230, 302 Basal Ganglia, 227, 229, 231, 233, 238 Basal Ganglia Diseases, 229, 231, 238 Base, 32, 44, 120, 124, 130, 135, 164, 167, 171, 221, 231, 245, 254, 255, 265, 272, 281, 302 Basement Membrane, 231, 252 Benzene, 231, 265 Beta carotene, 137, 231 Beta Rays, 231, 249 Bezafibrate, 69, 231 Bilateral, 231, 301 Bile, 3, 108, 152, 180, 184, 231, 238, 254, 259, 260, 261, 268, 297 Bile Acids, 108, 152, 231, 297 Bile Acids and Salts, 231 Bile Ducts, 231, 254 Biliary, 174, 231, 234, 259, 279 Biliary Tract, 231, 234, 279 Bilirubin, 182, 223, 231, 254 Binding Sites, 34, 231 Bioavailability, 129, 147, 158, 162, 231, 263 Biochemical, 17, 21, 26, 30, 39, 43, 61, 71, 149, 224, 227, 232, 257, 293 Biodegradation, 155, 232 Biological Factors, 41, 232 Biological therapy, 232, 258 Biomarkers, 44, 232 Biomass, 121, 232 Biopsy, 18, 26, 44, 232, 252 Biosynthesis, 13, 179, 228, 230, 232, 268, 287, 293, 294 Biotechnology, 62, 64, 68, 92, 179, 190, 201, 203, 204, 205, 206, 232 Biotransformation, 232 Bladder, 115, 143, 232, 263, 273, 286, 302, 303 Blastomycosis, 232, 265 Bloating, 232, 255, 265 Blood Coagulation, 232, 234, 299 Blood Glucose, 5, 19, 44, 139, 146, 184, 232, 259, 262, 264 Blood urea, 182, 233 Body Composition, 14, 42, 46, 56, 75, 233 Body Fluids, 26, 169, 232, 233, 234, 248, 283, 295, 302 Body Mass Index, 28, 32, 41, 46, 60, 183, 233, 278
Bolus, 40, 113, 233 Bolus infusion, 233 Bolus injection, 40, 233 Bone Marrow, 16, 27, 231, 233, 243, 262, 269, 295 Bone Remodeling, 114, 233 Bone Resorption, 233 Bowel, 182, 225, 233, 246, 263, 264, 266, 277, 280, 297 Bowel Movement, 233, 246, 297 Brachial, 12, 21, 60, 233, 289 Brachial Artery, 12, 21, 233, 289 Bradykinin, 233, 276, 282 Brain Infarction, 146, 233 Brain Stem, 233, 234, 237 Brain Stem Infarctions, 233, 234 Branch, 187, 215, 234, 269, 279, 288, 296, 299 Breakdown, 12, 49, 233, 234, 237, 246, 255, 277, 294 Bronchial, 234, 260 Bronchopulmonary, 25, 234 Bronchopulmonary Dysplasia, 25, 234 Buccal, 234, 268 Burns, 55, 234 Burns, Electric, 234 Bypass, 82, 234 C Calcification, 12, 21, 47, 50, 229, 234 Calcium Carbonate, 141, 234 Calcium channel blocker, 181, 227, 234 Calcium Channel Blockers, 181, 227, 234 Calculi, 234, 257 Callus, 234, 249 Caloric intake, 116, 137, 184, 235 Capillary, 233, 235, 267, 284, 292, 304 Capsaicin, 181, 235 Capsular, 129, 235 Capsules, 42, 115, 129, 235, 247, 250, 254, 255 Captopril, 18, 235 Carbohydrate, 10, 32, 38, 52, 54, 76, 82, 180, 235, 256, 257, 284, 293 Carbon Dioxide, 235, 239, 282, 290, 303 Carboxy, 8, 235 Carboxylic Acids, 130, 235 Carcinogen, 235, 302 Carcinogenesis, 19, 235, 238 Carcinogenic, 231, 235, 263, 286, 297 Cardiac, 17, 34, 43, 59, 63, 76, 222, 235, 243, 244, 245, 251, 274, 297 Cardiomyopathy, 17, 33, 58, 63, 235
310 Triglycerides
Cardiorespiratory, 222, 235 Cardiovascular System, 17, 235 Carnitine, 33, 43, 54, 86, 87, 115, 143, 221, 235 Carotene, 10, 231, 235, 291 Carotenoids, 231, 235 Carotid Arteries, 50, 236 Case report, 236, 239 Case series, 236, 239 Castor Oil, 124, 236 Catabolism, 34, 47, 72, 152, 236 Catecholamine, 45, 236, 247, 281 Catheterization, 225, 236 Catheters, 55, 236 Cathode, 231, 236, 249 Cations, 36, 236, 265 Causal, 27, 44, 236, 251 Cause of Death, 112, 117, 236, 244 Cell Adhesion, 17, 236 Cell Adhesion Molecules, 17, 236 Cell Cycle, 57, 236, 303 Cell Death, 228, 236, 237, 274 Cell Differentiation, 236, 294 Cell Division, 123, 204, 230, 236, 237, 256, 258, 272, 282 Cell Lineage, 57, 237 Cell membrane, 149, 234, 237, 245, 281 Cell Physiology, 51, 237 Cell proliferation, 18, 44, 229, 237, 294 Cell Respiration, 237, 272, 291 Cell Survival, 237, 258 Cellobiose, 237 Cellular metabolism, 147, 237 Cellulose, 93, 125, 171, 237, 254, 271, 282 Central Nervous System, 38, 221, 230, 231, 237, 254, 256, 258, 266, 273, 277, 293 Centrifugation, 237, 272 Ceramide, 56, 237 Cerebellar, 229, 237, 290 Cerebellum, 233, 237, 290 Cerebral, 152, 169, 226, 229, 231, 233, 237, 238, 242, 245, 251, 254, 301 Cerebral hemispheres, 231, 233, 237, 238 Cerebral Infarction, 152, 169, 233, 237 Cerebrospinal, 182, 237, 238 Cerebrospinal fluid, 182, 238 Cerebrovascular, 7, 75, 117, 144, 231, 234, 235, 238, 299 Cerebrum, 237, 238, 301 Character, 225, 238, 245 Chemopreventive, 150, 238 Chemoreceptor, 227, 238
Chemotactic Factors, 238, 241 Chest Pain, 141, 238 Chlamydia, 37, 238 Chlorophyll, 238, 254 Cholangitis, 182, 238 Cholecystectomy, 182, 238 Cholelithiasis, 182, 238 Cholesterol Esters, 51, 54, 61, 151, 238, 267 Cholinergic, 227, 238 Chorea, 227, 238 Choroid, 238, 291 Chromatin, 57, 228, 238, 296 Chromium, 87, 117, 238 Chromosomal, 224, 238, 239 Chromosome, 23, 25, 36, 222, 239, 258, 267 Chronic Disease, 10, 239 Chronic renal, 72, 185, 239, 283, 302 Chyle, 179, 239 Chylomicrons, 58, 191, 239, 267 Circulatory system, 149, 239, 249 CIS, 133, 164, 239, 291 Citric Acid, 36, 239 Citric Acid Cycle, 36, 239 Citrus, 229, 239 Civilization, 12, 239 Clamp, 40, 45, 239 Claviceps, 239, 292 Clear cell carcinoma, 239, 245 Clinical study, 12, 239, 242 Clinical trial, 4, 6, 9, 12, 27, 32, 46, 53, 55, 107, 110, 150, 201, 239, 242, 243, 287, 289 Cloning, 14, 36, 232, 239 Coagulation, 5, 12, 55, 65, 182, 232, 240, 282, 299 Coal, 120, 231, 240 Cod Liver Oil, 240, 249 Coenzyme, 62, 115, 117, 137, 229, 240, 268, 294 Cofactor, 240, 287, 299 Cohort Studies, 17, 240, 251 Colitis, 182, 240, 263, 265 Collagen, 114, 222, 231, 240, 253, 255, 283, 286 Collapse, 234, 240, 295 Colloidal, 223, 240, 249, 271, 281, 294 Colorectal, 18, 240 Colorectal Cancer, 18, 240 Combination Therapy, 240, 252 Combinatorial, 22, 240 Communis, 236, 240 Comorbidity, 41, 240 Complement, 225, 241, 255, 269, 282
Index 311
Complementary and alternative medicine, 91, 103, 241 Complementary medicine, 91, 241 Computational Biology, 201, 203, 241 Computed tomography, 21, 46, 113, 241 Computerized axial tomography, 241 Computerized tomography, 35, 47, 241 Conception, 242, 253, 297 Concomitant, 11, 242 Condyloma, 130, 242 Cones, 242, 291 Confounding, 32, 242 Congestion, 227, 242, 251 Congestive heart failure, 60, 242 Conjugated, 95, 133, 144, 164, 173, 174, 231, 242, 244 Conjunctiva, 242, 263 Connective Tissue, 229, 233, 240, 242, 253, 254, 255, 268, 280, 291, 298 Consciousness, 225, 242, 245, 247 Constipation, 181, 227, 242, 265, 280 Constitutional, 31, 242 Consumption, 16, 20, 67, 92, 129, 144, 145, 152, 171, 242, 276, 278 Contact dermatitis, 64, 242 Contraceptive, 242, 270 Contraindications, ii, 242 Contrast Media, 113, 242 Contrast Sensitivity, 242, 277 Control group, 18, 28, 42, 242, 285, 289 Controlled clinical trial, 14, 18, 21, 242 Convulsions, 242, 248, 285 Coronary Angiography, 71, 243 Coronary Circulation, 225, 243 Coronary Disease, 10, 41, 108, 109, 184, 243 Coronary Thrombosis, 243, 271, 274 Coronary Vessels, 243 Corpus, 243, 285 Corpus Luteum, 243, 285 Corrosion, 133, 243 Cortex, 229, 243, 290 Corticosteroids, 243, 256 Cortisol, 12, 14, 223, 243 Creatine, 87, 182, 243 Creatinine, 60, 182, 243, 302 Cross-Sectional Studies, 243, 251 Crystallization, 105, 121, 129, 131, 175, 243 Curative, 243, 276, 299 Cutaneous, 15, 232, 242, 243, 268 Cyclic, 124, 159, 243, 258, 276, 286, 294 Cyclosporine, 168, 243
Cysteine, 244, 250, 297 Cysteine Endopeptidases, 244, 250 Cytochrome, 116, 244 Cytokine, 29, 56, 244 Cytoplasm, 49, 140, 228, 237, 244, 252, 258, 292, 304 Cytoskeleton, 15, 244, 272 Cytotoxic, 235, 244, 294 D Dairy Products, 165, 244, 292 Data Collection, 5, 8, 26, 32, 244 Databases, Bibliographic, 201, 244 De novo, 54, 151, 244 Deamination, 244, 302 Death Certificates, 60, 244 Decidua, 79, 95, 244, 282 Decompensation, 7, 38, 244 Decubitus, 244, 295 Decubitus Ulcer, 244, 295 Degenerative, 245, 273, 291 Dehydroepiandrosterone, 29, 245 Deletion, 65, 228, 245 Delirium, 227, 245 Delivery of Health Care, 245, 258 Dementia, 227, 245 Dental Caries, 245, 254 Depolarization, 245, 294 Deprivation, 12, 49, 56, 245 Dermal, 166, 245 Dermatitis, 64, 143, 245 Dermatosis, 166, 245 DES, 225, 245 Desmin, 19, 245 Detergents, 245, 254, 295 Deuterium, 46, 246, 261 Dextrans, 113, 246 Diagnostic procedure, 111, 190, 246 Dialyzer, 246, 259 Diastole, 246 Diastolic, 33, 41, 50, 246, 261, 269 Diastolic blood pressure, 33, 41, 246 Diastolic pressure, 246, 261, 269 Diathermy, 246, 272 Diatrizoate, 114, 246 Dietary Fats, 117, 208, 246, 267 Dietetics, 48, 179, 184, 185, 246 Dietitian, 177, 246 Diffusion, 246, 247 Digestion, 181, 224, 231, 233, 246, 255, 264, 267, 268, 297, 303 Digestive system, 110, 124, 246, 255 Digestive tract, 246, 295, 305
312 Triglycerides
Dihydrotestosterone, 246, 290 Dihydroxy, 141, 223, 246, 292 Dilatation, 225, 246, 285, 303 Dilatation, Pathologic, 246, 303 Dilation, 233, 246, 303 Dilution, 40, 46, 125, 247, 282 Dimethyl, 127, 141, 157, 247 Diploid, 247, 282 Direct, iii, 13, 20, 27, 37, 46, 51, 54, 63, 127, 193, 247, 289, 290 Disinfectant, 247, 252 Dissection, 247, 301 Dissociation, 69, 223, 247 Dissociative Disorders, 247 Diuretic, 247, 296 Diuretics, Thiazide, 227, 247 Domesticated, 247, 258 Dopamine, 227, 247, 271, 281 Dormancy, 130, 247 Dosage Forms, 168, 247 Drive, ii, vi, 11, 81, 247, 266 Drug Interactions, 194, 247 Drug Tolerance, 248, 300 Duct, 236, 238, 248, 250, 252, 292 Duodenum, 231, 248, 255, 297 Dura mater, 248, 270, 278 Dyskinesia, 227, 248 Dyslipidemia, 6, 17, 19, 20, 27, 31, 40, 46, 51, 59, 66, 112, 248 Dyspareunia, 248, 252 Dysplasia, 205, 248 Dyspnea, 244, 248, 288 Dystonia, 227, 248 Dystrophy, 204, 248 E Echocardiography, 8, 248 Eclampsia, 248, 285 Ectopic, 13, 114, 248 Edema, 126, 242, 244, 248, 266, 275, 285, 302 Effector, 57, 221, 241, 248, 275 Efficacy, 4, 6, 9, 17, 20, 28, 32, 39, 44, 64, 107, 150, 248 Elasticity, 126, 229, 248 Elastin, 240, 248 Elastomers, 248, 284 Electrocardiogram, 72, 248 Electrocoagulation, 240, 248 Electrolysis, 226, 236, 248 Electrolyte, 223, 245, 249, 284, 295, 302 Electrons, 116, 227, 231, 236, 249, 264, 269, 278, 289
Electrophoresis, 43, 154, 249, 285 Elementary Particles, 249, 269, 276, 287 Embolus, 249, 263 Embryo, 34, 147, 236, 237, 249, 250, 255, 263, 271, 283, 305 Embryogenesis, 58, 249 Emollient, 126, 132, 134, 135, 249, 257, 272, 277 Empirical, 10, 127, 249 Emulsion, 73, 77, 91, 95, 113, 122, 123, 131, 159, 162, 168, 171, 172, 182, 249 Enamel, 245, 249, 265 Encapsulated, 129, 147, 158, 249 Encephalopathy, 249 Endarterectomy, 225, 249 Endocrine System, 249, 250, 275 Endocrinology, 14, 69, 73, 74, 79, 82, 83, 249 Endocytosis, 34, 250 Endoderm, 34, 250, 305 Endolymph, 181, 250 Endolymphatic Duct, 250 Endolymphatic Sac, 181, 250 Endometrial, 147, 250 Endometrium, 244, 250, 270 Endopeptidases, 15, 229, 244, 250, 271, 280, 287, 293 Endothelial cell, 15, 37, 109, 126, 250, 299 Endothelium, 29, 91, 250, 276, 283 Endothelium, Lymphatic, 250 Endothelium, Vascular, 250 Endothelium-derived, 250, 276 Endotoxic, 250, 267 Endotoxin, 66, 250, 302 End-stage renal, 184, 239, 250, 283 Energy balance, 44, 49, 56, 57, 250, 266 Energy Intake, 10, 56, 250 Enhancer, 13, 49, 170, 171, 250 Enteric-coated, 109, 250 Environmental Exposure, 250, 277 Environmental Health, 200, 202, 251 Enzymatic, 31, 121, 168, 170, 234, 235, 241, 245, 251, 252, 253, 260, 291 Epidemic, 58, 251, 296 Epidemiologic Studies, 108, 251 Epidemiological, 37, 251 Epidermal, 251, 270, 305 Epidermis, 251, 265 Epigastric, 251, 279 Epinephrine, 222, 247, 251, 276, 302 Epithelial, 18, 57, 244, 251, 279 Epithelial Cells, 57, 251
Index 313
Epithelium, 18, 152, 231, 242, 250, 251, 291 Erectile, 251 Erection, 181, 251 Ergot, 251, 292 Erythema, 242, 251 Erythrocytes, 225, 233, 251, 290 Erythromycin, 181, 251 Esophagus, 246, 252, 255, 281, 297 Essential Tremor, 204, 252 Esterification, 50, 56, 71, 121, 129, 133, 142, 164, 167, 252 Estradiol, 5, 252 Estrogen, 4, 20, 24, 46, 48, 55, 69, 181, 184, 252 Estrogen receptor, 20, 252 Estrogen Replacement Therapy, 24, 252 Ethanol, 158, 163, 167, 252, 253 Ether, 163, 252, 282 Ethnic Groups, 8, 252 Ethylenes, 155, 252 Eukaryotic Cells, 156, 252, 277, 302 Evacuation, 242, 252, 255, 266, 288 Excisional, 15, 252 Exhaustion, 226, 252 Exocrine, 252, 279 Exogenous, 43, 46, 57, 116, 130, 137, 139, 162, 170, 179, 222, 232, 235, 252, 287, 302 Exons, 144, 252 Extensor, 252, 287 Extracellular, 15, 54, 242, 250, 252, 253, 295 Extracellular Matrix, 15, 242, 252, 253 Extracellular Space, 252, 253 Extraction, 135, 253, 291 Extrapyramidal, 223, 227, 247, 253 Extravascular, 113, 253 Extremity, 60, 253 Eye Infections, 222, 253 F Faecal, 77, 253 Family Planning, 201, 253 Fatigue, 116, 253, 259 Fatty acids, 11, 12, 13, 15, 17, 20, 26, 30, 31, 39, 42, 43, 45, 47, 49, 50, 51, 54, 56, 58, 61, 64, 70, 77, 83, 84, 91, 93, 114, 115, 120, 121, 122, 123, 126, 128, 129, 131, 132, 133, 138, 143, 144, 145, 146, 147, 151, 152, 153, 157, 158, 161, 163, 164, 165, 167, 170, 172, 175, 179, 180, 221, 223, 235, 253, 257, 267, 277, 286, 295 Fatty Liver, 180, 253 Feces, 242, 253, 297 Fermentation, 130, 253
Ferrets, 171, 253 Fertilizers, 164, 253 Fetus, 253, 282, 285, 303 Fibrin, 232, 253, 280, 282, 299, 300 Fibrinogen, 5, 6, 9, 21, 55, 60, 73, 253, 282, 299 Fibrinolysis, 55, 253 Fibroblasts, 13, 64, 114, 253 Fibrosis, 70, 93, 97, 205, 253, 288, 292 Filarioidea, 254, 265 Filler, 84, 254 Fish Oils, 121, 138, 164, 254 Flatus, 254, 255 Fluorine, 118, 254 Flush, 149, 254 Foam Cells, 16, 254 Fold, 7, 30, 36, 52, 174, 254 Forearm, 232, 254, 289 Frontal Lobe, 226, 237, 254 Fructans, 93, 254 Fructose, 254, 256 Fungi, 125, 227, 229, 239, 253, 254, 258, 271, 272, 305 Fungus, 130, 251, 254, 292 G Gallbladder, 182, 221, 231, 238, 246, 254, 255 Gallstones, 97, 182, 231, 238, 254, 260 Ganglia, 221, 231, 254, 275, 280, 298 Ganglionic Blockers, 227, 254 Gas, 36, 224, 235, 246, 252, 254, 255, 261, 265, 276, 304 Gastric, 173, 179, 230, 235, 247, 255, 260 Gastric Emptying, 173, 255 Gastrin, 255, 260 Gastroenterology, 18, 255 Gastrointestinal, 116, 117, 168, 233, 246, 251, 252, 255, 266, 293, 295, 297, 302 Gastrointestinal tract, 116, 252, 255, 266, 293, 302 Gastroparesis, 181, 255 Gelatin, 158, 255, 298 Gels, 149, 255 Gemfibrozil, 6, 47, 69, 82, 83, 100, 190, 194, 255 Gene Expression, 11, 14, 24, 47, 49, 52, 57, 59, 205, 255, 296 Genetic Code, 255, 276 Genetic Engineering, 232, 239, 255 Genetics, 16, 36, 38, 77, 255 Genotype, 31, 38, 47, 55, 65, 255, 281 Germ Cells, 255, 278, 296, 298, 306
314 Triglycerides
Germ Layers, 250, 255 Gestation, 255, 280, 282, 285 Gestational, 26, 255 Gestational Age, 26, 255 Gibberellin, 130, 256 Ginseng, 84, 102, 256 Gland, 222, 256, 261, 268, 279, 286, 293, 297, 299 Glucocorticoid, 13, 256 Gluconeogenesis, 35, 38, 256 Glucose Intolerance, 246, 256 Glucose tolerance, 6, 12, 36, 46, 67, 72, 74, 139, 182, 183, 256 Glucose Tolerance Test, 36, 46, 139, 182, 183, 256 Glucuronic Acid, 256, 259 Glutamic Acid, 256, 286 Glutamine, 123, 256 Glutathione Peroxidase, 256, 293 Glyburide, 168, 256 Glycerol, 36, 38, 40, 45, 70, 71, 121, 124, 160, 161, 164, 167, 257, 281, 282 Glycerol Kinase, 38, 257 Glycerophospholipids, 257, 281, 282 Glycogen, 26, 43, 238, 257 Glycols, 130, 257 Glycolysis, 26, 257 Glycoprotein, 56, 147, 253, 257, 299, 302 Glycosidic, 237, 257, 277 Glycosylation, 15, 257 Goats, 244, 257 Gonad, 139, 257 Gonadal, 14, 257, 297 Gonadotropin, 146, 257 Gout, 97, 174, 257 Governing Board, 257, 285 Grade, 48, 164, 257 Graft, 38, 114, 257, 260 Graft Rejection, 38, 257 Grafting, 258, 262 Gram-negative, 238, 250, 258 Granulocytes, 258, 294, 305 Grasses, 130, 239, 258 Growth factors, 114, 258 Growth Substances, 130, 258 Guanylate Cyclase, 258, 276 Guinea Pigs, 39, 94, 171, 258 H Haloperidol, 80, 258 Haploid, 258, 282 Haplotypes, 22, 23, 46, 258 Haptens, 223, 258
Headache, 258, 263 Health Care Costs, 10, 117, 258 Health Education, 28, 48, 258 Health Expenditures, 258 Health Status, 183, 259, 305 Heart attack, 3, 82, 117, 149, 151, 169, 174, 235, 259 Heart failure, 116, 225, 259, 288 Heartbeat, 259, 269, 297 Hematology, 182, 259 Heme, 231, 244, 259 Hemodialysis, 73, 84, 185, 234, 246, 259, 266 Hemoglobin, 16, 60, 225, 251, 259, 266 Hemoglobinuria, 204, 259 Hemorrhage, 248, 258, 259, 297 Heparin, 50, 72, 259 Hepatic, 13, 19, 24, 36, 39, 50, 51, 54, 58, 70, 74, 113, 223, 245, 256, 259, 284, 294 Hepatobiliary, 180, 259 Hepatocyte, 9, 71, 94, 259 Hereditary, 257, 259, 273, 291 Heredity, 181, 255, 259 Heritability, 62, 259 Heterodimer, 147, 259 Heterogeneity, 223, 259 Heterotrophic, 254, 259 Heterozygotes, 52, 259 High blood cholesterol, 145, 260 High-density lipoproteins, 66, 69, 260 Hirsutism, 260, 261 Histamine, 225, 227, 260 Histology, 19, 260, 279 Homeostasis, 7, 8, 13, 16, 40, 49, 61, 68, 108, 147, 166, 233, 260, 295 Homogeneous, 22, 123, 229, 260, 281 Homologous, 224, 259, 260, 298 Homozygotes, 52, 260 Hormonal, 20, 43, 46, 181, 230, 252, 260, 280 Hormone Replacement Therapy, 46, 48, 53, 55, 260 Hormone therapy, 46, 260 Hospital Records, 60, 260 Host, 54, 154, 230, 260, 262, 266, 292, 303, 304 Humoral, 14, 257, 260 Humour, 260, 261 Hybrid, 14, 261, 292 Hydrogen, 142, 221, 231, 235, 246, 256, 261, 267, 272, 276, 278, 287 Hydrogen Peroxide, 256, 261, 267
Index 315
Hydrolysis, 20, 24, 56, 115, 121, 124, 133, 143, 229, 232, 237, 261, 267, 280, 281, 284, 287, 292 Hydrophilic, 114, 122, 167, 168, 172, 246, 261 Hydrophobic, 9, 56, 122, 134, 158, 159, 168, 246, 257, 261, 267 Hydroxylation, 109, 261 Hydroxylysine, 240, 261 Hydroxyproline, 240, 261 Hygienic, 261, 295 Hyperandrogenism, 50, 261 Hypercholesterolemia, 20, 42, 65, 95, 97, 107, 109, 146, 153, 248, 261 Hyperglycemia, 6, 11, 15, 39, 50, 54, 109, 139, 149, 153, 261 Hyperlipidemia, 15, 33, 38, 41, 42, 47, 66, 67, 76, 83, 108, 109, 115, 143, 146, 149, 153, 248, 261 Hyperlipoproteinemia, 108, 261, 267 Hypersensitivity, 14, 261, 266 Hyperuricemia, 257, 261 Hypobetalipoproteinemia, 36, 70, 262 Hypoglycemic, 141, 262 Hypotension, 227, 242, 254, 262 Hypothalamic, 14, 28, 262, 296 Hypothalamus, 230, 262 Hysterosalpingography, 221, 262 I Id, 74, 85, 96, 209, 214, 216, 262 Ileum, 262, 305 Imaging procedures, 262, 300 Immaturity, 25, 262 Immune response, 7, 37, 222, 227, 230, 257, 258, 262, 269, 297, 303, 304 Immune system, 226, 232, 262, 266, 269, 273, 274, 303, 305 Immunity, 54, 262, 277 Immunization, 262, 285 Immunodeficiency, 73, 204, 262 Immunogenic, 262, 267 Immunoglobulin, 226, 252, 262, 273 Immunologic, 238, 256, 262 Immunology, 222, 223, 262 Immunosuppressive, 38, 256, 262 Impairment, 229, 245, 248, 253, 262, 270, 288 Implantation, 114, 147, 242, 262 Impotence, 181, 251, 262 Impregnation, 125, 262 In vitro, 8, 16, 19, 24, 27, 34, 39, 56, 57, 66, 73, 126, 168, 262, 299
In vivo, 8, 9, 10, 14, 16, 19, 21, 27, 36, 39, 42, 51, 56, 57, 61, 66, 73, 76, 144, 168, 259, 262, 299 Incision, 263, 264 Incontinence, 263, 278 Indicative, 126, 137, 178, 263, 279, 303 Indinavir, 27, 74, 263 Induction, 13, 18, 51, 57, 152, 225, 227, 246, 254, 263, 289, 294 Infantile, 263, 267 Infarction, 59, 237, 263 Infection, 14, 37, 181, 229, 230, 232, 238, 245, 253, 262, 263, 266, 268, 269, 275, 279, 297, 305 Inflammatory bowel disease, 182, 263 Influenza, 174, 263 Infusion, 40, 47, 55, 113, 233, 263 Ingestion, 20, 30, 116, 117, 152, 162, 165, 254, 256, 263, 271, 283 Initiation, 13, 35, 55, 57, 263, 301 Initiator, 148, 263 Inlay, 263, 291 Inorganic, 125, 263, 297 Inositol, 117, 263 Insight, 17, 38, 263 Insulin-dependent diabetes mellitus, 12, 45, 264 Insulin-like, 11, 18, 264 Interindividual, 24, 264 Interleukin-1, 26, 133, 264 Interleukin-2, 264 Intermittent, 264, 268, 280 Internal Medicine, 29, 32, 36, 50, 55, 56, 77, 84, 249, 255, 259, 264 Intestinal, 58, 94, 116, 117, 137, 152, 156, 182, 235, 256, 264, 269, 306 Intestine, 34, 58, 147, 152, 231, 233, 240, 264, 266 Intracellular, 15, 16, 31, 36, 47, 51, 58, 62, 63, 71, 149, 234, 263, 264, 276, 284, 286, 293, 294 Intramuscular, 20, 74, 264, 279 Intraocular, 264, 300 Intraocular pressure, 264, 300 Intravenous, 35, 46, 73, 74, 79, 93, 233, 263, 264, 279 Intrinsic, 223, 231, 264 Invasive, 113, 262, 264, 269 Involuntary, 231, 238, 252, 264, 274, 296 Iodine, 182, 264 Ion Channels, 54, 264, 276
316 Triglycerides
Ions, 132, 231, 247, 249, 261, 264, 271, 272, 287, 292 Irritable Bowel Syndrome, 265, 278 Ischemia, 229, 244, 265 Ischemic stroke, 8, 265 Isocyanates, 148, 265 Isoflavones, 53, 95, 101, 265 Itraconazole, 168, 265 Ivermectin, 124, 265 J Joint, 23, 265, 298 K Kb, 200, 265 Keratin, 170, 265, 293 Keratolytic, 245, 265, 283 Keto, 265, 300 Ketone Bodies, 30, 52, 221, 265 Ketosis, 139, 265 Kidney Disease, 110, 181, 182, 200, 205, 223, 266 Kidney Failure, 250, 266 Kidney stone, 266, 302 Kinetic, 33, 36, 38, 40, 50, 92, 266 L Labile, 241, 266 Labyrinth, 250, 266, 278, 304 Large Intestine, 240, 246, 264, 266, 290, 295 Latent, 122, 266, 285 Laxative, 165, 223, 266, 271, 272, 296 Lens, 149, 235, 266, 305 Leprosy, 141, 266 Leptin, 28, 51, 52, 63, 78, 80, 152, 266 Lesion, 11, 27, 232, 266, 268, 298 Leucine, 47, 266 Leukemia, 204, 266 Leukocytes, 233, 238, 258, 266, 302 Leukotrienes, 228, 266, 268 Libido, 14, 225, 266 Library Services, 214, 266 Life cycle, 14, 254, 267 Ligament, 267, 286 Ligands, 9, 63, 75, 236, 267 Linkage, 22, 24, 25, 36, 237, 267, 282 Linkage Disequilibrium, 25, 267 Lipaemia, 79, 83, 267 Lipase, 11, 24, 30, 39, 45, 56, 62, 63, 70, 74, 101, 121, 136, 267, 277 Lipid A, 3, 7, 8, 9, 17, 25, 30, 39, 46, 49, 50, 52, 112, 144, 147, 267, 277 Lipid Peroxidation, 31, 267, 278 Lipodystrophy, 41, 47, 49, 267
Lipolysis, 8, 19, 30, 40, 45, 50, 63, 73, 75, 136, 137, 179, 267 Lipophilic, 113, 147, 167, 168, 267 Lipopolysaccharide, 37, 258, 267 Lipoprotein Lipase, 7, 11, 31, 39, 42, 57, 63, 68, 74, 75, 76, 169, 267 Lipoprotein(a), 6, 32, 33, 40, 47, 82, 92, 108, 267 Lipoxygenase, 10, 228, 266, 267, 268 Lipoxygenase Inhibitors, 11, 268 Lithium, 227, 268 Lobe, 226, 237, 268 Localization, 19, 144, 268 Localized, 76, 245, 249, 260, 263, 267, 268, 282 Locomotion, 268, 282 Long-Term Care, 38, 268 Loop, 28, 268 Lovastatin, 87, 268, 294 Low-density lipoprotein, 46, 53, 64, 73, 108, 169, 248, 267, 268 Lubricants, 120, 158, 268, 281 Luciferase, 24, 268 Lumen, 140, 250, 268 Lupus, 7, 9, 268, 298 Lymph, 230, 239, 250, 261, 268, 269 Lymph node, 230, 268, 269 Lymphatic, 115, 129, 143, 239, 250, 263, 268, 269, 295, 296, 299 Lymphatic system, 115, 129, 143, 239, 268, 269, 295, 296, 299 Lymphocyte, 227, 269, 270 Lymphoid, 226, 243, 269 Lymphoma, 204, 269 Lysine, 101, 261, 269 M Macrophage, 11, 16, 27, 264, 269 Magnetic Resonance Imaging, 48, 113, 269 Magnetic Resonance Spectroscopy, 36, 269 Major Histocompatibility Complex, 258, 269 Malabsorption, 115, 143, 204, 269 Malignant, 204, 227, 229, 269, 274 Malnutrition, 140, 185, 223, 229, 269, 273 Mammary, 267, 269 Mammogram, 234, 269, 271 Manic, 227, 268, 269, 288 Mannans, 254, 269 Mean blood pressure, 183, 269 Meat, 246, 269, 292 Meat Products, 246, 269
Index 317
Mechanical ventilation, 25, 234, 269 Medial, 37, 229, 270, 292 Mediate, 13, 21, 27, 33, 34, 58, 236, 247, 270 Mediator, 15, 78, 264, 270, 293 Medical Records, 60, 260, 270 Medicament, 270, 298 MEDLINE, 201, 203, 205, 270 Medroxyprogesterone, 69, 270 Medroxyprogesterone Acetate, 69, 270 Meglumine, 246, 270 Melanin, 270, 281, 302 Melanocytes, 270 Melanoma, 204, 270 Memory, 226, 245, 270 Meninges, 237, 248, 270 Meningitis, 174, 181, 265, 270 Menopause, 4, 24, 46, 53, 97, 270, 284 Menstrual Cycle, 270, 286 Menstruation, 244, 270, 285 Mental Disorders, 110, 270, 285, 288 Mental Health, iv, 4, 110, 200, 202, 270, 285, 288 Mental Processes, 247, 271, 287 Mentors, 21, 271 Mercaptopurine, 182, 271 Mesoderm, 271, 305 Mesolimbic, 227, 271 Meta-Analysis, 32, 271 Metabolic disorder, 12, 38, 56, 153, 257, 271 Metabolite, 13, 232, 247, 268, 271, 285 Metalloendopeptidases, 250, 271 Metastasis, 236, 271 Methanol, 163, 167, 271 Methionine, 247, 271, 298 Methylcellulose, 114, 271 Metoclopramide, 181, 271 MI, 12, 28, 113, 168, 183, 219, 271 Micelles, 163, 271 Microbe, 271, 300 Microbiology, 221, 230, 271 Microcalcifications, 234, 271 Microfilaments, 16, 271 Microorganism, 240, 271, 305 Micro-organism, 125, 245, 272 Microscopy, 19, 30, 231, 272 Microsomal, 47, 62, 71, 75, 94, 140, 142, 154, 204, 272 Microtubules, 16, 272 Microwaves, 119, 272, 289 Midaxillary line, 272, 305 Migration, 113, 272
Millimeter, 272, 305 Mineral Oil, 132, 135, 272 Mitochondria, 30, 33, 116, 137, 221, 272, 277 Mitochondrial Swelling, 272, 274 Mitosis, 228, 272, 296 Mobilization, 31, 35, 272 Modeling, 10, 36, 43, 46, 47, 50, 272 Modification, 24, 48, 73, 112, 153, 255, 272, 288 Modulator, 23, 63, 272 Molecular Structure, 272, 294, 301 Monitor, 243, 273, 276 Monoclonal, 34, 273 Monoclonal antibodies, 34, 273 Monocyte, 11, 16, 273 Mononuclear, 29, 273, 302 Monophosphate, 124, 273 Monotherapy, 40, 273 Monounsaturated fat, 33, 51, 151, 273 Morphine, 273, 274 Morphological, 8, 223, 249, 254, 270, 273 Morphology, 30, 259, 273 Motion Sickness, 273, 274 Movement Disorders, 227, 273, 299 Mucosa, 268, 273, 306 Multiple sclerosis, 273, 277 Muscle Contraction, 273, 292 Muscle Fibers, 273 Muscular Atrophy, 204, 273 Muscular Dystrophies, 248, 273 Musculoskeletal System, 174, 273 Mutagenesis, 144, 273 Mutagens, 274 Myalgia, 263, 274 Myocardial infarction, 12, 59, 60, 152, 169, 243, 271, 274 Myocardial Ischemia, 225, 243, 274 Myocardium, 17, 33, 43, 225, 271, 274 Myopathy, 137, 274 Myotonic Dystrophy, 204, 274 N N-acetyl, 15, 274 N-acetyl cysteine, 15, 274 Naive, 35, 274 Narcosis, 274 Narcotic, 181, 273, 274 Nasal Mucosa, 263, 274 Nausea, 113, 227, 247, 255, 265, 274, 302 NCI, 1, 110, 199, 239, 274 Necrosis, 70, 228, 233, 237, 263, 271, 274, 291
318 Triglycerides
Neoplasia, 204, 274, 275 Neoplasm, 274, 275, 279 Neoplastic, 147, 269, 275 Nephropathy, 37, 266, 275 Nephrosis, 275 Nephrotic, 7, 126, 275 Nephrotic Syndrome, 7, 126, 275 Nerve, 15, 149, 222, 223, 229, 230, 255, 270, 273, 275, 277, 284, 293, 297, 301, 303 Nerve Fibers, 15, 275 Networks, 22, 275 Neural, 22, 222, 254, 260, 275, 280, 291 Neuritis, 275, 277 Neuroendocrine, 173, 275 Neuroleptic, 223, 227, 275 Neurologic, 275, 301 Neuromuscular, 221, 275, 302 Neuromuscular Junction, 221, 275 Neuronal, 54, 274, 275, 280 Neurons, 254, 275, 298 Neuropathy, 181, 223, 275 Neuropeptide, 15, 275 Neurotoxic, 275 Neurotoxins, 54, 275 Neurotransmitters, 273, 275, 295 Neutrons, 224, 276, 289 Niacin, 39, 82, 86, 92, 107, 149, 276, 301 Nitric Oxide, 21, 276 Nitrogen, 26, 115, 123, 143, 170, 182, 224, 225, 256, 276, 301 Norepinephrine, 222, 247, 276 Nuclear, 13, 19, 231, 249, 252, 274, 276, 289 Nuclei, 14, 224, 226, 249, 252, 255, 269, 272, 276, 277, 287 Nucleic acid, 45, 124, 140, 154, 156, 160, 230, 255, 274, 276 Nucleus, 226, 228, 231, 238, 243, 244, 246, 249, 252, 273, 276, 287, 295, 299 Nutritional Status, 47, 276 O Observational study, 73, 276 Occult, 41, 277 Odds Ratio, 9, 277, 290 Odour, 228, 277, 302 Ointments, 247, 277, 279, 295 Oleic Acids, 125, 277 Oligosaccharides, 100, 277 Omega-3 fatty acid, 17, 76, 94, 277 Oncogene, 204, 277 Opacity, 245, 277 Opsin, 277, 291 Optic disc, 277
Optic Nerve, 277, 278, 291 Optic Neuritis, 174, 277 Orbital, 240, 277 Organelles, 116, 137, 237, 244, 270, 277, 283 Organoleptic, 144, 277 Orlistat, 83, 277 Orthostatic, 227, 278 Osmolality, 182, 278 Osmoles, 278 Osmosis, 278 Osmotic, 149, 223, 272, 278, 294 Ossicles, 278 Osteoporosis, 233, 252, 278 Otosclerosis, 181, 278 Ovaries, 261, 278, 294 Ovary, 50, 243, 252, 257, 261, 278, 283 Overexpress, 40, 59, 278 Overweight, 66, 75, 82, 85, 92, 174, 191, 278 Ovulation, 226, 278 Ovum, 243, 244, 255, 267, 278, 286, 305 Oxidative Stress, 11, 21, 30, 45, 278 Oxygen Consumption, 30, 105, 278, 291 P Pachymeningitis, 270, 278 Palliative, 279, 299 Palmitic Acid, 115, 143, 167, 279 Pancreas, 78, 221, 232, 246, 255, 264, 267, 279, 302 Pancreatic, 6, 58, 97, 136, 173, 204, 235, 279 Pancreatic cancer, 204, 279 Pancreatitis, 47, 65, 72, 97, 182, 279 Papilloma, 242, 279 Paraffin, 121, 155, 175, 279 Parasite, 265, 279 Parenteral, 77, 93, 138, 182, 250, 279 Parenteral Nutrition, 93, 182, 279 Parkinsonism, 227, 279 Paroxysmal, 204, 225, 279 Particle, 6, 9, 22, 34, 53, 59, 60, 66, 82, 113, 114, 159, 172, 279, 301 Pathogenesis, 30, 33, 37, 38, 45, 56, 279 Pathologic, 43, 228, 232, 243, 261, 279, 287, 290 Pathologic Processes, 228, 279 Pathophysiology, 6, 9, 180, 279 Pelvic, 279, 286 Penicillin, 226, 279 Peptide, 18, 51, 136, 250, 265, 266, 279, 284, 286, 287, 296 Peptide Hydrolases, 250, 279
Index 319
Perfusion, 280, 299 Perianal, 242, 280 Pericardium, 280, 298 Pericytes, 37, 280 Perinatal, 30, 280 Periodicity, 280 Peripheral blood, 29, 224, 280 Peripheral Nerves, 266, 280 Peripheral Nervous System, 280, 297 Peripheral Vascular Disease, 60, 98, 127, 144, 280 Peritoneal, 27, 177, 184, 185, 280 Peritoneal Cavity, 280 Peritoneal Dialysis, 177, 184, 185, 280 Peritoneum, 280 Peritonitis, 184, 280 Pesticides, 232, 280 Petrolatum, 249, 281 Petroleum, 120, 134, 155, 163, 272, 279, 281 Pharmaceutical Preparations, 130, 237, 252, 255, 281, 286 Pharmaceutical Solutions, 247, 281 Pharmacokinetic, 281 Pharmacologic, 281, 299, 300 Pharmacotherapy, 39, 53, 71, 94, 281 Pharynx, 263, 281, 303 Phenolphthalein, 249, 281 Phenotype, 7, 19, 34, 36, 38, 39, 56, 65, 281 Phenylalanine, 229, 281, 302 Phospholipases, 281, 294 Phosphorus, 177, 182, 184, 185, 234, 281 Phosphorylated, 240, 281 Phosphorylates, 38, 281 Phosphorylation, 19, 39, 56, 281 Photocoagulation, 240, 281 Physical Examination, 183, 256, 260, 281 Physical Fitness, 116, 282 Physiologic, 50, 223, 232, 270, 282, 286, 289, 290 Physiology, 25, 27, 33, 43, 56, 68, 74, 78, 185, 250, 255, 259, 282, 304 Pigment, 231, 270, 282, 291 Pilot study, 28, 44, 282 Placenta, 252, 282, 285 Plant sterols, 162, 282 Plaque, 109, 117, 149, 225, 229, 282 Plasma, 5, 6, 8, 10, 11, 16, 17, 20, 23, 24, 25, 26, 29, 30, 31, 33, 34, 36, 46, 47, 51, 52, 53, 54, 56, 58, 59, 61, 63, 65, 66, 67, 68, 70, 73, 76, 77, 79, 83, 84, 92, 93, 94, 95, 105, 108, 112, 126, 144, 145, 146, 149, 150, 152, 153, 162, 169, 170, 183, 223,
226, 237, 238, 246, 250, 253, 255, 256, 259, 261, 266, 267, 282, 287, 290, 293, 294, 300, 305 Plasma cells, 226, 282 Plasma protein, 223, 250, 282, 287, 294 Plasma Volume, 246, 282 Plasmalogens, 38, 282 Plasmin, 282, 283, 300, 303 Plasminogen, 40, 55, 84, 282, 283, 300, 303 Plasminogen Activators, 282, 283 Plasticity, 161, 283 Plasticizers, 161, 283 Plastids, 277, 283 Platelet Activation, 283, 294 Platelet Aggregation, 224, 225, 276, 283, 299 Platelets, 105, 228, 276, 283, 293, 299 Platinum, 268, 283 Platyhelminths, 265, 283 Pleated, 265, 283 Podophyllotoxin, 130, 283 Poisoning, 245, 251, 274, 283 Pollen, 283, 288 Poly U, 115, 140, 283 Polycystic, 50, 205, 261, 283 Polyesters, 118, 165, 283 Polyethylene, 155, 158, 283, 284 Polymerase, 228, 284, 291 Polymers, 118, 148, 155, 159, 161, 246, 283, 284, 287, 294, 297 Polymorphic, 24, 284 Polymorphism, 62, 77, 79, 284 Polyp, 18, 44, 284 Polypeptide, 11, 147, 154, 156, 160, 173, 224, 240, 253, 282, 284, 287, 306 Polyposis, 240, 284 Polysaccharide, 227, 237, 284 Polyunsaturated fat, 10, 42, 45, 67, 92, 115, 121, 133, 138, 143, 145, 164, 284, 299 Polyurethanes, 148, 284 Polyuria, 139, 284 Portal System, 115, 143, 284 Posterior, 225, 229, 237, 238, 272, 277, 279, 284 Postmenopausal, 4, 46, 48, 53, 252, 278, 284 Postnatal, 284, 297 Postprandial, 16, 22, 45, 65, 68, 69, 76, 79, 93, 179, 284 Postsynaptic, 284, 294 Potassium, 178, 184, 185, 224, 247, 284, 295 Potentiates, 264, 284
320 Triglycerides
Potentiation, 285, 294 Practice Guidelines, 202, 285 Prealbumin, 26, 285 Precancerous, 238, 285 Precipitation, 124, 168, 285 Precursor, 226, 228, 231, 247, 248, 251, 276, 281, 282, 285, 287, 301, 302 Predisposition, 9, 285 Preeclampsia, 30, 79, 126, 127, 285 Pre-Eclampsia, 78, 285 Pregnancy Tests, 256, 285 Premenstrual, 181, 285 Prenatal, 249, 285 Prevalence, 6, 7, 24, 25, 31, 48, 50, 53, 60, 67, 182, 277, 285 Primary endpoint, 21, 48, 285 Primary Prevention, 23, 179, 285 Probe, 58, 285 Prodrug, 147, 285 Progesterone, 4, 168, 285, 297 Progression, 6, 11, 19, 41, 48, 50, 226, 286 Progressive, 229, 236, 239, 245, 248, 252, 258, 273, 274, 283, 286, 288 Proline, 240, 261, 286 Promoter, 24, 31, 38, 79, 153, 286 Prone, 168, 286 Prophylaxis, 228, 286, 291, 303 Propofol, 73, 95, 286 Proportional, 166, 278, 286 Propylene Glycol, 124, 286 Prospective study, 7, 32, 35, 286 Prostaglandin, 18, 19, 44, 225, 286, 299 Prostaglandins A, 286 Prostate, 204, 232, 286, 302 Protease, 27, 35, 47, 190, 240, 263, 286, 287, 292, 300 Protease Inhibitors, 27, 47, 287 Protective Agents, 234, 287 Protein Binding, 287, 300 Protein C, 53, 54, 92, 115, 143, 223, 224, 228, 230, 265, 267, 287, 302 Protein Conformation, 224, 265, 287 Protein S, 57, 154, 179, 205, 228, 232, 251, 255, 287, 292, 299 Proteins, 13, 14, 30, 34, 43, 49, 56, 58, 61, 123, 137, 139, 146, 147, 157, 183, 224, 227, 228, 229, 237, 238, 240, 241, 251, 257, 259, 264, 265, 272, 276, 279, 282, 284, 287, 292, 294, 300, 301, 304 Proteinuria, 275, 285, 287 Proteolytic, 241, 253, 282, 283, 287, 300, 303
Prothrombin, 9, 55, 66, 92, 287, 299 Protocol, 36, 42, 45, 287 Protons, 36, 224, 261, 269, 287, 289 Protozoa, 265, 271, 287 Psoriasis, 98, 116, 130, 147, 287, 291 Psychic, 266, 287, 293 Psychology, 247, 287 Psychosis, 227, 255, 288 Psyllium, 102, 116, 117, 288 Puberty, 5, 288 Public Health, 5, 17, 32, 33, 51, 53, 59, 60, 179, 180, 202, 288 Public Policy, 201, 288 Publishing, 3, 62, 288 Pulmonary, 84, 232, 234, 242, 266, 288, 298, 304 Pulmonary Artery, 232, 288, 304 Pulmonary Fibrosis, 84, 288 Pulse, 21, 48, 273, 288 Pupil, 246, 277, 288 Purgative, 266, 288 Purifying, 161, 245, 288 Q Quality of Life, 18, 29, 53, 288 Quercetin, 94, 288 Quinones, 288 R Race, 8, 32, 50, 272, 288 Radial Artery, 48, 289 Radiation, 148, 225, 249, 251, 289, 305 Radio Waves, 246, 272, 289 Radioactive, 42, 50, 55, 113, 182, 261, 262, 273, 276, 289 Radioactivity, 43, 289 Radiography, 225, 242, 243, 256, 262, 289, 303 Radioisotope, 289, 300 Radiolabeled, 34, 289 Radius, 289 Random Allocation, 289 Randomization, 14, 21, 53, 289 Randomized, 4, 6, 12, 15, 17, 18, 21, 22, 28, 29, 33, 39, 41, 42, 44, 48, 53, 64, 74, 109, 248, 289 Randomized clinical trial, 53, 74, 289 Rape, 94, 175, 289 Reaction Time, 122, 289 Reagent, 136, 137, 268, 289 Recombinant, 34, 289, 303 Rectal, 18, 44, 290 Rectum, 228, 233, 240, 246, 254, 255, 263, 266, 286, 290, 298
Index 321
Recur, 280, 290 Recurrence, 8, 280, 290 Red blood cells, 182, 251, 290, 292 Red Nucleus, 229, 290 Reductase, 3, 16, 69, 149, 169, 184, 223, 268, 290, 294 Refer, 1, 171, 234, 241, 254, 268, 274, 275, 276, 288, 290, 304 Refraction, 290, 296 Regeneration, 57, 290 Regimen, 4, 184, 248, 281, 290 Relative risk, 55, 290 Remission, 290 Renin, 69, 225, 226, 235, 290 Renin-Angiotensin System, 225, 235, 290 Research Design, 21, 290 Resorption, 233, 290 Respiration, 228, 235, 238, 273, 290 Respirator, 269, 291, 304 Respiratory distress syndrome, 234, 291 Restoration, 15, 291, 305 Retina, 132, 149, 238, 242, 266, 277, 291, 292, 305 Retinal, 37, 60, 277, 291, 294 Retinal Detachment, 291, 294 Retinoblastoma, 204, 291 Retinoids, 291, 305 Retinol, 83, 291 Retinopathy, 37, 223, 281, 291 Retrobulbar, 277, 291 Reverse Transcriptase Inhibitors, 74, 291 Rhabdomyolysis, 63, 291 Rheology, 134, 291 Rheumatism, 70, 291, 292 Rheumatoid, 74, 292 Ribose, 124, 222, 283, 292 Ribosome, 292, 301 Rigidity, 279, 282, 292 Ritonavir, 27, 47, 292 Rod, 230, 239, 292 Rutin, 288, 292 Ryanodine, 19, 292 Rye, 130, 239, 251, 292 S Sagittal, 49, 292 Salivary, 246, 279, 292 Salivary glands, 246, 292 Saponification, 135, 292 Saponins, 292, 297 Sarcoplasmic Reticulum, 19, 292 Saturated fat, 32, 42, 47, 51, 137, 138, 151, 164, 172, 184, 191, 279, 292
Schizophrenia, 80, 292 Scleroproteins, 265, 292 Sclerosis, 204, 229, 273, 292 Screening, 61, 143, 144, 151, 157, 184, 239, 293, 302 Sebaceous, 293 Sebaceous gland, 293 Sebum, 166, 293 Secretion, 8, 9, 21, 39, 47, 50, 51, 58, 62, 71, 78, 94, 140, 142, 173, 179, 260, 261, 264, 293, 303 Secretory, 51, 56, 58, 293 Sedentary, 18, 20, 115, 117, 293 Sediment, 293, 302 Seizures, 245, 279, 293 Selenium, 117, 293 Semen, 286, 293 Semisynthetic, 265, 293 Senescence, 130, 293 Sensor, 92, 293 Sepsis, 56, 293 Septic, 77, 229, 293 Sequence Analysis, 23, 293 Sequencing, 36, 46, 293 Serine, 250, 293, 300 Serine Endopeptidases, 250, 293 Serotonin, 227, 281, 293, 301 Serous, 250, 294 Serum Albumin, 285, 294 Sex Characteristics, 222, 225, 288, 294, 298 Sex Determination, 205, 294 Sharks, 294 Shock, 98, 294, 301 Side effect, 61, 149, 150, 165, 193, 222, 223, 227, 232, 261, 294, 300 Signal Transduction, 11, 39, 263, 294 Silicone Oils, 135, 159, 294 Siloxanes, 294 Simvastatin, 64, 69, 87, 294 Skeleton, 221, 233, 265, 286, 294 Skin Care, 127, 135, 157, 295 Sleep apnea, 52, 295 Small intestine, 137, 147, 152, 163, 173, 231, 239, 248, 260, 262, 264, 295 Smooth muscle, 11, 19, 225, 234, 254, 260, 273, 280, 290, 295, 296, 297 Soaps, 254, 295 Social Environment, 288, 295 Social Support, 12, 44, 295 Socioeconomic Factors, 10, 295 Sodium Dodecyl Sulfate, 154, 295 Soft tissue, 233, 294, 295
322 Triglycerides
Solid tumor, 225, 295 Solitary Nucleus, 230, 295 Somatic, 222, 249, 260, 272, 280, 295, 303 Somatotropin, 296 Sorbitol, 122, 149, 223, 270, 296 Soybean Oil, 66, 70, 92, 93, 153, 284, 296, 305 Spasm, 228, 296 Specialist, 209, 246, 296 Species, 58, 130, 224, 235, 238, 245, 247, 251, 258, 261, 272, 273, 279, 288, 294, 296, 297, 301, 304, 305 Specificity, 147, 151, 223, 228, 250, 296, 300 Spectrometer, 36, 296 Spectrum, 14, 272, 289, 296 Sperm, 156, 225, 239, 283, 296, 302 Sperm Maturation, 156, 296 Spermatozoa, 293, 296 Sphincter, 165, 296 Spinal cord, 233, 237, 238, 248, 270, 275, 278, 280, 296, 298 Spleen, 16, 114, 269, 296 Sporadic, 291, 296 Stabilizer, 159, 296 Steatosis, 70, 92, 180, 253, 296 Steel, 239, 296 Stem Cells, 13, 114, 297 Sterility, 141, 297 Steroid, 5, 13, 14, 231, 243, 260, 292, 294, 297 Stimulants, 256, 297 Stimulus, 247, 264, 289, 297, 299 Stool, 18, 263, 265, 266, 297 Stress, 15, 21, 45, 55, 68, 116, 122, 132, 135, 181, 230, 236, 243, 265, 274, 278, 285, 297 Stroke, 8, 60, 75, 110, 118, 126, 127, 149, 169, 200, 235, 265, 297 Stupor, 274, 297 Styrene, 159, 161, 297 Subacute, 263, 297 Subclinical, 12, 21, 48, 50, 108, 182, 263, 293, 297 Subcutaneous, 173, 222, 248, 267, 279, 297, 305 Subspecies, 296, 297 Substance P, 125, 251, 271, 293, 297 Substrate, 13, 36, 38, 43, 125, 167, 268, 297 Sudden death, 169, 297 Sulfates, 295, 297 Sulfur, 170, 271, 297 Supplementation, 21, 47, 53, 70, 76, 93, 94, 95, 116, 137, 298
Suppositories, 255, 298 Suppression, 13, 20, 39, 152, 173, 298 Surfactant, 56, 129, 134, 167, 172, 295, 298 Sympathetic Nervous System, 225, 230, 298 Symphysis, 286, 298 Symptomatic, 38, 279, 298 Synaptic, 294, 298 Synergistic, 116, 117, 298 Systemic, 7, 48, 51, 70, 139, 194, 228, 232, 245, 251, 263, 284, 298 Systemic disease, 139, 298 Systemic lupus erythematosus, 70, 298 Systolic, 33, 41, 50, 76, 261, 269, 298 Systolic blood pressure, 33, 41, 50, 298 Systolic pressure, 269, 298 T Tardive, 227, 298 Telangiectasia, 205, 298 Testis, 252, 298 Testosterone, 5, 290, 298 Tetracycline, 180, 298 Thalamic, 229, 299 Thalamic Diseases, 229, 299 Therapeutics, 64, 173, 195, 299 Thermal, 121, 122, 247, 276, 299 Thigh, 46, 48, 299 Thorax, 221, 299, 303 Threshold, 261, 299 Thrombin, 253, 283, 287, 299 Thrombolytic, 282, 299 Thrombomodulin, 287, 299 Thrombosis, 55, 66, 78, 79, 92, 152, 287, 297, 299 Thromboxanes, 228, 299 Thrombus, 243, 263, 265, 274, 283, 299 Thymus, 262, 269, 299 Thyroid, 146, 182, 264, 299, 302 Thyroxine, 223, 281, 299 Tissue Culture, 299, 304 Tissue Distribution, 49, 299 Tissue Plasminogen Activator, 6, 40, 300 Tolerance, 46, 68, 73, 77, 84, 183, 256, 300 Tomography, 43, 48, 269, 300 Tonometry, 21, 48, 300 Tooth Preparation, 221, 300 Toothache, 141, 300 Topical, 229, 252, 261, 279, 281, 295, 300 Torsion, 263, 300 Toxaemia, 285, 300 Toxic, iv, 57, 59, 125, 231, 239, 251, 258, 262, 271, 275, 283, 292, 293, 297, 300
Index 323
Toxicity, 127, 247, 300 Toxicokinetics, 300 Toxicology, 150, 202, 300 Toxins, 227, 256, 263, 273, 300, 303 Trace element, 238, 254, 300 Tracer, 36, 43, 300 Trachea, 281, 299, 300 Traction, 239, 300 Transaminases, 22, 182, 300 Transcriptase, 291, 300 Transcription Factors, 13, 38, 49, 301 Transduction, 294, 301 Transfection, 14, 232, 301 Transferases, 257, 301 Transgenes, 7, 301 Transient Ischemic Attacks, 60, 301 Translation, 9, 39, 251, 301 Translocation, 9, 54, 58, 251, 301 Transmitter, 221, 247, 264, 270, 276, 301 Transplantation, 239, 262, 269, 301 Trauma, 48, 77, 181, 231, 245, 258, 274, 279, 299, 301 Trauma Centers, 49, 301 Triad, 31, 301 Tricyclic, 181, 301 Trigger zone, 227, 301 Troglitazone, 20, 301 Truncal, 5, 29, 301 Tryptophan, 240, 293, 301 Tuberculosis, 242, 268, 301 Tuberous Sclerosis, 205, 301 Tubulin, 272, 302 Tumor marker, 232, 302 Tumor Necrosis Factor, 26, 56, 70, 302 Type 2 diabetes, 15, 17, 28, 29, 39, 45, 51, 58, 59, 70, 73, 78, 79, 82, 174, 183, 302 Tyrosine, 19, 247, 302 U Ubiquitin, 58, 140, 302 Ultrasonography, 256, 302 Unconscious, 262, 302 Unsaturated Fats, 51, 124, 184, 254, 302 Uraemia, 279, 302 Urea, 121, 233, 302 Urethane, 148, 302 Urethra, 286, 302, 303 Uric, 182, 257, 261, 302 Urinalysis, 182, 302 Urinary, 21, 60, 230, 234, 263, 284, 300, 302, 303 Urinary Plasminogen Activator, 300, 303
Urine, 60, 139, 223, 230, 232, 243, 247, 259, 263, 265, 266, 284, 287, 302, 303 Urography, 246, 303 Uterus, 53, 243, 244, 250, 262, 270, 278, 286, 303 V Vaccination, 174, 303 Vaccine, 222, 287, 303 Vacuoles, 250, 277, 303 Vagina, 5, 245, 270, 303 Vaginal, 5, 303 Vagus Nerve, 295, 301, 303 Vasculitis, 279, 303 Vasodilation, 12, 29, 225, 303 Vasodilator, 78, 224, 227, 233, 247, 260, 303 Vasomotor, 4, 252, 303 Vector, 301, 303 Vegetative, 232, 303 Vein, 18, 55, 225, 264, 276, 303 Venoms, 275, 303 Venous, 55, 60, 233, 237, 244, 287, 303 Venous blood, 233, 237, 303 Ventilation, 304 Ventilator, 269, 291, 304 Ventricle, 262, 288, 298, 304 Ventricular, 12, 304 Venules, 233, 235, 250, 304 Very low-density lipoprotein, 57, 191, 304 Vesicular, 272, 304 Vestibular, 180, 181, 304 Vestibule, 304 Veterinary Medicine, 84, 201, 304 Vimentin, 19, 304 Viral, 8, 14, 174, 181, 228, 263, 301, 304, 305 Viral vector, 8, 304 Virilism, 261, 304 Virulence, 230, 300, 304 Virus, 73, 228, 230, 247, 250, 255, 282, 301, 304 Virus Diseases, 228, 304 Visceral, 19, 27, 29, 35, 48, 74, 230, 280, 303, 304, 305 Visceral Afferents, 230, 303, 304 Visceral fat, 20, 29, 35, 74, 305 Viscosity, 123, 125, 134, 135, 291, 305 Vitamin A, 124, 137, 263, 291, 305 Vitamin E, 114, 115, 137, 305 Vitamin K, 305 Vitelline Membrane, 305, 306 Vitreous Body, 291, 305 Vitro, 16, 34, 39, 259, 305 Vivo, 8, 14, 57, 305
324 Triglycerides
W Waist circumference, 29, 48, 305 Warts, 116, 283, 305 Weight Gain, 5, 28, 48, 133, 305 White blood cell, 182, 226, 266, 269, 273, 282, 305 Windpipe, 281, 299, 305 Womb, 303, 305 World Health, 58, 72, 218, 305 Wound Healing, 143, 236, 305
X Xenograft, 226, 305 X-ray, 5, 35, 46, 113, 236, 241, 246, 269, 276, 296, 305 Y Yeasts, 62, 254, 281, 305 Yolk Sac, 34, 305 Z Zymogen, 287, 306
Index 325
326 Triglycerides
Index 327
328 Triglycerides
