Glucose Tolerance Test - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

GLUCOSE TOLERANCE TEST 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., 1960Glucose Tolerance Test: 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: 0-497-00487-9 1. Glucose Tolerance Test-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.

Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail: [email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International, Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.

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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 glucose tolerance test. 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 GLUCOSE TOLERANCE TEST ..................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Glucose Tolerance Test.................................................................. 6 E-Journals: PubMed Central ....................................................................................................... 60 The National Library of Medicine: PubMed ................................................................................ 61 CHAPTER 2. ALTERNATIVE MEDICINE AND GLUCOSE TOLERANCE TEST ................................... 107 Overview.................................................................................................................................... 107 National Center for Complementary and Alternative Medicine................................................ 107 Additional Web Resources ......................................................................................................... 109 General References ..................................................................................................................... 110 CHAPTER 3. BOOKS ON GLUCOSE TOLERANCE TEST ................................................................... 113 Overview.................................................................................................................................... 113 Book Summaries: Federal Agencies............................................................................................ 113 Chapters on Glucose Tolerance Test .......................................................................................... 115 CHAPTER 4. MULTIMEDIA ON GLUCOSE TOLERANCE TEST ........................................................ 121 Overview.................................................................................................................................... 121 Video Recordings ....................................................................................................................... 121 CHAPTER 5. PERIODICALS AND NEWS ON GLUCOSE TOLERANCE TEST ..................................... 123 Overview.................................................................................................................................... 123 News Services and Press Releases.............................................................................................. 123 Newsletter Articles .................................................................................................................... 125 Academic Periodicals covering Glucose Tolerance Test............................................................. 125 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 129 Overview.................................................................................................................................... 129 NIH Guidelines.......................................................................................................................... 129 NIH Databases........................................................................................................................... 131 Other Commercial Databases..................................................................................................... 133 APPENDIX B. PATIENT RESOURCES ............................................................................................... 135 Overview.................................................................................................................................... 135 Patient Guideline Sources.......................................................................................................... 135 Finding Associations.................................................................................................................. 140 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 143 Overview.................................................................................................................................... 143 Preparation................................................................................................................................. 143 Finding a Local Medical Library................................................................................................ 143 Medical Libraries in the U.S. and Canada ................................................................................. 143 ONLINE GLOSSARIES................................................................................................................ 149 Online Dictionary Directories ................................................................................................... 150 GLUCOSE TOLERANCE TEST DICTIONARY ...................................................................... 151 INDEX .............................................................................................................................................. 213

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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 glucose tolerance test 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 glucose tolerance test, 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 glucose tolerance test, 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 glucose tolerance test. 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 glucose tolerance test, 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 glucose tolerance test. The Editors

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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.

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CHAPTER 1. STUDIES ON GLUCOSE TOLERANCE TEST Overview In this chapter, we will show you how to locate peer-reviewed references and studies on glucose tolerance test.

The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and glucose tolerance test, 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 “glucose tolerance test” (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: •

Oral Glucose Tolerance Test in Clinical Practice Source: Practical Diabetology. 9(1): 1-6. January-February 1990. Summary: The oral glucose tolerance test has many potential uses in the evaluation of patients with disorders of glucose homeostasis. Care has to be taken in properly interpreting the results, because of the multiple factors that affect the test. This review summarizes a practical approach to use of the test in routine clinical practice. The author focuses on the use of the glucose tolerance test in diagnosing diabetes mellitus, hypoglycemia, and gestational diabetes. The editor's commentary includes three case examples of the material covered in the text. 2 figures. 3 tables. 9 references.

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Identification of Persons at High Risk for Type 2 Diabetes Mellitus: Do We Need the Oral Glucose Tolerance Test? Source: Annals of Internal Medicine. 136(8): 575-581. April 16, 2002. Contact: Available from American College of Physicians. American Society of Internal Medicine. 190 North Independence Mall West, Philadelphia, PA 19106-1572. Website: www.acponline.org. Summary: The standard method of identifying persons at high risk for type 2 diabetes mellitus involves detection of impaired glucose tolerance, which requires a costly and inconvenient 2 hour oral glucose tolerance test (OGTT). Because clinical trials have indicated that diabetes is preventable by using behavioral or pharmacologic interventions, less expensive methods of identifying high risk persons are needed. This article reports on a study undertaken to determine whether multivariable models are superior to glucose tolerance tests for identifying persons at high risk for diabetes mellitus. The prospective cohort study took place in San Antonio, Texas, and included 1,791 Mexican Americans and 1,112 nonHispanic whites without diabetes at baseline who were randomly selected from census tracts. The study included measurements of medical history, body mass index (BMI), blood pressure, blood glucose levels, and lipoprotein and triglyceride levels. The results showed that persons at high risk for diabetes mellitus are better identified by using a simple prediction model than by relying exclusively on the results of a 2 hour OGTT. Although adding the 2 hour glucose variable to the model enhanced prediction, the resulting slight improvement entails greater cost and inconvenience. 1 figure. 2 tables. 19 references.

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75-g Glucose Tolerance Test in Pregnancy: A Reference Range Determined on a LowRisk Population and Related to Selected Pregnancy Outcomes Source: Diabetes Care. 21(11): 1807-1811. November 1998. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article describes a study that used a group of women at low risk for gestational diabetes mellitus (GDM)to determine a reference range for the 75-g glucose tolerance test (GTT) in pregnancy. The study also determined the validity of this reference range by examining selected pregnancy outcomes for glucose tolerant women with a 2 hour result on the GTT up to 1.0 mmol/L below the diagnostic level for GDM compared with treated women with GDM. The study was conducted in the Illawarra area, New South Wales, Australia. Between January 1993 and June 1994, all women attending the prenatal clinics at two hospitals were tested for GDM. The reference range for the GTT was determined in 573 low-risk Caucasian women who were less than 25 years old and who had a body mass index of less than 25 kg/m2. Selected pregnancy outcomes were compared for 272 treated women with GDM and 308 women with a 2 hour glucose level of 7.0 to 7.9 mmol/L. Results show that GDM was found in 183 of the total population of 2,907 and in 16 of the 573 low-risk women. Overall, GDM in the lowrisk women accounted for 16 of the 183 cases. In addition, there was 95 percent confidence that at least 95 percent of all the fasting glucose levels were 5.1 mmol/L or less and 95 percent confidence that at least 95 percent of all the 2 hour glucose levels were 7.8 mmol/L or less. Compared with glucose-tolerant women, treated women with GDM had a significantly reduced rate of large for gestational age infants, without any increase in the rate of small for gestational age infants or obstetric interventions. The article concludes that the reference range for the GTT in pregnancy should be determined on a low-risk population rather than on a total population. Consideration

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should be given to lowering the fasting glucose level to 5.0 mmol/L and the 2 hour level to 7.8 mmol/L. Glucose-tolerant women below this relatively low reference range have an increased rate of large-for-gestational age infants and may benefit from treatment. 1 table. 32 references. (AA-M). •

Glucose Tolerance Test: Degree of Glucose Abnormality Correlates With Neonatal Outcome Source: Obstetrics and Gynecology. 81(3): 344-348. March 1993. Summary: This article describes a study undertaken to determine how well the extent of glucose abnormality (as reflected by the number of abnormal values on the 3-hour oral glucose tolerance test, or GTT) correlates with the level of carbohydrate intolerance during pregnancy and with the severity of adverse outcome. The researchers followed 764 women with gestational diabetes under a once-per-week fasting and 2-hour postprandial serum glucose monitoring system. The subjects were stratified by the number of abnormal values on their GTTs. The level of glucose control and incidence of large-for-gestational-age (LGA) infants were then determined and compared with the findings in 636 gravidas with abnormal screening but all normal GTT values. The researchers concluded that one or more abnormal GTT values were associated with comparably elevated incidences of LGA infants in patients with poor glycemic control. Achievement of recommended glucose control decreased adverse outcomes to near normal levels. 3 figures. 3 tables. 13 references. (AA-M).

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Comparison of a Clinical Model, the Oral Glucose Tolerance Test, and Fasting glucose for Prediction of Type 2 Diabetes Risk in Japanese Americans Source: Diabetes Care. 26(3): 758-763. March 2003. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to test the validity of a published clinical model for predicting incident (new) diabetes in Japanese Americans. A total of 465 nondiabetic Japanese Americans (243 men, 22 women), aged 34 to 75 years, were studied at baseline and at 5 to 6 years. A total of 412 subjects were studied at 10 years. The clinical model included age, sex, ethnicity, body mass index (BMI), systolic blood pressure, fasting plasma glucose (FPG), HDL cholesterol, and family history of diabetes at baseline. The diabetes risk associated with body mass index (BMI), sex, and HDL cholesterol differed by age. The authors conclude that in Japanese Americans older than 55 years, a clinical model was better than FPG for predicting diabetes after 5 to 6 years, but not after 10 years. The model was not useful in older Japanese Americans, whereas 2 hour glucose testing was useful for predicting diabetes risk regardless of age. 3 tables. 22 references.

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Gestational Diabetes Mellitus Diagnosed with a 2-h 75-g Oral Glucose Tolerance Test and Adverse Pregnancy Outcomes Source: Diabetes Care. 24(7): 1151-1155. July 2001. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This review article describes a cohort study that evaluated American Diabetes Association (ADA) and World Health Organization (WHO) diagnostic criteria for gestational diabetes mellitus (GDM) against pregnancy outcomes. Although the

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ADA recommends a 3 hour 100 gram oral glucose tolerance test (OGTT) for the diagnosis of GDM, it has also recently included in its recommendations the use of a 2 hour 75 gram OGTT. GDM is defined by the new ADA test recommendations for the two hour 75 gram OGTT as at least two values greater than a fasting glucose of 5.3 mmol per liter, a 1 hour glucose of 10 mmol per liter, and a 2 hour glucose of 8.6 mmol per liter. WHO criteria require a fasting plasma glucose of equal to or greater than 7.0 mmol per liter or a 2 hour glucose of equal to or greater than 7.8 mmol per liter. The study population consisted of 4,977 Brazilian adult women attending general prenatal clinics who underwent a standardized 2 hour 75 gram OGTT between their estimated 24th to 28th gestational weeks. Among the women, 2.4 percent presented with GDM by ADA criteria and 7.2 percent by WHO criteria. After adjustment for the effects of age, obesity, and other risk factors, GDM by ADA criteria predicted an increased risk of macrosomia, preeclampsia, and perinatal death. Similarly, GDM by WHO criteria predicted increased risk for macrosomia, preeclampsia, and perinatal death. Of women positive by WHO criteria, 260 were negative by ADA criteria. Conversely, 22 women positive by ADA criteria were negative by WHO criteria. The article concludes that GDM based on a 2 hour 75 gram OGTT defined by either WHO or ADA criteria predicts adverse pregnancy outcomes. Thus, until consensual criteria are reached, these two criteria are valid options for the detection of a glucose tolerance state predictive of adverse pregnancy outcomes. 1 appendix. 1 figure. 2 tables. 18 references. (AA-M).

Federally Funded Research on Glucose Tolerance Test The U.S. Government supports a variety of research studies relating to glucose tolerance test. 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 glucose tolerance test. 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 glucose tolerance test. The following is typical of the type of information found when searching the CRISP database for glucose tolerance test: •

Project Title: "RAT MIODELS FOR CHRONIC SLEEP RESTRICTION IN AGING" Principal Investigator & Institution: Turek, Fred W.; Professor; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2003; Project Start 01-DEC-2002; Project End 30-NOV-2007 Summary: Despite the high prevalence of chronic sleep loss in modern society, no animal models have been developed to systematically examine the effects of chronic partial sleep loss on sleep architecture and indices of health. Furthermore, nothing is

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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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known about the effects of age or circadian rhythmicity on sleep during adaptation to or recovery from partial sleep restriction. The proposed studies will develop the rat as an animal model to test hypotheses about the impact of age and circadian rhythms on sleep during and following partial chronic sleep restriction. Most of the studies will involve young, middle age and old F344 and WKY rats in which sleep will be moderately (8 hours) or severely (4 hours) restricted for 1, 5 or 10 days. Sleep will be recorded under baseline conditions as well as during and for five days after the sleep restriction period. The circadian rhythms of body temperature and total locomotor activity will be monitored via biotelemetry. Old animals will be divided into two groups for data analysis: those that have robust and intact circadian rhythms and those where the rhythms are severely fragmented. This division, along with studies on animals with lesions of the SCN, will address questions about the importance of the integrity of the circadian system in the response to repeated sleep restriction. Use of F344 and WKY rats will test the hypothesis that the homeostatic sleep recovery process during and following a period of repeated sleep restriction is dependent on baseline sleep architecture. The endocrine and metabolic consequences of chronic partial sleep restriction will be evaluated by examining stress hormones and glucose metabolism under baseline and responsive conditions. The partial chronic sleep restriction paradigm will also be used on an animal model diabetes, the Zucker Fatty Diabetic rat, to determine whether the onset of diabetes occurs prematurely or is more severe in chronically sleep restricted animals. The completion of the proposed studies is expected to provide new insights on the effects of aging on sleep quantity and quality during and following chronic partial sleep loss, and on the physiological consequences of chronic sleep loss as a function of age. These studies will provide new information on the integration of the circadian and homeostatic processes in the regulation of the sleep wake cycle as a function of age, and will lead to new animal models for preventing or attenuating the effects of sleep loss on human health and disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ANDROGENIZED FEMALE AS A MODEL FOR P0LYCYSTIC OVARIAN SY Principal Investigator & Institution: Abbott, David H.; Primate Research Center; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2002; Project Start 01-AUG-1999; Project End 31-JUL-2004 Summary: Polycystic ovarian syndrome (PCOS) affects 10 percent of reproductive-aged women and is characterized by hyperandrogenic anovulation. Hyperinsulinemia plays a key role in the mechanism of hyperandrogenic anovulation. The etiology of PCOS in the human, however, is unknown. Prenatal androgen excess in female rhesus monkeys results in ovarian, endocrinological and metabolic features in adulthood which closely resemble PCOS. In this nonhuman primate model for PCOS, we will test the hypothesis that a double insult is required to evoke hyperandrogenic anovulation. We propose that hyperandrogenism is required for hyperinsulinemia to effect hyperandrogenic anovulation (PCOS). Without hyperandrogenism, hyperinsulinemia may induce ovarian hyperandrogenism, but it will fail to induce hyperandrogenic anovulation. The Specific Aims of the proposed research are to (1) use an insulin-sensitizing agent to ameliorate hyperinsulinemia and induce ovulatory cycles in prenatally androgenized female rhesus monkeys that exhibit hyperandrogenic anovulation, (2) produce hyperinsulinemia in normo-insulinemic, hyperandrogenic, prenatally androgenized females and induce hyperandrogenic anovulation, and (3) use an anti-androgen in combination with hyperinsulinemia in normo-insulinemic hyperandrogenic, prenatally androgenized

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females to block insulin-induced hyperandrogenic anovulation. Eight anovulatory and 10 ovulatory prenatally androgenized females will be matched for age and body composition with 18 ovulatory controls. The 8 anovulatory androgenized females and their controls will receive 4 mg/kg of troglitazone (RezulinTm, Parke-Davis) daily for 6 months to ameliorate their hyperinsulinemia. The 10 ovulatory androgenized females and their controls will receive daily injections of insulin (Ultralente insulin, Eli Lilly) for 6 months, starting at 5U/day and incrementing to 20U/day. A 6-month Control Phase will be counterbalanced with each Treatment Phase. During all Phases, data will be collected on ovarian function and morphology, hyperandrogenism in the ovary and adrenal, changes in intra-ovarian follicular fluid content, degree of LH hypersecretion, glucose/insulin homeodynamics, and CT/DXA-determined body composition. If our hypothesis is correct, these data will establish that hyperinsulinemia results in hyperandrogenic anovulation only in prenatally androgenized female monkeys. Such results would offer novel insights into the origin and mechanism of PCOS, and would provide a unifying determinant for a multifactorial syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BIOLOGICAL EFFECTS OF DHEA IN THE ELDERLY Principal Investigator & Institution: Kohrt, Wendy M.; Professor; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2002; Project Start 01-MAY-2000; Project End 31-MAR-2004 Summary: (adapted from Investigator's abstract) The central hypothesis is that restoring circulating DHEA levels of older people with low levels to more youthful levels will be associated with beneficial changes in body composition. The specific aims are to examine in 65-85 yr-old women and men the effects of 1yr DHEA replacement on: a) fat mass and fat-free mass; b) intra-abdominal fat volume and thigh muscle area by MRI; c) bone mineral density; d) glucose tolerance and insulin response evaluated using an oral glucose tolerance test. The hypothesis is that DHEA replacement will increase fat-free mass and bone mineral density and decrease fat mass. Additional hypotheses are that: 1) The increase in fat-free mass will be due to an increase in muscle mass. 2) The decrease in fat mass will be predominantly in the trunk regions. And 3) The increase in bone mineral density will be due to a decrease in bone resorption and a reduced insulin response to an oral glucose load will occur despite no change in the glucose response, indicating enhanced insulin action. The role of IGF-1 will be examined, as measured from IGF-1 and IGHBP-3, by examining whether these hormones predict changes in the aforementioned variables. The volunteers will be 72 men and 72 women, aged 56-85 yr who are healthy. They will be randomized to receive either a replacement dose of DHEA or placebo. If these results are confirmed, this will suggest the DHEA deficiency and its replacement may play an important role in the prevention of sarcopenia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CAFFEINE AND GLUCOSE REGULATION Principal Investigator & Institution: Lane, James D.; Psychiatry; Duke University Durham, Nc 27710 Timing: Fiscal Year 2004; Project Start 01-JUL-2004; Project End 31-MAY-2007 Summary: (provided by applicant): Caffeine has widespread effects in the 90 percent of US adults who consume it daily. Recent research in our laboratory indicates that caffeine has disruptive effects on glucose metabolism that may seriously impair glycemic control

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in type 2 diabetes and aggravate insulin resistance in pre-diabetic individuals. We propose 4 studies to determine the nature and extent of caffeine's effects and their potential importance to diabetes. A replication and extension of our preliminary study will examine the effects of a controlled dose of caffeine on fasting glucose and insulin and responses to the oral glucose tolerance test (OGTT) to determine whether caffeine aggravates hyperglycemic and hyperinsulinemic responses in type 2 diabetes patients. We will test a variety of clinical and physiological factors that could account for individual differences in caffeine's effects, to identify patients at greatest risk of impairment and to elucidate potential mechanisms of action. A similar study will determine caffeine's effects on glucose metabolism in subjects who are currently "prediabetic," but at risk of developing clinical diabetes. Confirming that caffeine increases insulin resistance and may elicit hyperglycemia in this group would establish caffeine as a factor that could aggravate and contribute to the metabolic processes that lead to the development of diabetes in this high-risk group. A third study will extend our laboratory findings into the natural environment and explore the use of continuous glucose monitoring system (CGMS) methodologies to determine the effects of caffeine consumption on blood glucose during normal daily activities. These ambulatory measurements will complement the controlled laboratory studies and establish the ecological importance of these effects. Together these studies will establish a foundation of evidence regarding caffeine's effects on glucose metabolism and their importance to clinical glucose management in type 2 diabetes. This foundation will support later studies of mechanism as well as clinical intervention trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CALORIC RESTRICTION AND AGING IN HUMANS 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 30-SEP-2001; Project End 31-AUG-2008 Summary: (provided by applicant) Primary aging is the progressive deterioration in structure and function with advancing age that occurs independently of disease and lifestyle/environmental factors. Slowing of primary aging results in an increase in maximal life span. Caloric restriction (CR) slows primary aging in various short-lived organisms, such as guppies, flies, mice and rats. It is not known if CR slows primary aging in humans. Secondary aging is due to disease processes and harmful lifestyle/environmental factors. Protection against secondary aging results in rectangularization of the mortality curve without an extension of maximal life span. Available evidence suggests that CR protects against some aspects of secondary aging in primates. In contrast to CR, an exercise-induced, caloric deficit does not slow primary aging in rats, suggesting that the effect of CR on primary aging is mediated by decreased intake and metabolism of food rather than by decreased energy availability. In this context, the specific aims of Phase 1 of this study are: 1) To determine the feasibility of achieving prolonged 20% restriction of energy intake or prolonged 20% increase of energy expenditure by exercise, in overweight, 50-60 yr old women and men and refine the techniques needed to achieve adherence to the CR and exercise protocols. The efficaciousness of two approaches will be evaluated for CR (meal plans versus meal replacement) and for exercise (supervised versus independent exercise programs); and 2) To evaluate and compare the effects of 12 mo of the CR and exercise interventions on a number of potential markers of aging, on body composition and on risk factors for CAD and type 2 diabetes. In Phase 1, volunteers will be randomized to one of five groups: 2 CR groups, 2 exercise groups and one control group. There will be 16

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participants per intervention group (i.e. 32 CR, 32 exercise) and 20 in the control, no intervention, group. We anticipate a drop out rate of approximately 25% based on previous experience. Our goal is to have at least 12 women and 12 men complete 1 yr of CR, and 12 women and 12 men complete 1 yr of exercise in Phase 1. The information obtained from the first 2 yrs, Phase 1, of this research, will be used in the planning and design of Phase 2. It should be possible to more accurately estimate the number of participants per group in Phase 2 based on our experience in Phase 1. In Phase 2, there will be 3 groups of healthy, overweight men and women aged 50-60 yr: CR, exercise and control. The CR and exercise protocols will be designed on the basis of our experience, and that of the other investigators, in Phase 1. In Phase 2, the duration of the CR and exercise interventions will be two years. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CARDIOVASCULAR DISEASE FOLLOWING HYPERTENSIVE PREGNANCY Principal Investigator & Institution: Wolf, Myles S.; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Candidate: Dr. Myles Wolf received the M.D. degree in 1996 from SUNY-Brooklyn. He completed internal medicine and nephrology training at MGH. In 2002, he received the Master of Medical Sciences degree in clinical physiological investigation from Harvard Medical School through its NIH K30supported Scholars in Clinical Science Program. Mentor: David Nathan, M.D., is a world-renowned clinical investigator who has trained numerous investigators in the areas of diabetes and insulin resistance, a field in which he has published extensively. As Director of the MGH GCRC and as a founding member of the Scholars in Clinical Science Program, Dr. Nathan will ensure the success of Dr. Wolf's research training, project and overall career development. Research: cardiovascular disease (CVD) is the leading cause of mortality among women in the U.S. Reducing its burden requires further understanding of its early mechanisms. Women with hypertensive disorders of pregnancy (HDP), including preeclampsia and gestational hypertension, return to their normotensive baseline soon after delivery, yet they are at increased risk for CVD in later years. Therefore, these women represent in-vivo human models of the pre-CVD state in whom its early mechanisms may be studied. In their first study, they will test the hypothesis that otherwise asymptomatic women with prior HDP display evidence of increased CVD risk relative to those with normal pregnancy as early as one year postpartum. In addition to examining traditional CVD risk factors, they will focus on insulin resistance, inflammation and microalbuminuria, factors that are associated with HDP but have been understudied in the postpartum period. In a second physiological study, they will examine vascular reactivity using brachial artery ultrasound, and insulin sensitivity using intravenous glucose tolerance tests. The hypotheses to be tested are that women with HDP display evidence of endothelial dysfunction during the early postpartum period and that this alteration is related to insulin resistance. All subjects will be identified from the MGH Obstetric Maternal Study, the largest pregnancy cohort in Massachusetts, and the source of several important studies during pregnancy. The proposed study is sufficiently powered (>90%), IRB-approved and pilot data support its feasibility. They believe the results will provide critical insight into mechanisms of CVD in women and potentially suggest means to alter their CVD risk. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CARDIOVASCULAR RISK Principal Investigator & Institution: Diez Roux, Ana V.; Assistant Professor; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): Over the past years there has been increasing interest in the role of prenatal and early childhood factors in influencing chronic disease risk in adulthood. In the field of cardiovascular disease (CVD), a growing body of literature has reported inverse associations between birthweight and CVD risk in adults. However, there is still debate on whether this association reflects an underlying etiologic process or is simply the result of confounding by socioeconomic status. In addition: there is little information on the mechanisms that may underlie the observed associations, on maternal factors that may be important, or on how prenatal factors may interact with later growth and with CVD risk factors in adulthood. We propose to use extensive prenatal, perinatal, and early childhood data collected as part of unique birth cohorts established approximately 40 years ago supplemented by assessments in adulthood, to investigate the early determinants of CVD risk. We will examine at total of 1000 sibling-sets who are offspring of pregnant women enrolled during 1959 to 1967 in two New England sites (Boston and Providence) of the National Collaborative Perinatal Project (NCPP) and in the Childhood Health and Development Study (CHDS). The use of a sibling-set design will enhance our ability to control for family influences. Oversampling of sibling sets with at least one low birthweight infant will ensure sufficient power to detect low birthweight effects. Extensive prenatal, perinatal, and early childhood information will be linked to assessments in adulthood. The outcomes investigated will include blood pressure, measures of glucose tolerance, carotid distensibility and intimal-medial thickness (IMT) and heart period variability. We will (1) examine whether associations between birthweight and adult CVD risk factors persist after stringent control for SES;: (2) establish to what extent it is fetal growth, rather than birthweight per se, that is a predictor of CVD risk; (3) investigate the role maternal characteristics; and (4) examine how fetal growth interacts with childhood growth trajectories and adult body size. We will also build on previous research by examining the relation of prenatal factors not only to selected CVD risk factors, but also to outcomes which may help us begin to understand the mechanisms and physiopathologic processes linking early life experiences to cardiovascular risk in adulthood. Thus we will also examine the relation of early life factors to large artery elasticity (as assessed by carotid distensibility), to subclinical atherosclerosis (as assessed by carotid intimal-medial wall thickness (IMT)), and to heart period variability (HPV). Addressing the aims we propose will contribute to our understanding of the causes of CVD generally, and may have important policy implications. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CHARACTERIZING THE OBESITY OF LONG-TERM CANCER SURVIVORS Principal Investigator & Institution: Nunez, Susan B.; Attending Physician; Children's Research Institute Washington, D.C., Dc 20010 Timing: Fiscal Year 2004; Project Start 25-JUN-2004; Project End 31-MAY-2006 Summary: (provided by applicant) We have more than 1000 long-term survivors of childhood cancer followed in our Late Effects and Neuro-Oncology Clinics. With improved treatment modalities, more patients diagnosed with childhood cancer are surviving into adulthood. Endocrine and cardiovascular late effects have been described

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Glucose Tolerance Test

by our group and others in long-term survivors of childhood cancer. This includes obesity and the Metabolic Syndrome (1-8). The atherosclerotic cardiovascular disease component of the Metabolic Syndrome continue to be one of the leading cause of death in the general population and may occur earlier and with increased frequency in survivors of childhood cancer. Obesity is major component of the Metabolic Syndrome. There is little information on the mechanism of obesity in long-term cancer survivors. This project is a pilot study to determine the role of neuropeptides in the development of obesity in cancer survivors treated with cranial irradiation with or without surgery. We plan to enroll obese cancer survivors and perform a 2-hr oral glucose tolerance test (OGTT) measuring glucose, insulin and obesity-related peptides levels. We hypothesize that childhood cancer survivors exposed to cranial irradiation and/or cranial surgery experience disruption in the hypothalamus that increases the risk for the development of hypothalamic obesity and insulin resistance, both components of the Metabolic Syndrome many years after completion of therapy. Obese survivors with these treatments will have abnormal levels of obesity-related peptides compared to obese survivors without those treatments. Among obese survivors, the proportion of insulin resistant patients is higher among those who had cranial irradiation and/or cranial surgery and who also have abnormal levels of the obesity-related peptides. A successful conclusion to this project will not only result in the development of preventive and intervention therapy to minimize the cardiovascular risks in these patients but also open the way to more focused studies of neuropeptide involvement in the pathogenesis of osteopenia/osteoporosis, a less well-described but recently recognized to have a higher incidence in long-term survivors of childhood cancers (22). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CHICAGO CHILDHOOD DIABETES REGISTRY Principal Investigator & Institution: Lipton, Rebecca B.; Associate Professor; Pediatrics; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2003; Project Start 30-SEP-1992; Project End 31-MAY-2008 Summary: (provided by applicant): Recent increases in childhood diabetes present an urgent public health challenge: to mount effective primary and secondary prevention efforts as soon as possible. We must therefore understand the mechanisms underlying the current epidemic, particularly the interaction of genetics with the changing epidemiology of behavioral risk factors. We propose to investigate the determinants of childhood diabetes risk in affected probands and their family members. This is a competing continuation application for the population-based Chicago Childhood Diabetes Registry. This database represents the largest number of non-Hispanic black children with diabetes worldwide, and the largest patient database for Latino children in the continental US. Ongoing ascertainment of incident cases will provide basic epidemiologic data and will anchor a further effort, in families of affected children, to describe the spectrum of youth-onset glucose intolerance in terms of inheritance and the expression of disease susceptibility alleles within families. We will specifically address these hypotheses: 1. That diabetes in youth is caused by a spectrum of etiologic processes, from the insulinopenia of autoimmune type 1 to obesity-related, insulinresistant type 2 diabetes. A subset of children demonstrate a mixed etiology, with autoimmune beta-cell destruction aggravated by the presence of insulin resistance due to genetic susceptibility, obesity and/or physical inactivity. 2. That secular changes in the epidemiology of childhood diabetes are directly related to changes in the prevalence of both type 1 and type 2 risk factors, including obesity, physical inactivity, and perinatal exposures. 3. That familial aggregation of specific traits affects the risk of

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chronic complications in young people with diabetes, over and above that of glycemic control. Ultimately, this approach will permit a truly population-based molecular epidemiologic study of early-onset diabetes in families from a range of ethnic groups. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CORE--CLINICAL RESOURCES Principal Investigator & Institution: Rainwater, David L.; Scientist; Southwest Foundation for Biomedical Res San Antonio, Tx 782450549 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 31-MAY-2007 Summary: (provided by the applicant): Core A will serve as a resource for all projects and cores. Its principal objective is to recruit and re-examine 950 members of our original cohort of participants in the San Antonio Family Heart Study. The examination will take place in the Frederick C. Bartter General Clinical Research Center which is located at the Audie Murphy Memorial Veterans Hospital in San Antonio. The clinic examination will consist of four elements: verification and consent; an interview detailing medical and reproductive history, medications and vitamin usage, and lifestyle behaviors; physical measurements (heart rate, blood pressure, and various assessments of adiposity); and phlebotomy. The data and blood samples will be transported to Southwest Foundation for Biomedical Research where Core A personnel will: edit blood samples; conduct biochemical measurements of glucose, insulin, cholesterol and triglyceride concentrations and lipoprotein size phenotypes; and check all data for plausibility and consistency before making the data files available to program investigators. (End of abstract) The Clinical Core led by Dr. Rainwater has primary responsibility for the collection of data and samples, processing and storage of samples, the measurement of a large number of phenotypes from the blood samples and data entry and validation. A total of 809 individuals were seen during the current program project; 950 individuals will be brought back during the first four years of SAFHS3. The examinations will take place in the GCRC in the Audie Murphy Memorial Veterans Hospital and all supplies for the examination will be provided by the GCRC. Core A staff will be responsible for data management and sample handling. The investigators have shown that they are capable of getting good participation from family members in the follow-up study and will make extra efforts to follow key pedigree members. A similar battery of questionnaires and measurements will be used as was used in the previous study. The investigators have decided not to follow-up on family information in the interest of time. It might be worthwhile to at least assess vital status and health status of individuals who are not returning. It is also a shame that carotid artery measurements cannot be obtained again for a longitudinal study, especially since the initial heritabilities were so strong however this would likely be very costly and time consuming. This core is vital to the success of the project as a whole as new samples are required for the endocrinological function of adipose tissue and change in phenotypes in project 1 and the oxidative stress phenotypes in project 2. The general protocols for sample handling, sample storage, lipoprotein analysis and quality control are excellent. More information is needed on protocols for handling samples for the new phenotypes to be measured and how transfer of samples to outside laboratories and return of information will be accomplished. A key strength of this core is the continuity of personnel working with the families and in the clinic. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Glucose Tolerance Test

Project Title: CORE--MOUSE PHENOTYPING Principal Investigator & Institution: Chua, Streamson C,.; Associate Professor of Pediatrics; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2003; Project Start 01-SEP-2002; Project End 31-AUG-2007 Summary: The mouse phenotyping core will provide expertise and training in the characterization of rodent models of diabetes. To achieve this mission, the Core will provide assistance in the histopathological characterization of mouse models of diabetes and training in the performance of basic metabolic assays, such as glucose and insulin tolerance tests. The Core will also provide consultation on the proper approach to generating recombinant and inbred strains of transgenic and knockout mice, and interact with the Genomics Core to help investigators design appropriate genotyping strategies for genome scans. In addition, the Core is in the process of developing expertise in performing glucose clamp studies to investigate whole body and organspecific metabolic parameters. Through collaborative efforts with the other Cores of the proposed DERC, the effects of defined genetic alterations in rodents can be thoroughly characterized for their effects on metabolism, ingestive behavior, energy balance, body composition, and endocrine function. The Core will serve an important training and education function for many DERC investigators by providing advice on how to prevent common mistakes in breeding programs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CORE--MOUSE PHENOTYPING CORE Principal Investigator & Institution: Hsueh, Willa A.; Professor of Medicine and Chief; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2003; Project Start 01-DEC-2002; Project End 30-NOV-2007 Summary: The overall objectives of the Mouse Phenotyping Core will be to provide DERC investigators with consultation, accurate and easily accessible mouse phenotyping, and the availability of both standard and certain unique mouse models of diabetes and its complications. Services provided by the Mouse Phenotyping Core to DERC investigators concentrate heavily on mouse metabolic, cardiovascular and pathologic phenotyping. These services particularly focus on interests of DERC members: 1) metabolic phenotyping relevant to the genesis of insulin resistance and the progression to type 2 diabetes; 2) cardiovascular physiological phenotyping relevant to models of atherosclerosis, diabetic cardiomyopathy and hypertension; 3) renal phenotyping relevant to hypertension and diabetic nephropathy. The existing strengths at UCSD in metabolic phenotyping and at UCLA in renal-cardiovascular phenotyping will be standardized and merged into one central, partially mobile Core. Seamless integration of phenotyping among DERC investigators at UCLA and UCSD will be facilitated by the Mobile Mouse Physiology Unit. This exciting and innovative concept permits delivery of many phenotyping services directly to the laboratory of DERC investigators, as well as provides needed transport of animals, cryopreserved embryos, equipment and other precious materials. Increased quality of data and substantial savings in costs to individual DERC investigators and the Core are anticipated through implementation of this unique concept. Dr. Gerald Levey, Provost UCLA, has committed to purchasing and equipping this Unit. Currently, the most heavily used services of the DERC include: oral glucose tolerance testing, plasma glucose determinations, renal function tests, non-invasive blood pressure measurements, osmotic minipump placement, cardiac fibrosis quantification, echocardiography, cardiac

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catheterization, and quantification of atherosclerosis. DERC funding will allow expansion of services and development of a new assay development component of this Core. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: COUPLING OF D-CHIRO-INOSITOL TO INSULIN IN PCOS WOMEN Principal Investigator & Institution: Iuorno, Maria J.; Internal Medicine; Virginia Commonwealth University Richmond, Va 232980568 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2005 Summary: (provided by applicant): Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism and chronic anovulation and it is the most common form of female infertility in the U.S. It has been demonstrated that insulin resistance accompanied by compensatory hyperinsulinemia is, in part, responsible for the hyperandrogenism and anovulation of this disorder. The cellular mechanisms of insulin resistance in PCOS are still largely unknown. D-chiro-inositol phosphoglycan (DCI-IPG) is a nonclassical mediator of insulin action that has been demonstrated to increase glucose utilization. Previous studies have shown that administering a drug similar to the native mediator to women with PCOS increases insulin sensitivity, reduces ovarian androgen production and improves ovulation in these women. Therefore, it seems likely that women with PCOS have a defect in DCI-IPG cellular activity that leads to insulin resistance. The aim of this application is to determine whether a defect in coupling between D-chiro-inositol phosphoglycan and insulin plays a role in the insulin resistance of PCOS. We propose to assess the coupling of the DCI-IPG to insulin in women with PCOS and normal women: 1) by administering diazoxide to these women in order to temporarily suppress their pancreatic insulin secretion and measure a change in activity in DCI-IPG in plasma of these women following suppression of insulin and 2) by restoring insulin following diazoxide administration using an insulin clamp and measuring the degree to which DCI-IPG activity is also restored during the clamp in normal women versus women with PCOS. Hence, both PCOS women and normal control women will be evaluated for this insulin to DCI-IPG activity relationship. It is our hypothesis that at least one mechanism of insulin resistance in PCOS is due to defective coupling between insulin and DCI-IPG activity. The results of these studies will 1) describe the physiologic, in vivo relationship between insulin and DCI-IPG in normal women; 2) provide a mechanism for insulin resistance in PCOS as it relates to the DCI-IPG insulin signaling cascade; 3) provide the groundwork for further clinical studies to explore the role of defective coupling in other insulin resistant human conditions (such obesity or type 2 diabetes); and 4) lead to novel specific therapies for the insulin resistance of PCOS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DEPRESSION AND INSULIN RESISTANCE IN TYPE 2 DIABETES Principal Investigator & Institution: Lustman, Patrick J.; Professor of Psychiatry; Psychiatry; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): The overall purpose of this study is to determine the impact of depression on insulin resistance (IR) in diabetes. IR characterizes type 2 diabetes (T2DM) and is a predictor of diabetes complications, particularly coronary heart disease (CHD). CHD, in turn, accounts for more than 50% of deaths and 75% of

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hospitalizations among diabetic patients. Because of this, potentially modifiable factors contributing to IR are being sought. There is evidence linking IR to depression in nondiabetic subjects, and IR may improve with depression treatment in these subjects. Depression is present in approximately 20% of patients with type 2 diabetes (T2DM), precedes the onset of diabetes diagnosis by more than 5 years on average, and may be responsible for some of the IR typifying T2DM and its CHD risk. In a 10-year prospective study of diabetic women with and without depression, we found that depression accelerated the development of (p <0.01) and increased the risk for CHD (OR 3.1, 95%CI 1.1-8.9) and was retained as an independent predictor of CHD in multivariate analysis. In the proposed study, we plan to recruit 160 untreated subjects with a provisional diagnosis of T2DM, 80 with and 80 without major depression (per DSM-IV) matched for gender and BMI. IR (from oral glucose tolerance tests), as well as measures of mood, glycemic control, HPA-axis activity, central adiposity, diet, and physical activity, will be determined at baseline for all subjects. Depressed subjects also will undergo frequently sampled intravenous glucose tolerance tests (FSIGTT) and more detailed analyses of activity, adiposity, and intramyocellular fat. Depressed subjects will be randomly assigned to 12 weeks of cognitive behavior therapy or usual depression care; nondepressed subjects will be observed for comparison. All baseline measures (including FSIGTT and the additional tests in the initially-depressed) will be repeated alter intervention/observation. Univariate tests, analyses of covariance, and least squares regression techniques will be used to assess the independent effects of depression and change in the severity of depression symptoms on IR and change in IR over time. The effect of depression treatment and of depression remission on IR (controlling for baseline differences) and potential mediators of a depression-IR relationship also will be determined in the initially depressed subjects. We hypothesize that depression is associated with increased IR in untreated T2DM and that IR improves with successful depression treatment. The findings from this study could identify a potentially modifiable factor for improving the course and outcome of those living with T2DM. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DEPRESSION/METABOLIC SYNDROME IN MEXICAN-AMERICAN WOMEN. Principal Investigator & Institution: Licinio, Julio; Professor of Psychiatry and Medicine/En; Psychiatry; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): This grant application has been developed to test the hypothesis that insulin resistance and hyperglycemic trends parallel plasma cortisol levels in major depressive disorder (MDD). We will also test the more focused hypothesis that treatment of depressive symptoms ameliorates state of insulin resistance. We will approach these hypotheses by studying depressed MexicanAmerican women from a rigorously characterized cohort of patients who have been recruited into our NIGMS-funded project in pharmacogenomics of antidepressant treatment response (GM61394). This application builds on the enormous resource provided by that prospective study, which provides the opportunity to recruit and treat these individuals. That project is a carefully designed, prospective clinical phase IIA randomized longitudinal study, using two pharmacological agents (desipramine and fluoxetine) with demonstrated efficacy in the treatment of MDD in the MexicanAmerican population. Clinical status is assessed with clinical interview and ratings such

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as the Hamilton Ratings Scale for Depression, Beck Depression Inventory, and Hamilton Anxiety Rating Scale. These instruments have been extensively validated in Spanish. That project is a treatment study with single- and double-masking, with random assignment of treatment, and with outcomes assessed with clinical measures. All subjects will undergo comprehensive intake assessments, and will then have follow-up assessments. Treatment will be provided according to our approved protocol. We propose to conduct detailed endocrine, nutritional, and metabolic studies in normalweight Mexican-American women, who are otherwise medically healthy and who will be extensively characterized for our pharmacogenomic study. This proposal will permit the ascertainment of degree of insulin resistance in MDD through the assessment of endocrine (HPA axis and leptin measurements), nutritional, body composition, and metabolic function (insulin sensitivity will be assessed by oral glucose tolerance test, glucose clamp and arginine stimulation test) before and after treatment. Treatment outcome data will be correlated with endocrine and metabolic endpoints. Several lines of evidence suggest diabetes mellitus is often associated with depression and that depression increases the risk of developing diabetes. This work will address this important area by the study of an population group who is markedly under represented in patient-oriented investigation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DIABETES MECHANISMS

IN

HEMOCHROMATOSIS:

PREVALENCE

AND

Principal Investigator & Institution: Mcclain, Donald A.; Professor and Director; Internal Medicine; University of Utah Salt Lake City, Ut 84102 Timing: Fiscal Year 2002; Project Start 01-MAR-2002; Project End 31-OCT-2006 Summary: Although the hemochromatosis gene (HFE) has been identified there is little information about the diabetes that often accompanies the disease. We hypothesize nondiabetic homozygotes for mutations in HFE will exhibit a defect in insulin secretion as iron overload develops. This notion is supported by preliminary data obtained in HFE mutant mice. The insulin deficiency will progress to type 2 diabetes only if insulin resistance also occurs, either from cirrhosis or inheritance of type 2 diabetes genes. Insulin resistance from cirrhosis is hypothesized to result from excess carbohydrate delivery to peripheral tissues, resulting in excess hexosamine generation, an established cause of insulin resistance. Our specific aims are to: 1. Determine the prevalence of impaired glucose intolerance (IGT) and diabetes in clinically unselected individuals with hemochromatosis by oral glucose tolerance criteria. 2. Determine if a defect in insulin secretion exists in nondiabetic homozygotes with or without iron overload. This will be accomplished using the frequently sampled intravenous glucose tolerance test (FSIVGTT) with insulin levels. Reversibility of the defect will be examined after subjects have undergone phlebotomy. The hypothesis will be verified in studies of isolated islets from mice carrying disrupted or mutant HFE genes. 3. Using animal models, determine if diabetes in hemochromatosis results only when insulin resistance is superimposed on an iron- mediated defect in insulin secretion. 4. Determine the sequence and relative contributions of insulin resistance and hepatic glucose production (HGP) in the evolution of diabetes in human hemochromatosis. Insulin resistance and HGP will be quantified by the hyperinsulinemic euglycemic clamp and stable isotope techniques in subjects with hemochromatosis who have normal or IGT, with or without hepatic involvement. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DIABETES PREVENTION PROGRAM Principal Investigator & Institution: Orchard, Trevor J.; Professor; Epidemiology; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2003; Project Start 15-AUG-1994; Project End 31-JAN-2008 Summary: (provided by applicant): The Diabetes Prevention Program is a multicenter controlled clinical trial examining the efficacy of an intensive life-style intervention or metformin to prevent or delay the development of diabetes in a population selected to be at high risk due to the presence of impaired glucose tolerance (IGT). Development of diabetes, defined by 1997 ADA criteria, is the primary outcome while cardiovascular disease and its risk factors are important secondary outcomes. The DPP began recruitment in mid-1996. At the time of this application, total study exposure is a mean of approximately 3 years (range 2 to 5) with a total of approximately 10,000 patient years in the 3,234 volunteers in the 3-arm study. On the basis of a statistically significant and clinically compelling decrease in the development of diabetes in the life-style intervention and metformin-treated groups (58% and 31% reductions, respectively) compared with the placebo treated group, the DPP Data Monitoring Board and NIDDK ended the masked treatment phase of the study in May, 2001, one year earlier than originally planned. This application is designed to take further advantage of the scientifically and clinically valuable cohort of DPP volunteers and the large volume of data collected during the study. The highly compliant DPP cohort, including 45% minorities, is the largest IGT population ever studied. Moreover, the subcohort that has developed diabetes (n approximately 700) has been followed from near the exact time of diabetes onset. Clinically important research questions remain in the wake of the DPP. The carefully collected, centrally measured and graded data in this cohort should help to answer, definitively, a number of important questions regarding the clinical course of IGT and early onset type 2 diabetes. Specific aims include: 1. Examine the long-term effects and durability of prior DPP intervention on the major DPP outcomes including diabetes, clinical cardiovascular disease, atherosclerosis, CVD risk factors, quality of life and cost-benefit; 2. Determine the clinical course of new onset type 2 diabetes and IGT, in particular regarding microvascular and neurologic complications; 3. Determine the incidence of cardiovascular disease (CVD), CVD risk factors and atherosclerosis in new onset type 2 diabetes and IGT; and 4. Examine topics 1-3 in minority populations, men vs. women, and in older subjects in the DPP. The current application is for 5 years of funding, although the some of the goals of the projects described will require a 10-year study. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DIET METABOLISM

AND

EXERCISE:

RACE,

POSTMENOPAUSE

AND

Principal Investigator & Institution: Ryan, Alice S.; Associate Professor; Medicine; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-AUG-2006 Summary: (Verbatim from application) African American women are more obese and insulin resistant than Caucasian women. This research is designed to determine whether overweight African American women respond differently to hypocaloric weight loss (WL) or aerobic exercise plus weight loss (AEX+WL) than do Caucasian women. The hypothesis is that ethnic differences (African American vs. Caucasian) in the mechanisms by which WL affects insulin sensitivity in overweight, insulin resistant African American postmenopausal women requires that the WL be accompanied by

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AEX in African American women to improve insulin sensitivity. Specific aims determine 1) the race effects of WL vs. AEX+WL on insulin action on glucose and fat metabolism in African American compared to Caucasian women by assessing insulin sensitivity (EC50), and FFA suppression during hyperinsulinemia; and 2) the cellular mechanisms by which the addition of AEX to WL affects insulin sensitivity in African American compared to Caucasian women by ascertaining the effects of WL vs. AEX+WL on proteins affecting insulin action (GLUT4, IRS 1 and Pl-3 kinase) in skeletal muscle, and insulin suppression of lipolysis in adipocytes. We will study healthy, overweight (Body Mass Index, 27-35 kg/rn2) 50-60 year old postmenopausal African American and Caucasian women. Metabolic studies will be performed before and after either hypocaloric weight loss treatment (n=30 per race) or aerobic exercise training plus weight loss (n=30 per race). Insulin sensitivity and free fatty acid concentrations will be determined during a 3-step hyperinsulinemic-euglycemic clamp. We will measure total body fat (DXA scans), visceral fat and mid-thigh low density lean tissue (CT scans), glucose and insulin responses during an oral glucose tolerance test, skeletal muscle GLUT4, IRS 1, Pl 3-kinase, and insulin suppression of lipolysis in adipocytes. These findings may provide a rationale for targeting specific populations of women who might improve glucose and fat metabolism more from the addition of exercise to hypocaloric weight loss than weight loss alone. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DO FREE GLUCOSE TEST STRIPS INCREASE SELF-MONITORING? Principal Investigator & Institution: Karter, Andrew J.; Investigator; Kaiser Foundation Research Institute 1800 Harrison St, 16Th Fl Oakland, Ca 946123433 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2004 Summary: (provided by applicant): Self-monitoring of blood glucose (SMBG) is considered the cornerstone of diabetes self-management; however, the test strips used for this practice are costly. On January 1, 2000, California enacted into law Senate Bill 64 (SB64) which resulted in Kaiser Permanente (KP) providing SMBG test strips free of charge to diabetic health plan members. Prior to this legislation, members paid varying amounts of copayments for test strip prescriptions. The broad, long-term objective of this proposal is to assess the impact of providing free test strips to patients with diabetes. Proposed Specific Aims include: 1) assessing legislation effects on individual level utilization of test strips (as a proxy for SMBG practice) and glycemic control, with special attention to disparities across ethnicity, socioeconomic status (SES) and disease severity; 2) evaluating the population-level impact of changes in glycemic control attributable to changes in adherence to recommended monitoring frequency; and 3) the cost-effectiveness of potential benefits. We hypothesize that after SB64, 1) test strip utilization increased on an individual level ("price-elastic demand"); 2) changes in strip utilization "explain" (mediate) a relationship between change in cost and change in glycemic control; and 3) on a population level, the elimination of financial barriers will reduce ethnic and socioeconomic disparities in monitoring frequency. This cohort study will include about 200,000 eligible Northern and Southern California KP health plan members identified as having diabetes. Standard hypothesis testing (regression) and estimation methods will be used for continuous and categorical variables to compare changes between the pre- (1999) and post- (2000-2001) legislation periods. We will also quantify the "legislation effect" by calculating a Generalized Impact Fraction, which assesses the reduction in poor glycemic control resulting from the increased frequency of adherent SMBG practice in the post-legislation period. We will use standard costeffectiveness methods to assess the relationship between incremental costs and benefits

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in terms of improved adherence and glycemic control. The global and abrupt change caused by SB64 created a unique natural experiment, positioning us to study the influence of legislative policy on diabetes self-management practices, whether eliminating financial barriers decreases ethnic and socioeconomic health disparities, and to what extent changes in SMBG practice impact glycemic control. Proposal strengths also include a longitudinal design, substantial statistical power, low cost data acquisition, and an ethnically diverse population with uniform access to care. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DOES HYPERGLYCEMIA PREDICT PANCREATIC CANCER DIAGNOSIS? Principal Investigator & Institution: Chari, Suresh T.; Mayo Clinic Coll of Medicine, Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Pancreatic cancer causes glucose intolerance and diabetes in up to 80% of patients. Pancreatic cancer induced diabetes (PaCDM) is often asymptomatic, of short duration (50 years of age may have PaCDM. We propose to establish whether newly elevated fasting blood glucose (FBG) is indicative of underlying pancreatic cancer as evidenced by diagnosis of pancreatic cancer within 3 years of the FBG measurement. If so, this would provide an entirely novel approach to screening for sporadic pancreatic cancer. We hypothesize that the 3-year likelihood of diagnosis of pancreatic cancer will be high in subjects: a) equal to or > 50 years of age with newly elevated FBG, b) with elevated fasting glucose who have known risk factors for pancreatic cancer (e.g. smoking), and/or c) who manifest an abrupt increase in FBG in serial measurements over time. We will identify visits to Mayo Clinic between years 1988 to 2002 by subjects equal to or >50 years of age who resided in its surrounding catchment area and had a routine physical examination that included a FBG. Preliminary data reveal that about 150,000 different subjects made >300,000 such visits during this time period providing >1 million person-years of follow-up. We will electronically retrieve clinical, and laboratory data and examine 3-year follow-up from date of FBG measurement to identify those diagnosed with pancreatic cancer. We expect 340 to 510 pancreatic cancer events in this cohort. Our Specific Aims are: Aim 1A). To test if FBG drawn during routine physical examination predicts likelihood of underlying pancreatic cancer and to test for non-linearity of this association. Aim 1B) To establish a FBG threshold that predicts a high 3-year likelihood of diagnosis of pancreatic cancer. Aim 2). To estimate the extent to which known risk factors for pancreatic cancer (age, smoking, obesity and family history) modify the likelihood of underlying pancreatic cancer in subjects with FBG greater than the threshold defined by Aim 1B. Aim 3). To test if patterns of change in serial measurements of FBG over time predict likelihood of underlying pancreatic cancer. The clinical and research implications of this study are considerable. These data may lead to delineation of individuals who have a high likelihood of existing pancreatic cancer, and who may be ideal candidates for more intensive screening or early detection regimens. The research described in this application is 100% relevant to pancreatic cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DPT-1 / TRIALNET Principal Investigator & Institution: Chase, H Peter.; B Davis Ctr/Childhood Diabetes; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508

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Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-AUG-2008 Summary: (provided by applicant) Long Term Objective: to determine whether early interventional therapies can delay, prevent, or reverse the development of Type 1 diabetes. Specific Aims: intervention trials for subjects with pre-diabetes and new onset diabetes The Diabetes Prevention Trial - Type 1 (DPT-1): to determine whether the early intervention use of insulin in nondiabetic relatives of persons with Type 1 diabetes can delay their development of Type 1 diabetes as a clinical disease. Insulin is used for this purpose since it is a well characterized antigen specifically produced by beta cells. Research design: the parenteral antigen protocol enrolled subjects found to be at high risk (greater than 50 percent) for development of diabetes in the next 5 years. Subjects randomized to the insulin-treated group received insulin intravenously for 4 days each year and two injections of Ultralente each day (before breakfast and before bedtime). The oral antigen protocol enrolls subjects found to be at intermediate risk (25-50 percent) for the development of Type 1 diabetes in the next 5 years. This is a double-blind study and all subjects take 1 capsule daily, with half receiving the antigen and the others receiving a placebo. Levels of antibodies, insulin, C-peptide, HbA1C and glucose are followed. The main study endpoint is two ?diabetic? oral glucose tolerance tests (OGTT) performed on different days. Immunotherapy Trial in New Onset Type 1 Diabetes: to test the hypothesis that mycophenolate mofetil (MMF alone or with daclizumab (DZB) will prolong the period of C-peptide production in subjects with new onset Type 1 diabetes. A secondary aim is to provide the clinical material for the validation of surrogate markers for immunity to islet beta-cells. This study is innovative in that these agents have not been previously evaluated but are rational choices for intervention in an autoimmune disorder. Research design: Levels of autoantibodies and T cell reactivity to islet autoantigens, both of which are surrogate immunological parameters specific for Type 1 diabetes will be followed. Measures of immune modulation will include serologic and T cell reactivity to recall antigens. The metabolic end-points of this study will be fasting and stimulated C-peptide, hemoglobin A1C, and total insulin dose. If this study has a positive outcome, then we would propose a similar study in people at high risk for developing Type 1 diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ENDOMETRIAL CANCER CHEMOPREVENTION STRATEGY FOR OBESE WO Principal Investigator & Institution: Lu, Karen H.; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2008 Summary: Obesity affects over 25% of adult women in the United States and continues to increase in prevalence. Minority women are disproportionately affected by obesity: 37% of African American women and 33% of Mexican American women are obese (body mass index equal to or more than 30 kg/m2). In addition to cardiovascular risks, obese women clearly are at increased risk for developing endometrial cancer. Obese women have a 9-10% lifetime risk of endometrial cancer and account for almost 50% of all cases. It is presumed that the increased peripheral conversion of adrenal steroids to estrone in adipose tissue, the increased bioavailability of adrenal steroids, and the increased bioavailablity of free estrogens due to decreased sex hormone binding globulin (SHBG) contribute to a "hyper-estrogenic state", resulting in the development of endometrial hyperplasia and endometrial cancer. However, excess circulating estrogens are unlikely to fully account for this increased cancer risk. We hypothesize that insulin resistance and hyperinsulinemia are causally related factors that promote

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Glucose Tolerance Test

endometrial carcinogenesis by altering estrogen regulated pathways in the endometrium. In addition, we hypothesize that correction of insulin resistance may be a rational cancer chemopreventive strategy for obese women. We plan to identify, using an animal model of obesity and insulin resistance, molecular markers in the endometrium associated with dysregulated estrogen-controlled growth pathways. A clinical chemoprevention trial will be performed to determine if normalization of insulin resistance is accompanied by modulation of surrogate biomarkers. Aim 1: To test the hypothesis that obesity and insulin resistance increase estrogen-dependent proliferation in the endometrium. Animal models of obesity and insulin resistance will be used to evaluate the effects of obesity on estrogen-regulated endometrial gene expression. In addition, the ability of insulin sensitizers to reverse this effect will be studied. Specific genes involved in estrogen-regulated proliferation pathways will be examined by quantitative PCR, including hormone receptors and co-activators, and genes involved in the Wnt pathway, IGF pathway, TGF-beta and retinoid pathway. Aim 2: To identify novel genes and pathways associated with insulin resistance and estrogenization, and to identify relevant and specific biomarkers that are modulated by normalization of insulin resistance. Expression profiling with cDNA microarrays will be used to explore the effects of obesity and insulin resistance on both estrogen-dependent and estrogenindependent endometrial gene expression. In addition, specific biomarkers of the endometrium that are modulated by insulin-sensitizers will be identified. Aim 3: To assess the ability of an insulin-sensitizing agent to modulate surrogate endometrial biomarkers in a post-menopausal cohort of obese, insulin resistant women. The postmenopausal cohort includes obese women (body mass index equal to or more than 30kg/m2) who demonstrate insulin resistance based on an oral glucose tolerance test, but who do not fulfill criteria for Type II Diabetes. We hypothesize that rosiglitazone, an insulin-sensitizing agent, will modulate relevant endometrial proliferation biomarkers. In pre-and post-treatment endometrial biopsies, we will assess expression levels of genes involved in estrogen-regulated gro,aedapathways, specific biomarkers as defined in Aim 2, and histologic and proliferation markers. As secondary endpoints, we will establish a point estimate of the baseline frequency of endometrial abnormalities in this cohort and we will determine changes in serum levels of estradiol, estrone, testosterone, DHEA-S and SHBG in obese, post-menopausal women taking rosiglitazone. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ESTROGENS AND INSULIN RESISTANCE IN WOMEN Principal Investigator & Institution: Olefsky, Jerrold M.; Professor; Medicine; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 31-MAY-2007 Summary: (provided by applicant): There are genetic and environmental causes of insulin resistance, and clearly these two inputs can be additive and interactive. A high fat intake is an important environmental factor which can cause, or exacerbate, insulin resistance and enhance the risk for the development of Type II diabetes. Our recent studies have shown that lipid/heparin infusions lead to insulin resistance in men, but not in pre-menopausal women. We also have preliminary data showing that postmenopausal women are fully susceptible to fat-induced insulin resistance and that estrogen replacement therapy re-establishes the protective state. In addition, we have conducted a series of studies in rats, demonstrating that estrogenization (endogenous or exogenous) will protect females from fat -induced insulin resistance. Based on these findings, we propose that men and non-replaced post-menopausal women will exhibit fat-induced insulin resistance, whereas, adequately estrogenized women will be

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protected. We will test these ideas, not only by employing the lipid/heparin infusion glucose clamp technique, but also by placing experimental subjects on control and high fat diets. It is also possible that adequate estrogen can ameliorate the effects of other physiologic causes of insulin resistance. Thus, we also will conduct studies to determine whether estrogenization can protect women from the insulin resistance induced by obesity and aging. Using muscle biopsy samples collected during the glucose clamp studies, we will conduct experiments aimed at identifying cellular mechanisms for these protective effects of estrogens. We also propose an extensive series of animal studies, in which we will explore in more detail the mechanisms of estrogen protection from fatinduced insulin resistance. We will conduct studies in normal male and female rats, ovariectomized rats, and old estrogen deficient female rats+/- treatment with estradiol, an estrogen antagonist, or estrogen receptor isoform specific agonists. Studies in mice with deletion of the alpha or beta forms of the estrogen receptor, as well as muscle specific estrogen receptor specific knockout animals are also proposed. We will also determine whether the fat cell secreted protein ACRP3O is modulated by estrogen status, and whether the insulin sensitizing effects of ACRP3O are responsible for the estrogen induced protection from insulin resistance. If the concepts contained in this application prove correct, then these findings could have significant implications concerning the mechanisms of insulin resistance as well as the treatment and possibly prevention of this disorder. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ETHNIC DIFFERENCES IN INSULIN SENSITIVITY Principal Investigator & Institution: Gower, Barbara A.; Associate Professor; Nutrition Sciences; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-AUG-2004 Summary: This is an application in response to a program announcement for studies to examine racial/ethnic differences in the etiology of type 2 diabetes. The PI proposed a cross-sectional design to examine the time course of change in insulin and insulin resistance that lead to diabetes. The proposed project will: 1) characterize insulin sensitivity, secretion and clearance in African-Americans (AA) and CaucasianAmericans, and 2) determine whether depressed insulin sensitivity (greater insulin resistance) or hyperinsulinemia is likely to be the primary defect. All information regarding differences in insulin sensitivity, secretion and clearance will be obtained from a single frequently sampled intravenous tolerance test and subsequent minimal modeling. A stable isotope of glucose will be used to differentiate glucose uptake from glucose production. Measurement of C-peptide will be performed to differentiate insulin secretion from insulin clearance. Both obese and non-obese AA and C individuals will be studied to examine obesity-ethnic interactions. Free fatty acid concentrations will be measured throughout the glucose tolerance test to begin to address the potential physiological ramifications of chronic hyperinsulinemia among AA subject. The PI believes that the primary defect in conferring lower insulin sensitivity in AA vs C subjects is a defect in hepatic insulin extraction (clearance). The chronic hyperinsulinemia that results from this defect will ultimately result in peripheral (skeletal muscle) insulin resistance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ETIOLOGY AND EPIDEMIOLOGY OF INSULIN DEPENDENT DIABETES MELLITUS Principal Investigator & Institution: Becker, Dorothy J.; Professor; Children's Hosp Pittsburgh/Upmc Hlth Sys of Upmc Health Systems Pittsburgh, Pa 152132583 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: The incident population of children with IDDM and their families are evaluated to determine genetic autoimmune viral causes of the disorder. Heterogeniety of metabolic alterations at presentation is correlated with genetic and autoimmune markers. Oral and intravenous tolerance tests are performed where indicated on nondiabetic subjects and insulin sensitivity assessed using the minimal model technique. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: EVALUATION OF BODY COMPOSITION AND FAT DISTRIBUTION IN CHILDREN Principal Investigator & Institution: Catalano, Patrick M.; Professor; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: The aim of this protocol is to determine if the increase and central distribution of fat found in neonates of women with gestational diabetes as compared with women with normal glucose tolerance during gestation persists through one year of age. We plan to achieve this aim by evaluating control infants and infants of gestational diabetic women at birth and at 4, 8, and 12 months of age. All subjects will have body composition evaluated by total body electrical conductivity and fat distribution using skinfold calipers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: EXERCISE TRAINING IN OBESITY-PRONE BLACK AND WHITE WOMEN Principal Investigator & Institution: Weinsier, Roland L.; Professor and Director; Nutrition Sciences; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-MAY-1995; Project End 30-NOV-2005 Summary: Rationale: Identifying ways to increase physical activity (PA) is paramount to controlling the epidemic of obesity and its co-morbidities, including type 2 diabetes. For unknown reasons, post-obese women and black women appear to be especially prone to weight gain. Data from our current RO1 study suggest that inherent variations in resting energy expenditure and fuel utilization do not distinguish obesity-prone from obesityresistant women or predict weight gain. By contrast, being of black race and having reduced strength, lower free-living PA, and lower total daily energy expenditure are strongly predictive of future weight gain. Objective: To extend our current studies in order to examine the effectiveness of exercise training to improve free-living PA and, in turn, energy balance and weight control. Specifically, we hypothesize that resistance exercise training will be more effective than aerobic and no exercise training in 1) increasing the physiologic ease of, and spontaneous engagement in physical activities of daily living, and 2) increasing total daily energy expenditure and weight-loss maintenance of obese black and white women. Design & Methods: Obese premenopausal black and white women will be randomized to either diet-only, diet+aerobic or diet+resistance exercise training groups. Diet/behavior intervention,

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with or without the aerobic or resistance exercise training, will be provided throughout the 18 months of study. Testing will be done in the obese state, 6 months later in the normal-weight post-obese state, and after 1 year of weight-loss maintenance. All testing will be under tightly controlled General Clinical Research Center conditions following 4 weeks of diet-controlled energy balance. Changes in body composition will be assessed by the 4-compartment model, and insulin resistance by the insulin modified, frequentlysampled intravenous glucose tolerance test. Major outcomes will include measures of perceived and physiologic difficulty of exercise (cardiac, ventilatory, electromyographic responses to standardized exercise tasks); aerobic fitness; strength fitness (isometric tests); and spontaneous free-living PA, activity-related energy expenditure, non-exercise activity thermogenesis, and total daily free-living energy expenditure (all derived from doubly labeled water). Significance: The results will provide insight into the effectiveness of, and the mechanisms by which, different types of exercise training can improve physical fitness, spontaneous engagement in physical activities of daily living and, in turn, weight-loss maintenance, especially in obesity-prone black women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FAT MEDIATED INSULIN SECRETION AND DIABETES IN ELDERLY Principal Investigator & Institution: Boden, Guenther; Professor; Medicine; Temple University 406 Usb, 083-45 Philadelphia, Pa 19122 Timing: Fiscal Year 2002; Project Start 01-DEC-1998; Project End 30-NOV-2003 Summary: Physiological elevations of plasma free fatty acids (FFA) have been shown to produce insulin resistance dose-dependently in healthy and in diabetic subjects and to increase insulin secretion chronically in healthy subjects. However, FFA stimulated insulin secretion less in diabetic (NIDDM) than in non-diabetic subjects. These findings suggested that in most obese subjects, FFA increased insulin secretion sufficiently to compensate for the insulin resistance that they had generated and thus prevented deterioration of glucose tolerance. The objective of the current project is to determine the reason why a minority of obese subjects develop diabetes (NIDDM). Specifically, we plan to test the hypothesis 1) that in obese subjects, who are genetically predisposed to develop NIDDM, FFA fail to appropriate stimulate insulin secretion and 2) that this would then leave peripheral and hepatic insulin resistance, at least partially, uncompensated, resulting in NIDDM. To test this hypothesis, we propose to study effects of a wide spectrum of a wide plasma FFA concentrations on insulin secretions in 3 groups of subjects, representing 3 stages in the development of NIDDM. The 3 groups will consist of 1) first degree relatives of patients with NIDDM. These subjects are normally glucose tolerant, but are considered to be at high risk to develop NIDDM; 2) subjects who have impaired glucose tolerance, i.e., individuals in whom glucose tolerance has not yet deteriorated to the point of frank diabetes and 3) patients with newly diagnosed NIDDM (< 1 year). In all subjects, plasma FFA levels will be either lowered (with nicotinic acid, Test 1) or maintained at basal levels (with saline plus glycerol, Test 2) or increased (with IV lipid plus heparin, Test 3). Plasma glucose concentrations will be clamped at euglycemic levels (all subjects). To assess hepatic actions FFA in more detail we will test effects of elevated plasma FFA (IV lipid/heparin) on rates of gluconeogenesis and glycogenolysis in patients with NIDDM and controls. NIDDM affects between 20 and 30% of the elderly population in the US and is responsible for a large amount of morbidity and mortality. We hope that this project will help to better understand the mechanisms by which obesity contributes to the development of NIDDM.

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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FUNCTIONAL ANALYSIS OF THE BETA-CELL Principal Investigator & Institution: Davis, Roger J.; Professor; Molecular Medicine; Univ of Massachusetts Med Sch Worcester Office of Research Funding Worcester, Ma 01655 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): The overall goal of this research program is to understand the role of the c-Jun N-terminal kinase (JNK) group of mitogen-activated protein (MAP) kinases. Many of the components of the JNK protein kinase cascade have been identified by molecular cloning and have been characterized in biochemical studies. However, an understanding of the physiological role of the JNK signaling pathway has remained elusive. The long-term goal of this research is to define function of the JNK signaling pathway in the beta cell. Previous studies have demonstrated that JNK can phosphorylate and inhibit the function of insulin receptor substrate (IRS) proteins. In addition, the JIP scaffold proteins that co-ordinate the JNK protein kinase cascade have been found to be mutated in diabetic humans. We have constructed several mouse models with defects in the JNK signaling pathway, including mice with defects in the JIP scaffold proteins. These mouse models will be used to study the function of these proteins in beta cells Achievement of the goals of this proposal will increase understanding of signal transduction; mechanisms that contribute to normal beta cell function. This information may represent a basis for the design of novel therapeutic strategies for the treatment of diabetes. The Specific Aims of this proposal are to employ mouse models to: Define the role of JNK in beta cells. Define the role of JIP scaffold proteins in beta cells Define the function of diabetes-associated mutations in JIP1 Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GENE EXPRESSION IN PREDIABETES: POTENTIAL ROLE OF PGC-1 Principal Investigator & Institution: Patti, Mary E.; Assistant Professor of Medicine; Joslin Diabetes Center Boston, Ma 02215 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Since both genotype and environmental risk factors for diabetes, including obesity and inactivity, converge to influence cellular function at the level of gene and protein expression, we hypothesize that alterations in gene expression in nondiabetic individuals at high risk for developing diabetes ("prediabetes") mediate this risk. In our recent array studies of differential gene expression in skeletal muscle from Mexican-American subjects, we identified a pattern of coordinate reduction in expression of multiple nuclear respiratory factor (NRF)regulated genes of oxidative metabolism and mitochondrial function in insulin resistant and diabetic subjects. We have now identified a potential molecular mechanism for these changes: decreased expression of PGC-1, a coactivator of both NRF and PPARgamma-dependent transcription linked to mitochondrial biogenesis and function. Quantitative RT-PCR demonstrates that PGC-1 expression is reduced in insulin resistant and diabetic subjects and correlates with obesity, insulin resistance, and free fatty acid levels. Taken together, these data form the basis of our hypothesis that reductions in PGC-1 and NRF-dependent metabolic gene transcription play an important role in metabolic changes characteristic of insulin resistance and diabetes progression, including inabililty to modulate lipid oxidation, intramuscular lipid accumulation, and

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further insulin resistance. We will test this hypothesis in 2 additional populations at high risk for diabetes: subjects with a family history of diabetes and African-American ethnicity. Moreover, we will test the specific hypotheses that obesity and inactivity mediate risk in prediabetes via reduction in PGC-1 and NRF-dependent gene expression, and evaluate whether weight loss and physical training can increase PGC-1 expression and reverse abnormal patterns of metabolic gene expression in parallel with improved insulin sensitivity. Finally, since it is difficult to dissect the contribution of individual metabolic risk factors to reductions in PGC-1 expression in humans, we will utilize cultured cells to test whether nutrient excess and/or insulin resistance can directly reduce PGC-1 expression, and determine whether experimental reductions in PGC-1 expression can directly induce intracellular triglyceride accumulation and/or insulin resistance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETIC LIPODYSTROPHIES

AND

METABOLIC

BASIS

OF

FAMILIAL

Principal Investigator & Institution: Garg, Abhimanyu; Professor of Internal Medicine; Internal Medicine; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2003; Project Start 15-MAY-1999; Project End 31-MAR-2007 Summary: (provided by applicant): Obesity is a major health problem in the U.S. However, how adipose tissue disorders cause metabolic diseases is not well understood. Study of familial lipodystrophies which are characterized by partial (familial partial lipodystrophies; FPL) or almost complete lack of body fat (congenital generalized lipodystrophy, CGL) and metabolic complications may elucidate the mechanisms involved. Recently, FPL was reported to be due to defects in lamin A/C (LMNA) and peroxisome proliferator-activated receptor-g (PPARG) genes and CGL due to mutations in 1- acylglycerol-3-phosphate O-acyltransferase 2 (AGPA T2) or Seipin genes on chromosome 9q34 and 11q13, respectively. The main aim of this proposal is to identify additional gene(s) that cause CGL and FPL. Another aim is to define the role of AGPAT2 mutations in adipose tissue biology and development by conducting functional studies and by developing a knockout Agpat2 mouse model. To accomplish these aims, we have collected a number of well-characterized CGL pedigrees, which do not harbor substantial alterations in AGPAT2 and Seipin and FPL pedigrees without alterations in LMNA and PPARG. We will carefully characterize minor changes in the phenotype by studying body fat distribution by anthropometry and whole body magnetic resonance imaging and will ascertain severity of metabolic complications by measuring insulin sensitivity, plasma lipoproteins, free fatty acids, glycerol, leptin and other metabolic variables. Additional locus (loci) for CGL and FPL will be determined by genome-wide linkage analysis. Following chromosomal localization and fine mapping, candidate genes, already mapped or identified in these regions will be examined for mutations using direct sequencing. The identification of novel genes responsible for CGL and FPL and understanding of the role of AGPATs in adipocyte biology will lead to a better understanding of how common adipose tissue disorders such as obesity cause insulin resistance and other metabolic complications. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETICS OF BETA CELL FAILURE IN MEXICAN AMERICANS Principal Investigator & Institution: Buchanan, Thomas A.; Professor; Medicine; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033

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Timing: Fiscal Year 2003; Project Start 20-JAN-2003; Project End 31-DEC-2007 Summary: (provided by applicant): In young Hispanic women who developed gestational diabetes mellitus (GDM) during pregnancy, we have identified relatively early-onset and progressive loss of insulin secretion that precedes and predicts the development of type 2 diabetes mellitus (T2DM). The defect in insulin secretion appears to be caused or worsened by insulin resistance and it is highly heritable in families of GDM probands. Based on these observations, we hypothesize that there are genetic determinants of the defect in insulin secretion that leads to T2DM in these young women. We have extensive experience with the performance of detailed phenotyping to quantify insulin secretion and insulin resistance in large cohorts of Hispanic Americans, including one large family-based cohort. We also have access to a large number of large families with a GDM proband. Accordingly, we propose to search for genetic determinants of the beta-cell defect that we have identified, using detailed phenotyping combined with candidate gene and genome-wide QTL linkage analysis. The present application is focused on the recruitment and phenotyping of Mexican American women with GDM and their siblings and first cousins (i.e., families enriched with the Bcell defect) and of matched control women who maintained normal glucose tolerance during pregnancy (robust B-cell function). All of these individuals will have detailed studies of B-cell function, insulin sensitivity and body composition. Additional family members will provide DNA for assessment of identity-by-descent and for future construction of haplotypes in GDM probands and matched controls. Studies of selected candidate genes for GDM and T2DM will be conducted during this award period. Support for a genome-wide scan will be sought separately and will be followed by fine mapping and association studies of positional candidate regions and genes. Ultimately, the results of this project will be crucial in attaining our long-term goals of (a) understanding the fundamental cause(s) of T2DM in young Hispanic Americans and (b) developing strategies to predict and prevent that disease at relatively early stages in its evolution. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OUTCOMES

GESTATIONAL

DIABETES:

DIAGNOSTIC

CRITERIA

AND

Principal Investigator & Institution: Ferrara, Assiamira; Research Scientist Ii; Kaiser Foundation Research Institute 1800 Harrison St, 16Th Fl Oakland, Ca 946123433 Timing: Fiscal Year 2002; Project Start 01-SEP-2000; Project End 31-AUG-2004 Summary: (Adapted from Investigator's Abstract) Gestational diabetes mellitus (GDM) is associated with increased risk of several adverse infant and maternal outcomes and its clinical recognition can reduce these risks. There is concern that the current criteria for GDM may be to restrictive and that residual excess risk of perinatal complications exists below present cutoff values. The proposed study will evaluate whether among women without GDM (as defined by current criteria), increasing levels of maternal glycemia are associated with increased risk of selected perinatal complications: infant severe macrosomia, severe hyperbilirubinemia, hypoglycemia, respiratory distress syndrome, and maternal preeclampsia/eclampsia. To accomplish this, the investigators propose to conduct five nested case-control studies, one for each of the complications of interest, within a large multiethnic cohort of approximately 74,000 women who were screened at 24 to 28 weeks of gestation at Kaiser Permanente, Northern California between 1995 and 1998. In this setting nearly 94 percent of the pregnant women are screened for GDM by a 50 gm., 1 hr. oral glucose tolerance test (50 g, 1-h OGTT) and approximately 15 percent have are abnormal screening and go on to receive the diagnostic (100-g, 3-h OGTT) test.

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Potential cases of each type of complication will be identified by searching computerized hospitalization and laboratory databases. For each of the infant complications, 500 cases will be randomly selected without knowledge of the maternal glucose values. A single control group for the infant complication case groups will be 1,000 infants randomly selected from all births and frequency matched on gestational age to the distribution of the combined case group. Five hundred women with either preeclampsia or eclampsia and 500 age-matched controls will be randomly selected. The medical records of the 3,000 mother-infant pairs in the four case-control studies on infant complications, and 1,000 women for the case-control study of preeclampsia/eclampsia, will be abstracted to confirm eligibility, and, if so, to ascertain data on possible maternal and infant covariates. Logistic regression will be used to estimate the odds ratios associated with several levels of pregnancy glycemia and perinatal complications. The investigators state that the proposed study will provide important knowledge about the magnitude of the risk of severe perinatal complications associated with degrees of maternal hyperglycemia below the glucose cutpoints currently used to diagnose GDM. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GLP-1 TO ENHANCE ISLET TRANSPLANTATION Principal Investigator & Institution: Powers, Alvin C.; Professor of Medicine; Medicine; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2005 Summary: (provided by applicant): Pancreatic islet transplantation holds great promise for the treatment of type 1 diabetes; recent advances in islet isolation and immunosuppression have led to greatly improved results. However, major obstacles and gaps in our current scientific knowledge preclude islet transplantation from being widely adapted as a treatment for type 1 diabetes. For example, most patients require islets isolated from two pancreata to become insulin-independent and often insulinindependence is not permanent. Safe, clinically applicable approaches to increase or sustain islet mass after transplantation in humans are hampered by the inability to study islets or assess islet mass after transplantation in humans. Using a multidisciplinary approach and the transplantation of murine, non-human primate, and human islets, our team proposes to test the hypothesis that glucagon-like peptide-1 (GLP-1), a promising therapy for improving islet function in type 2 diabetes, will increase or sustain islet mass after transplantation. In response to the RFA, the proposed studies will progress from basic science studies in cultured islets and genetically modified mice (bench) to studies of islet transplantation in non-human primates (bedside). In the R-21 phase of the research, we propose the following specific aims: 1) Ascertain the physiological importance of GLP-1 R signaling in murine islet transplantation using genetically modified mice with increased or decreased GLP-1 action. 2) Determine if GLP-1 administration before and/or after transplantation improves the survival of non-human primate islets into an immunodeficient mouse model that allows for in vivo study of xenotransplanted human islets. If these results are informative, we propose a R-33 phase with the following specific aims: 1) Determine the optimal parameters for GLP-1 administration using non-human primate and human islets transplanted into an immunodeficient mouse model that allows for in vivo study of xenotransplanted human islets. 2) Determine if GLP-1 administration increases or sustains islet mass in a nonhuman primate model of islet transplantation. 3) Determine the optimal parameters for GLP-1 administration in a non-human primate model of islet transplantation. As multiple GLP-1 analogues are in clinical trials for the treatment of diabetes, we

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anticipate that information from these models will be directly relevant and quickly applicable to islet transplantation in humans and should lead to a new approach to increase or sustain islet mass after transplantation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HAPO: DATA COORDINATING CENTER Principal Investigator & Institution: Dyer, Alan R.; Professor and Associate Chair; Preventive Medicine; Northwestern University Office of Sponsored Research Chicago, Il 60611 Timing: Fiscal Year 2002; Project Start 04-MAY-1999; Project End 31-MAR-2004 Summary: There is a consensus that overt diabetes mellitus (DM), whether or not accompanied by symptoms or signs of metabolic decompensation, is associated with a significant risk of adverse pregnancy outcome. On the other hand, the risk of adverse outcome associated with degrees of glucose intolerance less severe than overt DM is controversial. The Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study is a basic epidemiologic investigation aiming to clarify unanswered questions on the association of various levels of glucose intolerance during the third trimester of pregnancy and risk of adverse outcomes. Its General Aim -- by means of an international cooperative study involving 16 centers and approximately 25,000 pregnant women -- is to achieve a major advance in knowledge on levels of glucose during pregnancy that place the mother, fetus, and neonate at increased risk. The primary hypothesis is that hyperglycemia during pregnancy, less severe than overt DM, is associated with increased risk of adverse maternal, fetal, and neonatal outcome that is independently related to the degree of metabolic disturbance. Specific Aims of HAPO are: 1. to examine glucose tolerance in a large, heterogeneous, multinational, multicultural, ethnically diverse cohort of women in the third trimester of gestation with medical caregivers "blinded" to status of glucose tolerance (except in those instances where fasting and/or two hour OGTT plasma glucose concentration exceeds a predefined cutoff value); and 2. to derive internationally acceptable criteria for the diagnosis and classification of gestational diabetes mellitus (GDM) based on the specific relationships between maternal glycemia and the risk of specific adverse outcomes that are established through this study. The study is to be accomplished with high quality standardized data collection on the women during the third trimester of gestation (including the OGTT) and at time of delivery for assessment of adverse outcomes, including operative delivery (caesarean section), increased fetal size (macrosomia/obesity), neonatal morbidity (hypoglycemia), and fetal hyperinsulinism. HAPO is to include a Clinical Coordinating Center and Data Coordinating Center, both located at the Northwestern University Medical School in Chicago, as well as a Central Laboratory located in Belfast, United Kingdom. This application requests support for the Data Coordinating Center for HAPO. Cost effectiveness for HAPO is enhanced through cost sharing by colleagues in non-U.S. centers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: HEPATIC FATTY ACID METABOLISM AND INSULIN RESISTANCE Principal Investigator & Institution: Stefanovic-Racic, Maja; Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 31-MAR-2009 Summary: (provided by applicant): Insulin resistance is a hallmark feature of type 2 diabetes mellitus (DM) and is also present in many obese individuals and the majority

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of those with the metabolic syndrome. Fasting plasma free fatty acids (FFA) are frequently elevated in these subjects and significant controversy surrounds the role of hepatic FFA oxidation in the development of insulin resistance. Previous studies have been limited by the absence of a specific activator of this pathway. However, our preliminary data demonstrate that this issue can be addressed directly for the first time by overexpression of the enzyme carnitine palmitoyltransferase I (CPT I), a major intracellular regulator of beta-oxidation. This proposal has two primary goals. The first is to provide the applicant with the skills necessary to become an independent clinical investigator in the field of lipid metabolism and type 2 DM. Training aims; 1. To expand the candidate's theoretical background in the biochemistry of metabolic disorders. 2. To gain experience in the design and interpretation of metabolic studies. 3. To learn many of the practical techniques necessary to pursue a career in metabolic research. The second goal is to perform novel research into the role of L-CPT I in hepatic fatty acid metabolism, particularly as it relates to the development of insulin resistance, liver steatosis and type 2 DM. Research aims: In Aim 1, we will test the hypothesis that increased activity of L-CPT I in hepatocytes in vitro will promote fatty acid oxidation, while reducing acyl-CoA esterification, intracellular triglyceride (TG) accumulation and very low-density lipoprotein (VLDL) secretion. In Aims 2, 3 and 4, CPT I will be overexpressed in vivo, in the liver of normal rats, high-fat fed obese/insulin resistant rats and ZDF obese/diabetic rats, respectively. Elevated hepatic L-CPT I is expected to have similar effects on lipid metabolism as proposed for in vitro studies. We hypothesize that such alterations will decrease or prevent lipid accumulation in the liver. This is expected to: (1) enhance insulin sensitivity in normal rats (Aim 2); (2) ameliorate the disregulation of liver fatty acid metabolism associated with the development of insulin resistance in the high-fat fed animals (Aim 3); and (3) prevent or reverse the abnormalities of fatty acid metabolism that accompany the fully diabetic phenotype in ZDF rats (Aim 4). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HERITAGE: GENETICS, RESPONSE TO EXERCISE, RISK FACTORS Principal Investigator & Institution: Wilmore, Jack H.; Professor and Head; Health and Kinesiology; Texas A&M University System College Station, Tx 778433578 Timing: Fiscal Year 2002; Project Start 01-JUL-1992; Project End 31-AUG-2004 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: HERITAGE:GENETICS RESPONSE TO EXERCISE RISK FACTORS-III Principal Investigator & Institution: Leon, Arthur S.; Kinesiology; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2002; Project Start 01-JUL-1992; Project End 31-AUG-2004 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: HIV ANTIRETROVIRAL DRUGS AND GLUCOSE METABOLISM Principal Investigator & Institution: Grunfeld, Carl; Professor of Medicine; Northern California Institute Res & Educ 4150 Clement Street (151-Nc) San Francisco, Ca 941211545 Timing: Fiscal Year 2004; Project Start 01-MAR-2004; Project End 31-DEC-2007

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Summary: (provided by applicant): The development of highly active anti-retroviral therapy with protease inhibitors (PIs) has been associated with metabolic abnormalities including disturbances in glucose metabolism, dyslipidemia, and fat distribution/lipodystrophy. However their cause is debated. Data show that not all of the metabolic effects of PIs are direct toxic effects, as some are due to restoration to health, reconstitution of immune system or changes in fat distribution. A role for NRTI is emerging. To design future HIV drugs that have the least metabolic effects it is necessary to determine which metabolic effects of these drugs are direct toxic drug effects vs. secondary to changes in disease status. Given the difficulty in dissecting out the different contributors in HIV-positive patients, we have begun studies of the metabolic effects of ARV in HIV-negative controls. We have evidence that the metabolic effects are drug-specific and not class-specific with independent effects of PIs on glucose and lipid metabolism. Our preliminary data suggest that PIs affect several pathways in glucose metabolism including peripheral insulin resistance, insulin secretion and hepatic glucose production. These three lesions are key contributors to the development of type 2 diabetes. Therefore we propose to test the effects of PIs and NRTIs as follows: Specific Aim 1a: To determine which Pls inhibit insulin secretion in humans. Specific Aim 1b: To determine which PIs acutely block insulin mediated glucose disposal in humans. Specific Aim 1c: To determine which PIs increase hepatic glucose production and to determine the mechanisms by quantifying gluconeogenesis and glycogenolysis. Specific Aim 2a: To demonstrate that in subjects with elements of Metabolic Syndrome compared to thin healthy controls, PIs induce more diabetes and impaired glucose tolerance on oral glucose tolerance testing. Specific Aim 2b: To determine if the effects of PIs in Metabolic Syndrome are more severe at the level of resistance to insulin-mediated glucose disposal, insulin secretion and hepatic glucose production. Specific Aim 3a: To demonstrate that NRTI combinations, alone or with a PI, affect glucose metabolism in HIV negative subjects using the OGTT in acute or four-week studies. Specific Aim 3b: To determine the mechanisms by which NRTI adversely affect glucose metabolism, we will assess their effects on insulin mediated glucose disposal, insulin secretion and/or hepatic glucose production. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HOSTILITY, RACE, AND GLUCOSE METABOLISM Principal Investigator & Institution: Surwit, Richard S.; Professor; Psychiatry; Duke University Durham, Nc 27710 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2007 Summary: (provided by applicant): Recent research in our laboratory has provided evidence that the metabolic correlates of hostility may play a role in the racial disparity in the prevalence of type 2 diabetes. We propose to study how hostility is differentially related to glucose metabolism in healthy African-Americans and Caucasians, to determine the underlying behavioral and physiologic mechanisms of these relationships, and to investigate the possibility that race and sex interact in determining this relationship. We will assess the multi-factorial nature of hostility in 400 healthy African-American and Caucasian men and women. These psychometric measures will be examined in relation to fasting and two-hour post-prandial glucose and insulin as well as hemoglobin AIC (HbAIC) on all subjects. We will test the hypothesis that hostility is related to insulin resistance in Caucasians and to glucose production and defective glucose-stimulated insulin secretion in African-Americans, putting hostile African-Americans at greater risk for developing diabetes. Accordingly, we will assess glucose-stimulated insulin release, insulin resistance, hepatic glucose production and

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glucose effectiveness utilizing an IV GTT with labeled glucose in a subset of our sample. We will begin to determine the mechanism by which hostility impacts glucose metabolism in an African-American and Caucasian population. Three sets of mediators will be examined in the subjects studied parameters of hypothalamic-pituitary-adrenal (HPA) axis activity, measures of body mass and fat distribution, and measures of behavioral factors including calorie intake and exercise habits. It is further hypothesized that while the relationship of hostility to fasting insulin and insulin sensitivity in Caucasians is mediated by BMI and behavioral variables, the relationship of hostility to fasting glucose in African-Americans will depend on neuroendocrine factors influencing hepatic glucose production and insulin secretion. These studies will further our understanding of the differences in the etiology of diabetes in these ethnic groups and may help explain the racial disparity in this disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INSULIN RESISTANCE AND ADENOMAS OF THE COLORECTUM Principal Investigator & Institution: Haffner, Steven M.; Professor of Medicine; Medicine; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2002; Project Start 20-AUG-2001; Project End 31-JUL-2004 Summary: There is considerable evidence that insulin and/or insulin-like growth factors (IGFs) can increase risk of colorectal neoplasia. Epidemiologic risk factors for colorectal neoplasia are similar to those for insulin resistance syndromes, and prospective studies have shown both diabetes and higher levels of IGF-1 to be associated with colorectal cancer risk. No previous studies have included direct measures of insulin resistance, nor have any included complete ascertainment of colorectal neoplasia by direct examination of the entire colorectum. This study will assess the relationship between insulin resistance and colorectal neoplasia by taking advantage of a unique opportunity to examine a multi-ethnic cohort on whom prior measures of insulin sensitivity have been made. The Insulin Resistance and Atherosclerosis Study (IRAS) is a cohort study supported by the National Heart Lung and Blood Institute. IRAS examined 1628 people of average age 55 in 1991-1994 for atherosclerosis risk factors. The cohort, assembled in four clinical centers (Alamosa, Co., Los Angeles, Oakland, and San Antonio) was established to be multi-ethnic (34 percent Hispanic, 28 percent African American, and 38 percent non-Hispanic white), bi-gender, and varied in diabetes risk. In 1998-1999 over 85 percent of the surviving cohort was re-examined. Both of the examinations have included measures of self-reported risk factors for atherosclerosis (diet, physical activity, tobacco use, family history) as well as anthropometry and, most importantly, oral glucose tolerance testing and frequently-sampled intravenous glucose tolerance tests (FSIGT). The FSIGT is a sensitive and specific measure of insulin resistance. All surviving cohort members (estimated 1518) will be invited to have a screening colonoscopy. Feasibility data indicate that 1000 will agree to have a colonoscopic exam, among whom we estimate 240 (range 206- 274) will have adenomas. Mucosal biopsies will be taken from the cecum and rectum of all subjects, and all adenomas will be removed and examined for histologic features, Ki-ras mutations, proliferation, and apoptosis. Serum samples will be assayed for insulin, IGF-1, IGFBP1, and IGFBP3 levels for all cohort members at both the time of colonoscopy, as well as at the time of two earlier examinations (1991-4 and 1998-9) using stored serum samples. This study offers the advantage of the availability of prospective measures of glucose tolerance, insulin resistance, measurements of most colorectal neoplasia risk factors, and the availability of stored blood samples from a multi-ethnic and bi- gender cohort. Complete colorectal

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visualization of this entire cohort will enable unbiased estimates of colorectal neoplasia risk related to these factors. This study therefore offers a time-efficient and a costefficient method to test the hypothesis that colorectal neoplasia risk is increased substantially by factors related to insulin resistance, and to examine the biologic mechanisms whereby that risk is increased. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INSULIN RESISTANCE AND CARDIOVASCULAR RISK FACTORS Principal Investigator & Institution: Egan, Brent M.; Associate Professor; Pharmacology; Medical University of South Carolina P O Box 250854 Charleston, Sc 29425 Timing: Fiscal Year 2002; Project Start 15-SEP-2000; Project End 31-AUG-2005 Summary: This K-24 application includes a mentoring plan and two research components which are linked together by the common theme of insulin resistance and cardiovascular risk factor clustering. In part 1 of the research plan, we plan to continue work under the current R01 and a subsequent competitive renewal to test the hypothesis that fatty acids and angiotensin induce a synergistic enhancement of oxidative stress in humans. The three specific aims are to determine (1) the effects of raising fatty acids and angiotensin singly and in combination on markers of platelet PKC activity and oxidative stress (2) the effects of a low NaCl diet, which raises plasma angiotensin II, on markers of oxidative stress in obese hypertensive patients during treatment, with an AT1 receptor antagonist compared to placebo 3) which protein kinase C (PKC) isoform isoform(s) are stimulated by oleic acid and lead to the generation of reactive oxygen species and activation of extracellular signal-regulated kinases in human aortic smooth muscle cells by using antisense oligonucleotides to specific PKCs. Each of these specific aims will be addressed using methods which are well established in our patientoriented clinical and bench research. In part 2, with the support of this K-24 Award, we plan to extend the generalizability of our findings to the wider community and by addressing important gaps in the literature on low birth weight and cardiovascular risk. We will test the hypothesis that low birth weight contributes to cardiovascular risk and salt sensitivity in a biracial sample of young adults at two college campuses in South Carolina. Three specific aims will be addressed to determine the relationships of low birth weight (<2500 grams) to (1) metabolic components of insulin resistance (oral glucose tolerance test and dyslipidemia (NMR lipid profile) (2) hemodynamic components of the insulin resistance syndrome including laboratory and 24-hour ambulatory blood pressure (BP), baroreflex sensitivity (cross spectral analysis of systolic BP and heart rate), proximal and distal arterial compliance (HDI pulse-wave) and postischemic forearm vascular resistance (venous occlusion plethysmography). (3) Salt sensitivity defined by the differences in BP on 180 vs. 80 mmol/d NaCl diets. All of the mentoring activities, which would be supported by the K-24 Award, also relate to various facets of the insulin resistance syndrome. "Access to excess" calories and labor saving devices has produced an epidemic of obesity and cardiovascular risk factors related to insulin resistance. While lifestyle changes are important and the PI and his colleagues work diligently in this area most people are unable to normalize their risk through lifestyle changes alone. We believe that a better definition of the pathophysiological common denominators and key intracellular signaling events mediating these effects will provide the basis for novel therapeutic approaches to cardiovascular disease prevention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: INSULIN RESISTANCE AND POLYCYSTIC OVARY SYNDROME Principal Investigator & Institution: Brown, Ann J.; Medicine; Duke University Durham, Nc 27710 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): This career development proposal details a plan for the Principal Investigator to obtain the training and experience necessary to develop an independent career as a clinical investigator. By conducting the proposed study, the PI will develop skills that will enable her to study the effects of exercise on insulin resistance in polycystic ovary syndrome (PCOS), and that will be relevant to many career pathways. PCOS is a common disorder affecting up to 10% of young women. It is characterized clinically by hirsutism and oligo/amenorrhea. Recent studies have documented significant insulin resistance in this population suggesting an important predisposition to long-term complications such as diabetes and cardiovascular disease. The early onset and large affected population create a powerful opportunity to harness the positive effects of lifestyle changes for purposes of disease prevention. However, the hirsutism and obesity associated with PCOS may create psychological barriers to change. For this reason, effective management may require a tailored approach that takes into account psychosocial issues as well as metabolic profile. Physical activity is an ideal intervention for this group. Exercise reduces insulin resistance, improves cardiovascular health and enhances sense of wellbeing. However, the type, duration and intensity of exercise that will optimally reduce insulin resistance, and that is well tolerated, has not been established. This study is meant to address these issues by answering the following questions about women with PCOS: 1. In a randomized controlled clinical trial, does a 12 week program of monitored exercise of moderate intensity, without weight loss, significantly improve insulin sensitivity as measured by an intravenous glucose tolerance test? What is the relative magnitude of the acute effect compared to the chronic effect of exercise on insulin sensitivity? 2. Does exercise that reduces insulin resistance also decrease androgen levels? 3. Does exercise improve indicators of perceived body image, quality of life, stress and depression? Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: INSULIN RESISTANCE IN ADOLESCENTS AT HIGH RISK FOR PCOS Principal Investigator & Institution: Geller, David H.; Cedars-Sinai Medical Center Box 48750, 8700 Beverly Blvd Los Angeles, Ca 900481804 Timing: Fiscal Year 2002; Project Start 20-SEP-2001; Project End 31-AUG-2006 Summary: (provided by applicant): The applicant previously focused his research on molecular aspects of steroid hormone biosynthesis. He recently assumed a position as Assistant Professor of Pediatrics in the UCLA School of Medicine. To further his career, as an independent investigator, he has established relationships with experts in the fields of ovarian physiology, insulin signaling, sensitivity and secretion. Under their mentored supervision, the candidate will initiate studies to address the childhood origins of the polycystic ovary syndrome (PCOS). PCOS is a heterogeneous clinical entity characterized by the post-pubertal onset of menstrual irregularities and excessive production of male hormones. PCOS is the most common endocrine disorder of women of reproductive age, affecting 5-10% of women worldwide. Insulin resistance is a necessary antecedent of both type 2 diabetes mellitus (T2DM) and the hormonal imbalances characteristic of PCOS. As insulin resistance is a transient physiologic phenomenon of normal pubertal maturation, the applicant hypothesizes that the

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requisite insulin resistance of PCOS must be expressed initially during pubertal progression. Cross- sectional and longitudinal studies will describe the patterns of insulin sensitivity that emerge throughout puberty in young women. Initially, the applicant will contrast the insulin sensitivity achieved on frequently sampled intravenous (iv) glucose tolerance tests between two matched sets of 25 subjects from families with, and without, histories of PCOS, at each of two distinct stages of puberty. He will then test the hypothesis that insulin resistance evolving throughout puberty in 40 girls at high risk for development of PCOS differs qualitatively and quantitatively in its pattern of expression, when compared with an equal number of adolescent controls. The applicant will measure specific biophysical and biochemical parameters to determine whether changes in these easily-obtained indices correlate with and predict changes in insulin sensitivity. To begin to elucidate the cellular mechanism for this unique form of insulin resistance, the applicant further proposes to obtain needle biopsies of insulin-responsive muscle from select subjects who demonstrate extremes of insulin sensitivity in the cross- sectional study. The applicant will assess the integrity and function of specific molecules necessary for cellular transmission of the insulin signal, to determine whether changes in these effectors might be responsible for evolving insulin resistance in at-risk individuals. This work will provide insight into the earliest relationship between PCOS and insulin resistance, at the whole-body and cellular level. Enhanced understanding of these fundamental events may permit earlier detection and intervention, thus preventing the profound physiological consequences of unabated T2DM associated with PCOS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INSULIN RESISTANCE IN PCOS--SEQUELAE AND TREATMENT Principal Investigator & Institution: Legro, Richard S.; Associate Professor; ObstetricsGynecology; Pennsylvania State Univ Hershey Med Ctr 500 University Drive Hershey, Pa 170332390 Timing: Fiscal Year 2002; Project Start 01-APR-2001; Project End 31-MAR-2006 Summary: (Adapted from the applicant's description): The immediate goals of the PI are to expand the focus of his research from familial forms of polycystic ovary syndrome (PCOS), and genetic influences on the development of the syndrome into areas with even greater clinical impact. Specifically the goals of this application are to 1) identify other unrecognized morbidity that results from insulin resistance in PCOS and in the long term. 2) expand the clinical trials of improving insulin sensitivity as a primary treatment modality in PCOS. Another long-term goal is to develop within the medical center a cadre of investigators interested in PCOS patient-oriented research. The overall hypothesis of this proposal is that insulin resistance is the fundamental pathophysiologic defect in women with PCOS, that its effects can be protean and unrecognized, and that metabolic abnormalities worsen with age. Our preliminary studies suggest that insulin resistance is major contributor to both the etiology of PCOS and its association with sleep apnea. We propose further studies to clarify the role of insulin resistance in both PCOS and control female populations on sleep disorders. We theorize that there is enhanced steroidogenesis in endometrial glandular and stromal cells from women with PCOS and this is further stimulated by hyperinsulinemia. We intend to study these hypotheses in endometrial tissue form PCOS women and appropriate controls. Our preliminary experience suggests that insulin resistance over time will lead to a worsening of glucose tolerance and other metabolic markers in PCOS women with an improvement in reproductive abnormalities such as anovulation and hyperandrogenemia. We propose to identify clinical interventions in PCOS women that

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will improve insulin sensitivity and manifestations of the syndrome. Improving insulin action through diet and exercise, with and without weight loss, will result in lowered circulating insulin levels, lowered androgens and increased ovulatory frequency rate in PCOS women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INSULIN RESISTANCE IN TISSUE SPECIFIC IKKB TRANSGENICS Principal Investigator & Institution: Lee, Jongsoon; Joslin Diabetes Center Boston, Ma 02215 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2004 Summary: (provided by applicant): Our studies in insulin resistant cells and animals, and type 2 diabetic patients showed that the IkappaB kinase, IKKbeta, plays a central role in acquired insulin resistance. In 3T3-L1 adipocytes and Fao hepatoma cells, activation of IKKbeta by treatment of TNF or by transfection of upstream kinase, NIK, or constitutively active IKK, induced cellular insulin resistance-decreased insulinstimulated Tyr phosphorylation of IR and IRSs. Inhibition of IKKbeta by specific inhibitors- high doses of salicylates (NaS) or aspirin (ASA)- or by transfection of dominant negative IKKbeta reversed TNF-induced insulin resistance. Treatment of high doses of NaS or ASA to type 2 diabetes patients or obese and insulin resistant animals reversed insulin resistance as judged by glucose tolerance test (GTT), insulin tolerance test (ITT) and hyperinsulinemic, euglycemic clamp studies. Hyperglycemia, hyperinsulinemia, and dyslipidemia are normalized by ASA treatment. Insulin signaling studies conducted with tissues isolated from the rodents show that insulinstimulated Tyr phosphorylation of IR and IRS are increased due to decrease in inhibitory Ser/Thr phosphorylation of IRSs. Heterozygous deletion (IkkBeta +/-) in mice reduced fasting glucose and insulin concentrations, and protected against the development of insulin resistance during high-fat feeding and in obese Lep-ob/ob mice. We also found that obese animals have higher IKK kinase activity than control animals. To study which tissue(s) are important for IKK-mediated insulin resistance and for the reversal of insulin resistance by salicylates, we generated mice expressing constitutively active IKKbeta in fat, muscle and liver with the hypothesis that increasing IKKbeta activity in animal tissues may itself induce insulin resistance. We now have colonies of all three tissue transgenic mice and found that fat- and liver-specific transgenic mice have developed insulin resistance as early as 4 week-old. We will characterize these mice to determine which tissue is responsible for IKKbeta-induced insulin resistance and how activation of IKKbeta in one tissue can induce whole body insulin resistance. These experiments will validate IKKbeta as a major mediator of insulin resistance and as a useful target for the discovery of new drugs to treat type 2 diabetes and insulin resistance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: INSULIN SCHIZOPHRENIA

SENSITIVITY/SECRETION/

GLUCOSE

IN

Principal Investigator & Institution: Henderson, David C.; Executive Secretary (Dfo); Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: INTRA-ABDOMINAL ADOLESCENTS

FAT

AND

RISK

OF

DISEASE

IN

Principal Investigator & Institution: Goran, Michael I.; Associate Director and Professor; Preventive Medicine; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033 Timing: Fiscal Year 2002; Project Start 01-JUN-1997; Project End 31-MAY-2005 Summary: (provided by applicant): The specific aim of this competitive renewal application is to extend data collection in our existing cohort of Caucasian and African American children, so that data on changes in body composition, abdominal fat distribution and insulin action and secretion are obtained in all children to the point of achieving full maturation. Progress: We have established a successful cohort study and made considerable progress towards understanding differences in metabolic risk factors that occur during early pubertal growth (to the point of mid-puberty), how these are influenced by body fat and visceral fat, and especially how these differ between African American and Caucasian children. We have shown that African American children have unfavorable differences in glucose metabolism (hyperinsulinemia, reduced insulin sensitivity, and increased acute insulin response) that remain highly significant even after adjusting for differences in body composition, fat distribution, physical activity and dietary factors. We have shown that the transition from Tanner Ito Ill is associated with a 33% reduction in insulin sensitivity with a lower than expected rise in the acute insulin response. This pubertal fall in insulin sensitivity is independent of obesity status and consistent across gender and ethnic groups. Based on these findings and other preliminary data we are proposing two new hypotheses. Hypothesis 1: Insulin sensitivity will increase and the acute insulin response will decrease from Tanner Ill to Tanner V towards the levels observed prior to puberty. However, the overall recovery of insulin sensitivity and the acute insulin response, as indicated by the change in the disposition index will be poorer in African American children and more obese children; Hypothesis 2:Glucose tolerance will be maintained during puberty by an increase in first-phase insulin secretion except in the most susceptible of individuals (e.g. AfricanAmerican females) who will show an impairment in first-phase insulin secretion with progression of puberty. Summary: This competitive renewal provides a unique opportunity to examine the nature of transient insulin resistance during puberty, and especially how this may differ in African American children who are at increased risk for type 2 diabetes during puberty. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INTRAISLET COMMUNICATION IN SURGICALLY-ALTERED PANCREAS Principal Investigator & Institution: Brunicardi, F. Charles.; Professor; Surgery; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2004; Project Start 01-MAY-1993; Project End 31-JAN-2008 Summary: (provided by applicant): Preliminary data suggest the presence of a delta-tobeta cell endocrine axis within the islet in which intraislet somatostatin inhibits insulin secretion. The somatostatin receptor subtypes responsible for the inhibition of insulin are unknown, however, preliminary data suggest that SSTR1 and SSTR5 are important regulators of insulin secretion and that there are species differences. We have also demonstrated the importance of the axis in that gene ablation of SSTR5 and/or SSTR1 in mice results in significant age- and sex-dependent alterations in insulin secretion, glucose regulation and islet morphology, and ultimately in diabetes. The purpose of this

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competitive renewal proposal is to prove the hypotheses that a) intraislet somatostatin is an important inhibitory regulator of insulin secretion via SSTR5, b) systemic somatostatin is an important inhibitory regulator of insulin secretion via SSTR1 and c) disruption of the inhibitory effect of intraislet and/or systemic somatostatin by gene ablation of SSTR5 and/or SSTR1 will result in diabetes in mice. We hope to translate the observations in mice to human islets and determine the role of SSTR5 and SSTR1 in the human endocrine pancreas in three specific aims: Specific Aim 1. to determine whether a) intraislet somatostatin inhibits insulin secretion via SSTR5 in mice, b) disruption of the inhibitory effect of intraislet somatostatin by gene ablation of SSTR5 results in altered insulin secretion, glucose homeostasis and islet morphology and ultimately diabetes in older mice and c) the alterations are age- and sex-dependent. Specific Aim 2. to determine whether a) intraislet somatostatin inhibits insulin secretion via SSTR1 in mice, b) disruption of the inhibitory effect of intraislet somatostatin by gene ablation of SSTR1 results in altered insulin secretion, glucose homeostasis and islet morphology and ultimately diabetes in younger mice, and c) the alterations are age- and sexdependent, and d) double gene ablation of SSTRI/SSTR5 results in altered insulin secretion, glucose homeostasis and islet morphology and ultimately diabetes in mice. Specific Aim 3. to determine whether a) intraislet somatostatin inhibits insulin secretion via SSTR1 and SSTR5 in human islets and b) the regulatory effects of SSTR1 and SSTR5 are age- and sex-dependent. For this proposal, four mouse colonies, already established in our laboratory, will be studied over time: 1) SSTR5 1/- mice, 2) beta cell-specific SSTR5 -/- mice, 3) SSTR1 -/-mice and 4) SSTRI&5 -/- mice. One additional mouse colony will be developed: 1) beta cell-specific SSTR-/- mice. In vivo and in vitro physiology studies will be performed using the following techniques: 1) intraperitoneal glucose tolerance tests in mice 2) isolated perfused mouse pancreas, 3) isolated mouse islet cultures, and 4) isolated perfused human pancreas. The role of SSTR1 and SSTR5 on human and mouse insulin secretion will be determined by examining insulin responses to varying levels of glucose, selective SSTR1 and SSTR5 agonists and to a potent somatostatin monoclonal antibody. Immunohistochemistry, Western blot, Northern blot, Southern blot and RT-PCR will be used to determine whether SSTR1 and SSTR5 gene ablation alters expression of selected regulatory proteins, such as other SSTRs, PDX-1, PCNA, c-Myc, and TGF-beta and Smads in mouse islets. Light microscopy will be used to study alterations in structure of the endocrine pancreas following SSTR1 and SSTR5 gene ablation in mice. The proposed studies will determine whether SSTR1 and SSTR5 are the predominant inhibitory regulators of insulin secretion in human and mouse islets and whether there are pathophysiologic consequences to ablating these receptors in mouse beta cells. Translation of observation in these molecularlyengineered mouse islets to human islets will hopefully provide greater insights into physiologic pathways regulating human insulin secretion, which potentially could benefit in the diagnosis and treatment of patients with diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IRAS FAMILY STUDY: GENETICS OF INSULIN RESISTANCE Principal Investigator & Institution: Saad, Mohammed F.; Professor; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 15-SEP-1999; Project End 31-AUG-2004 Summary: Insulin resistance is an important risk factor for atherosclerosis. Insulin sensitivity varies widely within populations and substantial evidence indicates that much of the variation can be attributed to genetic factors. Visceral adiposity, another

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important atherosclerosis risk factor, appears also to be genetically determined and correlates strongly with insulin resistance. The overall goals of this proposal are to: 1) identify the genetic determinants of insulin sensitivity and visceral adiposity; 2) determine the extent to which insulin sensitivity, visceral adiposity, and metabolic cardiovascular risk factors share common genetic influences. To address these goals, we will enroll family members of 160 African-American and Hispanic men and women who are currently participating in the Insulin Resistance Atherosclerosis Study (IRAS). Approximately 1280 family members will be recruited. Insulin sensitivity will be measured using the frequently sampled intravenous glucose tolerance test with minimal model analysis. Visceral adiposity will be assessed with computed tomography and traditional metabolic cardiovascular risk factors will be measured. A panel of 370 microsatellite markers will be genotyped from DNA and a genome-wide scan will be performed to detect chromosomal regions containing loci that influence phenotypic variation. We will then saturate the regions of linkage identified in these analyses with additional markers and will perform linkage disequilibrium analysis to localize further the putative loci. The organization of this study will be similar to that of IRAS, with three clinical centers, a coordinating center, a central laboratory, and a genetic laboratory. Our center will examine 432 family members of 54 African-American participants in the IRAS. This project will contribute substantially to our understanding of the genetic determinants of insulin sensitivity, visceral adiposity, and the risk of atherosclerosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IRAS FAMILY STUDY--GENETICS OF INSULIN RESISTANCE Principal Investigator & Institution: Bergman, Richard N.; Physiology and Biophysics; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033 Timing: Fiscal Year 2002; Project Start 15-AUG-1999; Project End 31-JUL-2004 Summary: Insulin resistance is an important risk factor for atherosclerosis. Insulin resistance varies widely within populations, and substantial evidence indicates that much of this variation can be attributed to genetic sources. Visceral adiposity, another important atherosclerosis risk factor, is strongly correlated with insulin resistance, and this trait also appears to be under substantial genetic control. The overall goals of the proposed research project are to: 1) identify the genetic determinants of insulin resistance and visceral adiposity; and 2) determine the extent to which insulin resistance visceral adiposity, and metabolic cardiovascular disease risk factors share common genetic influences. To address these goals, we will enroll 160 families of AfricanAmerican and Hispanic background who are participating in the Insulin Resistance Atherosclerosis Study (ERAS). Approximately 1280 additional family members will be recruited. Insulin resistance will be measured using the frequently sampled intravenous glucose tolerance test, and visceral adiposity will be measured using computed tomography. A panel of other metabolic cardiovascular disease risk factors will also be assessed. A panel of 370 microsatellite markers will be genotyped from DNA, and a genome-wide scan will be performed to detect chromosomal regions containing loci that influence phenotypic variation. We will then saturate the regions of linkage identified in these analyses with additional markers and will then perform linkage disequilibrium analyses in effort to localize further the putative loci. The organization of this study will be similar to that of IRAS, with three clinical centers, a coordinating center, a central laboratory and a genetic laboratory. This center at the University of Southern California will be responsible for performing and coordinating laboratory measurements, as well as for analysis of insulin sensitivity and other metabolic parameters. This project will

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contribute substantially to our understanding of the genetic determinants of insulin sensitivity, and consequently to risk of atherosclerosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IRAS FAMILY STUDY--MOLECULAR GENETICS Principal Investigator & Institution: Bowden, Donald W.; Professor; Biochemistry; Wake Forest University Health Sciences Winston-Salem, Nc 27157 Timing: Fiscal Year 2002; Project Start 15-AUG-1999; Project End 31-JUL-2004 Summary: Insulin resistance is an important risk factor for atherosclerosis. Insulin resistance varies widely within populations, and substantial evidence indicates that much of this variation can be attributed to genetic sources. Visceral adiposity, another important atherosclerosis risk factor, is strongly correlated with insulin resistance, and this trait also appears to be under substantial genetic control. The overall goals of the proposed research project are to: 1) identify the genetic determinants of insulin resistance and visceral adiposity; and 2) determine the extent to which insulin resistance, visceral adiposity, and metabolic cardiovascular disease risk factors share common genetic influences. To address these goals, we will enroll 160 families of African-American and Hispanic background who are participating in the Insulin Resistance Atherosclerosis Study (IRAS). Approximately 1280 additional family members will be recruited. Insulin resistance will be measured using the frequently sampled intravenous glucose tolerance test, and visceral adiposity will be measured using computed tomography. A panel of other metabolic cardiovascular disease risk factors will also be assessed. A panel of 370 microsatellite markers will be genotyped from DNA, and a genome-wide scan will be performed at the Mammalian Genotyping Service to detect chromosomal regions containing loci that influence phenotypic variation. We will then saturate the regions of linkage identified in these analyses with additional markers and will then perform linkage disequilibrium analyses in effort to localize further the putative loci. The organization of this study will be similar to that of IRAS, with three clinical centers, a coordinating center, a central laboratory and a genetics laboratory. This Molecular Genetics component of the study will (1) carry out genomic DNA isolation and quality control, (2) fill significant gaps and correct errors in data from the whole genome screen, and (3) carry out detailed analysis of chromosome regions which show evidence for linkage. This project will contribute substantially to our understanding of the genetic determinants of insulin sensitivity, and consequently to risk of atherosclerosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ISLET ALLOGRAFT GENE THERAPY FOR PRIMATE DIABETES Principal Investigator & Institution: Stewart, Andrew F.; Professor; Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2006 Summary: (provided by applicant): This application is written in response to RFA DK03-001, "Bench to Bedside Research in Type 1 Diabetes and Its Complications". The application represents a joint effort of two groups, one in Miami and one in Pittsburgh. The Miami group has a strong record of expertise and achievement in non-human primate and human islet transplantation, as well as fluency in islet transplant immunology. The Pittsburgh group has a strong track record using the transgenic and viral delivery of growth factors to the pancreatic islet. This application, therefore, in accord with the goals of the RFA, brings together basic scientists with expertise in beta

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cell molecular and cellular biology, beta cell gene therapy, and beta cell immunology, with animal physiologists expert in islet transgenic mouse development, rodent islet transplant, and non-human primate islet transplant, with clinicians with expertise in human islet transplantation and clinical management of diabetes. Specifically, the Pittsburgh group has shown that: 1) transgenic or adenoviral gene delivery of hepatocyte growth factor (HGF) to rodent islets prior to islet transplantation markedly improves transplant outcomes and islet graft function, 2) that this markedly reduces the number of islets required to achieve successful transplant outcomes in rodents, and 3) that HGF can be readily delivered to non-human primate islets using gene transfer techniques. The Miami group has demonstrated that the steroid-free immunosuppression protocol developed by the Edmonton group for humans can be successfully applied to non-human primates, and have developed an ideal marginal islet mass transplant model in non-human primates. This confluence of methodology and expertise allow the combined groups to test the hypothesis that delivery of HGF to nonhuman primate islets will very significantly enhance the engraftment and performance of these islets, and will therefore very significantly reduce the number of islets required to achieve normal glycemic control. We are optimistic that these studies will likely achieve their goal, and will serve in the near term as the third and final preclinical step required for similar studies in humans with diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: JAPANESE AMERICAN COMMUNITY DIABETES STUDY Principal Investigator & Institution: Boyko, Edward J.; Professor; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: This longitudinal study examines the relationship of environmental factors in the development of the insulin resistance syndrome (hyperinsulinemia, central obesity, glucose intolerance, hypertension, dyslipidemia, and coronary heart disease) in Japanese Americans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: LEPTIN TREATMENT OF HIV-ASSOCIATED LIPODYSTROPHY Principal Investigator & Institution: Schambelan, Morris; Professor; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2005 Summary: (provided by applicant): The past 5 years have witnessed a dramatic reduction in HIV-associated morbidity and mortality in the developed world, an event that is generally attributed to the advent of highly active antiretroviral therapy. However, the enthusiasm generated by this therapeutic advance has been tempered by widespread reports of potentially deleterious metabolic side effects, including insulin resistance, dyslipidemia, peripheral and/or facial lipoatrophy, and central/visceral fat accumulation, findings reminiscent of syndrome X and commonly referred to as the HIV-associated lipodystrophy syndrome. A major goal of our laboratory has been to not only understand the pathogenesis of HIV-associated metabolic and morphologic abnormalities but also to evaluate novel therapies, using a paradigm based on intensive metabolic ward assessments in which each subject serves as his or her own control. The goal of the present proposal is to evaluate the effects of recombinant human leptin, an adipocyte-derived hormone that appears to have dramatic salutary effects in both murine and human models of lipodystrophy, in HIV-infected patients with

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lipodystrophy. Two studies will be performed: in the first, we will utilize an open-label design to evaluate the effects of leptin replacement therapy in 12 patients with HIVlipodystrophy who are also hypoleptinemic, hyperinsulinemic, and hypertriglyceridemic; in the second we will utilize a randomized placebo-control design to extend our investigation of the efficacy of leptin treatment to a group of 40 non-obese HIV-positive patients with diabetes and lipodystrophy. These two studies are designed to test the hypotheses that treatment with leptin will: 1) improve hepatic and peripheral insulin sensitivity and overall carbohydrate metabolism as measured by oral glucose tolerance testing, a euglycemic hyperinsulinemic clamp and stable isotope tracer studies of hepatic glucose production, gluconeogenesis, and glycogen flux; 2) ameliorate abnormalities in lipid metabolism, as measured by plasma lipid and lipoprotein levels and stable isotope studies of whole-body lipolysis and de novo hepatic lipogenesis and cholesterolgenesis; and 3) decrease visceral adiposity, hepatic mass, and intramyocellular lipids, as measured by magnetic resonance imaging and spectroscopy, respectively. To evaluate the effects of leptin on whole-body and regional fat and lean tissue distribution, we will also perform whole-body dual-energy X-ray (DEXA) scanning. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISM(S) FOR METABOLIC COMPLICATIONS IN HIV Principal Investigator & Institution: Yarasheski, Kevin E.; Associate Professor of Metabolism; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 30-SEP-1994; Project End 31-AUG-2004 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MECHANISMS OF NEONATAL PROTEIN ACCRETION Principal Investigator & Institution: Denne, Scott C.; Professor of Pediatrics; Pediatrics; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2003; Project Start 01-MAY-1992; Project End 31-DEC-2007 Summary: (provided by applicant): Despite continually improving survival rates, growth outcomes for premature extremely low birth weight (ELBW) infants remain exceptionally poor. Growth failure is nearly universal in these infants as they near term gestation. High rates of protein loss and elevated energy expenditures uncompensated by adequate nutritional intake appear to be primary factors in producing this growth failure, perhaps producing metabolic changes that prioritize survival over growth. There is accumulating experimental, clinical, and epidemiologic evidence that abnormal fetal growth can result in adaptations which persist throughout the lifespan and increase the risk of disease. Growth restriction in ELBW infants occurs in the extrauterine environment during the last third of gestation, and although adaptive responses might be expected, they have not been examined. The goal of the present proposal is to test the overall hypothesis that nutritional inadequacies of the extrauterine environment induce adaptive responses in protein metabolism, energy expenditure, insulin sensitivity, and endothelial function in ELBW infants which persist throughout infancy. Studies will be performed in ELBW and normal control infants at term gestation, 4 and 18 months of age. The following specific aims will be pursued: 1) To assess protein kinetics and protein catabolism during enteral feeding and in response to

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increased protein intake in ELBW infants throughout infancy. Proteolysis, protein synthesis and protein catabolism will be measured using stable isotopic tracers of leucine, phenylalanine, and urea 2) To determine the rate of total energy expenditure, resting energy expenditure, and energy of activity in ELBW infants throughout infancy. Total energy expenditure, resting energy expenditure and the energy of activity will be assessed using the doubly labeled water method and respiratory calorimetry 3) To examine insulin sensitivity in ELBW infants throughout infancy. A glucose tolerance test will be performed and glucose oxidation measured. 4) To evaluate endothelial function in ELBW infants throughout infancy. Endothelial function will be by determining acetylcholine induced vasodilation using the laser doppler technique. These studies may form the basis for improved clinical and nutritional strategies for these infants, as well as a future opportunity to more thoroughly explore the potential mechanisms underlying these adaptations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISMS OF THE GLUCOSE INTOLERANCE OF AGING Principal Investigator & Institution: Ader, Marilyn; Associate Professor; Physiology and Biophysics; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033 Timing: Fiscal Year 2002; Project Start 02-DEC-1998; Project End 30-NOV-2002 Summary: Impaired glucose tolerance is a hallmark of aging even in the absence of attendant pathology, and is associated with increased mortality due to enhanced risk for development of diabetes and cardiovascular disease. Intolerance of aging is typically attributed to the development of insulin resistance, resulting from changes in adiposity, diet, and/or sedentary lifestyle, and studies to understand the pathogenesis of intolerance have focused on the relative contributions of insulin resistance and pancreatic islet dysfunction. We have demonstrated that insulin-independent mechanisms of glucose regulation are equally important in determining glucose tolerance. These processes, termed "glucose effectiveness", are defined as the actions of glucose to regulate its own utilization (Rd) and hepatic production (HGO) independent of elevated insulin. The purpose of this proposal is to examine the role of glucose effectiveness in the glucose intolerance of normal, non-diseased aging in the rat. We will test the hypothesis that in insulin-resistant states such as aging, efficient disposition of a carbohydrate challenge becomes increasingly dependent on metabolic factors which are independent of insulin action, i.e. glucose effectiveness. These studies will establish the role of glucose effectiveness in the glucose intolerance of normal, non-diseased aging. We will apply newly developed methods to quantify glucose effectiveness directly in young and old rats, and determine how aging alters the relative contributions of Rd vs HGO and the specific tissue sites and glucose transporters involved. We will examine the mechanisms by which glucose effectiveness may compensate in aging-associated insulin resistance. Finally, we propose to examine the ability of caloric restriction to improve tolerance through their actions on glucose effectiveness, and determine the tissue sites, mechanisms, and glucose transporters which may be involved. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MENOPAUSE, LPL GENOTYPE AND METABOLISM AFTER WEIGHT LOSS Principal Investigator & Institution: Goldberg, Andrew P.; Professor; Medicine; University of Maryland Balt Prof School Baltimore, Md 21201

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Timing: Fiscal Year 2002; Project Start 01-SEP-2000; Project End 31-JUL-2005 Summary: This research is designed to determine whether obese postmenopausal women with a common polymorphism in the lipoprotein lipase (LPL) PvuII gene, i.e. the (+) allele have less favorable metabolic responses to weight loss (WL) treatment than women without the LPL PvuII cut-site (-/-). The hypothesis is that the LPL PvuII genotype affects fasting muscle and adipose tissue and LPL activity and the metabolic responses to hypocaloric feeding-induced WL in a dose-dependent manner to affect the magnitude of the reduction of total and visceral fat, and improvements in glucose/insulin and lipoprotein lipid metabolism following WL in postmenopausal women. Specific aims determine whether obese women who are homozygous for the LPL PvuII (+) cut-site, i.e. the (+/+) genotype, have greater increases in adipose tissue LPL and decreases in muscle LPL activity and larger decreases in resting metabolic rate (RMR) and fat oxidation than heterozygotes during hypocaloric diets, that are associated with: 1) the loss of less total body and visceral fat; and 2) smaller improvements in lipid and glucose metabolism than women without the cut-site, i.e., (/-). We will study healthy, obese (Body Mass Index, 30-40 kg/m2) 50-60 year old women within 5 years of menopause. The statistical power to test our hypothesis is based on preliminary data showing differences in adipose tissue LPL responses to WL between LPL PvuII (+/+) and (-/-) genotypes, and requires 27 women/genotype. Subjects will be entered prospectively based on their LPL genotype to ensure a homogeneous group of obese menopausal women are studied to eliminate confounding factors of gender, age, duration from menopause and body composition on the metabolic responses to WL treatment. Metabolic studies are performed on prepared calculated weight maintaining eucaloric diets for 2-3 weeks at baseline and after 6-mo WL to ensure metabolic stability, and on hypocaloric diets after the short-term study to assess metabolic responses to negative energy balance. We will measure muscle and adipose tissue LPL activity, RMR, fat oxidation, total and visceral body fat (DXA and CT scans) lipoprotein lipids and. glucose/insulin responses during an oral glucose tolerance test. Following the post-WL metabolic evaluations, subjects enter a 6- mo follow-up period followed by metabolic testing to assess long- term metabolic adaptations and weight regain by genotype. Collectively, these findings will enhance our understanding of obesity by assessing the gene-metabolic mechanisms underlying the predisposition of some obese women to more favorable metabolic health benefits from WL. This would allow the targeting of WL treatments to women more likely to respond, and pharmacologic and other treatments to those less likely to respond to WL. This optimistic outcome would reduce prevalence of obesity and risk for CVD in older women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: METABOLIC EFFECTS OF PREGNANCY IN CYSTIC FIBROSIS (SS) Principal Investigator & Institution: Hardin, Dana S.; Associate Professor; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2002; Project Start 01-DEC-2000; Project End 31-MAR-2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: METABOLIC EFFECTS OF PROTEASE INHIBITORS IN HIV DISEASE Principal Investigator & Institution: Mulligan, Kathleen; Associate Professor; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 30-SEP-1998; Project End 31-AUG-2004 Summary: (Adapted from applicant's abstract). Reports of increased glucose triglyceride, and cholesterol levels in HIV-infected patients on protease inhibitors (PI) have prompter speculation that these agents have unique metabolic effects. Additionally, some HIV-infected patients have noted increased abdominal girth and buffalo humps that clinicians and patients attribute to the use of Pi's. In preliminary studies, we have observed significant increases in glucose, insulin, TG and total LDL cholesterol in a group of patients following initiation of therapy with a PI, whereas no such changes occurred in patients beginning therapy with lamivudine or maintaining constant regimen that did not include lamivudine or a PI. Because hyperglycemia, hypertriglyceridemia, hypercholesterolemia, and central obesity are associated with increased risk of cardiovascular disease, these effects may impact on the long-term prognosis in patients whose life expectancies are extended due to effective viral suppression. As yet, these metabolic and body composition changes have not been systematically characterized, nor is it known if these changes represent one year syndrome or are unrelated findings. Therefore, to evaluate the scope of and mechanisms underling these changes in carbohydrate and lipid metabolism and their relationship, if any, to changes in body composition, e propose to perform intensive metabolic ward studies in which we prospectively evaluate changes in glucose and lipid metabolism and body composition in separate cohorts of HIV-infected men and women before and after beginning Pi therapy. These studies are designed to: (1) test the hypothesis that PI's induce insulin resistance (as assessed by oral glucose tolerance test, hyperinsulinemic, euglycemic clamp, stable isotope studies of hepatic glucose production, gluconeogenesis and glycogenesis); 2) test the hypothesis that PI's produce an atherogenic lipid profile (plasma lipids and lipoprotein composition, intravenous fat tolerance test, stable isotope studies of whole body lipolysis, de novo hepatic lipogenesis, and cholesterolgenesis); and (3) to determine whether patients uniformly develop changes in regional fat distribution while on PI therapy and the relationship, if any, or changes in glucose and lipid metabolism to changes in body composition (dual-energy X-ray absorptiometry, computed tomography)> The role of glucoregulatory, adrenal, and gonadal hormones in mediating these effects will also be evaluated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: METABOLIC EFFECTS OF VALPROATE AND ANTIPSYCHOTIC THERAPY Principal Investigator & Institution: Haupt, Daniel W.; Instructor; Psychiatry; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 31-MAR-2009 Summary: (provided by applicant): This is a revision of a K23 application targeting the development of a clinical investigator in an area of pressing public health significance. A growing literature indicates that mental illness can be associated with an increased prevalence of obesity, diabetes mellitus, dyslipidemia and cardiovascular disease, in some cases building on already epidemic rates in the general population. Factors contributing to these problems, including medication effects can be studied using reliable and validated methodologies that rarely are applied in psychiatric research. This

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K23 will allow the Candidate to develop unique and needed expertise in techniques for studying alterations in whole-body glucose and lipid metabolism, and the regulation of body composition and weight. The career development plan is integrated with a related research plan that aims to study the effects of multi-class polypharmacy (antipsychotic plus valproate) on sensitive measures of insulin sensitivity, lipid metabolism and fat mass. Motivating this plan, the treatment of schizophrenia commonly utilizes multiclass polypharmacy, with up to 35% of atypical antipsychotic prescriptions accompanied by co-prescription of valproate. Due in part to increases in polypharmacy, psychotropic costs (e.g. Missouri Medicaid) have nearly doubled in the last 10 years, with similar increases nationwide. Polypharmacy is associated with increased risk for medication interactions, poorer compliance, confounding of medication effects, and can lead to additional polypharmacy to treat side effects. Glucoregulatory abnormalities, diabetes, dyslipidemia, and increased adiposity have all been associated with antipsychotic treatment, and the addition of valproate can further disturb glucose and lipid metabolism and weight regulation. Although sensitive methods are available, studies have not addressed the metabolic consequences of this common type of polypharmacy. The Candidate will combine and extend the knowledge of two Cosponsors to develop expertise in the assessment of lipid metabolism, insulin sensitivity and weight regulation. Schizophrenia patients suffer nearly twice the rate of cardiovascular death as the general population, and changes in lipid metabolism are strongly associated with changes in cardiovascular risk. Current NIH guidelines recommend reduction of lipids as the main intervention for prevention of cardiovascular disease. This project aims to evaluate the effects of olanzapine and risperidone in combination with valproate on glucose and lipid metabolism, abdominal fat, and total body fat using available gold standard methodologies. The aims will be addressed in non-diabetic schizophrenia patients chronically treated with olanzapine or risperidone who will be randomized to receive either concomitant valproate versus no additional treatment. Relevant data are critically needed to target basic research, identify long-term cardiovascular risks, and plan therapeutic interventions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEUROGLYCOPENIA: GENOTYPE-PHENOTYPE CORRELATION Principal Investigator & Institution: De Vivo, Darryl C.; Sidney Carter Professor of Neurology; Pediatrics; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2003; Project Start 01-AUG-1998; Project End 31-AUG-2008 Summary: (provided by applicant): Glucose transporter protein Type I (Glut1), when deficient (GlutlDS, OMIM 606777), causes chronic neuroglycopenia and developmental encephalopathy. The deficiency results from GLUT1 haploinsufficiency, genetically transmitted as an autosomal dominant trait. The long-term objectives of this research project are improved understanding of the pathogenesis, increased awareness of the phenotypic presentations, and better treatment of the neurodevelopmental syndrome. Four specific aims are proposed to achieve these long-term objectives: (1) To expand our understanding of the GlutlDS phenotypes associated with GLUT1 gene mutations; (2) To correlate genotypic pathogenicity with phenotypic severity; (3) To replicate the human disease in an animal model; (4) To explore alternative treatment options for patients with GlutlDS. The research design and methods have been developed to increase recruitment of patients; to assess phenotypic variability by multi-disciplinary methods; and to serially evaluate patients over time to assess the phenotypic durability during development and the influences of gender on clinical expression. The phenotype

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will be correlated with the genotype by assessing the nature of the mutation and the kinetic and structure-function perturbations that result from these mutations. The Xenopus oocyte expression system is used to evaluate functional disturbances related to missense mutations. GLUT1 polymorphisms will be determined in the GlutlDS population and compared to the presence/absence of similar polymorphisms in a control population. A transgenic antisense mouse model and gene targeted homologous recombination knock-out mouse model will be examined clinically and neuropathologically for evidence of regional brain injury and neuronal apoptosis. Emphasis will be placed on establishing the cellular types most affected by the disease. Cellular dysfunction and apoptosis will be assessed by the in vitro study of neuronal and glial cultures derived from the mutant mouse models. Treatment opportunities will be explored in the mouse models and applied to the patient population assessing the relative benefits of a ketogenic diet and a carbohydrate diet, and the advantages of sustained hyperglycemia using uncooked cornstarch supplements and diazoxide. A 5hour oral glucose tolerance test will be evaluated as a possible diagnostic tool measuring clinical, neuropsychological and electrographic changes associated with transient hyperglycemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEW APPROACHES TO EVALUATION AND TREATMENT OF ACROMEGALY Principal Investigator & Institution: Freda, Pamela U.; Medicine; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2002; Project Start 01-MAR-2002; Project End 31-DEC-2003 Summary: Acromegaly, a disorder of chronic, growth hormone excess, is associated with significant morbidity and mortality. Prevention of the long-term complications of acromegaly depends on both an accurate biochemical assessment of disease status and an understanding of the goals of therapy. The studies planned for the final two years of my K08 (DK02561) continue to examine new approaches to the evaluation and treatment of acromegaly utilizing a large cohort of patients with acromegaly and will focus on integrating the molecular, biochemical and clinical aspects of my initial studies. Studies will continue a careful biochemical assessment of this cohort with modern, sensitive techniques in order to further define the new criteria for cure suggested by our work to date. Studies will focus on a longitudinal follow up of this cohort examining detailed biochemical parameters and determining if certain patients are at risk for disease recurrence. Studies will now include a new direction, the assessment of a clinical marker of GH status, body composition analysis, and a correlation of this analysis with the biochemical measures. I will continue to analyze tumor specimens from this larger cohort for the presence of activating mutations in the alpha subunit of Gs and will determine if these mutations define a clinical phenotype and/or biochemical response to medical therapy. The studies in this proposal are a first step toward achieving a multifaceted understanding of the optimal biochemical and clinical goals for disease control of acromegaly and toward integrating the information from molecular analysis of these tumors into our treatment approach. The R03will proved vital added support in the final two years of my K08. The R03 funds will enable me to continue to employ a clinical research assistant whose help with my studies will allow me to devote the needed effort to broadening my clinical research projects and to developing my skills in clinical and basic research methods as well as new projects for future funding. My current environment continues to be ideally suited for achieving my goals. My collaboration with Dr. Kalmon Post, providing me with access to large numbers of both

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patients and pituitary tumor specimens, continues to be effective. I continue to receive instruction in the molecular techniques from Drs. Sharon Wardlaw and Streamson Chua. My new collaboration with Dr. Steven Heymsfield on the body composition studies will add an important new aspect to my studies. My sponsor, Dr. Wardlaw, continues to be committed to providing me with the guidance I need to pursue my research plans and to facilitate my transition to independent investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PARACRINE DYSREGULATION OF OOCYTE COMPETENCE IN PCOS Principal Investigator & Institution: Dumesic, Daniel A.; Professor; Mayo Clinic Coll of Medicine, Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2007 Summary: (provided by applicant): Polycystic ovary syndrome (PCOS) in women is characterized by anovulation, LH hypersecretion, hyperandrogenism and insulin resistance. As the most common endocrinopathy in females, affecting 4-7% of reproductive-aged women, and as a frequent cause of infertility, accounting for 75% of anovulation, PCOS has staggering adverse physiological, psychological and financial consequence on reproduction in women. During gonadotropin stimulation for in vitro fertilization (IVF), PCOS women experience decreased fecundity and increased pregnancy loss. Since experimental investigation of oocyte and embryo development in humans is limited by ethical constraints, we have developed the prenatally androgenized (PA) female rhesus monkey as a model for PCOS. PA female monkeys undergoing follicle stimulating hormone (FSH) therapy for IVF exhibit LH hypersecretion, circulating insulin excess, an exaggerated shift in intrafollicular steroidogenesis from estradiol (E2) and androstenedione (A4) to progesterone (P4), and impaired embryo development beginning with embryonic genome activation. Because insulin enhances FSH-induced granulose cell differentiation, leading to LH-induced P4 production, we hypothesize that a) premature follicle luteinization and b) impaired oocyte developmental competence in PA monkeys are caused by adverse effects of hyperinsulinemia on follicle maturation. We predict that such abnormalities in PA monkeys are reversed by improved insulin sensitivity from weight loss through dietary restriction and will test our prediction in Specific Aims 1 and 2. Based upon data from our recognized nonhuman primate model of PCOS, we also hypothesize that c) premature follicle luteinization is a cause of poor oocyte developmental competence in PCOS women undergoing FSH therapy for IVF. We predict that granulosa cell dysregulation of LH receptor, insulin receptor (IR) and growth differentiation factor-9 (GDF-9) transcription from premature follicle luteinization causes poor cumulus cell proliferation in PCOS women (Specific Aim 3). We further hypothesize that d) meiotically-competent and meiotically-incompetent oocytes of PCOS patients are impaired in expression of GDF-9 and other developmentally relevant messenger ribonucleic acids (mRNAs) (Specific Aim 4). The long-term objectives of this proposal are to: 1) define molecular markers of oocyte developmental competence that enhance IVF pregnancy outcome by improving rates of embryo cleavage and blastocyst formation; while minimizing pregnancy loss in women with PCOS and other insulin resistant states, such as obesity and Type II diabetes, and 2) to provide additional, unique, insight into the transgenerational effect of PCOS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PHYSIOLOGIC LIPODYSTROPHY

GROWTH

HORMONE

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IN

HIV

Principal Investigator & Institution: Grinspoon, Steven K.; Associate Professor of Medicine; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-JAN-2008 Summary: (provided by applicant): Changes in fat distribution, including increased abdominal visceral fat and reduced subcutaneous fat are increasingly recognized in HIV-infected patients receiving highly active antiretroviral therapy. We have previously shown that the changes in fat distribution are associated with a metabolic syndrome, including insulin resistance and dyslipidemia, hypertension, impaired thrombosis and bone loss. We have recently demonstrated reduced mean GH concentrations, and GH pulse amplitude among patients with HIV lipodystrophy and significant visceral fat accumulation using detailed frequent sampling and pulse detection algorithms. Using standard stimulation testing with arginine and GHRH, up to one third of such patients may be GH deficient. GH deficiency is associated with insulin resistance, dyslipidemia, increased cardiovascular risk parameters, fat redistribution, and bone loss among non HIV infected patients, in whom GH replacements attenuates increased cardiovascular risk parameters and improves bone density. Novel preliminary data presented with this grant application suggest that cardiovascular risk markers are increased in association with GH deficiency in HIV-infected patients with lipodystrophy and that bone density is inversely related to mean overnight GH levels and peak GH responses to secretogogue testing in this population, suggesting the potential utility of physiologic GH administration in this population. To date, short-term studies using very high doses of GH have been performed, with the anticipated negative effects on glucose homeostasis. In contrast, physiologic GH administration has been shown to improve insulin sensitivity in non HIV-infected patients with abdominal obesity and to improve cardiovascular risk markers, bone density, and fat redistribution in non HIV-infected patients with GH deficiency. Importantly, studies investigating the pathophysiology of GH deficiency, strategies to increase physiologic GH secretion, and the use of long-term physiologic GH to improve insulin sensitivity, cardiovascular risk indices and bone density have not been performed in the large group of HIV-infected patients with reduced GH. In the proposed grant, we will: 1) investigate the pathophysiology of reduced growth hormone, 2) determine the novel short-term effects of a GH secretogogue, GHRH, to restore physiologic GH levels, and 3) determine the long-term effects of physiologic GH administration on bone and metabolic parameters in patients with HIV lipodystrophy and reduced GH. The studies outlined in this grant proposal will investigate a novel approach to the treatment and management of critical metabolic abnormalities in patients with HIV lipodystrophy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: POST DPP (DIABETES PREVENTION PROGRAM) Principal Investigator & Institution: Barrett-Connor, Elizabeth L.; Professor; Medicine; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2003; Project Start 10-SEP-1994; Project End 31-JAN-2008 Summary: (provided by applicant): The Diabetes Prevention Program is a multicenter controlled clinical trial examining the efficacy of an intensive life-style intervention or metformin to prevent or delay the development of diabetes in a population selected to be at high risk due to the presence of impaired glucose tolerance (IGT). Development of diabetes, defined by 1997 ADA criteria, is the primary outcome while cardiovascular

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disease and its risk factors are important secondary outcomes. The DPP began recruitment in mid-1996. At the time of this application, total study exposure is a mean of approximately 3 years (range 2 to 5) with a total of approximately 10,000 patient years in the 3,234 volunteers in the 3-arm study. On the basis of a statistically significant and clinically compelling decrease in the development of diabetes in the life-style intervention and metformin-treated groups (58% and 31% reductions, respectively) compared with the placebo treated group, the DPP Data Monitoring Board and NIDDK ended the masked treatment phase of the study in May, 2001, one year earlier than originally planned. This application is designed to take further advantage of the scientifically and clinically valuable cohort of DPP volunteers and the large volume of data collected during the study. The highly compliant DPP cohort, including 45% minorities, is the largest IGT population ever studied. Moreover, the subcohort that has developed diabetes (n approximately 700) has been followed from near the exact time of diabetes onset. Clinically important research questions remain in the wake of the DPP. The carefully collected, centrally measured and graded data in this cohort should help to answer, definitively, a number of important questions regarding the clinical course of IGT and early onset type 2 diabetes. Specific aims include: 1. Examine the long-term effects and durability of prior DPP intervention on the major DPP outcomes including diabetes, clinical cardiovascular disease, atherosclerosis, CVD risk factors,quality of life and cost-benefit; 2. Determine the clinical course of new onset type 2 diabetes and IGT, in particular regarding microvascular and neurologic complications; 3. Determine the incidence of cardiovascular disease (CVD), CVD risk factors and atherosclerosis in new onset type 2 diabetes and IGT; and 4. Examine topics 1-3 in minority populations, men vs. women, and in older subjects in the DPP. The current application is for 5 years of funding, although the some of the goals of the projects described will require a 10-year study. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: POST-DPP FOLLOW-UP STUDY Principal Investigator & Institution: Crandall, Jill P.; Medicine; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2003; Project Start 15-AUG-1994; Project End 31-JAN-2008 Summary: (provided by applicant): The Diabetes Prevention Program is a multicenter controlled clinical trial examining the efficacy of an intensive life-style intervention or metformin to prevent or delay the development of diabetes in a population selected to be at high risk due to the presence of impaired glucose tolerance (IGT). Development of diabetes, defined by 1997 ADA criteria, is the primary outcome while cardiovascular disease and its risk factors are important secondary outcomes. The DPP began recruitment in mid-1996. At the time of this application, total study exposure is a mean of approximately 3 years (range 2 to 5) with a total of approximately 10,000 patient years in the 3,234 volunteers in the 3-arm study. On the basis of a statistically significant and clinically compelling decrease in the development of diabetes in the life-style intervention and metformin-treated groups (58% and 31% reductions, respectively) compared with the placebo treated group, the DPP Data Monitoring Board and NIDDK ended the masked treatment phase of the study in May, 2001, one year earlier than originally planned. This application is designed to take further advantage of the scientifically and clinically valuable cohort of DPP volunteers and the large volume of data collected during the study. The highly compliant DPP cohort, including 45% minorities, is the largest IGT population ever studied. Moreover, the subcohort that has developed diabetes (n approximately 700) has been followed from near the exact time of

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Glucose Tolerance Test

diabetes onset. Clinically important research questions remain in the wake of the DPP. The carefully collected, centrally measured and graded data in this cohort should help to answer, definitively, a number ofvolunteers with impaired glucose tolerance and volunteers whose diabetes developed during the DPP to determine the natural history of diabetic complications. This analysis will be epidemiologic in nature with all groups being pooled with prior treatment being used as a co-variate. Finally, the same data will be used to examine the effects of gender, age, and race/ethnicity on diabetes and its vascular complication. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PRENATAL MATERNAL STRESS AND PREMATURE OFFSPRING AGING Principal Investigator & Institution: Mcdonald, Thomas J.; Associate Professor; Obstetrics and Gynecology; New York University School of Medicine 550 1St Ave New York, Ny 10016 Timing: Fiscal Year 2002; Project Start 01-FEB-2002; Project End 31-JAN-2004 Summary: Compelling data from several species demonstrates that glucocorticoid treatments both antenatally and in early postnatal life have beneficial effects on lung development and surfactant production. However, they also cause growth retardation of organ systems and the placenta. In addition, such treatments are known to produce long term deficits in the function of various physiological systems (e.g., blood pressure, glucose metabolism) that are similar in many respects to changes seen with aging in normal individuals. However, these changes occur much earlier in life and follow inappropriate glucocorticoid exposure at during development. Human demographic data indicate that the majority of working women who become pregnant will work for a large proportion of their pregnancy. Central to the present proposal is the thesis that working during pregnancy represents a psychological stress to the mother that may increase as pregnancy progresses. While data from human and animal studies has accumulated on immediate perinatal outcomes of stress during pregnancy, little data exists on the long term consequences of such stress on the health or life span of progeny in later life. This application proposes to use pregnant rats subjected to psychological stress throughout pregnancy to study aging of offspring. The hypothesis is: Female rats subjected to daily stress through pregnancy produce offspring that age and die more quickly than progeny from non stress controls. The paradigm used places pregnant mothers in a standard rat restraint chamber for 45 min per day throughout pregnancy starting on the day of breeding. The endpoints examined are the baroreflex, glucose tolerance and aged at death. The rat is a well established model for studies in aging and the prenatal maternal psychological stress used in this model is known to cause long term deficits in the hippocampus (a critical aging-related brain area) of progeny. If funded, further development of this model will: 1) provide sorely needed information on long term consequences of psychological stress during pregnancy, 2) ultimately provide information on windows of risk for premature aging and 3) help in the design of strategies to minimize and/or prevent the occurrence of such undesirable consequences. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PREVENTION OF DIABETES IN OBESE HISPANIC ADOLESCENTS Principal Investigator & Institution: Cruz, Martha L.; Professor; Preventive Medicine; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033

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Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 31-MAR-2006 Summary: (provided by applicant): Overall Objective: to conduct a study of the safety and effects of treatment of obese, Hispanic adolescents at high risk for type 2 diabetes (T2D) with an insulin sensitizer. Overall Hypothesis: treatment of obese, Hispanic adolescents with pioglitazone, will result in enhanced insulin sensitivity, improved betacell function, normalization of glucose tolerance, improvements in cardiovascular disease (CVD) risk factors and atherosclerosis. Specific Aims and Approach: i) to conduct a randomized double blind placebo controlled pilot study of the safety and effects of treatment of overweight, Hispanic adolescents with pioglitazone (30 mg/day) for 12 weeks, ii) to compare changes in insulin sensitivity, insulin secretion, beta-cell function (measured via the frequently sampled intravenous glucose tolerance test), body composition (via dual energy x-ray absorptiometry) body fat distribution (via magnetic resonance imaging), CVD risk factors (lipids, lipoproteins, blood pressure) and atherosclerosis (via intima media thickness of the common carotid artery and arterial stiffness) in Hispanic youth, before and after 12 weeks of treatment (30 mg/day) with pioglitazone + standard care (n = 20) or placebo + standard care (n =20). Forty, obese, Hispanic adolescents, with impaired glucose tolerance, a positive family history for type 2 diabetes, and exposed in utero to gestational diabetes will be recruited for the study and randomized to either treatment with pioglitazone or placebo. Rationale: T2D is recent health problem in obese youth specially in ethnic minorities. 28% of obese Hispanic adolescents with a family history of T2D have impaired glucose tolerance (IGT). In youth exposed to gestational diabetes in utero this value increases to 41%. Furthermore, 30% of obese Hispanic youth have the metabolic syndrome. Data from a current NIDDK longitudinal study provide compelling preliminary evidence to suggest that chronic insulin resistance coupled with poor insulin secretory response are the key events contributing to hyperglycemia in this population, while insulin resistance may be additionally responsible for the high prevalence of the metabolic syndrome. Health implications: Interventions aimed at improving insulin resistance in susceptible individuals may be an effective means of preventing both type 2 diabetes and early cardiovascular disease (CVD). The applicant's previous training, and the clinical & scientific expertise available at the host institution will facilitate the successful completion of the proposal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: R21 PROJECT: ANTI-DIABETIC EFFECTS OF PANAX GINSENG Principal Investigator & Institution: Yuan, Chun-Su; Anesthesiology; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2002; Project Start 15-MAR-2002; Project End 31-JAN-2004 Summary: Diabetes mellitus or diabetes is a chronic metabolic disease that can cause blindness, kidney failure, nerve damage, and confers an increased risk of ischemic heart disease, stroke and peripheral vascular disease. Diabetes is divided into two major categories: type 1 or insulin- dependent diabetes mellitus (IDDM), and type 2 or noninsulin dependent diabetes mellitus (NIDDM). In this country, the incidence of diabetes is approximately 4.5%, of which 90% is type 2 diabetes. In 1992, diabetes care required roughly 14.6% of the total U.S. health care expenditure ($105 billion). Many of these patients also suffer from diabetic complications. Considering the heterogeneity of this disease, and the limitations of current therapies, such as high secondary failure rates and side effects, there is an urgent need to explore new anti- diabetic agents. This research project is related to the development of useful products in the field of complementary and alternative medicine. This proposal will focus on our studies on

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anti-diabetic effects of Panax ginseng, and this project is a continuation of our previous ginseng pharmacological studies. Recently, in our preliminary studies, we observed exciting results on anti-diabetic actions in ob/ob mice using Panax ginseng berry (or fruit) extract, other than the commonly used root extract. The ob/ob mice is a genetic model for type 2 diabetes, and these animals are extremely insulin resistant and have fasting blood glucose levels that are significantly higher than that of lean mice. Data from our pilot observation showed that extract of Panax ginseng berry normalized hyperglycemia and increased insulin sensitivity in ob/ob mice. In addition, we analyzed the constituents of the ginseng berry by HPLC analysis and found that, compared to ginseng root, the ginseng berry has a distinctive profile of ginsenosides, the vital constituent of ginseng. In this revised proposal, we will test the hypothesis that Panax ginseng berry extract has significant anti-hyperglycemic activity. The project aims to identify the anti-hyperglycemic constituents of Panax ginseng berry, and synergistic effects between these constituents. We will also investigate mechanisms of action of these active component(s). Our strategy is to use an in vivo-guided chemical fractionation method to isolate the pure, biologically active, anti-hyperglycemic compound(s) from Panax ginseng berry using the ob/ob mouse. Improvements in glucose homeostasis, glucose tolerance, and in vivo insulin sensitivity will be tested. The results of the proposed project will also help fill gaps in our knowledge before therapeutic agents can be developed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF HEPATIC AND PERIPHERAL GLUCOSE METABOLISM Principal Investigator & Institution: Defronzo, Ralph A.; Professor; Medicine; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2002; Project Start 01-JUL-1988; Project End 31-MAR-2005 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: REPRODUCTIVE ANDROGENIZATION

CONSEQUENCES

OF

PRENATAL

Principal Investigator & Institution: Padmanabhan, Vasantha; Professor of Pediatrics; Pediatrics & Communicable Dis; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 08-AUG-2001; Project End 31-MAY-2006 Summary: Polycystic ovarian syndrome (PCOS) is the most common endocrinopathy and it affects 10 percent of reproductive-aged women. The etiology of chronic hyperandrogenic anovulations, such as PCOS, may have genetic underpinnings. Although the underlying mechanisms are unknown, PCOS is now recognized as hyperandrogenism accompanied by anovulation. Polycystic ovarian morphology is highly correlated with conditions in which the fetus has been exposed to high amounts of sex steroids before birth. For example, women with classical 21-hydroxylase deficiency mimic PCOS, exhibit anovulation, ovarian hyperandrogenism, and LH hypersecretion. Perhaps excess sex steroids early in life may provide a hormonal "insult" that results in manifestation of PCOS later in adulthood. This proposal aims to use a new model, the prenatally-androgenized sheep (long gestation, mono-ovular species), to investigate causal mechanisms for the developmental origins of PCOS. Our preliminary studies indicate that these sheep develop ovulatory defects during adulthood similar to

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those of women with PCOS: anovulation, elevated LH levels, hyperandrogenemia, hyperinsulinemia, and multifollicular ovaries. In this proposal, we will test the following hypothesis: prenatal exposure to androgens disrupts adult reproductive function culminating in hyperandrogenic anovulation and that this disruption is mediated via reduced sensitivity to the positive feedback actions of estradiol, abnormal gonadotropic drive and/or altered ovarian sensitivity to FSH. The specific Aims of the proposed research are to determine 1) the extent to which fetal exposure to androgens disrupts reproductive cyclicity, ovarian function, ovulatory capacity and fertility in adulthood, (2) if reduced sensitivity to estradiol stimulatory feedback of gonadotropin secretion contributes to the disruptive effects of prenatal- androgenization on postnatal reproductive cyclicity, and (3) if abnormal gonadotropic drive and/or reduced ovarian sensitivity to FSH contributes to the disruptive effects of prenatal- androgenization on postnatal reproductive cyclicity. If our hyposthesis proves to be correct, this would form the basis for a distinct developmental origin of an important reproductive disease in adulthood. Specifically it will establish that discrete, experimentally induced androgen excess of fetal sheep provides the first clear etiology for hyperandrogenic anovulation in adulthood. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ROLE OF PERILIPIN IN LIPOLYSIS AND ENERGY METABOLISM Principal Investigator & Institution: Gullicksen, P Scott.; None; Tufts University Boston Boston, Ma 02111 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): Regulation of fat storage and breakdown (lipolysis) in cells and tissues is critical to understanding obesity. Perilipin (peri) proteins, which coat the intracellular lipid droplet in adipocytes, are thought to be critical regulators of fat storage and breakdown since they inhibit lipolysis and in the absence of peri, allow for greater constitutive lipolysis to occur. Peri null (knockout or KO) mice, which do not express perilipin, are resistant to diet-induced obesity (DIO) and lack ectopic fat. Obesity and insulin resistance is associated with increased lipolysis and circulating fatty acids (FA). FA stimulate uncoupling protein-1 (UCP1) activity in the brown adipose tissue (BAT) of rodents resulting in the generation of heat at the expense of the FA. We hypothesize those peri null mice are resistant to DIO due to enhanced constitutive lipolysis, resulting in increased FA flux to BAT and activation of UCPI. Also, we hypothesize that increased metabolism of FA via UCP1 will protect the mice from becoming insulin resistant. The phosphorylation of peri by cyclic-AMP dependent protein kinase A (PKA) abrogates its inhibitory actions on lipases. We have generated our own peri null mice to elucidate peri's actions and in vivo studies to define the critical role of peri and UCP1 in modulating energy metabolism and adipocyte biology. These studies will help us to understand the potentially important role of peri in obesity and its associated complications such as diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ROLE OF SH2-B IN GLUCOSE METABOLISM Principal Investigator & Institution: Rui, Liangyou; Molecular and Integrative Physiology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2004; Project Start 15-FEB-2004; Project End 31-DEC-2008

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Summary: (provided by applicant): Insulin is the primary hormone regulating glucose homeostasis. It binds to and activates the insulin receptor (IR), which subsequently tyrosine phosphorylates and activates multiple cell signaling proteins including IRS proteins, APS and SH2-B. Defects in activation of IR and/or its downstream signaling molecules result in insulin resistance, which is associated with and may be a driving force for type 2 diabetes. The long-term goal of my research program is to elucidate the molecular mechanisms of insulin signaling and resistance. We recently identified SH2-B as a binding protein for IR as well as for JAK2, a cytosolic tyrosine kinase required for cytokine action. SH2-B binds to JAK2 via its SH2 domain, and enhances JAK2 kinase activity; however, its role in insulin action is unclear. To study the physiological function of SH2-B in vivo, we generated mutant mice lacking SH2-B. Initial inspection revealed that the mutant mice homozygous for the SH2-B null allele develop insulin resistance and type 2 diabetes. Moreover, hepatic IRS2 is reduced significantly in SH2-B deficient mice. We hypothesize that SH2-B enhances IR activation and IRS2 expression independently, and that both contribute to maintaining normal insulin sensitivity in animals. To test this hypothesis, we shall determine whether deletion of SH2-B impairs insulin-stimulated IR activation and the subsequent phosphorylation of its substrates and activation of downstream pathways, and whether reintroduction of recombinant SH2-B can rescues normal insulin signaling and physiological responses in SH2-B deficient cells and tissues. We shall determine whether SH2-B activates IRS2 promoter independent of insulin stimulation. We shall use a variety of methods to identify molecular mechanisms by which SH2-B potentiates IR activation and promotes IRS2 expression. Thus, the Specific Aims of this proposal are to: 1. Determine whether SH2-B directly enhances insulin physiological responses and signal transduction in mice, tissues and cultured cells. 2. Determine whether and how SH2-B enhances IR activation in mice, tissues and cultured cells. 3. Determine whether and how SH2-B enhances the IRS2 expression in mice, tissues and cultured cells. The results of this proposal will lead to identification of SH2-B-initiated signaling events that may serve as targets for drug intervention of insulin resistance and type 2 diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INDUCTION

ROSIGLITAZONE

AND

CLOMIPHENE

FOR

OVULATION

Principal Investigator & Institution: Cataldo, Nicholas A.; Assistant Professor of Obstetrics and Gy; Gynecology and Obstetrics; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 01-AUG-2001; Project End 31-JUL-2004 Summary: This proposal will evaluate the effectiveness of a new drug combination, rosiglitazone and clomiphene, for the induction of ovulation in anovulatory women with polycystic ovary syndrome (PCOS). PCOS is a disorder affecting about 5% of women of reproductive age, characterized by anovulation with loss of menstrual cyclicity and hyperandrogenism, often resulting in hirsutism or acne. Anovulation leads to spontaneous infertility and poses a risk of endometrial carcinoma if untreated. A majority of women with PCOS have peripheral insulin resistance and compensatory hyperinsulinemia. These abnormalities may lead to a long-term increased rish of Type 2 diabetes mellitus, hypertension, and accelerated atherosclerosis. Induction of ovulation is necessary to restore fertility to women with PCOS. The standard initial treatment is oral clomiphene citrate, a selective estrogen-receptor modulator which increases endogenous FSH secretion. Clomiphene is successful in inducing ovulation in only about 70% of women with PCOS, and failure is associated with hyperinsulinemia. Women who fail clomiphene ovulation induction are usually treated with parenteral

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FSH, but this is associated with a greater risk than clomiphene of both multiple gestation and ovarian hyperstimulation syndrome, which in its severe form can be lifethreatening. This study will examine whether clomiphene can be more effective in inducing ovulation in women with PCOS when given concomitantly with rosiglitazone, an insulin sensitizer which lowers circulating insulin levels. Women with PCOS selected for previous resistance to clomiphene ovulation induction will be randomized to receive either rosiglitazone or placebo in double-bind fashion for 6 weeks, and then will undergo attempted ovulation induction with clomiphene. If unsuccessful, the clomiphene dose will be increased in up to 2 subsequent cycles in standard fashion in an effort to achieve ovulation. Spontaneous and clomiphene-induced ovulatory outcomes, assessed by serum progesterone levels, will be compared between rosiglitazone and placebo groups and correlated with changes in hyperinsulinemia, assessed on oral glucose tolerance testing (OGTT), and with changes in baseline LH, total and free testosterone, sex hormone binding globulin (SHBG), and insulin-like growth factor binding protein-1 (IGFBP-1) levels. The effects of rosiglitazone on insulin secretion on OGTT will be correlated with its effects on the levels of the above hormones and binding proteins. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SECRETION AND BIOSYNTHESIS OF INSULIN Principal Investigator & Institution: Mcdaniel, Michael L.; Professor; Pathology and Immunology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 01-MAY-1977; Project End 31-JAN-2007 Summary: (provided by applicant) Type 2 diabetes is associated with obesity and elevated plasma levels of free fatty acids (FFA) and triacylglycerides (TAG). Obesity is also associated with the development of insulin resistance in insulin-sensitive tissues that results in hyperglycemia and hyperinsulinemia. b-cell failure in obesity-associated type 2 diabetes is believed to correlate with the intracellular accumulation of lipids that contribute to defects in insulin secretion and/or insulin and growth factor signaling necessary to maintain sufficient b-ceIl mass. The overall goal of this proposal is to define the cellular mechanisms whereby FFA and TAG exert their inhibitory effects on b-cell function in obesity-associated type 2 diabetes. Our recent studies have identified lipoprotein lipase (LpL) in b-cells, a key enzyme for catalyzing the hydrolysis of lipoprotein-associated TAG, to produce FFA for local cellular uptake. Our overall hypothesis is that LpL serves as a gatekeeper for the physiological import of FFA into bcells analogous to that described for adipocytes. Furthermore, our new findings indicate that elevated concentrations of glucose and insulin enhance LpL enzyme activity in bcells that may explain how b-cells continue to accumulate lipids in the setting of hyperglycemia and hyperinsulinemia associated with type 2 diabetes. In specific aim 1, we will: 1) further characterize the ability of nutrients, glucose and amino acids, and insulin to regulate LpL activity, expression and intracellular localization in rodent and human islets and b-cell lines, 2) assess the role of rapamycin, an inhibitor of mTOR, to regulate LpL and: lipid levels, and 3) evaluate LpL function in vivo. In specific aim 2, we will 1) examine the effects of enhanced FFA uptake by overexpression of FATP1 and ACS1, 2) characterize lipid droplet associated proteins, ADRP, perilipins and HSL, and 3) determine the regulation of lipid droplet synthesis and breakdown by phosphorylation and overexpression of lipid droplet associated proteins. Mitochondria exert a major role in glucose-stimulated insulin secretion, and mitochondrial activation is required for normal signal transduction. Recent studies suggest that FFA up-regulate mitochondrial uncoupling proteins (UCP) proposed to dissipate the proton gradient

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across the mitochondrial inner membrane. In specific aim 3, we will: 1) determine the role of UCP in mediating b-cell function by overexpressing UCP-2 in islets and b-cell lines, 2) assess the modulation of UCP-2 by increased levels of FFA in vitro and in vivo as described in specific aims 1 and 2. This experimental approach will be used to delineate the link between FFA and b-cell mitochondrial dysfunction. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SERINE PHOSPHORYLATION OF P450C17 & 5 ALPHA REDUCTASE ACTIVITY Principal Investigator & Institution: Azziz, Ricardo; Professor and Chairman; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: There is no text on file for this abstract. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TELOMERE INDUCED GENOMIC INSTABILITY IN PREMATURE AGING Principal Investigator & Institution: Chang, Sandy S.; Assistant Professor; Molecular Genetics; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2004; Project Start 01-JUL-2004; Project End 31-MAY-2007 Summary: (provided by applicant): Genetic studies of human progeric syndromes have furthered our understanding of the molecular mechanisms of the aging process. Mutations in Wrn causes Wemer Syndrome (WS), a disease characterized by premature aging, elevated genomic instability and cancer. WS fibroblasts prematurely senescence due to telomere shortening, suggesting the possibility that telomere dysfunction collaborates with Wrn loss to generate WS. Telomeres function to prevent chromosomal ends from being recognized as double-strand DNA breaks and confer genome stability. It has been postulated that telomere shortening serves as a molecular clock that eventually signals replicative senescence. WS cells senescence while still possessing long telomeres, suggesting that they may be hypersensitive to telomere shortening. This hypothesis is supported by the observation that the senescence phenotype observed in WS cells can be rescued by overexpression of telomerase, suggesting that one consequence of the WS defect is the acceleration of normal telomere-based senescence. Mice lacking WRN do not display obvious aging phenotypes, and I hypothesize that manifestation of the WS phenotype requires the presence of critically short telomeres. Mouse telomeres are normally too long for the required telomere attrition to take place during the aging process. To test experimentally the hypothesis that manifestation of the WS phenotype in WRN-/- mice requires critical telomere shortening, telomere lengths were shortened genetically via successive intercrossings of WRN-/- mTERC-/- mice. Compound mutant mice with short dysfunctional telomeres exhibited early onset of aging phenotypes, including alopecia, cataract formation and glucose intolerance and died prematurely. These exciting results suggest that our mouse model recapitulates features of WS observed in human patients. Our immediate goal is to characterize additional aging phenotypes in these mice and to correlate the onset of premature aging with genomic instability induced by telomere dysfunction. We are also probing for molecular mechanisms that may be responsible for the observed aging phenotypes in our mouse model. These studies should illuminate the roles of Wrn and dysfunctional telomeres during human aging. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: THE IMPACT OF GAD ON PRESERVATION ON B CELL FUNCTION Principal Investigator & Institution: Wherrett, Diane K.; Hospital for Sick Chldrn (Toronto) 555 University Ave Toronto, On Timing: Fiscal Year 2002; Project Start 29-SEP-2001; Project End 31-AUG-2008 Summary: (provided by applicant) The objectives of this application are: to describe the capability of the Hospital for Sick Children/University of Toronto site as a Clinical Center for TrialNet and to describe studies to determine whether intravenous treatment with glutamic acid decarboxylase (GAD) alters the immune response directed at islet cells thereby preventing ongoing B cell destruction in two groups of subjects: (1) patients with newly diagnosed Type 1 diabetes (DM1), using preservation of C-peptide secretion as the primary endpoint (Intervention); and (2) relatives of patients with DM1 who are at significant risk of diabetes, as defined by the presence of two islet antibodies, using prevention/delay of loss of first phase insulin release as the primary endpoint (Prevention). The clinical center includes: Principal and Co-investigators Drs. Diane Wherrett, Denis Daneman and Jeffrey Mahon, who have extensive experience in clinical trials, diabetes prevention trials, study design and immunology of Type 1 diabetes; the strong infrastructure of the Hospital for Sick Children Research Institute which provides the facilities, clinical trials, methodological and statistical support and scientific environment to carry out these studies; a network of pediatric and adult institutions within the Greater Toronto Area and beyond which will supply a large subject pool for study participation and have a proven track record of high levels of participation in diabetes prevention trials, both in ENDIT and DPT-1. The Intervention study will use a randomized, double-blind, placebo-controlled design to assess the efficacy and safety of parenteral GAD to maintain residual insulin secretion in persons with new-onset DM1. 132 patients with DM1 will be identified within 4 weeks of onset of insulin therapy. They will be randomized 2:1 to 2 different doses of GAD or placebo. The study endpoint will compare the mean meal-stimulated C-peptide level at 12 months in the GAD treated group versus placebo by a two-sided t-test. An interim analysis for safety will be carried out. The Prevention study will use a randomized, double-blind, placebocontrolled design to assess the efficacy of parenteral GAD in the prevention of loss of first phase insulin release in first degree relatives of those with Type 1 diabetes. It involves: screening first degree relatives for antibodies to insulin, IA-2, and GAD (and ICA in those with 1 positive antibody), if 2 of GAD, IA-2 or insulin antibodies are greater than the 97th percentile, then; staging with intravenous glucose tolerance test (IVGTT) to measure first phase insulin release (FPIR), HLA typing to exclude DQB10602 and confirmation of islet antibody status, if FPIR is greater than the 1st percentile for age and normal oral glucose tolerance, then; randomization 1:1 to intervention with GAD or control; follow up with IVGTT every 6 months, repeated if less than the 1st percentile, if confirmed, subject has reached study endpoint. The primary analysis will test the difference in proportion of subjects and controls with FPIR below 1st percentile for age, using a two-sided Chi Square test with continuity correction. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: THE PATHOPHYSIOLOGY OF TYPE 2 DIABETES IN ADOLESCENTS Principal Investigator & Institution: Brickman, Wendy J.; Children's Memorial Hospital (Chicago) Chicago, Il 606143394 Timing: Fiscal Year 2002; Project Start 15-APR-2001; Project End 31-JAN-2005 Summary: (adapted from the application) In adults, type 2 diabetes represents a group of polygenic disorders with abnormalities in insulin sensitivity, insulin secretion, and

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hepatic glucose production. Recently, there have been increased reports of what appears to be type 2 diabetes in the pediatric population. This increase in type 2 diabetes in children has occurred amidst an environment of increasing insulin resistance, as noted by 1) the pubertal stage of many affected individuals, 2) the parallel increase in obesity within the pediatric population, 3) the parallel increase in sedentary lifestyle features, and 4) the frequent presence of acanthosis nigricans. However, all individuals with insulin resistance do not have type 2 diabetes. Little data is available on the pathophysiology of impaired glucose tolerance and type 2 diabetes in children and adolescents. In order to prove that type 2 diabetes in adolescents is characterized by severe insulin resistance and defects in B-cell function, adolescents with Type 2 diabetes followed at Children's Memorial Hospital will undergo a thorough history, physical examination, an oral gluocse tolerance and, in a subset of participants, a frequently sampled intravenous glucose tolerance test. In order to prove that adolescents with acanthosis nigricans and varying degrees of glucose tolerance are characterized by severe insulin resistance and defects in B-cell function, a group of adolescents with acanthosis nigricans will be recruited. Each will have a thorough history and targeted physical, and an oral glucose tolerance test to assess insulin sensitivity, insulin secretion, and glucose tolerance. A subset of these will also undergo a modified IVGTT as well. In order to prove that adolescents with insulin resistance have evidence of risk factors for later cardiovascular disease, a group of individuals with low insulin sensitivity will have cardiovascular studies to evaluate for pediatric antecedents of cardiovascular disease. A better understanding of the pathophysiology of type 2 diabetes and its development in adolescents, will enable us to predict which preventive and therapeutic interventions will be successful in hopes of improving the morbidity and mortality associated with type 2 diabetes and/or severe insulin resistance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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 “glucose tolerance test” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for glucose tolerance test in the PubMed Central database: •

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INTERPRETATION OF THE RAPID INTRAVENOUS GLUCOSE TOLERANCE TEST IN NORMAL INDIVIDUALS AND IN MILD DIABETES MELLITUS. by Amatuzio DS, Stutzman FL, Vanderbilt MJ, Nesbitt S.; 1953 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=438359

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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THE INTRAVENOUS GLUCOSE TOLERANCE TEST IN PREGNANCY. by Johnson DG, Bonsnes RW, Barad B.; 1948 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=439551

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THE RAPID INTRAVENOUS GLUCOSE TOLERANCE TEST IN PREGNANCY. by Silverstone FA, Solomons E, Rubricius J.; 1961 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=290927

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 glucose tolerance test, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “glucose tolerance test” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for glucose tolerance test (hyperlinks lead to article summaries): •

A comparison between a 75-g and 100-g oral glucose tolerance test in pregnant women. Author(s): Soonthornpun S, Soonthornpun K, Aksonteing J, Thamprasit A. Source: International Journal of Gynaecology and Obstetrics: the Official Organ of the International Federation of Gynaecology and Obstetrics. 2003 May; 81(2): 169-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12706274

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A comparison of the 3 H glucose tolerance test and the 2 H value in identifying risk for excessive fetal growth. Author(s): Curet LB, Izquierdo LA, Gilson GJ, Del Valle GO, Qualls C. Source: The Journal of Maternal-Fetal Medicine. 1997 January-February; 6(1): 28-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9029381

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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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A method to measure the degree of control per se in the oral glucose tolerance test. Author(s): Martin HF, Goldstein RB, Hologgitas J. Source: Computers and Biomedical Research, an International Journal. 1989 August; 22(4): 314-27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2673656

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A model-based method for assessing insulin sensitivity from the oral glucose tolerance test. Author(s): Mari A, Pacini G, Murphy E, Ludvik B, Nolan JJ. Source: Diabetes Care. 2001 March; 24(3): 539-48. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11289482

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A new index of insulin sensitivity obtained from the oral glucose tolerance test applicable to advanced type 2 diabetes. Author(s): Kanauchi M. Source: Diabetes Care. 2002 October; 25(10): 1891-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12351505

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A postnatal fasting plasma glucose is useful in determining which women with gestational diabetes should undergo a postnatal oral glucose tolerance test. Author(s): Holt RI, Goddard JR, Clarke P, Coleman MA. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 2003 July; 20(7): 594-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12823243

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A simple method for quantitation of insulin sensitivity and insulin release from an intravenous glucose tolerance test. Author(s): Galvin P, Ward G, Walters J, Pestell R, Koschmann M, Vaag A, Martin I, Best JD, Alford F. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 1992 December; 9(10): 921-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1478037

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A standardised breakfast tolerance test in pregnancy: comparison with the 75 g oral glucose tolerance test in unselected mothers and in those with impaired glucose tolerance. Author(s): Roberts RN, McManus J, Dobbs S, Hadden DR. Source: Ulster Med J. 1997 May; 66(1): 18-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9185485

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A study of oral glucose tolerance test in patients of hypertension receiving propranolol. Author(s): Gautam VK, Vasavada JP, Khanijo SK. Source: Indian Heart J. 1989 July-August; 41(4): 261-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2807363

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Abnormal blood glucose and insulin response during oral glucose tolerance test in familial renal glycosuria. Author(s): De Marchi S, Cecchin E, Zanello F, Bartoli E. Source: Contrib Nephrol. 1997; 122: 200-2. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9399067

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Abnormal glucose screening test followed by normal glucose tolerance test and pregnancy outcome. Author(s): Thomas A, Kaur S, Somville T. Source: Saudi Med J. 2002 July; 23(7): 814-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12174232

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Abnormal growth hormone and cortisol, but not thyroid-stimulating hormone, responses to an intravenous glucose tolerance test in normal-weight, bulimic women. Author(s): Coiro V, Volpi R, Marchesi C, Capretti L, Speroni G, Rossi G, Caffarri G, De Ferri A, Marcato A, Chiodera P. Source: Psychoneuroendocrinology. 1992 November; 17(6): 639-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1363137

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Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults. Author(s): Moore MC, Cherrington AD, Mann SL, Davis SN. Source: The Journal of Clinical Endocrinology and Metabolism. 2000 December; 85(12): 4515-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11134101

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Adrenocortical tumors: prevalence of impaired glucose tolerance and of "Paradoxical Rise" of cortisol during an oral glucose tolerance test. Author(s): Vierhapper H, Heinze G, Gessl A, Exner M. Source: Experimental and Clinical Endocrinology & Diabetes : Official Journal, German Society of Endocrinology [and] German Diabetes Association. 2003 October; 111(7): 41520. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14614648

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Amylin release during oral glucose tolerance test. Author(s): Thomaseth K, Pacini G, Clodi M, Kautzky-Willer A, Nolan JJ, Prager R, Olefsky JM, Ludvik B. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 1997 June; 14 Suppl 2: S29-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9212327

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An audit of oral glucose tolerance test requests. Author(s): Burnett L. Source: The Medical Journal of Australia. 1990 June 4; 152(11): 607-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2348787

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An evaluation of the WHO criteria for abnormal glucose tolerance test during pregnancy in Nigerian women. Author(s): Okonofua FE, Onwudiegwu U, Ugwu NC. Source: Afr J Med Med Sci. 1995 December; 24(4): 365-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8886152

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Androgen response to endogenous insulin secretion during the frequently sampled intravenous glucose tolerance test in normal and hyperandrogenic women. Author(s): Falcone T, Finegood DT, Fantus IG, Morris D. Source: The Journal of Clinical Endocrinology and Metabolism. 1990 December; 71(6): 1653-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2146285

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Antioxidant defences are reduced during the oral glucose tolerance test in normal and non-insulin-dependent diabetic subjects. Author(s): Ceriello A, Bortolotti N, Crescentini A, Motz E, Lizzio S, Russo A, Ezsol Z, Tonutti L, Taboga C. Source: European Journal of Clinical Investigation. 1998 April; 28(4): 329-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9615913

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Application of the SAAM modeling program to minimal model analysis of intravenous glucose tolerance test data. Author(s): Martin IK, Weber KM, Ward GM, Best JD, Boston RC. Source: Computer Methods and Programs in Biomedicine. 1990 December; 33(4): 193203. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2282786

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Are the current ACOG Glucose Tolerance Test criteria sensitive enough? Author(s): Neiger R, Coustan DR. Source: Obstetrics and Gynecology. 1991 December; 78(6): 1117-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1945219

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Are the WHO (1980) criteria for the 75 g oral glucose tolerance test appropriate for pregnant women? Author(s): Cheng LC, Salmon YM. Source: British Journal of Obstetrics and Gynaecology. 1993 July; 100(7): 645-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8369247

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Assessing the shape of the glucose curve during an oral glucose tolerance test. Author(s): Tschritter O, Fritsche A, Shirkavand F, Machicao F, Haring H, Stumvoll M. Source: Diabetes Care. 2003 April; 26(4): 1026-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12663568

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Assessment of beta-cell function during the oral glucose tolerance test by a minimal model of insulin secretion. Author(s): Cretti A, Lehtovirta M, Bonora E, Brunato B, Zenti MG, Tosi F, Caputo M, Caruso B, Groop LC, Muggeo M, Bonadonna RC. Source: European Journal of Clinical Investigation. 2001 May; 31(5): 405-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11380592

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Assessment of glucose tolerance test criteria for diagnosis of diabetes in Chinese subjects. Author(s): Cockram CS, Lau JT, Chan AY, Woo J, Swaminathan R. Source: Diabetes Care. 1992 August; 15(8): 988-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1505331

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Assessment of insulin secretion from the oral glucose tolerance test in white patients with type 2 diabetes. Author(s): Stumvoll M, Mitrakou A, Pimenta W, Jenssen T, Yki-Jarvinen H, Van Haeften T, Haring H, Fritsche A, Gerich J. Source: Diabetes Care. 2000 September; 23(9): 1440-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10977054

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Assessment of insulin sensitivity and beta-cell function from measurements in the fasting state and during an oral glucose tolerance test. Author(s): Albareda M, Rodriguez-Espinosa J, Murugo M, de Leiva A, Corcoy R. Source: Diabetologia. 2000 December; 43(12): 1507-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11151759

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Assessment of insulin sensitivity and insulin secretion from the oral glucose tolerance test in nonobese Japanese type 2 diabetic patients: comparison with minimal-model approach. Author(s): Taniguchi A, Nagasaka S, Fukushima M, Sakai M, Nagata I, Doi K, Tanaka H, Yoneda M, Tokuyama K, Nakai Y. Source: Diabetes Care. 2000 September; 23(9): 1439-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10977053

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Assessment of insulin sensitivity and secretion with the labelled intravenous glucose tolerance test: improved modelling analysis. Author(s): Mari A. Source: Diabetologia. 1998 September; 41(9): 1029-39. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9754821

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Assessment of the glucose tolerance test in unselected pregnancy using 75 g glucose load. Author(s): Li DF, Wang ZQ, Wong VC, Ma HK. Source: International Journal of Gynaecology and Obstetrics: the Official Organ of the International Federation of Gynaecology and Obstetrics. 1988 August; 27(1): 7-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2905302

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Beta-cell function during insulin-modified intravenous glucose tolerance test successfully assessed by the C-peptide minimal model. Author(s): Toffolo G, Cefalu WT, Cobelli C. Source: Metabolism: Clinical and Experimental. 1999 September; 48(9): 1162-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10484058

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Beta-endorphin response to oral glucose tolerance test in obese and non-obese preand postmenopausal women. Author(s): Stomati M, Bersi C, Bernardi F, Rubino S, Nappi L, Catarsi S, Ferrari A, Spinetti A, Cionini R, Petraglia F, Genazzani AR. Source: Gynecological Endocrinology : the Official Journal of the International Society of Gynecological Endocrinology. 1998 February; 12(1): 35-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9526708

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Beta-endorphin, insulin, ACTH and cortisol plasma levels during oral glucose tolerance test in obesity after weight loss. Author(s): Giovannini C, Ciucci E, Clementi R, Cugini P, Facchinetti F, Negri M. Source: Hormone and Metabolic Research. Hormon- Und Stoffwechselforschung. Hormones Et Metabolisme. 1990 February; 22(2): 96-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2157655

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Blood glucose and plasma insulin and glucagon response during intravenous glucose tolerance test in newborn infants affected by erythroblastosis foetalis. Author(s): Massi-Benedetti F, Marini A, Caccamo ML, Falorni A. Source: Acta Paediatr Scand. 1975 January; 64(1): 113-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1114890

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Blood glucose, free fatty acids and intravenous glucose tolerance test in obese patients on different diets. Author(s): Bjorntorp P, Jonsson A, Hood B. Source: Acta Med Scand. 1965 August; 178(2): 175-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5834917

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Blood inorganic phosphate, pyruvate and lactate during an intravenous glucose tolerance test in ischemic cardiovascular disease. Author(s): Hagenfeldt L, Wahlberg F. Source: Acta Med Scand. 1971 March; 189(3): 207-11. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5090205

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Blood levels of branched-chain alpha-keto acids in uremia: effect of an oral glucose tolerance test. Author(s): Schauder P, Matthaei D, Henning HV, Scheler F, Langenbeck U. Source: Klin Wochenschr. 1981 August 3; 59(15): 845-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7021997

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Caffeine ingestion elevates plasma insulin response in humans during an oral glucose tolerance test. Author(s): Graham TE, Sathasivam P, Rowland M, Marko N, Greer F, Battram D. Source: Canadian Journal of Physiology and Pharmacology. 2001 July; 79(7): 559-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11478588

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Can glucose tolerance test predict fetal hyperinsulinism? Author(s): Weiss PA, Haeusler M, Tamussino K, Haas J. Source: Bjog : an International Journal of Obstetrics and Gynaecology. 2000 December; 107(12): 1480-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11192103

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Change in retinal arterial blood flow in the contralateral eye of retinal vein occlusion during glucose tolerance test. Author(s): Kida T, Harino S, Sugiyama T, Kitanishi K, Iwahashi Y, Ikeda T. Source: Graefe's Archive for Clinical and Experimental Ophthalmology = Albrecht Von Graefes Archiv Fur Klinische Und Experimentelle Ophthalmologie. 2002 May; 240(5): 342-7. Epub 2002 March 20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12073056

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Changes in plasma, erythrocyte, and platelet magnesium levels in normotensive and hypertensive obese subjects during oral glucose tolerance test. Author(s): Corica F, Allegra A, Ientile R, Buemi M, Corsonello A, Bonanzinga S, Macaione S, Ceruso D. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 1999 February; 12(2 Pt 1): 128-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10090339

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Changes in sex hormones during an oral glucose tolerance test in healthy premenopausal women. Author(s): Ivandic A, Prpic-Krizevac I, Jakic M, Bacun T. Source: Fertility and Sterility. 1999 February; 71(2): 268-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9988396

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Changes in uterine artery doppler velocimetry in pregnant patients undergoing glucose tolerance test may predict adverse outcome in later pregnancy: a preliminary study. Author(s): Jaffe R, Friedman Z. Source: Fetal Diagnosis and Therapy. 1998 July-August; 13(4): 241-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9784646

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Changes of serum TSH level during oral glucose tolerance test: comparison of morning and evening test with plain circadian TSH rhythm. Author(s): Langer P, Martino E, Ksinantova L, Glasso L, Vigas M. Source: Endocrine Regulations. 2000 September; 34(3): 145-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11074659

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Circulating ghrelin levels in basal conditions and during glucose tolerance test in acromegalic patients. Author(s): Cappiello V, Ronchi C, Morpurgo PS, Epaminonda P, Arosio M, Beck-Peccoz P, Spada A. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2002 August; 147(2): 189-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12153739

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Clinical outcomes of pregnancy with one elevated glucose tolerance test value. Author(s): Kim HS, Chang KH, Yang JI, Yang SC, Lee HJ, Ryu HS. Source: International Journal of Gynaecology and Obstetrics: the Official Organ of the International Federation of Gynaecology and Obstetrics. 2002 August; 78(2): 131-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12175714

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Comments on the proposed revision of the oral glucose tolerance test. Author(s): Masse J. Source: Clinical Chemistry. 1990 May; 36(5): 819-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2338002

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Comparison of a clinical model, the oral glucose tolerance test, and fasting glucose for prediction of type 2 diabetes risk in Japanese Americans. Author(s): McNeely MJ, Boyko EJ, Leonetti DL, Kahn SE, Fujimoto WY. Source: Diabetes Care. 2003 March; 26(3): 758-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12610034

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Comparison of estimates of insulin sensitivity from minimal model analysis of the insulin-modified frequently sampled intravenous glucose tolerance test and the isoglycemic hyperinsulinemic clamp in subjects with NIDDM. Author(s): Coates PA, Luzio SD, Brunel P, Owens DR. Source: Diabetes. 1995 June; 44(6): 631-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7789626

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Comparison of estimates of insulin sensitivity in pre- and postmenopausal women using the insulin tolerance test and the frequently sampled intravenous glucose tolerance test. Author(s): Lindheim SR, Buchanan TA, Duffy DM, Vijod MA, Kojima T, Stanczyk FZ, Lobo RA. Source: Journal of the Society for Gynecologic Investigation. 1994 April-June; 1(2): 150-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9419764

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Comparison of the 50 g capillary plasma glucose tolerance test with the 75 g venous plasma glucose tolerance test in pregnancy. Author(s): Henry OA, Shelley-Jones DC, Oats JN, Wein P, Beischer NA. Source: The Journal of Obstetrics and Gynaecology Research. 1996 June; 22(3): 215-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8840705

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Comparison of the metabolic effects of mixed meal and standard oral glucose tolerance test on glucose, insulin and C-peptide response in healthy, impaired glucose tolerance, mild and severe non-insulin-dependent diabetic subjects. Author(s): Marena S, Montegrosso G, De Michieli F, Pisu E, Pagano G. Source: Acta Diabetologica. 1992; 29(1): 29-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1520903

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Comparison of the metabolic response to a glucose tolerance test and a standardized test meal and the response to serial test meals in normal healthy subjects. Author(s): Owens DR, Wragg KG, Briggs PI, Luzio S, Kimber G, Davies C. Source: Diabetes Care. 1979 November-December; 2(6): 409-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12085572

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Computerized analysis of fetal heart rate indices during oral glucose tolerance test. Author(s): Weissman A, Goldstick O, Geva A, Zimmer EZ. Source: Journal of Perinatal Medicine. 2003; 31(4): 302-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12951885

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Controlled oral glucose tolerance test: evaluation of insulin resistance with an insulin infusion algorithm that forces the OGTT glycaemic curve within the normal range. A feasibility study. Author(s): Volpicelli G, Iannello S, Belfiore F. Source: Clinical Physiology (Oxford, England). 1999 January; 19(1): 32-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10068865

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Correlation between fasting plasma glucose and two-hour plasma glucose during oral glucose tolerance test in South Indians. Author(s): Mohan V, Deepa R, Rema M. Source: Metabolism: Clinical and Experimental. 2000 April; 49(4): 455-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10778868

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Counterpoint: the oral glucose tolerance test is superfluous. Author(s): Davidson MB. Source: Diabetes Care. 2002 October; 25(10): 1883-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12351497

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Criteria for the oral glucose tolerance test in pregnant and non-pregnant Nigerian women. Author(s): Okonofua FE, Amole FA, Ayangade SO, Nimalaraj T. Source: International Journal of Gynaecology and Obstetrics: the Official Organ of the International Federation of Gynaecology and Obstetrics. 1988 August; 27(1): 85-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2905305

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Decrease in serum dopamine-beta-hydroxylase activity during oral glucose tolerance test. Author(s): Obermann Z, Herzberg M. Source: Isr J Med Sci. 1978 July; 14(7): 798-800. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=681172

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Depressive symptoms and the glucose tolerance test and insulin tolerance test. Author(s): Heninger GR, Mueller PS, Davis LS. Source: The Journal of Nervous and Mental Disease. 1975 December; 161(6): 421-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1194911

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Detection of diabetes in hospitalized patients using a simplified glucose tolerance test. Author(s): Zamrazil V, Nemec J, Havelka J. Source: Rev Czech Med. 1977; 23(3): 136-42. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=410080

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Diagnosing gestational diabetes mellitus: use of a glucose screen without administering the glucose tolerance test. Author(s): Chez RA. Source: Obstetrics and Gynecology. 1996 July; 88(1): 156. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8684751

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Diagnosing gestational diabetes mellitus: use of a glucose screen without administering the glucose tolerance test. Author(s): Landy HJ, Gomez-Marin O, O'Sullivan MJ. Source: Obstetrics and Gynecology. 1996 March; 87(3): 395-400. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8598962

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Diagnosis of cystic fibrosis related diabetes: a selective approach in performing the oral glucose tolerance test based on a combination of clinical and biochemical criteria. Author(s): Yung B, Kemp M, Hooper J, Hodson ME. Source: Thorax. 1999 January; 54(1): 40-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10343630

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Diagnosis of diabetes mellitus: pitfalls in the glucose tolerance test. Author(s): King H, Alberti KG, Keen H, Bennett PH. Source: British Medical Journal (Clinical Research Ed.). 1988 January 30; 296(6618): 357. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3125894

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Diagnosis of diabetes mellitus: pitfalls in the glucose tolerance test. Author(s): Wiener K. Source: British Medical Journal (Clinical Research Ed.). 1987 November 28; 295(6610): 1363. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3121015

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Diagnosis of reactive hypoglycemia: pitfalls in the use of the oral glucose tolerance test. Author(s): Chalew SA, Koetter H, Hoffman S, Levin PA, Kowarski AA. Source: Southern Medical Journal. 1986 March; 79(3): 285-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3952536

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Diagnostic capabilities of the intravenous glucose tolerance test. Author(s): O'Sullivan JB, Mahan CM. Source: J Chronic Dis. 1973 March; 26(3): 153-61. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4571891

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Diagnostic value of fasting capillary glucose, fructosamine and glycosylated haemoglobin in detecting diabetes and other glucose tolerance abnormalities compared to oral glucose tolerance test. Author(s): Herdzik E, Safranow K, Ciechanowski K. Source: Acta Diabetologica. 2002 April; 39(1): 15-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12043934

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Diagnostic value of the oral glucose tolerance test evaluated with a mathematical model. Author(s): Jansson L, Lindskog L, Norden NE. Source: Computers and Biomedical Research, an International Journal. 1980 December; 13(6): 512-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7460536

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Different responses of insulin, C-peptide, and testosterone to an oral glucose tolerance test in two groups of women with polycystic ovarian syndrome. Author(s): Ke WX, Shan GQ, Hua SY. Source: Acta Obstetricia Et Gynecologica Scandinavica. 1996 February; 75(2): 166-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8604605

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Dilution of the 75-g oral glucose tolerance test improves overall tolerability but not reproducibility in subjects with different body compositions. Author(s): Sievenpiper JL, Jenkins DJ, Josse RG, Vuksan V. Source: Diabetes Research and Clinical Practice. 2001 February; 51(2): 87-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11165688

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Dilution of the 75-g oral glucose tolerance test increases postprandial glycemia: implications for diagnostic criteria. Author(s): Sievenpiper JL, Jenkins DJ, Josse RG, Vuksan V. Source: Cmaj : Canadian Medical Association Journal = Journal De L'association Medicale Canadienne. 2000 April 4; 162(7): 993-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10763397

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Do impaired glucose tolerance and diabetes mellitus interfere with the interpretation of the growth hormone response to the oral glucose tolerance test? Author(s): Kayath MJ, Russo EM, Dib SA, Vieira JG. Source: Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas / Sociedade Brasileira De Biofisica. [et Al.]. 1992; 25(5): 449-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1342220

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Do we need the oral glucose tolerance test to identify future cases of type 2 diabetes? Author(s): Stern MP, Williams K, Haffner SM. Source: Diabetes Care. 2003 March; 26(3): 940-1. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12610061

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Does a high carbohydrate preparatory diet affect the 3-hour oral glucose tolerance test in pregnancy? Author(s): Entrekin K, Work B, Owen J. Source: The Journal of Maternal-Fetal Medicine. 1998 March-April; 7(2): 68-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9584817

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Does insulin secretion in patients with one abnormal glucose tolerance test value mimic gestational diabetes mellitus? Author(s): Ergin T, Lembet A, Duran H, Kuscu E, Bagis T, Saygili E, Batioglu S. Source: American Journal of Obstetrics and Gynecology. 2002 February; 186(2): 204-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11854636

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Effect of acitretin on the response to an intravenous glucose tolerance test in healthy volunteers. Author(s): Hartmann D, Forgo I, Dubach UC, Hennes U. Source: European Journal of Clinical Pharmacology. 1992; 42(5): 523-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1535045

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Effect of advancing pregnancy on the glucose tolerance test and on the 50-g oral glucose load screening test for gestational diabetes. Author(s): Benjamin F, Wilson SJ, Deutsch S, Seltzer VL, Droesch K, Droesch J. Source: Obstetrics and Gynecology. 1986 September; 68(3): 362-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3737059

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Effect of diltiazem on plasma glucose, insulin and glucagon during an oral glucose tolerance test in healthy volunteers. Author(s): Segrestaa JM, Caulin C, Dahan R, Houlbert D, Thiercelin JF, Herman P, Sauvanet JP, Larribaud J. Source: European Journal of Clinical Pharmacology. 1984; 26(4): 481-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6376146

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Effect of fetal hyperinsulinism on oral glucose tolerance test results in patients with gestational diabetes mellitus. Author(s): Weiss PA, Scholz HS, Haas J, Tamussino KF. Source: American Journal of Obstetrics and Gynecology. 2001 February; 184(3): 470-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11228505

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Effect of subject height on the result for the fifty-gram oral glucose tolerance test. Author(s): Phillipou G. Source: American Journal of Obstetrics and Gynecology. 1991 February; 164(2): 698. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1992724

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Effect of the 100-g oral glucose tolerance test on fetal acid-base balance. Author(s): Weissman A, Lowenstein L, Drugan A, Zimmer EZ. Source: Prenatal Diagnosis. 2003 April; 23(4): 281-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12673629

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Effects of collateral vessel occlusion on oral glucose tolerance test in liver cirrhosis. Author(s): Tanabe N, Ishii M, Sato Y, Akahane T, Kobayashi N, Gama H, Iwasaki T, Toyota T. Source: Digestive Diseases and Sciences. 2000 March; 45(3): 581-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10749336

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Effects of doxazosin, a selective alpha 1-inhibitor, on plasma insulin and blood glucose response to a glucose tolerance test in essential hypertension. Author(s): Giorda C, Appendino M. Source: Metabolism: Clinical and Experimental. 1993 November; 42(11): 1440-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8231840

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Effects of laparoscopic ovarian drilling on serum vascular endothelial growth factor and on insulin responses to the oral glucose tolerance test in women with polycystic ovary syndrome. Author(s): Tulandi T, Saleh A, Morris D, Jacobs HS, Payne NN, Tan SL. Source: Fertility and Sterility. 2000 September; 74(3): 585-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10973659

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Effects of metformin on glucose, insulin and lipid metabolism in patients with mild hypertriglyceridaemia and non-insulin dependent diabetes by glucose tolerance test criteria. Author(s): Hollenbeck CB, Johnston P, Varasteh BB, Chen YD, Reaven GM. Source: Diabete Metab. 1991 September-October; 17(5): 483-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1752350

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Effects of selective vagotomy with or without drainage on glucose tolerance test. Author(s): Akiyama H, Ohdate K, Iwasaki M, Yoshioka S, Kameya S, Izima N. Source: Jpn J Surg. 1984 January; 14(1): 15-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6376896

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Epinephrine exerts opposite effects on peripheral glucose disposal and glucosestimulated insulin secretion. A stable label intravenous glucose tolerance test minimal model study. Author(s): Avogaro A, Toffolo G, Valerio A, Cobelli C. Source: Diabetes. 1996 October; 45(10): 1373-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8826974

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Erythrocyte insulin receptor and glucose tolerance test in children treated with prednisolone. Author(s): Kan H, Fujimoto S, Matsuda I. Source: Endocrinol Jpn. 1985 June; 32(3): 347-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3899618

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Estimation of beta-cell sensitivity from intravenous glucose tolerance test C-peptide data. Knowledge of the kinetics avoids errors in modeling the secretion. Author(s): Toffolo G, De Grandi F, Cobelli C. Source: Diabetes. 1995 July; 44(7): 845-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7789653

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Evaluation of activity in postoperative acromegalics--plasma growth hormone levels during oral glucose tolerance test, daytime blood sampling and urinary GH excretion. Author(s): Hattori N, Shimatsu A, Tanoh T, Koshiyama H, Kato Y, Imura H. Source: Endocrinol Jpn. 1990 October; 37(5): 629-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2128272

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Evaluation of insulin release and relative peripheral resistance with use of the oral glucose tolerance test: a study in subjects with normoglycaemia, glucose intolerance and non-insulin-dependent diabetes mellitus. Author(s): Cederholm J, Wibell L. Source: Scandinavian Journal of Clinical and Laboratory Investigation. 1985 December; 45(8): 741-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3909372

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Evaluation of insulin response in glucose tolerance test in a patient with Werner's syndrome: a 16-year follow-up study. Author(s): Abe T, Yamaguchi Y, Izumino K, Ozaki M, Yamakawa K, Kondo H, Sera Y, Uotani S, Takino H, Kawasaki E, Yamasaki H, Eguchi K. Source: Diabetes Nutr Metab. 2000 April; 13(2): 113-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10898130

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Evaluation of suppression of growth hormone levels following a 75g oral glucose tolerance test. Author(s): Nazaimoon WM, Ng ML, Satgunasingam N, Khalid BA. Source: Med J Malaysia. 1992 June; 47(2): 103-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1494329

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Evaluation of the WHO criteria for 75 g oral glucose tolerance test in pregnancy. Author(s): Li DF, Wong VC, O'Hoy KM, Ma HK. Source: British Journal of Obstetrics and Gynaecology. 1987 September; 94(9): 847-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3663546

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False-positive result of a glucose tolerance test. Author(s): DeLeacy EA, Cowley DM, Wynne JM. Source: The Medical Journal of Australia. 1988 August 15; 149(4): 225-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3173184

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Familial resemblance for glucose and insulin metabolism indices derived from an intravenous glucose tolerance test in Blacks and Whites of the HERITAGE Family Study. Author(s): Hong Y, Weisnagel SJ, Rice T, Sun G, Mandel SA, Gu C, Rankinen T, Gagnon J, Leon AS, Skinner JS, Wilmore JH, Bergman RN, Bouchard C, Rao DC; HERITAGE Family Study. Source: Clinical Genetics. 2001 July; 60(1): 22-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11531966

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Fast fluctuations of glycosylated hemoglobins. II. Hemoglobin A1c determination and oral glucose tolerance test. Author(s): Kitzis A, Baudis M, Auge MC, Gachon AM, Dastugue B, Wajcman H. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1982 May 20; 121(2): 133-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7094334

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Fatty acid composition of plasma lipids in normal and obese children under fasting conditions and during an intravenous glucose tolerance test. Author(s): Bonnet F, Gosselin L, Chantraine J, Senterre J. Source: Rev Eur Etud Clin Biol. 1970 November; 15(9): 976-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5505089

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Fetal biophysical testing. The effects of prolonged maternal fasting and the oral glucose tolerance test. Author(s): Devoe LD, Searle N, Castillo RA, Searle J. Source: J Reprod Med. 1987 August; 32(8): 563-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3309287

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First-phase insulin release during the intravenous glucose tolerance test as a risk factor for type 1 diabetes. Author(s): Chase HP, Cuthbertson DD, Dolan LM, Kaufman F, Krischer JP, Schatz DA, White NH, Wilson DM, Wolfsdorf J. Source: The Journal of Pediatrics. 2001 February; 138(2): 244-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11174623

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Five-hour oral glucose tolerance test in obese children. Author(s): Court JM, Dunlop M, Leonard I, Leonard RF. Source: Archives of Disease in Childhood. 1971 December; 46(250): 791-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5129181

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Flat GTT. The significance of flat glucose tolerance test. Author(s): Shah S, Stoffer RP, McReynolds CR. Source: J Kans Med Soc. 1975 November; 76(11): 263-5, 267. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1185022

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Forearm glucose uptake during the oral glucose tolerance test in normal subjects. Author(s): Jackson RA, Peters N, Advani U, Perry G, Rogers J, Brough WH, Pilkington TR. Source: Diabetes. 1973 June; 22(6): 442-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4713669

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Free fatty acids curve in normals during the oral glucose tolerance test. Author(s): Gola A, Frydecka I, Slonczewski B. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1972 April; 38(1): 127-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5031776

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Free fatty-acid pattern in the plasma of normal and obese children during fasting and intravenous glucose tolerance test. Author(s): Bonnet F, Gosselin L, Chantraine J, Senterre J. Source: Arch Int Physiol Biochim. 1970 August; 78(3): 495-508. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4098000

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Further experience on glucose tolerance test during rifampicin therapy. Author(s): Sharma TN, Agarwal KC, Gupta PR, Purohit SD, Sharma VK, Mathur BB. Source: J Assoc Physicians India. 1986 February; 34(2): 131-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3711003

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Gestational diabetes mellitus and glucose tolerance test: value of the values. Author(s): Rohilla M. Source: American Journal of Obstetrics and Gynecology. 2002 November; 187(5): 1424; Author Reply 1424-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12439542

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Gestational diabetes mellitus diagnosed with a 2-h 75-g oral glucose tolerance test and adverse pregnancy outcomes. Author(s): Schmidt MI, Duncan BB, Reichelt AJ, Branchtein L, Matos MC, Costa e Forti A, Spichler ER, Pousada JM, Teixeira MM, Yamashita T; Brazilian Gestational Diabetes Study Group. Source: Diabetes Care. 2001 July; 24(7): 1151-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11423494

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GH, IGFBP-1, and IGFBP-3 response to oral glucose tolerance test in perimenopausal women: no influence of body mass index. Author(s): Bernardi F, Petraglia F, Seppala M, Spinetti A, Bertolini S, Driul L, Ferdeghini M, Genazzani AR. Source: Maturitas. 1999 October 24; 33(2): 163-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10597881

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Glucose and insulin responses to a glucose tolerance test in primary hyperparathyroidism before and after parathyroidectomy and during an acute calcium infusion. Author(s): Shapiro MS, Roitman A, Bernheim J. Source: Isr J Med Sci. 1990 October; 26(10): 577-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2249935

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Glucose metabolism in severe malaria: minimal model analysis of the intravenous glucose tolerance test incorporating a stable glucose label. Author(s): Binh TQ, Davis TM, Johnston W, Thu LT, Boston R, Danh PT, Anh TK. Source: Metabolism: Clinical and Experimental. 1997 December; 46(12): 1435-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9439539

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Glucose processing during the intravenous glucose tolerance test. Author(s): Henriksen JE, Alford F, Handberg A, Vaag A, Beck-Nielsen H. Source: Metabolism: Clinical and Experimental. 1996 May; 45(5): 598-605. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8622603

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Glucose tolerance test and glycosylated haemoglobin measurement for diagnosis of diabetes mellitus--an assessment of the criteria of the WHO Expert Committee on Diabetes Mellitus 1980. Author(s): Albutt EC, Nattrass M, Northam BE. Source: Annals of Clinical Biochemistry. 1985 January; 22 ( Pt 1): 67-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3985560

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Glucose tolerance test and insulin levels in children with transfusion-dependent thalassaemia. Author(s): Lee BW, Tan SH, Lee WK, Yap HK, Aw SE, Wong HB. Source: Annals of Tropical Paediatrics. 1985 December; 5(4): 215-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2418772

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Glucose tolerance test during antituberculous drug therapy. Author(s): Singh RP, Narang RK, Agarwal VB, Singh RK, Katiyar SK. Source: Indian J Chest Dis Allied Sci. 1988 July-September; 30(3): 183-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3243600

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Glucose tolerance test during pregnancy: the significance of one abnormal value. Author(s): Forest JC, Masse J, Garrido-Russo M. Source: Clinical Biochemistry. 1994 August; 27(4): 299-304. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8001292

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Glucose tolerance test in Israeli pregnant women. Author(s): Friedman S, May JY, Hod M, Rusecki Y, Ovadia J. Source: Isr J Med Sci. 1985 August; 21(8): 639-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4044228

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Glucose tolerance test in leprosy. Author(s): Garg R, Agrawal JK, Bajpai HS, Singh G, Srivastava PK. Source: Indian J Lepr. 1990 January-March; 62(1): 50-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2358705

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Glucose tolerance test periodicity as a descriptor of glucose tolerance abnormality. Author(s): Berkus MD, Xenakis EM, Langer O. Source: Obstetrics and Gynecology. 1992 June; 79(6): 931-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1579316

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Glucose tolerance test periodicity: the effect of glucose loading. Author(s): Berkus MD, Langer O. Source: Obstetrics and Gynecology. 1995 March; 85(3): 423-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7862384

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Glucose tolerance test: degree of glucose abnormality correlates with neonatal outcome. Author(s): Berkus MD, Langer O. Source: Obstetrics and Gynecology. 1993 March; 81(3): 344-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8437783

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Glucose, insulin and C-peptide kinetics during an oral glucose tolerance test in patients with chronic liver disease. Author(s): Min YK, Suh KI, Choi SJ, Lee HK, Kim CY, Koh CS, Min HK. Source: Korean J Intern Med. 1987 January; 2(1): 37-41. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3154815

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Glucose, insulin and C-peptide kinetics during intravenous glucose tolerance test in chronic liver disease. Author(s): Lee KU, Rhee BD, Lee HK, Kim CY, Koh CS, Min HK. Source: Diabetes Research and Clinical Practice. 1987 May-June; 3(3): 161-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3297592

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Glycogenesis and glucose oxidation during an intravenous glucose tolerance test in man. Author(s): Bluck LJ, Clapperton AT, Kidney CV, Coward WA. Source: Clinical Science (London, England : 1979). 2004 June; 106(6): 645-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14759220

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Glycosylated haemoglobin as an alternative to the glucose tolerance test for the diagnosis of diabetes mellitus. Author(s): Lester E, Frazer AD, Shepherd CA, Woodroffe FJ. Source: Annals of Clinical Biochemistry. 1985 January; 22 ( Pt 1): 74-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3985561

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Glycosylated haemoglobin values and their correlation to the glucose tolerance test in normal pregnancy. Author(s): Thalassinos NC, Yalouris A, Gania P, Vrakas G, Gnafakis N, Arapakis G. Source: Acta Endocrinol Suppl (Copenh). 1984; 265: 24-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6593982

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Health evaluation of the dentist and his wife. II. Three-hour oral glucose tolerance test. Author(s): Cheraskin E, Ringsdorf WM Jr. Source: The Journal of the American Dental Association. 1968 July; 77(1): 107-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5241371

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Heterogeneity of high-density lipoprotein particles and insulin output during oral glucose tolerance test in men with coronary artery disease. Author(s): Iwanejko J, Kwasniak M, Wybranska I, Hartwich J, Guevara I, Zdzienicka A, Kruszelnicka-Kwiatkowska O, Piwowarska W, Miszczuk-Jamska B, Dembinska-Kiec A. Source: Acta Diabetologica. 1996 March; 33(1): 58-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8777287

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Hyperinsulinemia during oral glucose tolerance test is associated with increased neointimal tissue proliferation after coronary stent implantation in nondiabetic patients: a serial intravascular ultrasound study. Author(s): Takagi T, Yoshida K, Akasaka T, Kaji S, Kawamoto T, Honda Y, Yamamuro A, Hozumi T, Morioka S. Source: Journal of the American College of Cardiology. 2000 September; 36(3): 731-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10987592

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Hyperinsulinism, neonatal obesity and placental immaturity in infants born to women with one abnormal glucose tolerance test value. Author(s): Schafer-Graf UM, Dupak J, Vogel M, Dudenhausen JW, Kjos SL, Buchanan TA, Vetter K. Source: Journal of Perinatal Medicine. 1998; 26(1): 27-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9595364

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Identification of persons at high risk for type 2 diabetes mellitus: do we need the oral glucose tolerance test? Author(s): Stern MP, Williams K, Haffner SM. Source: Annals of Internal Medicine. 2002 April 16; 136(8): 575-81. Summary for Patients In: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11955025

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Impact of overnight dexamethasone suppression on the adrenal androgen response to an oral glucose tolerance test in women with and without polycystic ovary syndrome. Author(s): Buyalos RP, Geffner ME, Azziz R, Judd HL. Source: Human Reproduction (Oxford, England). 1997 June; 12(6): 1138-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9221990

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Increased secretion of insulin during oral glucose tolerance test can be a predictor of stent restenosis in nondiabetic patients. Author(s): Babalik E, Gurmen T, Orhan L, Bulur H, Gulbaran M, Ersanli M, Ozturk S. Source: Catheterization and Cardiovascular Interventions : Official Journal of the Society for Cardiac Angiography & Interventions. 2003 March; 58(3): 306-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12594693

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Influence of sample type on the interpretation of the oral glucose tolerance test for gestational diabetes mellitus. Author(s): Neely RD, Kiwanuka JB, Hadden DR. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 1991 FebruaryMarch; 8(2): 129-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1827397

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Influence of two guar preparations on glucose and insulin levels during a glucose tolerance test in healthy volunteers. Author(s): Kirsten R, Nelson K, Storck J, Hubner-Steiner U, Speck U. Source: Int J Clin Pharmacol Ther Toxicol. 1991 January; 29(1): 19-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1848539

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83

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Inhibitory action of oral thyrotropin-releasing hormone on the glucoregulatory response of the oral glucose tolerance test. Author(s): Duntas LH, Papanastasiou L, Mantzou E, Jehle P, Mantzos I, Koutras DA. Source: Thyroid : Official Journal of the American Thyroid Association. 1998 October; 8(10): 929-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9827661

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Insulin independence and normalization of oral glucose tolerance test after islet cell allotransplantation. Author(s): Cretin N, Caulfield A, Fournier B, Buhler L, Becker C, Philippe J, Morel P. Source: Transplant International : Official Journal of the European Society for Organ Transplantation. 2001 September; 14(5): 343-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11692219

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Insulin levels during fasting and the glucose tolerance test and Homa's index predict subsequent development of hypertension. Author(s): Kashiwabara H, Inaba M, Maruno Y, Morita T, Awata T, Negishi K, Iitaka M, Katayama S. Source: Journal of Hypertension. 2000 January; 18(1): 83-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10678547

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Insulin release and peripheral sensitivity at the oral glucose tolerance test. Author(s): Cederholm J, Wibell L. Source: Diabetes Research and Clinical Practice. 1990 October; 10(2): 167-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2261853

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Insulin resistance in the oral glucose tolerance test--a link with hypertension. Author(s): Cederholm J, Wibell L. Source: Scandinavian Journal of Primary Health Care. 1991 March; 9(1): 53-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2041930

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Insulin secretion and sensitivity during oral glucose tolerance test in Korean lean elderly women. Author(s): Kim J, Choi S, Kong B, Oh Y, Shinn S. Source: Journal of Korean Medical Science. 2001 October; 16(5): 592-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11641528

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Insulin sensitivity and beta-cell secretion in thalassaemia major with secondary haemochromatosis: assessment by oral glucose tolerance test. Author(s): Cario H, Holl RW, Debatin KM, Kohne E. Source: European Journal of Pediatrics. 2003 March; 162(3): 139-46. Epub 2003 January 15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12655415

84

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Insulin sensitivity in type 2 diabetes: univariate and multivariate techniques to derive estimates of insulin sensitivity from the insulin modified intravenous glucose tolerance test (FSIGT). Author(s): Mehring GH, Coates PA, Brunel PC, Luzio SD, Owens DR. Source: Computer Methods and Programs in Biomedicine. 2002 May; 68(2): 161-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11932032

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Insulin sensitivity in women: a comparison among values derived from intravenous glucose tolerance tests with different sampling frequency, oral glucose tolerance test or fasting. Author(s): Cagnacci A, Arangino S, Renzi A, Cagnacci P, Volpe A. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2001 September; 145(3): 281-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11517008

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Insulin sensitivity indexes calculated from oral glucose tolerance test data. Author(s): Belfiore F. Source: Diabetes Care. 2000 October; 23(10): 1595-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11023159

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Intravenous glucose tolerance test-derived glucose effectiveness in bulimia nervosa. Author(s): Taniguchi A, Nakai Y, Fukushima M, Doi K, Tokuyama K, Kawamura H, Suzuki M, Higaki Y, Tanaka H, Sakai M, Nagata I. Source: Metabolism: Clinical and Experimental. 1997 May; 46(5): 484-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9160811

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Intravenous glucose tolerance test-derived glucose effectiveness in strength-trained humans. Author(s): Fujitani J, Higaki Y, Kagawa T, Sakamoto M, Kiyonaga A, Shindo M, Taniguchi A, Nakai Y, Tokuyama K, Tanaka H. Source: Metabolism: Clinical and Experimental. 1998 July; 47(7): 874-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9667238

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Intravenous glucose tolerance test-derived insulin sensitivity changes during the menstrual cycle. Author(s): Valdes CT, Elkind-Hirsch KE. Source: The Journal of Clinical Endocrinology and Metabolism. 1991 March; 72(3): 642-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1997519

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Is there any use for the oral glucose tolerance test? Author(s): Vaccaro O, Ruffa G, Riccardi G. Source: Diabetes Care. 2000 May; 23(5): 714-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10834445

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Isn't it time to retire the oral glucose tolerance test for diabetes screening and diagnosis? Author(s): Goldstein DE. Source: Diabetes Care. 1998 August; 21(8): 1215-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9702421

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Leptin concentrations during oral glucose tolerance test (OGTT) in obese and normal weight women. Author(s): Bougoulia M, Tzotzas T, Efthymiou H, Koliakos G, Konstantinidis T, Triantos A, Krassas GE. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 1999 June; 23(6): 625-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10411236

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Letter: Effect of vagotomy and pyloroplasty: the oral glucose tolerance test. Author(s): Somayaji BN. Source: Gastroenterology. 1974 February; 66(2): 326-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4810923

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Letter: Misuse of the glucose tolerance test? Author(s): Pickering LK, Feigin RD. Source: The Journal of Pediatrics. 1974 July; 85(1): 147. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4852863

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Limitations of the oral glucose tolerance test in diagnosis of early diabetes. Author(s): Sherwin RS. Source: Primary Care. 1977 June; 4(2): 255-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=586717

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Liver steatosis in juvenile obesity: correlations with lipid profile, hepatic biochemical parameters and glycemic and insulinemic responses to an oral glucose tolerance test. Author(s): Guzzaloni G, Grugni G, Minocci A, Moro D, Morabito F. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2000 June; 24(6): 772-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10878685

86

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Longitudinal changes in plasma glucose values of the 75-g glucose tolerance test in triplet pregnancies. Author(s): Sameshima H, Higo T, Ikenoue T. Source: American Journal of Perinatology. 2004 February; 21(2): 49-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15017466

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Lower extremity blood flow in intermittent claudication--the role of oral glucose tolerance test. Author(s): Hanson M. Source: Angiology. 1987 October; 38(10): 756-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3662104

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Management of women with one abnormal oral glucose tolerance test value reduces adverse outcome in pregnancy. Author(s): Langer O, Anyaegbunam A, Brustman L, Divon M. Source: American Journal of Obstetrics and Gynecology. 1989 September; 161(3): 593-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2675597

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Maternal mean arterial pressure and oral glucose tolerance test results. Relationship in normotensive women. Author(s): Ma RM, Lao TT. Source: J Reprod Med. 2001 August; 46(8): 747-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11547650

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Mathematical modelling of the intravenous glucose tolerance test. Author(s): De Gaetano A, Arino O. Source: Journal of Mathematical Biology. 2000 February; 40(2): 136-68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10743599

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Measurement of insulin sensitivity by the minimal model method using a simplified intravenous glucose tolerance test: validity and reproducibility. Author(s): Duysinx BC, Scheen AJ, Gerard PL, Letiexhe MR, Paquot N, Lefebvre PJ. Source: Diabete Metab. 1994 July-August; 20(4): 425-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7843475

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Measurement of interstitial muscle glucose and lactate concentrations during an oral glucose tolerance test. Author(s): Muller M, Holmang A, Andersson OK, Eichler HG, Lonnroth P. Source: The American Journal of Physiology. 1996 December; 271(6 Pt 1): E1003-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8997218

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Mechanism of the cortisone-modified glucose tolerance test. Author(s): Berger S, Downey JL, Traisman HS, Metz R. Source: The New England Journal of Medicine. 1966 June 30; 274(26): 1460-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5939845

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Menstrual cycle carbohydrate metabolism. Studies on plasma insulin and blood glucose levels during an intravenous glucose tolerance test. Author(s): Spellacy WN, Carlson KL, Schade SL. Source: American Journal of Obstetrics and Gynecology. 1967 October 1; 99(3): 382-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6042615

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Metabolic observations in infants of strictly controlled diabetic mothers. II. Plasma insulin, FFA, glycerol, beta-hydroxybutyrate during intravenous glucose tolerance test. Author(s): Persson B, Gentz J, Kellum M, Thorell J. Source: Acta Paediatr Scand. 1976 January; 65(1): 1-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1251714

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Mild insulin resistance during oral glucose tolerance test (OGTT) in women with acne. Author(s): Aizawa H, Niimura M. Source: The Journal of Dermatology. 1996 August; 23(8): 526-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8854583

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Minimal model analysis of intravenous glucose tolerance test-derived insulin sensitivity in diabetic subjects. Author(s): Welch S, Gebhart SS, Bergman RN, Phillips LS. Source: The Journal of Clinical Endocrinology and Metabolism. 1990 December; 71(6): 1508-18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2229309

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MINMOD: a computer program to calculate insulin sensitivity and pancreatic responsivity from the frequently sampled intravenous glucose tolerance test. Author(s): Pacini G, Bergman RN. Source: Computer Methods and Programs in Biomedicine. 1986 October; 23(2): 113-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3640682

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Minor physiological relevance of oral glucose tolerance test. Author(s): Kuhl C, Vandsted M, Olsen PG. Source: Diabete Metab. 1982 September; 8(3): 203-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6754492

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Modification of response to the triamcinolone glucose tolerance test by treatment with oral hypoglycemic agents. Author(s): Navarrete VN, Torres IH, Castelazo Ayala L, Alger CR, Flores HV. Source: Diabetes. 1966 October; 15(10): 726-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5332532

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Modify the oral glucose tolerance test? Author(s): Colley CM. Source: Clinical Chemistry. 1990 September; 36(9): 1704-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2208726

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Muscarinic cholinergic modulation of insulin response to an intravenous glucose tolerance test in normal man. Author(s): Coiro V, Chiodera P, Volpi R, d'Amato L, Camellini L, Rossi G, Pignatti D, Butturini U. Source: J Endocrinol Invest. 1986 February; 9(1): 27-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3517121

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Natural history of glucose tolerance in relatives of diabetic patients: low prognostic value of the oral glucose tolerance test. Author(s): Kobberling J, Berninger D. Source: Diabetes Care. 1980 January-February; 3(1): 21-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7408614

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New criteria for interpretation of the 75 g oral glucose tolerance test in pregnancy. Author(s): Nasrat HA, Sabbagh SA, Salleh M, Ardawi M. Source: Metabolism: Clinical and Experimental. 1990 January; 39(1): 51-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2403620

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New index for evaluation of oral glucose tolerance test results. Author(s): Billewicz WZ, Anderson J, Lind T. Source: British Medical Journal. 1973 March 10; 1(5853): 573-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4694403

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New model out-performs glucose tolerance test in predicting risk of diabetes. Author(s): Rollins G. Source: Rep Med Guidel Outcomes Res. 2002 May 17; 13(10): 10, 12. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12492090

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Normal growth hormone response to the 75 g oral glucose tolerance test measured by immunoradiometric assay. Author(s): Stewart PM, Smith S, Seth J, Stewart SE, Cole D, Edwards CR. Source: Annals of Clinical Biochemistry. 1989 March; 26 ( Pt 2): 205-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2729870

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Normal initial insulin response in elderly people with glucose tolerance test diabetes. Author(s): Johansen K. Source: Isr J Med Sci. 1972 June; 8(6): 918. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5051845

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Novel insulin sensitivity index derived from oral glucose tolerance test. Author(s): Soonthornpun S, Setasuban W, Thamprasit A, Chayanunnukul W, Rattarasarn C, Geater A. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 March; 88(3): 101923. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12629079

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Occurrence of gestational diabetes mellitus and the value of different screening indicators for the oral glucose tolerance test. Author(s): Ostlund I, Hanson U. Source: Acta Obstetricia Et Gynecologica Scandinavica. 2003 February; 82(2): 103-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12648169

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On estimating biological variation in diagnostic tests: application to the oral glucose tolerance test. Author(s): Dix D, Cohen P. Source: Am J Med Technol. 1983 December; 49(12): 873-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6670667

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Oral glucose tolerance test and the preparatory diet. Author(s): Crowe SM, Mastrobattista JM, Monga M. Source: American Journal of Obstetrics and Gynecology. 2000 May; 182(5): 1052-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10819825

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Oral glucose tolerance test at each trimester of pregnancy. Author(s): Manassakorn J, Wankrue P, Tantisirin P, Cheunwatana P, Intramax L. Source: J Med Assoc Thai. 1988 January; 71(1): 25-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3361252

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Oral glucose tolerance test in children with sickle cell anaemia. Author(s): Adekile AD, Olusi SO, Oyebola DD. Source: East Afr Med J. 1985 March; 62(3): 213-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4017922

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Oral glucose tolerance test in general practice--when is it worthwhile? Author(s): Rutle O, Bruusgaard D, Furuseth K, Vaaler S. Source: Scandinavian Journal of Primary Health Care. 1994 December; 12(4): 255-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7863143

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Oral glucose tolerance test in healthy pregnant Nigerian women. Author(s): Famuyiwa OO, Amadin RA, Adelusi BO. Source: Diabetes Care. 1988 May; 11(5): 412-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3391091

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Oral glucose tolerance test in liver recipients treated with FK 506. Author(s): Mieles L, Todo S, Fung JJ, Jain A, Furukawa H, Susuki M, Starzl TE. Source: Transplantation Proceedings. 1990 February; 22(1): 41-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1689894

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Oral glucose tolerance test in myoma uterus. Author(s): Khandelwal S, Khandelwal PD, Bhu N, Bafna N. Source: J Indian Med Assoc. 1983 October; 81(7-8): 114-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6676357

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Oral glucose tolerance test in pregnancy. Evaluation of a simplified procedure. Author(s): Hanson U, Kallner A. Source: Acta Obstetricia Et Gynecologica Scandinavica. 1984; 63(3): 249-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6730941

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Oral glucose tolerance test in unselected pregnant Indian women. Author(s): Srinivasan P, Ponniah V, Kasthuri M. Source: Diabetes Care. 1985 November-December; 8(6): 619-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4075951

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Oral glucose tolerance test indexes for insulin sensitivity and secretion based on various availabilities of sampling times. Author(s): Stumvoll M, Van Haeften T, Fritsche A, Gerich J. Source: Diabetes Care. 2001 April; 24(4): 796-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11315860

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Oral glucose tolerance test is a poor predictor of hyperglycemia during pregnancy. Author(s): Backx CJ, Lotgering FK, Cornelis H, Wallenburg S. Source: Journal of Perinatal Medicine. 1989; 17(4): 253-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2625650

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Oral glucose tolerance test minimal model indexes of beta-cell function and insulin sensitivity. Author(s): Breda E, Cavaghan MK, Toffolo G, Polonsky KS, Cobelli C. Source: Diabetes. 2001 January; 50(1): 150-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11147781

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Oral glucose tolerance test. Author(s): Greenspoon JS. Source: Mayo Clinic Proceedings. 1988 August; 63(8): 838. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3398602

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Oral glucose tolerance test: an inhibitory or a stimulatory input to growth hormone secretion? Author(s): Valcavi R. Source: J Endocrinol Invest. 1996 April; 19(4): 253-5. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8862507

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Oral glucose tolerance test: indications and limitations. Author(s): Nelson RL. Source: Mayo Clinic Proceedings. 1988 March; 63(3): 263-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3278175

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Oral glucose tolerance test: to be or not to be performed? Author(s): Ann Intern Med. 2002 Apr 16;136(8):I29 Source: Clin Lab. 2002; 48(3-4): 143-52. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11955045

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Oral glucose tolerance test--can the reflectance meter replace laboratory-based methods? Author(s): Tan KT, Hsu AA, Wang KW. Source: Ann Acad Med Singapore. 1990 July; 19(4): 452-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2221801

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Paraoxonase-1 L55M polymorphism is associated with an abnormal oral glucose tolerance test and differentiates high risk coronary disease families. Author(s): Deakin S, Leviev I, Nicaud V, Brulhart Meynet MC, Tiret L, James RW; European Atherosclerosis Risk Study Group. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 March; 87(3): 126873. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11889198

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Physical properties of starch meals in vivo and in vitro and their influence on gastric emptying and oral glucose tolerance test. Author(s): Chang TM, Passaro E Jr, Shain LR, Chen WL. Source: Nutrition (Burbank, Los Angeles County, Calif.). 1991 November-December; 7(6): 410-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1802230

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Physiologic modeling of the intravenous glucose tolerance test in type 2 diabetes: a new approach to the insulin compartment. Author(s): Ward GM, Walters JM, Barton J, Alford FP, Boston RC. Source: Metabolism: Clinical and Experimental. 2001 May; 50(5): 512-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11319711

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Plasma androgens and oestradiol during oral glucose tolerance test in patients with polycystic ovaries. Author(s): Tiitinen A, Pekonen F, Stenman UH, Laatikainen T. Source: Human Reproduction (Oxford, England). 1990 April; 5(3): 242-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2191000

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Plasma glycohydrolase levels in patients with type 1 diabetes at onset and in subjects undergoing an intravenous glucose tolerance test. Author(s): Goi G, Bairati C, Burlina A, Massaccesi L, Monciotti C, Segalini G, Testa R, Lombardo A. Source: Metabolism: Clinical and Experimental. 2000 October; 49(10): 1352-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11079828

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Plasma insulin and blood pressure response to oral glucose tolerance test in young borderline hypertensives. Author(s): Narkiewicz K, Rynkiewicz A, Furmanski J, Gan J, Narwojsz E, Bieniaszewski L, Krupa-Wojciechowska B. Source: Mater Med Pol. 1993 January-March; 25(1): 23-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8412338

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Plasma levels of active form of ghrelin during oral glucose tolerance test in patients with anorexia nervosa. Author(s): Nakai Y, Hosoda H, Nin K, Ooya C, Hayashi H, Akamizu T, Kangawa K. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2003 July; 149(1): R1-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12824869

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Plasma neurotransmitters throughout an oral glucose tolerance test in non-depressed essential hypertension patients. Author(s): Lechin F, van der Dijs B, Lechin M, Jara H, Lechin A, Baez S, Orozco B, Rada I, Cabrera A, Arocha L, et al. Source: Clinical and Experimental Hypertension (New York, N.Y. : 1993). 1993 January; 15(1): 209-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8096777

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Point: a glucose tolerance test is important for clinical practice. Author(s): Tuomilehto J. Source: Diabetes Care. 2002 October; 25(10): 1880-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12351496

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Predicting future cardiovascular disease: do we need the oral glucose tolerance test? Author(s): Stern MP, Fatehi P, Williams K, Haffner SM. Source: Diabetes Care. 2002 October; 25(10): 1851-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12351490

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Prediction of diabetes with body mass index, oral glucose tolerance test and islet cell autoantibodies in a regional population. Author(s): Rolandsson O, Hagg E, Nilsson M, Hallmans G, Mincheva-Nilsson L, Lernmark A. Source: Journal of Internal Medicine. 2001 April; 249(4): 279-88. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11298847

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Predictive value of 1 hour 50 g oral glucose load screening test for gestational diabetes mellitus compared to 3 hour oral glucose tolerance test in high risk pregnant women. Author(s): Jirapinyo M, Puavilai G, Chanprasertyotin S, Tangtrakul S. Source: Asia Oceania J Obstet Gynaecol. 1993 March; 19(1): 7-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8489471

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Predictive value of intravenous glucose tolerance test insulin secretion less than or greater than the first percentile in islet cell antibody positive relatives of type 1 (insulin-dependent) diabetic patients. Author(s): Vardi P, Crisa L, Jackson RA. Source: Diabetologia. 1991 February; 34(2): 93-102. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2065854

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Prehepatic beta-cell secretion during the intravenous glucose tolerance test in humans: application of a combined model of insulin and C-peptide kinetics. Author(s): Watanabe RM, Volund A, Roy S, Bergman RN. Source: The Journal of Clinical Endocrinology and Metabolism. 1989 October; 69(4): 7907. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2674187

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Preoperative growth hormone response to thyrotropin-releasing hormone and oral glucose tolerance test in acromegaly: a retrospective evaluation of 50 patients. Author(s): De Marinis L, Mancini A, Bianchi A, Gentilella R, Valle D, Giampietro A, Zuppi P, Anile C, Maira G, Giustina A. Source: Metabolism: Clinical and Experimental. 2002 May; 51(5): 616-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11979395

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Prevalence of diabetes in Catalonia (Spain): an oral glucose tolerance test-based population study. Author(s): Castell C, Tresserras R, Serra J, Goday A, Lloveras G, Salleras L. Source: Diabetes Research and Clinical Practice. 1999 January; 43(1): 33-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10199586

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Prevalence of islet cell antibodies and its correlation with glucose and insulin response to oral glucose tolerance test in 1st degree relatives of insulin dependent diabetes mellitus probands. Author(s): Merchant PC, Godse CS, Varthakavi PK, Patel KL, Nihalani KD. Source: J Assoc Physicians India. 1998 May; 46(5): 417-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11273280

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Proinsulin and specific insulin responses to an oral glucose tolerance test in a healthy population. Author(s): Chevenne D, Leger J, Levy-Marchal C, Noel M, Collin D, Czernichow P, Porquet D. Source: Diabetes & Metabolism. 1998 June; 24(3): 260-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9690061

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Prolonged oral glucose tolerance test combined with indirect calorimetry and estimation of several substrates and hormones in obese subjects. Author(s): Sonka J, Svacina S, Sucharda P, Hilgertova J, Kalvach Z, Limanova Z. Source: Acta Univ Carol [med] (Praha). 1993; 39(1-4): 39-47. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9355660

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Proposed diagnostic thresholds for gestational diabetes mellitus according to a 75-g oral glucose tolerance test. Maternal and perinatal outcomes in 3260 Danish women. Author(s): Jensen DM, Damm P, Sorensen B, Molsted-Pedersen L, Westergaard JG, Korsholm L, Ovesen P, Beck-Nielsen H. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 2003 January; 20(1): 51-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12519320

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Racial differences in glucagon-like peptide-1 (GLP-1) concentrations and insulin dynamics during oral glucose tolerance test in obese subjects. Author(s): Velasquez-Mieyer PA, Cowan PA, Umpierrez GE, Lustig RH, Cashion AK, Burghen GA. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 November; 27(11): 1359-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14574347

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Re.: Nielsen GL, Nielsen PH. Results of oral glucose tolerance test performed following birth of a baby with birthweight above 4500 gr. Author(s): Geirsson RT. Source: Acta Obstetricia Et Gynecologica Scandinavica. 1991; 70(3): 251-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1927306

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Reference values for 75 g oral glucose tolerance test in pregnancy. Author(s): Nasrat AA. Source: British Medical Journal (Clinical Research Ed.). 1988 May 7; 296(6632): 1330. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3133072

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Reference values for glucose tolerance test in the urban Zimbabwean pregnant woman. Author(s): Wellington M, Mahomed K, Ndoro E. Source: Cent Afr J Med. 1992 May; 38(5): 182-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1423546

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Relation of fetal growth to maternal responses to oral glucose tolerance test throughout gestation. Author(s): Giampietro O, Bay P, Orlandi MC, Ferdeghini M, Boldrini E, Forotti G, Matteucci E. Source: Acta Diabetologica. 1999 September; 36(3): 127-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10664316

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Relationship between normal oral glucose tolerance test in women at risk for gestational diabetes and large for gestational age infants. Author(s): Phillipou G. Source: Diabetes Care. 1991 November; 14(11): 1092-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1797495

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Relative contribution of insulin sensitivity and beta-cell function to plasma glucose and insulin concentrations during the oral glucose tolerance test. Author(s): Chiu KC, Martinez DS, Yoon C, Chuang LM. Source: Metabolism: Clinical and Experimental. 2002 January; 51(1): 115-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11782882

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Reliability of the oral glucose tolerance test in the early postoperative assessment of acromegaly remission. Author(s): Kristof RA, Neuloh G, Redel L, Klingmuller D, Schramm J. Source: Journal of Neurosurgery. 2002 December; 97(6): 1282-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12507124

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Repeatability of the oral glucose tolerance test for the diagnosis of impaired glucose tolerance and diabetes mellitus. Author(s): Balkau B, Eschwege E. Source: Diabetologia. 1991 March; 34(3): 201-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1884894

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Reproducibility and comparability of insulin sensitivity indices measured by stablelabel intravenous glucose tolerance test. Author(s): Hovorka R, Bannister P, Eckland DJ, Halliday D, Murley DN, Rees SE, Young MA. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 1998 March; 15(3): 234-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9545125

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Reproducibility of the first-phase insulin release in the intravenous glucose tolerance test. Author(s): Chen CC, Chen RH, Chang CT, Cheah N. Source: J Formos Med Assoc. 1996 August; 95(8): 639-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8870437

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Reproducibility of the oral glucose tolerance test in pregnancy. Author(s): Harlass FE, Brady K, Read JA. Source: American Journal of Obstetrics and Gynecology. 1991 February; 164(2): 564-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1992702

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Reproducibility of the oral glucose tolerance test in pregnant women. Author(s): Catalano PM, Avallone DA, Drago NM, Amini SB. Source: American Journal of Obstetrics and Gynecology. 1993 October; 169(4): 874-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8238142

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Resistance exercise and growth hormone administration in older men: effects on insulin sensitivity and secretion during a stable-label intravenous glucose tolerance test. Author(s): Zachwieja JJ, Toffolo G, Cobelli C, Bier DM, Yarasheski KE. Source: Metabolism: Clinical and Experimental. 1996 February; 45(2): 254-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8596499

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Response of plasma beta-endorphin and insulin to oral glucose tolerance test in nonobese women with polycystic ovaries. Author(s): Laatikainen TJ, Tiitinen AE, Salminen-Lappalainen KR, Pekonen F. Source: Gynecological Endocrinology : the Official Journal of the International Society of Gynecological Endocrinology. 1989 September; 3(3): 241-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2531535

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Response of sex hormone binding globulin and insulin-like growth factor binding protein-1 to an oral glucose tolerance test in obese women with polycystic ovary syndrome before and after calorie restriction. Author(s): Hamilton-Fairley D, Kiddy D, Anyaoku V, Koistinen R, Seppala M, Franks S. Source: Clinical Endocrinology. 1993 September; 39(3): 363-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7693380

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Results of oral glucose tolerance test performed following birth of a baby with birthweight above 4,500 grams. Author(s): Nielsen GL, Nielsen PH. Source: Acta Obstetricia Et Gynecologica Scandinavica. 1990; 69(6): 501-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2284899

98

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Retrograde versus antegrade cannulation in the intravenous glucose tolerance test. Author(s): Rowe RE, Leech NJ, Finegood DT, McCulloch DK. Source: Diabetes Research and Clinical Practice. 1994 September; 25(2): 131-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7821192

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Revision of the oral glucose tolerance test: a pilot study. Author(s): Schwartz JG, Phillips WT, Aghebat-Khairy B. Source: Clinical Chemistry. 1990 January; 36(1): 125-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2297902

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Revisiting the oral glucose tolerance test criterion for the diagnosis of diabetes. Author(s): Davidson MB, Schriger DL, Peters AL, Lorber B. Source: Journal of General Internal Medicine : Official Journal of the Society for Research and Education in Primary Care Internal Medicine. 2000 August; 15(8): 551-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10940146

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Screened glucosuria during pregnancy. Correlation with intravenous glucose tolerance test and serum lipids. Author(s): Castren O, Kallio V, Ruponen S. Source: Acta Obstetricia Et Gynecologica Scandinavica. 1974; 53(4): 323-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4440459

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Serum growth hormone response to bromocriptine during a glucose tolerance test in acromegaly. Author(s): Cassar J, Mashiter K, Sullivan G, Joplin GF. Source: Acta Endocrinol (Copenh). 1976 May; 82(1): 39-46. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=946714

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Serum insulin and growth hormone values in children during the oral glucose tolerance test. Author(s): Cole HS, Epel R. Source: Diabetes. 1972 January; 21(1): 16-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5008083

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Serum insulin values during oral glucose tolerance test in various age groups. Author(s): Kerpel-Fronius E, Gacs G. Source: Acta Paediatr Acad Sci Hung. 1975; 16(3-4): 197-202. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1241502

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99

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Short-term secretory regulation of the active form of ghrelin and total ghrelin during an oral glucose tolerance test in patients with anorexia nervosa. Author(s): Nakai Y, Hosoda H, Nin K, Ooya C, Hayashi H, Akamizu T, Kangawa K. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2004 June; 150(6): 913-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15191363

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Should we do an oral glucose tolerance test in hypertensive men with normal fasting blood-glucose? Author(s): Agewall S. Source: Journal of Human Hypertension. 2001 January; 15(1): 71-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11224005

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Significance of oral glucose tolerance test for the diagnosis of diabetes mellitus in patients with liver cirrhosis. Author(s): Imano E, Nishida T, Shibata M, Kanda T. Source: Intern Med. 1999 November; 38(11): 918. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10563758

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Significance of the oral glucose tolerance test performed on the third day after delivery for the diagnosis of diabetes in pregnancy. Author(s): Salzberger M, Sharon A, Liban E. Source: Isr J Med Sci. 1975 June; 11(6): 629-31. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1158671

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Simplifying the intravenous glucose tolerance test. Author(s): Posner NA, Silverstone FA, Breuer J, Heller M. Source: J Reprod Med. 1982 October; 27(10): 633-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7175833

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Some effects of triamcinolone pretreatment on intravenous glucose tolerance test in patients with different thyroid function. Author(s): Zamrazil V, Nemec J, Nedvidkova J, Felt V, Havelka J, Bednar J. Source: Endokrinologie. 1981 October; 78(1): 73-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7032896

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Stable-label intravenous glucose tolerance test minimal model. Author(s): Avogaro A, Bristow JD, Bier DM, Cobelli C, Toffolo G. Source: Diabetes. 1989 August; 38(8): 1048-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2753235

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Standardization of the oral glucose tolerance test and the criteria for diagnosis of chemical diabetes in children. Author(s): Guthrie RA, Guthrie DW, Murthy DY, Jackson RL, Lang J. Source: Metabolism: Clinical and Experimental. 1973 February; 22(2): 275-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4687949

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Standardization of the oral glucose tolerance test. Author(s): Baron DN. Source: Annals of Clinical Biochemistry. 1989 March; 26 ( Pt 2): 210-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2729876

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Statistical analysis of the reproducibility of the intravenous glucose tolerance test and the serum insulin response to this test in the middle-aged men. Author(s): Hedstrand H, Boberg J. Source: Scandinavian Journal of Clinical and Laboratory Investigation. 1975 July; 35(4): 331-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1103265

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Studies on diagnostic criteria for gestational diabetes mellitus by 75 g glucose tolerance test. Author(s): Hamada T, Tetsuou M, Yoshimatsu K, Amagase N, Ooshima T, Kubo N. Source: Asia Oceania J Obstet Gynaecol. 1987 June; 13(2): 187-93. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3632467

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Studies on normal blood glucose level - statistical approach to interpretation of glucose tolerance test. Author(s): Sasaki A, Horiuchi N. Source: J Chronic Dis. 1976 February; 29(2): 129-40. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=947927

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Study of glucose tolerance and the dynamic property of insulin secretion. Analysis of intravenous glucose tolerance test with the aid of a control theory. Author(s): Kawamori R, Shichiri M, Murata T, Nomura M, Shigeta Y, Abe H. Source: Acta Endocrinol (Copenh). 1979 February; 90(2): 283-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=419917

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Suppression of circulating delta 4-androstenedione and dehydroepiandrosterone sulfate during oral glucose tolerance test in normal females. Author(s): Hubert GD, Schriock ED, Givens JR, Buster JE. Source: The Journal of Clinical Endocrinology and Metabolism. 1991 October; 73(4): 7814. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1832424

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Suppression of serum prolactin levels after an oral glucose tolerance test in patients with polycystic ovarian syndrome. Author(s): Rousso D, Skiadopoulos S, Rousso I, Kalahanis J, Petropoulos P, Mavromatidis G, Panidis D. Source: Gynecologic and Obstetric Investigation. 1997; 44(2): 120-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9286726

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Symptomatic reactive hypoglycemia during glucose tolerance test in lithium-treated patients. Author(s): Shah JH, DeLeon-Jones FA, Schickler R, Nasr S, Mayer M, Hurks C. Source: Metabolism: Clinical and Experimental. 1986 July; 35(7): 634-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3523117

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Testosterone levels in pregnant women correlate with the insulin response during the glucose tolerance test. Author(s): Dokras A, Spaczynski RZ, Behrman HR, Duleba AJ. Source: Fertility and Sterility. 2003 March; 79(3): 492-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12620428

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The 75-g oral glucose tolerance test in pregnancy. Author(s): Pettitt DJ. Source: Diabetes Care. 2001 July; 24(7): 1129. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11423490

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The abbreviated glucose tolerance test in screening for diabetes: the Islington Diabetes Survey. Author(s): Forrest RD, Jackson CA, Yudkin JS. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 1988 September; 5(6): 557-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2974779

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The effect of low-oestrogen combined pill, progestogen-only pill and medroxyprogesterone acetate on oral glucose tolerance test. Author(s): Kamau RK, Maina FW, Kigondu C, Mati JK. Source: East Afr Med J. 1990 August; 67(8): 550-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2148146

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The iterative two-stage population approach to IVGTT minimal modeling: improved precision with reduced sampling. Intravenous glucose tolerance test. Author(s): Vicini P, Cobelli C. Source: American Journal of Physiology. Endocrinology and Metabolism. 2001 January; 280(1): E179-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11120672

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The ketosis-resistance in fibro-calculous-pancreatic-diabetes. 1. Clinical observations and endocrine-metabolic measurements during oral glucose tolerance test. Author(s): Yajnik CS, Shelgikar KM, Naik SS, Kanitkar SV, Orskov H, Alberti KG, Hockaday TD. Source: Diabetes Research and Clinical Practice. 1992 February; 15(2): 149-56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1563331

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The number of abnormal plasma glucose values in the oral glucose tolerance test and the feto-maternal outcome of pregnancy. Author(s): Gruendhammer M, Brezinka C, Lechleitner M. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 2003 June 10; 108(2): 131-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12781399

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The oral glucose tolerance test is a poor predictor of hyperglycemia during pregnancy. Author(s): Rudge MV, Peracoli JC, Berezowski AT, Calderon IM, Brasil MA. Source: Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas / Sociedade Brasileira De Biofisica. [et Al.]. 1990; 23(11): 1079-89. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2133015

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The oral glucose tolerance test reveals a high frequency of both impaired glucose tolerance and undiagnosed Type 2 diabetes mellitus in primary hyperparathyroidism. Author(s): Procopio M, Magro G, Cesario F, Piovesan A, Pia A, Molineri N, Borretta G. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 2002 November; 19(11): 958-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12421435

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The oral glucose tolerance test with one abnormal value. Author(s): Philipson EH, Kalhan SC, Hertz RH. Source: American Journal of Obstetrics and Gynecology. 1989 January; 160(1): 271-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2912092

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The oral glucose tolerance test, revisited. Author(s): Barrett-Connor E. Source: European Heart Journal. 2002 August; 23(16): 1229-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12175655

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The oral glucose tolerance test--an assessment of the quality of its performance. Author(s): Evans SJ, Longland PW. Source: Annals of Clinical Biochemistry. 1988 September; 25 ( Pt 5): 589-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3232965

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The relationship of one abnormal glucose tolerance test value and pregnancy complications. Author(s): Scialli AR. Source: Obstetrics and Gynecology. 1989 July; 74(1): 134-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2733933

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The relationship of one abnormal glucose tolerance test value and pregnancy complications. Author(s): Lindsay MK, Graves W, Klein L. Source: Obstetrics and Gynecology. 1989 January; 73(1): 103-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2909030

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The use of the intravenous glucose tolerance test to evaluate nonobese hyperandrogenemic women. Author(s): Herbert CM 3rd, Hill GA, Diamond MP. Source: Fertility and Sterility. 1990 April; 53(4): 647-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2138572

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Three-hour spontaneous GH secretion profile is as reliable as oral glucose tolerance test for the diagnosis of acromegaly. Author(s): Grottoli S, Razzore P, Gaia D, Gasperi M, Giusti M, Colao A, Ciccarelli E, Gasco V, Martino E, Ghigo E, Camanni F. Source: J Endocrinol Invest. 2003 February; 26(2): 123-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12739738

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Thyrotropin secretion during oral glucose tolerance test in acromegalic patients and control subjects. Author(s): Hubina E, Kovacs L, Gorombey Z, Szabolcs I, Czirjak S, Goth MI. Source: Endocrine. 2003 November; 22(2): 177-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14665723

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Time to abolish the five hour glucose tolerance test? Author(s): Simmons D. Source: N Z Med J. 1991 April 10; 104(909): 141-2. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2011310

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Two-hour 75-g oral glucose tolerance test early in pregnancy detects most cases of gestational diabetes. Author(s): Dashora U, Dashora V, Kennedy L. Source: Diabetes Care. 2002 April; 25(4): 803; Author Reply 804. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11919147

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Type I diabetes manifested solely by 2-h oral glucose tolerance test criteria. Author(s): Greenbaum CJ, Cuthbertson D, Krischer JP; Disease Prevention Trial of Type I Diabetes Study Group. Source: Diabetes. 2001 February; 50(2): 470-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11272162

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Understanding oral glucose tolerance: comparison of glucose or insulin measurements during the oral glucose tolerance test with specific measurements of insulin resistance and insulin secretion. Author(s): Phillips DI, Clark PM, Hales CN, Osmond C. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 1994 April; 11(3): 286-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8033528

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Undiagnosed glucose intolerance encountered in clinical practice: reappraisal of the use of the oral glucose tolerance test. Author(s): Hwu CM, Kwok CF, Ku BI, Lin YT, Lee YS, Hsiao LC, Lee SH, Ho LT. Source: Zhonghua Yi Xue Za Zhi (Taipei). 2001 August; 64(8): 435-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11720141

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Urinary excretion of ceruloplasmin is elevated in the subjects with "borderline glucose tolerance test". Author(s): Murata M, Narita T, Koshimura J, Ito S. Source: The Tohoku Journal of Experimental Medicine. 1999 May; 188(1): 1-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10494895

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Urine sodium excretion in response to an oral glucose tolerance test in obese and nonobese adolescents. Author(s): Finta KM, Rocchini AP, Moorehead C, Key J, Katch V. Source: Pediatrics. 1992 September; 90(3): 442-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1518704

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Use of a standard preparatory diet for the oral glucose tolerance test. Is it necessary? Author(s): Harlass FE, McClure GB, Read JA, Brady K. Source: J Reprod Med. 1991 February; 36(2): 147-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2010899

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Use of the insulin sensitivity index obtained from oral glucose tolerance test in Japanese subjects. Author(s): Taniguchi T, Okamoto M, Ueno H, Tanaka J, Okamoto M, Hamasaki A, Yamada Y, Seino Y. Source: Diabetes Research and Clinical Practice. 2001 November; 54(2): 143-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11640998

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Use of the oral glucose tolerance test to assess insulin release and insulin sensitivity. Author(s): Stumvoll M, Mitrakou A, Pimenta W, Jenssen T, Yki-Jarvinen H, Van Haeften T, Renn W, Gerich J. Source: Diabetes Care. 2000 March; 23(3): 295-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10868854

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Use of the oral glucose tolerance test to define remission in acromegaly. Author(s): Vierhapper H, Heinze G, Gessl A, Exner M, Bieglmayr C. Source: Metabolism: Clinical and Experimental. 2003 February; 52(2): 181-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12601629

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Usefulness of enhanced insulin secretion during an oral glucose tolerance test as a predictor of restenosis after direct percutaneous transluminal coronary angioplasty during acute myocardial infarction in patients without diabetes mellitus. Author(s): Osanai H, Kanayama H, Miyazaki Y, Fukushima A, Shinoda M, Ito T. Source: The American Journal of Cardiology. 1998 March 15; 81(6): 698-701. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9527077

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Using glucose tolerance test results to predict insulin requirement in women with gestational diabetes. Author(s): Tan YY, Liauw PC, Yeo GS. Source: The Australian & New Zealand Journal of Obstetrics & Gynaecology. 1995 August; 35(3): 262-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8546639

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Validation of insulin sensitivity indices from oral glucose tolerance test parameters in obese children and adolescents. Author(s): Yeckel CW, Weiss R, Dziura J, Taksali SE, Dufour S, Burgert TS, Tamborlane WV, Caprio S. Source: The Journal of Clinical Endocrinology and Metabolism. 2004 March; 89(3): 1096101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15001593

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Validation of simple indices to assess insulin sensitivity based on the oral glucose tolerance test in the Japanese population. Author(s): Kanauchi M, Tsujimoto N, Hashimoto T. Source: Diabetes Research and Clinical Practice. 2002 March; 55(3): 229-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11850099

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Variability of glucose tolerance test in pregnancy diminished by use of a glucose polymer. Author(s): De Leacy EA, Cowley DM. Source: Clinical Chemistry. 1992 July; 38(7): 1388-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1623616

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Variance in capillary and venous glucose levels during a glucose tolerance test. Author(s): Melnik J, Potter JL. Source: Am J Med Technol. 1982 June; 48(6): 543-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7114087

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Variations in the level of human serum albumin during glucose tolerance test. Author(s): Awdeh ZL, Islam MR, Samra SA. Source: Biochemical and Biophysical Research Communications. 1974 January 23; 56(2): 358-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4823871

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Vector autoregressive modeling analysis of frequently sampled oral glucose tolerance test results. 1. A new method for quantifying insulin resistance and secretion. Author(s): Ito K, Wada T, Makimura H, Matsuoka A. Source: The Keio Journal of Medicine. 1998 March; 47(1): 28-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9560529

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Vector autoregressive modeling analysis of frequently sampled oral glucose tolerance test results. 2. Insulin resistance and secretion after gastrectomy. Author(s): Ito K, Wada T, Makimura H, Matsuoka A, Maruyama H, Saruta T. Source: The Keio Journal of Medicine. 1998 June; 47(2): 78-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9659817

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Why use the oral glucose tolerance test? Author(s): Stolk RP, Orchard TJ, Grobbee DE. Source: Diabetes Care. 1995 July; 18(7): 1045-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7555541

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Xylose absorption and oral glucose tolerance test in pregnant and non-pregnant Nigerian women. Author(s): Egwuatu VE. Source: Trop Geogr Med. 1982; 34(4): 313-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7167999

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CHAPTER 2. ALTERNATIVE MEDICINE AND GLUCOSE TOLERANCE TEST Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to glucose tolerance test. 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 glucose tolerance test 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 “glucose tolerance test” (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 glucose tolerance test: •

“Karella” in the treatment of diabetes mellitus. Author(s): Patel JC, Dhirawani MK, Doshi JC. Source: Indian Journal of Medical Sciences. 1968 January; 22(1): 30-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5654713

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4-Hydroxyisoleucine: experimental evidence of its insulinotropic and antidiabetic properties. Author(s): Broca C, Gross R, Petit P, Sauvaire Y, Manteghetti M, Tournier M, Masiello P, Gomis R, Ribes G. Source: The American Journal of Physiology. 1999 October; 277(4 Pt 1): E617-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10516120

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A comparative study of two diets in the treatment of primary exogenous obesity in children. Author(s): Pena L, Pena M, Gonzalez J, Claro A. Source: Acta Paediatr Acad Sci Hung. 1979; 20(1): 99-103. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=532631

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A fermentation product of Cordyceps sinensis increases whole-body insulin sensitivity in rats. Author(s): Balon TW, Jasman AP, Zhu JS. Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 June; 8(3): 315-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12165189

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A modified high-fat diet induces insulin resistance in rat skeletal muscle but not adipocytes. Author(s): Wilkes JJ, Bonen A, Bell RC. Source: The American Journal of Physiology. 1998 October; 275(4 Pt 1): E679-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9755088

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A physiological level of rhubarb fiber increases proglucagon gene expression and modulates intestinal glucose uptake in rats. Author(s): Reimer RA, Thomson AB, Rajotte RV, Basu TK, Ooraikul B, McBurney MI. Source: The Journal of Nutrition. 1997 October; 127(10): 1923-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9311946

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Digitalis-like factor response to hyperinsulinemia accompanying a euglycemic hyperinsulinemic clamp or oral glucose tolerance test. Author(s): Carroll JS, Seely EW, Tao QF, Graves SW. Source: Life Sciences. 2001 July 6; 69(7): 829-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11487094

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Effect of Plantago psyllium mucilage on the glucose tolerance test. Author(s): Frati-Munari AC, Castillo-Insunza MR, de la Riva-Pinal H, Ariza-Andraca CR, Banales-Ham M. Source: Arch Invest Med (Mex). 1985 April-June; 16(2): 191-7. English, Spanish. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3907568

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Escins-Ia, Ib, IIa, IIb, and IIIa, bioactive triterpene oligoglycosides from the seeds of Aesculus hippocastanum L.: their inhibitory effects on ethanol absorption and hypoglycemic activity on glucose tolerance test. Author(s): Yoshikawa M, Harada E, Murakami T, Matsuda H, Wariishi N, Yamahara J, Murakami N, Kitagawa I.

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Source: Chemical & Pharmaceutical Bulletin. 1994 June; 42(6): 1357-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8069982 •

No influence of high- and low-carbohydrate diet on the oral glucose tolerance test in pregnancy. Author(s): Buhling KJ, Elsner E, Wolf C, Harder T, Engel B, Wascher C, Siebert G, Dudenhausen JW. Source: Clinical Biochemistry. 2004 April; 37(4): 323-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15003736

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Oral glucose tolerance test after high-dose i.v. biotin administration in normoglucemic hemodialysis patients. Author(s): Koutsikos D, Fourtounas C, Kapetanaki A, Agroyannis B, Tzanatos H, Rammos G, Kopelias I, Bosiolis B, Bovoleti O, Darema M, Sallum G. Source: Renal Failure. 1996 January; 18(1): 131-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8820510

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Preliminary studies on the inorganic constituents of some indigenous hypoglycaemic herbs on oral glucose tolerance test. Author(s): Kar A, Choudhary BK, Bandyopadhyay NG. Source: Journal of Ethnopharmacology. 1999 February; 64(2): 179-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10197754

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The effect of age and diet on the oral glucose tolerance test in ponies. Author(s): Murphy D, Reid SW, Love S. Source: Equine Veterinary Journal. 1997 November; 29(6): 467-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9413720

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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WebMDHealth: 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 glucose tolerance test; 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 Diabetes Mellitus Source: Integrative Medicine Communications; www.drkoop.com Hypoglycemia Source: Integrative Medicine Communications; www.drkoop.com Low Blood Sugar Source: Integrative Medicine Communications; www.drkoop.com Migraine Headaches Source: Healthnotes, Inc.; www.healthnotes.com

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Herbs and Supplements Aralia Alternative names: Spikenard; Aralia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Eugenia Clove Alternative names: Cloves; Eugenia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Trigonella Alternative names: Fenugreek; Trigonella foenum graecum L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org

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.

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This Web site provides a general overview of various topics and can lead to a number of general sources.

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CHAPTER 3. BOOKS ON GLUCOSE TOLERANCE TEST Overview This chapter provides bibliographic book references relating to glucose tolerance test. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on glucose tolerance test 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 “glucose tolerance test” (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 glucose tolerance test: •

Manual for Management of Diabetes Mellitus: A Hong Kong Chinese Perspective Source: Hong Kong: Chinese University Press. 1998. 144 p. Contact: Available from Chinese University Press. Chinese University of Hong Kong, Sha Tin, N.T., Hong Kong. (852) 2609 6508. Fax (852) 2603 6692. E-mail: cup @cuhk.hk. PRICE: $19.00 plus shipping and handling. ISBN: 9622017576. Summary: This manual, which combines the latest international and Chinese information on diabetes, serves as a quick reference to all health care personnel involved in the management of diabetes. The manual begins with a chapter on the classification and pathogenesis of diabetes, focusing on intermediary metabolism, insulin, and counterregulatory hormones; the classification, presentation, and pathogenesis of diabetes; the overlap between type 1 and type 2 diabetes; and diabetes in Chinese people. This is followed by a chapter on the diagnosis of diabetes. Topics include the

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American Diabetes Association and World Health Organization diagnostic criteria and the oral glucose tolerance test. The third chapter recommends standards of medical care for patients who have diabetes, focusing on the initial visit, continuing care, the annual assessment, target values, hospital admission criteria, and referral for specialist assessment. The next chapter addresses the issue of patient education. Topics include health beliefs and affective responses, knowledge and skills, patient rights and roles, obstacles to glycemic control, self monitoring of blood glucose, insulin administration, sick day management, hypoglycemia, diabetic complications, treatment noncompliance, psychosociological problems, and finances. The fifth chapter focuses on the dietary management of diabetes and exercise in diabetes. Diet-related topics include the goals of dietary management, diet composition, healthy eating and dining out guidelines, food choices, weight control, and sweeteners. This is followed by a chapter on oral drugs for treating diabetes, including sulfonylureas, biguanides, antiabsorptive drugs, antiobesity drugs, and insulin and oral agent combinations. The next chapter discusses insulin use in terms of indications for use, actions and duration, types, regimen, dosage, adjustment of dosage, and use while travelling. The eighth chapter describes diabetic complications, including ophthalmic complications, diabetic foot, diabetic neuropathy, and microalbuminuria and renal involvement. This is followed by chapters on the treatment of hypertension and dyslipidemia. Perioperative management of people who have poorly and well controlled type 1 or type 2 diabetes is the topic of the next chapter. This is followed by a chapter on diabetic emergencies such as diabetic ketoacidosis, hyperosmolar nonketotic coma, and lactic acidosis. Remaining chapters discusses the diagnosis and management of gestational diabetes and the primary, secondary, and tertiary prevention of diabetes. 2 appendices. 9 figures. 1 table. •

Type II Diabetes Sourcebook Source: Los Angeles, CA: Lowell House, and Chicago, IL: Contemporary Books. 1997. 336 p. Contact: Available from Contemporary Books, Inc. 2 Prudential Plaza, Suite 1200, Chicago, IL 60601. Also available from Lowell House, 2020 Avenue of the Stars, Suite 300, Los Angeles, CA 90067. (310) 552-7555. Fax (310) 552-7573. PRICE: $25.00 (cloth). ISBN: 1565656466. Summary: This sourcebook provides people with diabetes a comprehensive manual of self care for noninsulin-dependent diabetes mellitus (NIDDM, or Type II). The authors stress the importance of active patient participation and self management in caring for diabetes and in preventing complications. Sixteen chapters cover an introduction to diabetes, self empowerment, the patient care team and elements of a good treatment plan, the biology of diabetes and the role of insulin, stress management, blood glucose and its monitoring, food and nutrition, exercise, medications, laboratory tests and why each is important, daily hygiene and self care steps to prevent complications, pregnancy, the social and psychological aspects of diabetes, financial considerations, complications, and research being undertaken in this area. The chapter on laboratory tests covers blood pressure, hemoglobin A1C testing, lipid profile, urine tests, oral glucose tolerance test (OGTT), and the fructosamine assay. The chapter on mental health covers family problems, social support, communication skills, professional counseling, support groups, and diabetes burnout. The book includes two appendices: a listing of resources and a glossary of common terms. A subject index concludes the volume.

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Chapters on Glucose Tolerance Test In order to find chapters that specifically relate to glucose tolerance test, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and glucose tolerance test 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 “glucose tolerance test” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on glucose tolerance test: •

Diabetic Syndrome Source: in Patel, A. Diabetes in Focus. 2nd ed. Lewisville, TX: Pharmaceutical Press. 2003. p. 5-10. Contact: Available from Pharmaceutical Press. c/o JAMCO Distribution, 1401 Lakeway Drive, Lewisville, TX 75057. (800) 538-1287. (972) 353-1303. E-mail: [email protected] or [email protected]. Website: www.pharmpress.org. PRICE: L29.95. ISBN: 853695059. Summary: Diabetes mellitus is a common chronic disorder and represents a serious health care challenge. The prevalence of diabetes is increasing worldwide and considerable progress has been made in the understanding of diabetes management. This overview chapter on the diabetic syndrome is from a textbook that details the practical pharmaceutical care that pharmacists can provide for people with diabetes. In this chapter, the author presents the World Health Organization (WHO) diagnostic criteria, and the WHO classification criteria for type 1 diabetes mellitus, type 2 diabetes mellitus, and other specific types. One sidebar explains the oral glucose tolerance test. 6 references.

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Testing for Gestational Diabetes Source: in Reece, E.A. and Coustan, D.R., eds. Diabetes Mellitus in Pregnancy. 2nd ed. New York, NY: Churchill Livingstone. 1995. p. 261-275. Contact: Available from Churchill Livingstone. 300 Lighting Way, Secaucus, NJ 07094. (800) 553-5426. PRICE: $92.00. ISBN: 0443089795. Summary: This chapter covers diagnostic criteria for the oral glucose tolerance test and for the intravenous glucose tolerance test (IVGTT) in testing for gestational diabetes. In addition, the author examines proposed screening tests, including historical factors, glycosylated hemoglobin and other blood protein levels, and other oral challenge tests. The diagnostic use of amniotic fluid glucose, insulin, and C-peptide, as well as postpartum evaluation of women with suspected diabetic fetopathy, are also discussed. 6 tables. 90 references. (AA-M).

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Hormones and Glands Source: in Kelly, R.B., ed. Family Health and Medical Guide. Dallas, TX: Word Publishing. 1996. p. 207-219. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237. Website: www.aafp.org.

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PRICE: $30.00 for members; $35.00 for non-members; plus shipping and handling. ISBN: 0849908396. Summary: This chapter discusses the role of hormones in regulating the body's activities. Hormones are made by glands or organs. Endocrine and exocrine glands are the two main types. Endocrine glands release hormones directly into the bloodstream and they travel in the blood to the part of the body where they are needed. The adrenal glands, thyroid gland, pituitary gland, testes, and ovaries are endocrine glands. The exocrine glands (the pancreas, salivary glands, sweat glands, mammary glands, mucous glands, and sebaceous glands) release chemicals through a tube or duct. The chapter describes the location and function of the adrenal glands, the pancreas, the parathyroid glands, the pituitary gland, and the thyroid gland. In addition, the chapter presents the features, diagnosis, and treatment of various conditions caused by endocrine and exocrine glands dysfunction, including diabetes and hypoglycemia. Diabetes occurs when the body either does not make enough insulin or does not use the insulin it makes properly. There are two types of diabetes. In type 1, the pancreas produces little or no insulin; in type 2, the body is resistant to insulin. A simple blood test can indicate blood sugar level, and a glucose tolerance test can be used to determine the body's response to a sugary drink. Although controlling diabetes requires a different treatment plan for each person who has it, a combination of diet, exercise, and medication is generally required. Diabetes can cause various complications. Home monitoring of blood glucose is important because careful control of blood sugar can reduce the risk of complications. Hypoglycemia occurs when the sugar level in the blood drops below normal. Although anyone can experience hypoglycemia when he or she is hungry, the condition occurs most commonly in people who have diabetes. Treatment may be as simple as eating a piece of candy or drinking some fruit juice. Changing dietary habits is the most effective way to prevent dietary or stress-induced hypoglycemia. 5 figures. •

Laboratory Tests Source: in Lockhart, P.B. Oral Medicine and Hospital Practice. Chicago, IL: Special Care Dentistry. 1997. p. 10.3-10.12. 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.

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Classification, Diagnostic Criteria, and Screening for 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. 15-36. Contact: Available from National Diabetes Information Clearinghouse (NDIC). 1 Information Way, Bethesda, MD 20892-3560. (800) 860-8747 or (301) 654-3327. E-mail: [email protected]. Also available at http://www.niddk.nih.gov/. PRICE: Fulltext available online at no charge. Summary: This chapter on the classification, diagnostic criteria, and screening for diabetes is from a compilation and assessment of data on diabetes and its complications in the United States. Four major types of diabetes have been defined: insulin dependent diabetes mellitus (Type 1 Diabetes), noninsulin dependent diabetes mellitus (Type 2 Diabetes), gestational diabetes mellitus (GDM), and diabetes secondary to other conditions. Impaired glucose tolerance (IGT) is a class that encompasses persons whose glucose tolerance is intermediate between normal and diabetes ranges. Screening is most appropriately carried out in groups at high risk for NIDDM. Major risk factors for NIDDM include older age, obesity, family history of diabetes, race or ethnicity of black, Hispanic or American Indian, and the presence of complications related to diabetes. The author outlines the scientific basis for the diagnostic criteria, the circumstances and methods for the diagnosis of diabetes in the United States, the use of the oral glucose tolerance test, the frequency and methods of screening for diabetes in the United States, the principles of screening for undiagnosed NIDDM, controversies in screening for NIDDM, and screening in high risk populations. The author concludes that the choice of screening method and criteria to be used depends on the screening situation. In public screening programs, considerations of cost and efficiency are important and it might be considered important to screen only very high risk groups to ensure high yields of positive screenees, although this would miss significant numbers of persons with NIDDM. In physicians' offices, where the focus is on care of the individual patient, it would appear appropriate to relax the screening exclusions and be more inclusive. Screening for undiagnosed NIDDM can also be accomplished in the context of programs directed toward other medical conditions that are frequent in people with diabetes, such as hypertension and hypercholesterolemia. 15 figures. 13 tables. 87 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. 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

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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). •

Diabetes Mellitus Source: in Wilson, J.D., et al., eds. Williams Textbook of Endocrinology. 9th ed. Philadelphia, PA: W.B. Saunders Company. 1998. p. 973-1059. Contact: Available from W.B. Saunders Company. Book Order Fulfillment Department. 11830 Westline Industrial Drive, Saint Louis, MO 63146-9988. (800) 545-2522 or (314) 4537010. Fax (800) 568-5136 or (314) 453-7095. E-mail: [email protected]. Website: www.wbsaunders.com. PRICE: $150.00 plus shipping and handling. ISBN: 0721661521. Summary: This chapter provides an overview of diabetes mellitus. This condition comprises a heterogenous group of hyperglycemic disorders. The chapter begins with a description of the tests used to diagnose diabetes, including measurement of fasting plasma glucose, glycosylated hemoglobin, and the muscle capillary basement membrane; the oral glucose tolerance test; and the intravenous glucose tolerance test. This is followed by a discussion of nomenclature and definitions. The chapter then provides detailed information on type 1 and type 2 diabetes. Topics related to both types of diabetes include their prevalence, incidence, genetics, and clinical features. Other topics relevant to type 1 diabetes include environmental-genetic interactions, islet antibodies, and superantigens. In addition, the natural history, prevention, and hormonal pathophysiology of type 1 diabetes are discussed. Topics related to the prevention of type 1 diabetes include potential prophylactic agents, immunomodulation in autoimmune diabetes, and the pathology of the Islets of Langerhans in type 1 diabetes. Topics concerning type 2 diabetes include islet cell function, hormonal pathophysiology, and molecular genetics. Molecular genetic topics include mutations in genes involved in insulin resistance, mutations in genes encoding beta cell proteins involved in the quality and quantity of secreted insulin, mutations in genes involved in lipid metabolism and obesity, mutations in genes relevant to insulin action, miscellaneous mutations in genes without known diabetogenicity, the current state of candidate genes, the inheritance of type 2 diabetes, and autoimmune type 2 diabetes. The chapter continues with a discussion of insulin resistance, management of the diabetic pregnancy, gestational diabetes, and surgery in diabetic patients. Information is

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provided on the complications of diabetes, including the role of metabolic control in preventing complications and the potential mechanisms in the pathogenesis of complications. Complications discussed include cardiomyopathy, dermopathy, diabetic foot syndrome, nephropathy, retinopathy, cataracts, neuropathy, and peripheral vascular disease. The issue of treatment is also addressed. Topics include the treatment of type 1 diabetes with insulin, diet, and exercise; the treatment of type 2 diabetes with diet, oral antihyperglycemic drugs, and insulin; the treatment of diabetic ketoacidosis and nonketotic hyperosmolar coma; the prevention and treatment of vascular complications; and pancreas and islet transplantation. 49 figures. 28 tables. 1207 references. •

Diagnostic Tests in Diabetes Mellitus and Hypoglycaemia Source: in Diagnostic Tests in Endocrinology and Diabetes. Bouloux, P.-M.G. and Rees, L.H., eds. New York, NY: Chapman and Hall Medical. 1994. p. 187-214. Contact: Available from Chapman and Hall. One Penn Plaza, 41st floor, New York, NY 10119. (212) 244-6412. Fax (212) 268-9964. PRICE: $49.95. ISBN: 0412352001. Summary: This chapter, from a book on diagnostic tests in endocrinology and diabetes, discusses diagnostic tests in diabetes mellitus and hypoglycemia. The section on diabetes covers the classification and types of diabetes; the oral glucose tolerance test; the diagnosis of diabetes mellitus in pregnancy; predictive tests for diabetes mellitus; monitoring diabetes and its complications, including measurement of blood glucose, urine versus blood tests, home blood glucose monitoring, urine tests for ketones, glycation products, and fructosamine tests; screening for complications, including measurement of renal function, tests for urine albumin, measurements of renal function in established disease, assessment of retinopathy, assessment of diabetic neuropathy, laboratory tests of nerve function, the diabetic foot, ischemic heart disease and early atheroma, and bone changes in diabetes mellitus; screening people with diabetes mellitus; and screening populations for diabetes. The section on hypoglycemia discusses clinical presentation, including acute neuroglycopenia, subacute neuroglycopenia, and chronic neuroglycopenia; insulinoma, including clinical presentation, biochemical investigation, tumor localization, and preoperative investigation; factitious hypoglycemia; and endocrine causes. 4 tables. 95 references.

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CHAPTER 4. MULTIMEDIA ON GLUCOSE TOLERANCE TEST Overview In this chapter, we show you how to keep current on multimedia sources of information on glucose tolerance test. 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.

Video Recordings An excellent source of multimedia information on glucose tolerance test is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “glucose tolerance test” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, 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 “Videorecording (videotape, videocassette, etc.).” Type “glucose tolerance test” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on glucose tolerance test: •

Living with Diabetes: Making the Diagnosis Source: Madison, WI: University of Wisconsin Hospitals and Clinics, Department of Outreach Education. 1999. (videocassette). Contact: Available from University of Wisconsin Hospital and Clinics. Picture of Health, 702 North Blackhawk Avenue, Suite 215, Madison, WI 53705-3357. (800) 757-4354 or (608) 263-6510. Fax (608) 262-7172. PRICE: $19.95 plus shipping and handling; bulk copies available. Order number 071899A. Summary: This videotape, part of a series on living with diabetes, focuses on the diagnosis of diabetes. A moderator discusses the new criteria for the diagnosis and classification of diabetes, the rise in the incidence of diabetes, the symptoms of diabetes, and the prevention of diabetes with an endocrinologist. The videotape begins with a discussion of what diabetes is, how insulin works, the types of diabetes, and risk factors for diabetes. Type 1 diabetes, which was formerly known as insulin dependent diabetes,

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usually develops quickly, whereas type 2 diabetes, which was formerly known as noninsulin dependent diabetes, usually has a gradual onset. The symptoms of diabetes, which are generally the same regardless of the type, are related to high blood sugar. They include excessive urination and thirst, fatigue, hunger, weight loss, and blurred vision. Risk factors for type 1 diabetes include a genetic predisposition for developing the disease. Risk factors for type 2 diabetes include being overweight, sedentary, and over 45 years old; having a history of stillbirth or gestational diabetes; having high blood pressure and high cholesterol; being African American, Hispanic, or Native American; and having previously been identified with impaired glucose tolerance. The acute complications of diabetes include ketoacidosis, nonketotic hyperosmolar syndrome, and hypoglycemia. The chronic complications are divided into microvascular and macrovascular complications. Microvascular complications include retinopathy, neuropathy, and nephropathy. Macrovascular complications include heart attack, stroke, and peripheral vascular disease. Early diagnosis is important in preventing complications. Diagnosis is based on blood sugar levels obtained from a blood glucose test, a fasting plasma glucose test, or an oral glucose tolerance test. The risk of developing type 2 diabetes may be reduced by eating properly, maintaining an ideal weight, and exercising. The videotape includes a self test that viewers can take to assess their risk of developing type 2 diabetes.

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CHAPTER 5. PERIODICALS AND NEWS ON GLUCOSE TOLERANCE TEST Overview In this chapter, we suggest a number of news sources and present various periodicals that cover glucose tolerance test.

News Services and Press Releases One of the simplest ways of tracking press releases on glucose tolerance test 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 “glucose tolerance test” (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 glucose tolerance test. 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 “glucose tolerance test” (or synonyms). The following was recently listed in this archive for glucose tolerance test: •

Oral glucose tolerance test superior to fasting glucose for Japanese Americans Source: Reuters Medical News Date: January 15, 2001

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Oral glucose tolerance test necessary to detect diabetes in Chinese Source: Reuters Medical News Date: September 20, 1999 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 “glucose tolerance test” (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 “glucose tolerance test” (or synonyms). If you know the name of a company that is relevant to glucose tolerance test, 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/. 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 “glucose tolerance test” (or synonyms).

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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 “glucose tolerance test” (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 glucose tolerance test: •

American College of Physicians Home Medical Guide to Diabetes Source: New York, NY: Dorling Kindersley Publishing, Inc. 2000. 96 p. Contact: Available from Dorling Kindersley Publishing, Inc. 95 Madison Avenue, New York, NY 10016. (212) 213-4800. Fax (212) 213-5240. E-mail: [email protected]. Website: www.dk.com. PRICE: $6.95 plus shipping and handling. ISBN: 0789452006. Summary: This illustrated guide provides people who have diabetes with expert advice on understanding and living with this chronic disease. The guide begins with a section that explains what diabetes is and what causes it. Known causes include heredity, infection, and environmental factors. The next section focuses on tests used to diagnosis diabetes, including the oral glucose tolerance test and urine tests. This is followed by sections that discuss the treatment of diabetes with diet and medications such as sulfonylureas, benzoic acid derivatives, biguanides, acarbose, thiazolidinediones, and insulin. The next section is devoted to monitoring blood glucose levels through blood and urine tests. Hypoglycemia is the focus of the next section. Topics include preventing and treating this acute complication. This is followed by a section that discusses exercising, socializing, traveling, coping with illness, and having a baby. The next section deals with issues related to children who have diabetes, including home monitoring, hypoglycemia, food difficulties, family reactions, and behavioral issues. The topic of the next section is complications of diabetes, including diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, erectile dysfunction, skin problems, cardiovascular problems, and foot problems. This is followed by a section that explains the medical procedures and information that a person who has diabetes should expect from his or her health care professional. The final section addresses the issues of preventing, curing, and treating diabetes in the future. In addition, the guide presents answers to some common questions about diabetes and provides information on useful resources and online sites. 12 figures.

Academic Periodicals covering Glucose Tolerance Test Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to glucose tolerance test. In addition to these sources, you can search for articles covering glucose tolerance test 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.”

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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 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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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 Institute7: •

Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm

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National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/

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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html

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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25

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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm

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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm

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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/

7

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

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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/

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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm

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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm

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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/

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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/

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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm

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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html

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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm

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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm

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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

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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html

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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm

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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp

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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/

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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp

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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html

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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.8 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:9 •

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

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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html

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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/

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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

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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

8

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). 9 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 Gateway10 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.11 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “glucose tolerance test” (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 22422 133 988 52 71 23666

HSTAT12 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.13 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.14 Simply search by “glucose tolerance test” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

10

Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.

11

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). 12 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 13 14

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 Biologists15 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.16 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.17 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/.

15 Adapted 16

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. 17 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.

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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 glucose tolerance test 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 glucose tolerance test. 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 glucose tolerance test. 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 “glucose tolerance test”:

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Diabetes http://www.nlm.nih.gov/medlineplus/diabetes.html Diabetes and Pregnancy http://www.nlm.nih.gov/medlineplus/diabetesandpregnancy.html Hypoglycemia http://www.nlm.nih.gov/medlineplus/hypoglycemia.html Juvenile Diabetes http://www.nlm.nih.gov/medlineplus/juvenilediabetes.html Laboratory Tests http://www.nlm.nih.gov/medlineplus/laboratorytests.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. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on glucose tolerance test. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •

All About Pre-Diabetes Source: Alexandria, VA: American Diabetes Association. 2004. 2 p. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. E-mail: [email protected]. Fax: (770) 442-9742. Website: www.diabetes.org. PRICE: Full-text available online at no charge. Item number: Toolkit No. 1. Summary: Cardiovascular disease (CVD) is the leading cause of death among people with diabetes, accounting for at least two out of three diabetes-related deaths. This fact sheet on pre-diabetes is from a set of 26 reproducible patient education handouts on topics related to diabetes CVD. Pre-diabetes is a condition in which blood glucose (sugar) levels are higher than normal but are not high enough to be considered diabetes (type 2 diabetes). Readers are encouraged to incorporate lifestyle changes that can delay or prevent the development of type 2 diabetes. These changes include cutting down on calories and fat, being physically active, and losing weight. The fact sheet describes these strategies, and discusses risk factors for diabetes, diagnostic tests that might be used to confirm pre-diabetes (fasting plasma glucose test, and oral glucose tolerance test), how to reverse pre-diabetes, and the use of medications to treat pre-diabetes. The fact sheet includes blank space for readers to record their goals for behavior changes.

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Insulin Resistance and Pre-Diabetes Source: Bethesda, MD: National Diabetes Information Clearinghouse (NDIC). 2003. 8 p. 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 available online at no charge; $5.00 for package of 25. Order number: 03-4893. Summary: Insulin resistance is a silent condition that increases the changes of developing diabetes and heart disease. This fact sheet describes insulin resistance and pre-diabetes and how readers can make lifestyle changes to help prevent diabetes and other health problems. Topics include the role of insulin; the interplay between insulin resistance, prediabetes and type 2 diabetes; the causes of insulin resistance; symptoms; metabolic syndrome; diagnostic tests used to confirm the presence of diabetes and prediabetes, including fasting blood glucose tests, glucose tolerance test, and insulin measure; strategies to reverse insulin resistance, including physical activity, appropriate weight loss, control of blood pressure, control of cholesterol levels, and stopping smoking; and the drugs that are used to improve response to insulin. One additional section briefly reports on future research projects in this area. The fact sheet concludes with a brief description of the goals and activities of the National Diabetes Information Clearinghouse (NDIC).

•

Prediabetes: Staying Healthy Source: Scotts Valley, CA: ETR Associates. 2003. 4 p. Contact: Available from ETR Associates. 4 Carbonero Way, Scotts Valley, CA 950664200. (800) 321-4407. Fax (800) 435-8433. Website: www.etr.org. PRICE: Single copy free; $16.00 for 50 copies, discounts for larger orders. Item number: 262. Summary: Sometimes people have high blood glucose levels (high sugar) but it is not high enough to be considered diabetes. This condition is called prediabetes and includes a higher likelihood of getting diabetes or having a heart attack or stroke. This brochure helps readers with prediabetes understand how to lower blood glucose to a healthy level, prevent or delay getting diabetes, and lower the chances of having a heart attack or stroke. The brochure reviews risk factors, encourages readers to get tested for prediabetes, explains the test results for the fasting plasma glucose test (FPG) and the oral glucose tolerance test (OGTT), and notes the symptoms of diabetes. One sidebar lists strategies to help blood glucose stay at healthy levels: eat healthy foods more often, eat smaller servings of less-healthy foods, choose low-fat foods, cook in healthy ways, be active, achieve and maintain a healthy weight, and stop smoking. The brochure concludes with the contact information for the American Diabetes Association (800-3422383 or www.diabetes.org). 1 figure. 1 table.

•

Inside Look at Managing Diabetes Source: South Deerfield, MA: Channing L. Bete Co., Inc. 2000. 15 p. Contact: Available from Channing L. Bete, Co., Inc. 200 State Road, South Deerfield, MA 01373-0200. (800) 628-7733. Fax (800) 499-6464. PRICE: $1.60 each; plus shipping and handling; quantity discounts available. Order number 75226. Summary: This booklet provides an overview of diabetes management. The booklet begins by explaining how glucose gets into cells in a person who is healthy. This is

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followed by a description of type 1, type 2, and gestational diabetes. Risk factors for each type of diabetes are identified. The booklet then discusses the laboratory tests that can confirm a diagnosis of diabetes, including the fasting plasma glucose test, the random plasma glucose test, and the oral glucose tolerance test. Other topics include the effects of damage to the heart and large blood vessels and impact of damage to the small blood vessels. Small blood vessel damage can lead to eye and kidney disease, reduced circulation to the feet and legs, and nerve damage. In addition, the booklet presents steps that people who have diabetes can take to improve their quality of life, including following a healthy meal plan, engaging in regular physical activity, controlling their weight, performing regular self tests of blood glucose, and testing for ketones. The booklet concludes with information on the use of insulin and diabetes pills to manage the disease and other ways to determine the effectiveness of a treatment and self care plan. •

Gestational Diabetes: Diabetes When You're Pregnant Source: Santa Cruz, CA: ETR Associates. 2000. 6 p. Contact: Available from ETR Associates. 4 Carbonero Way, Scotts Valley, CA 950664200. (800) 321-4407. Fax (800) 435-8433. Website: www.etr.org. PRICE: Single copy free; $16.00 for 50 copies, discounts for larger orders. Summary: This brochure focuses on gestational diabetes. This form of diabetes occurs during pregnancy if a woman has too much sugar in her blood. A one hour glucose test and a glucose tolerance test are used to diagnose gestational diabetes. The brochure provides a checklist of health risks for gestational diabetes and suggests ways women can manage gestational diabetes. Tips include eating healthy foods every day, eating small meals and snacks, drinking eight glasses of water per day, drinking caffeine free drinks, taking vitamin supplements, avoiding foods that increase blood sugar, avoiding alcoholic beverages, checking blood sugar levels, quitting smoking, being physically active, and keeping track of weight gain. Other topics include labor, delivery, and follow up.

•

Questions Most Frequently Asked About Hypoglycemia Source: Washington, D.C.: Sugar Association, Inc. 1993. 4 p. Contact: Available from Sugar Association, Inc. 1101 15th Street, N.W., Suite 600, Washington, D.C. 20005. (202) 785-1122. PRICE: Up to 100 copies free. Summary: This brochure, written in a question-and-answer format, discusses hypoglycemia. The brochure addresses the causes of hypoglycemia; how hypoglycemia is treated; the use of special diets; how to find out if low blood glucose is causing symptoms; how blood glucose is measured; low blood glucose levels; the incidence of hypoglycemia; the use of oral glucose tolerance tests (OGTT); hypoglycemia in diabetes; how blood glucose levels are controlled; and steps to take if a reader suspects he or she has hypoglycemia.

•

Diabetes Diagnosis Source: Alexandria, VA: American Diabetes Association. 199x. 4 p. Contact: Available from American Diabetes Association, Inc. Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. PRICE: $9.95 (members), $11.95 (nonmembers) for 50 copies; single copy free. Order number CDBD11.

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Summary: This fact sheet, which is one in a series of 42 fact sheets about daily living and coping with diabetes, covers how doctors diagnosis diabetes on the basis of too-high levels of glucose on the blood. Topics include high blood glucose levels, urine tests, blood tests, fasting plasma glucose tests, random plasma glucose tests, oral glucose tolerance tests, and glycohemoglobin (or glycated hemoglobin) tests, and insulindependent diabetes mellitus (IDDM, or Type I) versus noninsulin-dependent diabetes mellitus (NIDDM, or Type II). The fact sheet notes that glucose tolerance tests may lead to one of the following diagnoses: normal response, impaired glucose tolerance, diabetes, or gestational diabetes. While test results are important in diagnosing diabetes, doctors also consider the individual's physical exam, symptoms, and medical history. Whatever type of diabetes one has, the goal of treatment will be to get blood glucose levels as close to normal as possible. (AA-M). •

Blood Sugar and Fats Contact: University of New Mexico School of Medicine, Infectious Diseases Division, New Mexico AIDS Education and Training Center, New Mexico AIDS InfoNet, PO Box 810, Arroyo Seco, NM, 87514-0810, (505) 776-8032, http://www.aidsinfonet.org. Summary: This information sheet discusses the impact of the human immunodeficiency virus (HIV) on blood sugar (glucose) and fats. Anti-HIV drugs seem to cause abnormally high levels of blood sugar and fats, so people with HIV test their blood sugar and blood fat levels frequently. Ways to test for blood glucose levels are a random blood glucose test, a fasting glucose test, and a glucose tolerance test. Blood fats that can be measured are triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. These blood fats are measured as the amount, in milligrams, contained in one tenth of a liter of blood.

•

Tests For Diabetes Source: San Diego, CA: Sweet Success: California Diabetes and Pregnancy Program. 1990. 6 p. Contact: Available from Education Programs Associates,Inc. 1 West Campbell Avenue, Building D, Campbell, CA 95008. (408) 374-3720. PRICE: $.35 for CDAPP members or $.50 for non-members. Summary: This simple, fold-out informational booklet briefly reviews the diagnostic test for gestational diabetes that may be performed during pregnancy. Written in clear, easyto-understand language, the booklet outlines the procedures followed during the 3-hour glucose tolerance test. Simple drawings illustrate the topics covered. Space is included for patient notes. This booklet is also available in Spanish (See DMBR01820). 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 glucose tolerance test. 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

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rare or 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/

•

WebMDHealth: 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 glucose tolerance test. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with glucose tolerance test. 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 glucose tolerance test. 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 “glucose tolerance test” (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 “glucose tolerance test”. 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 “glucose tolerance test” (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 “glucose tolerance test” (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.18

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

18

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)19: •

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

•

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/

19

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

•

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/

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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

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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

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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

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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

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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/

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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html

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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/

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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html

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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/

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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm

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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp

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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/

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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/

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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml

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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html

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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html

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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml

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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp

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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm

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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

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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/

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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/

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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

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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp

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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/

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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

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On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/

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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 glucose tolerance test: •

Basic Guidelines for Glucose Tolerance Test Glucose tolerance test Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003466.htm

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Signs & Symptoms for Glucose Tolerance Test Fainting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003092.htm Stress Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm

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Diagnostics and Tests for Glucose Tolerance Test Venipuncture Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003423.htm

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Background Topics for Glucose Tolerance Test Acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002215.htm 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 Exercise Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Infant test or procedure preparation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002055.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

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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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GLUCOSE TOLERANCE TEST DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 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] Ablation: The removal of an organ by surgery. [NIH] Abortion: 1. The premature expulsion from the uterus of the products of conception - of the embryo, or of a nonviable fetus. The four classic symptoms, usually present in each type of abortion, are uterine contractions, uterine haemorrhage, softening and dilatation of the cervix, and presentation or expulsion of all or part of the products of conception. 2. Premature stoppage of a natural or a pathological process. [EU] Acanthosis Nigricans: A circumscribed melanosis consisting of a brown-pigmented, velvety verrucosity or fine papillomatosis appearing in the axillae and other body folds. It occurs in association with endocrine disorders, underlying malignancy, administration of certain drugs, or as in inherited disorder. [NIH] 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] 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] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Acitretin: An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of etretinate with the advantage of a much shorter half-life when compared with etretinate. [NIH]

Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Activities of Daily Living: The performance of the basic activities of self care, such as dressing, ambulation, eating, etc., in rehabilitation. [NIH] Acyl: Chemical signal used by bacteria to communicate. [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]

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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] 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] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [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] 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] Aerobic Metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, oxidative metabolism, or cell respiration. [NIH] Aerobic Respiration: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as oxidative metabolism, cell respiration, or aerobic metabolism. [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 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] Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [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]

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Aged, 80 and Over: A person 80 years of age and older. [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] Alertness: A state of readiness to detect and respond to certain specified small changes occurring at random intervals in the environment. [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] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha-1: A protein with the property of inactivating proteolytic enzymes such as leucocyte collagenase and elastase. [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] Amenorrhea: Absence of menstruation. [NIH] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU]

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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] 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] Amnion: The extraembryonic membrane which contains the embryo and amniotic fluid. [NIH]

Amniotic Fluid: Amniotic cavity fluid which is produced by the amnion and fetal lungs and kidneys. [NIH] Anaemia: A reduction below normal in the number of erythrocytes per cu. mm., in the quantity of haemoglobin, or in the volume of packed red cells per 100 ml. of blood which occurs when the equilibrium between blood loss (through bleeding or destruction) and blood production is disturbed. [EU] 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] 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] Androstenedione: A steroid with androgenic properties that is produced in the testis, ovary, and adrenal cortex. It is a precursor to testosterone and other androgenic hormones. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anergy: Absence of immune response to particular substances. [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] Angiotensin I: The decapeptide precursor of angiotensin II, generated by the action of renin

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on angiotensinogen. It has limited pharmacologic activity. [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] 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] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [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] Anorexia Nervosa: The chief symptoms are inability to eat, weight loss, and amenorrhea. [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] Antecedent: Existing or occurring before in time or order often with consequential effects. [EU]

Anthropometry: The technique that deals with the measurement of the size, weight, and proportions of the human or other primate body. [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] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidiabetic: An agent that prevents or alleviates diabetes. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [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]

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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] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] 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] 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 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] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [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] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] 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

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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] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [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] Asymptomatic: Having no signs or symptoms of disease. [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, or hormonal changes. [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] Autonomic: Self-controlling; functionally independent. [EU] 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] 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] 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] Baroreflex: A negative feedback system which buffers short-term changes in blood pressure. Increased pressure stretches blood vessels which activates pressoreceptors (baroreceptors) in the vessel walls. The net response of the central nervous system is a reduction of central sympathetic outflow. This reduces blood pressure both by decreasing peripheral vascular resistance and by lowering cardiac output. Because the baroreceptors are tonically active, the baroreflex can compensate rapidly for both increases and decreases in blood pressure. [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] 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] Behavior Therapy: The application of modern theories of learning and conditioning in the treatment of behavior disorders. [NIH] Benzoic Acid: A fungistatic compound that is widely used as a food preservative. It is conjugated to glycine in the liver and excreted as hippuric acid. [NIH] Beta-Endorphin: A peptide consisting of amino acid sequence 61-91 of the endogenous pituitary hormone beta-lipotropin. The first four amino acids show a common tetrapeptide sequence with methionine- and leucine enkephalin. The compound shows opiate-like activity. Injection of beta-endorphin induces a profound analgesia of the whole body for several hours. This action is reversed after administration of naloxone. [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] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biogenesis: The origin of life. It includes studies of the potential basis for life in organic compounds but excludes studies of the development of altered forms of life through mutation and natural selection, which is evolution. [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] 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] Bladder: The organ that stores urine. [NIH]

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Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [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] 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] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [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 Image: Individuals' personal concept of their bodies as objects in and bound by space, independently and apart from all other objects. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Bone Density: The amount of mineral per square centimeter of bone. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by photon absorptiometry or x-ray computed tomography. [NIH] 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 Resorption: Bone loss due to osteoclastic activity. [NIH] Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [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] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH] Breast Feeding: The nursing of an infant at the mother's breast. [NIH] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH]

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Bromocriptine: A semisynthetic ergot alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion and is used to treat amenorrhea, galactorrhea, and female infertility, and has been proposed for Parkinson disease. [NIH] Buffers: A chemical system that functions to control the levels of specific ions in solution. When the level of hydrogen ion in solution is controlled the system is called a pH buffer. [NIH]

Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Caesarean section: A surgical incision through the abdominal and uterine walls in order to deliver a baby. [NIH] Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling. [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] 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] 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] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]

Cardiac: Having to do with the heart. [NIH] Cardiac catheterization: A procedure in which a thin, hollow tube is inserted into a blood vessel. The tube is then advanced through the vessel into the heart, enabling a physician to study the heart and its pumping activity. [NIH] Cardiac Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume

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(volume per beat). [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] Cardioselective: Having greater activity on heart tissue than on other tissue. [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] 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] Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Cataract: An opacity, partial or complete, of one or both eyes, on or in the lens or capsule, especially an opacity impairing vision or causing blindness. The many kinds of cataract are classified by their morphology (size, shape, location) or etiology (cause and time of occurrence). [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] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] 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] Cavernous Sinus: An irregularly shaped venous space in the dura mater at either side of the sphenoid bone. [NIH] Cecum: The beginning of the large intestine. The cecum is connected to the lower part of the small intestine, called the ileum. [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 Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH]

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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] Cell Division: The fission of a cell. [NIH] Cell motility: The ability of a cell to move. [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] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] 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] Chemoprevention: The use of drugs, vitamins, or other agents to try to reduce the risk of, or delay the development or recurrence of, cancer. [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] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [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]

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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] 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] 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] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Circadian: Repeated more or less daily, i. e. on a 23- to 25-hour cycle. [NIH] Circadian Rhythm: The regular recurrence, in cycles of about 24 hours, of biological processes or activities, such as sensitivity to drugs and stimuli, hormone secretion, sleeping, feeding, etc. This rhythm seems to be set by a 'biological clock' which seems to be set by recurring daylight and darkness. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [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] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [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] Clomiphene: A stilbene derivative that functions both as a partial estrogen agonist and complete estrogen antagonist depending on the target tissue. It antagonizes the estrogen receptor thereby initiating or augmenting ovulation in anovulatory women. [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] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognitive behavior therapy: A system of psychotherapy based on the premise that distorted or dysfunctional thinking, which influences a person's mood or behavior, is common to all psychosocial problems. The focus of therapy is to identify the distorted

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thinking and to replace it with more rational, adaptive thoughts and beliefs. [NIH] Cognitive restructuring: A method of identifying and replacing fear-promoting, irrational beliefs with more realistic and functional ones. [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] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colonoscopy: Endoscopic examination, therapy or surgery of the luminal surface of the colon. [NIH] 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] 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,

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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] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [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] 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] 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] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Conjugated: Acting or operating as if joined; simultaneous. [EU] 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] Constipation: Infrequent or difficult evacuation of feces. [NIH] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [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

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treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contralateral: Having to do with the opposite side of the body. [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, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] 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] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cost-benefit: A quantitative technique of economic analysis which, when applied to

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radiation practice, compares the health detriment from the radiation doses concerned with the cost of radiation dose reduction in that practice. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Cranial Irradiation: The exposure of the head to roentgen rays or other forms of radioactivity for therapeutic or preventive purposes. [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] Criterion: A standard by which something may be judged. [EU] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] 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] Cyst: A sac or capsule filled with fluid. [NIH] 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] Daclizumab: A monoclonal antibody that is being studied for treatment of adult T-cell leukemia. Also called dacliximab. Monoclonal antibodies are laboratory-produced substances that can locate and bind to cancer cells. [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] 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] 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] 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

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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] 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] Dentate Gyrus: Gray matter situated above the gyrus hippocampi. It is composed of three layers. The molecular layer is continuous with the hippocampus in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called granule cells, whose axons pass through the polymorphic layer ending on the dendrites of pyramidal cells in the hippocampus. [NIH] Deoxyribonucleic: A polymer of subunits called deoxyribonucleotides which is the primary genetic material of a cell, the material equivalent to genetic information. [NIH] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Dermis: A layer of vascular connective tissue underneath the epidermis. The surface of the dermis contains sensitive papillae. Embedded in or beneath the dermis are sweat glands, hair follicles, and sebaceous glands. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholingeric activity, through its affinity to muscarinic receptors. [NIH] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Foot: Ulcers of the foot as a complication of diabetes. Diabetic foot, often with infection, is a common serious complication of diabetes and may require hospitalization and disfiguring surgery. The foot ulcers are probably secondary to neuropathies and vascular problems. [NIH] Diabetic Ketoacidosis: Complication of diabetes resulting from severe insulin deficiency coupled with an absolute or relative increase in glucagon concentration. The metabolic acidosis is caused by the breakdown of adipose stores and resulting increased levels of free fatty acids. Glucagon accelerates the oxidation of the free fatty acids producing excess ketone bodies (ketosis). [NIH]

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Diabetic Retinopathy: Retinopathy associated with diabetes mellitus, which may be of the background type, progressively characterized by microaneurysms, interretinal punctuate macular edema, or of the proliferative type, characterized by neovascularization of the retina and optic disk, which may project into the vitreous, proliferation of fibrous tissue, vitreous hemorrhage, and retinal detachment. [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] Diastolic: Of or pertaining to the diastole. [EU] Diastolic pressure: The lowest pressure to which blood pressure falls between contractions of the ventricles. [NIH] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [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] Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of the calcium ion in membrane functions. It is also teratogenic. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Disposition: A tendency either physical or mental toward certain diseases. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] 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] Dose-dependent: Refers to the effects of treatment with a drug. If the effects change when the dose of the drug is changed, the effects are said to be dose dependent. [NIH]

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Double-blind: Pertaining to a clinical trial or other experiment in which neither the subject nor the person administering treatment knows which treatment any particular subject is receiving. [EU] Doxazosin: A selective alpha-1-adrenergic blocker that lowers serum cholesterol. It is also effective in the treatment of hypertension. [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] 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] 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] Dysphoric: A feeling of unpleasantness and discomfort. [NIH] Dyspnea: Difficult or labored breathing. [NIH] 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]

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] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [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] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elasticity: Resistance and recovery from distortion of shape. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU]

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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] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryo Transfer: Removal of a mammalian embryo from one environment and replacement in the same or a new environment. The embryo is usually in the pre-nidation phase, i.e., a blastocyst. The process includes embryo or blastocyst transplantation or transfer after in vitro fertilization and transfer of the inner cell mass of the blastocyst. It is not used for transfer of differentiated embryonic tissue, e.g., germ layer cells. [NIH] Embryology: The study of the development of an organism during the embryonic and fetal stages of life. [NIH] Emollient: Softening or soothing; called also malactic. [EU] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocrine Glands: Ductless glands that secrete substances which are released directly into the circulation and which influence metabolism and other body functions. [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] Endocrinologist: A doctor that specializes in diagnosing and treating hormone disorders. [NIH]

Endocrinology: A subspecialty of internal medicine concerned with the metabolism, physiology, and disorders of the endocrine system. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [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] Endorphin: Opioid peptides derived from beta-lipotropin. Endorphin is the most potent naturally occurring analgesic agent. It is present in pituitary, brain, and peripheral tissues. [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] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH]

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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] Enkephalin: A natural opiate painkiller, in the hypothalamus. [NIH] Entorhinal Cortex: Cortex where the signals are combined with those from other sensory systems. [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] Epidemiological: Relating to, or involving epidemiology. [EU] 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] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [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.

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[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]

Estrone: 3-Hydroxyestra-1,3,5(10)-trien-17-one. A metabolite of estradiol but possessing less biological activity. It is found in the urine of pregnant women and mares, in the human placenta, and in the urine of bulls and stallions. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), estrone may reasonably be anticipated to be a carcinogen (Merck, 11th ed). [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] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Etretinate: An oral retinoid used in the treatment of keratotic genodermatosis, lichen planus, and psoriasis. Beneficial effects have also been claimed in the prophylaxis of epithelial neoplasia. The compound may be teratogenic. [NIH] Evacuation: An emptying, as of the bowels. [EU] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Excrete: To get rid of waste from the body. [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] External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [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 dishes adhere. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Facial: Of or pertaining to the face. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fasting Blood Glucose Test: A method for finding out how much glucose (sugar) is in the blood. The test can show if a person has diabetes. A blood sample is taken in a lab or

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doctor's office. The test is usually done in the morning before the person has eaten. The normal, nondiabetic range for blood glucose is from 70 to 110 mg/dl, depending on the type of blood being tested. If the level is 126 mg/dl or greater, it means the person has diabetes (except for newborns and some pregnant women). [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]

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] Fertilization in Vitro: Fertilization of an egg outside the body when the egg is normally fertilized in the body. [NIH] Fetal Heart: The heart of the fetus of any viviparous animal. It refers to the heart in the postembryonic period and is differentiated from the embryonic heart (heart/embryology) only on the basis of time. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [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] Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Follicular Fluid: A fluid consisting of sex steroid hormones, plasma proteins, mucopolysaccharides, and electrolytes that is present in the vesicular ovarian follicle (Graafian follicle) surrounding the ovum. [NIH] Foot Ulcer: Lesion on the surface of the skin of the foot, usually accompanied by inflammation. The lesion may become infected or necrotic and is frequently associated with diabetes or leprosy. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Fructosamine: An amino sugar formed when glucose non-enzymatically reacts with the Nterminal amino group of proteins. The fructose moiety is dervied from glucose by the "classical" Amadori rearrangement. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] 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] Gastrectomy: An operation to remove all or part of the stomach. [NIH] Gastric: Having to do with the stomach. [NIH]

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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]

Gastritis: Inflammation of the stomach. [EU] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [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] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [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] 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, physical examination, early immunologic pregnancy tests, radiography, ultrasonography, and amniotic fluid analysis. [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

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therapeutically in fluid and nutrient replacement. [NIH] Glucose Clamp Technique: Maintenance of a constant blood glucose level by perfusion or infusion with glucose or insulin. It is used for the study of metabolic rates (e.g., in glucose, lipid, amino acid metabolism) at constant glucose concentration. [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] 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] Glutamate: Excitatory neurotransmitter of the brain. [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]

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]

Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [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] Glycosuria: The presence of glucose in the urine; especially the excretion of an abnormally large amount of sugar (glucose) in the urine, i.e., more than 1 gm. in 24 hours. [EU] 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] Gonadotropic: Stimulating the gonads; applied to hormones of the anterior pituitary which influence the gonads. [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] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [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] Grafting: The operation of transfer of tissue from one site to another. [NIH] Graft-versus-host disease: GVHD. A reaction of donated bone marrow or peripheral stem cells against a person's tissue. [NIH]

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Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [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] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [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] 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 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] 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] Hemochromatosis: A disease that occurs when the body absorbs too much iron. The body stores the excess iron in the liver, pancreas, and other organs. May cause cirrhosis of the liver. Also called iron overload disease. [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] Hemoglobin A: Normal adult human hemoglobin. The globin moiety consists of two alpha and two beta chains. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [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,

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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] Hepatocyte: A liver cell. [NIH] Hepatocyte Growth Factor: Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is proto-oncogene protein C-met. [NIH] Hepatoma: A liver tumor. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] 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]

Heterogenic: Derived from a different source or species. Also called heterogenous. [NIH] Heterogenous: Derived from a different source or species. Also called heterogenic. [NIH] Heterozygotes: Having unlike alleles at one or more corresponding loci on homologous chromosomes. [NIH] Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [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] 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] 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] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH]

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Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] 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] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [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] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthyroidism: Excessive functional activity of the thyroid gland. [NIH] Hypertrichosis: Localized or generalized excess hair. The concept does not include hirsutism, which is excess hair in females and children with an adult male pattern of distribution. [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] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypoglycemic: An orally active drug that produces a fall in blood glucose concentration. [NIH]

Hypoglycemic Agents: Agents which lower the blood glucose level. [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] 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]

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Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [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] Immunoradiometric Assay: Form of radioimmunoassay in which excess specific labeled antibody is added directly to the test antigen being measured. [NIH] Immunosuppression: Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [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] 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] Incision: A cut made in the body during surgery. [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] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infant, Newborn: An infant during the first month after birth. [NIH] 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,

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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]

Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] 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] 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] 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] Inotropic: Affecting the force or energy of muscular contractions. [EU] Insight: The capacity to understand one's own motives, to be aware of one's own 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] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Intermittent Claudication: A symptom complex characterized by leg pain and weakness brought on by walking, with the disappearance of the symptoms following a brief rest. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] 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] Intraperitoneal: IP. Within the peritoneal cavity (the area that contains the abdominal

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organs). [NIH] Intravascular: Within a vessel or vessels. [EU] 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]

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 positive charge are known as cations; those with a negative charge are anions. [NIH] Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Islet: Cell producing insulin in pancreas. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [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] Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [NIH] Ketoacidosis: Acidosis accompanied by the accumulation of ketone bodies (ketosis) in the body tissues and fluids, as in diabetic acidosis. [EU] 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] 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.

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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 Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH] Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [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] Lactation: The period of the secretion of milk. [EU] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Lamivudine: A reverse transcriptase inhibitor and zalcitabine analog in which a sulfur atom replaces the 3' carbon of the pentose ring. It is used to treat HIV disease. [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] 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] 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

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instincts in general that motivate behavior. [NIH] Ligaments: Shiny, flexible bands of fibrous tissue connecting together articular extremities of bones. They are pliant, tough, and inextensile. [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] 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] Lipopolysaccharides: 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] 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] Liver Cirrhosis: Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. [NIH] Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [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

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humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Locomotor: Of or pertaining to locomotion; pertaining to or affecting the locomotive apparatus of the body. [EU] Longitudinal Studies: Studies in which variables relating to an individual or group of individuals are assessed over a period of time. [NIH] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [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] Lutein Cells: The cells of the corpus luteum which are derived from the granulosa cells and the theca cells of the Graafian follicle. [NIH] 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] 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] Lymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] 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] 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] Malaria: A protozoan disease caused in humans by four species of the genus Plasmodium (P. falciparum (malaria, falciparum), P. vivax (malaria, vivax), P. ovale, and P. malariae) and transmitted by the bite of an infected female mosquito of the genus Anopheles. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high fever, sweating, shaking chills, and anemia. Malaria in animals is caused by other species of plasmodia. [NIH]

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Malaria, Falciparum: Malaria caused by Plasmodium falciparum. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations. [NIH] Malaria, Vivax: Malaria caused by Plasmodium vivax. This form of malaria is less severe than malaria, falciparum, but there is a higher probability for relapses to occur. Febrile paroxysms often occur every other day. [NIH] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] 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] Manic: Affected with mania. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] 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] 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] 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] Melanin: The substance that gives the skin its color. [NIH] Melanosis: Disorders of increased melanin pigmentation that develop without preceding inflammatory disease. [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] Menarche: The establishment or beginning of the menstrual function. [EU] Menopause: Permanent cessation of menstruation. [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal

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tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Health: The state wherein the person is well adjusted. [NIH] Mesolimbic: Inner brain region governing emotion and drives. [NIH] Metabolic acidosis: (met-ah-BOL-ik as-id-O-sis): A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). [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] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [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] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcirculation: The vascular network lying between the arterioles and venules; includes capillaries, metarterioles and arteriovenous anastomoses. Also, the flow of blood through this network. [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 organisms, they are sometimes classified as microorganisms. [NIH] Milliliter: A measure of volume for a liquid. A milliliter is approximately 950-times smaller than a quart and 30-times smaller than a fluid ounce. A milliliter of liquid and a cubic centimeter (cc) of liquid are the same. [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] 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] 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] 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] Morphological: Relating to the configuration or the structure of live organs. [NIH]

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Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Morula: The early embryo at the developmental stage in which the blastomeres, resulting from repeated mitotic divisions of the fertilized ovum, form a compact mass. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multivariate Analysis: A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables. [NIH] Mycophenolate mofetil: A drug that is being studied for its effectiveness in preventing graft-versus-host disease and autoimmune disorders. [NIH] 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] Natural selection: A part of the evolutionary process resulting in the survival and reproduction of the best adapted individuals. [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] 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] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Nephrology: A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney. [NIH] Nephropathy: Disease of the kidneys. [EU] 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] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [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] 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

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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] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] 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] 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] Normotensive: 1. Characterized by normal tone, tension, or pressure, as by normal blood pressure. 2. A person with normal blood pressure. [EU] 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] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio

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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] Oestradiol: Growth hormone. [NIH] Oestrogen: A generic term for oestrus-producing steroid compounds; the female sex hormones. In humans, oestrogen is formed in the ovary, possibly the adrenal cortex, the testis, and the foetoplacental unit; it has various functions in both sexes. It is responsible for the development of the female secondary sex characteristics, and during the menstrual cycle it acts on the female genitalia to produce an environment suitable for the fertilization, implantation, and nutrition of the early embryo. Oestrogen is used in oral contraceptives and as a palliative in cancer of the breast after menopause and cancer of the prostate; other uses include the relief of the discomforts of menopause, inhibition of lactation, and treatment of osteoporosis, threatened abortion, and various functional ovarian disorders. [EU]

Oligo: Chemical and mineral elements that exist in minimal (oligo) quantities in the body, in foods, in the air, in soil; name applied to any element observed as a microconstituent of plant or animal tissue and of beneficial, harmful, or even doubtful significance. [NIH] Oligomenorrhea: Abnormally infrequent menstruation. [NIH] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [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] Oocytes: Female germ cells in stages between the prophase of the first maturation division and the completion of the second maturation division. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Ophthalmic: Pertaining to the eye. [EU] Opiate: A remedy containing or derived from opium; also any drug that induces sleep. [EU] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [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] 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

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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] 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] Ovarian Follicle: Spheroidal cell aggregation in the ovary containing an ovum. It consists of an external fibro-vascular coat, an internal coat of nucleated cells, and a transparent, albuminous fluid in which the ovum is suspended. [NIH] Ovarian Hyperstimulation Syndrome: Syndrome composed of a combination of ovarian enlargement and an acute fluid shift out of the intravascular space. The enlargement is caused by ovarian cyst formation and the fluid shift may result in ascites, hydrothorax, or generalized edema. The syndrome is most usually seen as a complication of ovulation induction, a treatment for infertility. [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] 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] Ovulation Induction: Techniques for the artifical induction of ovulation. [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 metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, cell respiration, or aerobic metabolism. [NIH] 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] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] 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]

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Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Parathyroid hormone: A substance made by the parathyroid gland that helps the body store and use calcium. Also called parathormone, parathyrin, or PTH. [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] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Particle: A tiny mass of material. [EU] Parturition: The act or process of given birth to a child. [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] Patient Care Team: Care of patients by a multidisciplinary team usually organized under the leadership of a physician; each member of the team has specific responsibilities and the whole team contributes to the care of the patient. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]

Pedigree: A record of one's ancestors, offspring, siblings, and their offspring that may be used to determine the pattern of certain genes or disease inheritance within a family. [NIH] Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: An ulceration of the mucous membrane of the esophagus, stomach or duodenum, caused by the action of the acid gastric juice. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] 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

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vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Perimenopausal: The time of a woman's life when menstrual periods become irregular. Refers to the time near menopause. [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 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] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Pharmacists: Those persons legally qualified by education and training to engage in the practice of pharmacy. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] 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] Phlebotomy: The letting of blood from a vein. Although it is one of the techniques used in drawing blood to be used in diagnostic procedures, in modern medicine, it is used commonly in the treatment of erythrocytosis, hemochromocytosis, polycythemia vera, and porphyria cutanea tarda. Its historical counterpart is bloodletting. (From Cecil Textbook of Medicine, 19th ed & Wintrobe's Clinical Hematology, 9th ed) Venipuncture is not only for

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the letting of blood from a vein but also for the injecting of a drug into the vein for diagnostic analysis. [NIH] Phorbol: Class of chemicals that promotes the development of tumors. [NIH] Phorbol Esters: Tumor-promoting compounds obtained from croton oil (Croton tiglium). Some of these are used in cell biological experiments as activators of protein kinase C. [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] Phosphorylate: 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] Physical Examination: Systematic and thorough inspection of the patient for physical signs 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] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [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] 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

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other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plethysmography: Recording of change in the size of a part as modified by the circulation in it. [NIH] Pneumonia: Inflammation of the lungs. [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] Polycystic Ovary Syndrome: Clinical symptom complex characterized by oligomenorrhea or amenorrhea, anovulation, and regularly associated with bilateral polycystic ovaries. [NIH] Polymorphism: The occurrence together of two or more distinct forms in the same population. [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] Porphyria: A group of disorders characterized by the excessive production of porphyrins or their precursors that arises from abnormalities in the regulation of the porphyrin-heme pathway. The porphyrias are usually divided into three broad groups, erythropoietic, hepatic, and erythrohepatic, according to the major sites of abnormal porphyrin synthesis. [NIH]

Porphyria Cutanea Tarda: A form of hepatic porphyria (porphyria, hepatic) characterized by photosensitivity resulting in bullae that rupture easily to form shallow ulcers. This condition occurs in two forms: a sporadic, nonfamilial form that begins in middle age and has normal amounts of uroporphyrinogen decarboxylase with diminished activity in the liver; and a familial form in which there is an autosomal dominant inherited deficiency of uroporphyrinogen decarboxylase in the liver and red blood cells. [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] Postoperative: After surgery. [NIH] Postprandial: Occurring after dinner, or after a meal; postcibal. [EU] 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] 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

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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] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Preclinical: Before a disease becomes clinically recognizable. [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] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Preeclampsia: A toxaemia of late pregnancy characterized by hypertension, edema, and proteinuria, when convulsions and coma are associated, it is called eclampsia. [EU] Pre-eclamptic: A syndrome characterized by hypertension, albuminuria, and generalized oedema, occurring only in pregnancy. [NIH] Pregnancy Complications: The co-occurrence of pregnancy and a disease. The disease may precede or follow conception and it may or may not have a deleterious effect on the pregnant woman or fetus. [NIH] Pregnancy Outcome: Results of conception and ensuing pregnancy, including live birth, stillbirth, spontaneous abortion, induced abortion. The outcome may follow natural or artificial insemination or any of the various reproduction techniques, such as embryo transfer or fertilization in vitro. [NIH] Pregnancy Tests: Tests to determine whether or not an individual is pregnant. [NIH] Premenopausal: Refers to the time before menopause. Menopause is the time of life when a women's menstrual periods stop permanently; also called "change of life." [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Preoperative: Preceding an operation. [EU] Pressoreceptors: Receptors in the vascular system, particularly the aorta and carotid sinus, which are sensitive to stretch of the vessel walls. [NIH] 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] Progeny: The offspring produced in any generation. [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 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] Progestogen: A term applied to any substance possessing progestational activity. [EU]

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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] Prolactin: Pituitary lactogenic hormone. A polypeptide hormone with a molecular weight of about 23,000. It is essential in the induction of lactation in mammals at parturition and is synergistic with estrogen. The hormone also brings about the release of progesterone from lutein cells, which renders the uterine mucosa suited for the embedding of the ovum should fertilization occur. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol is used in the treatment or prevention of many disorders including acute myocardial infarction, arrhythmias, angina pectoris, hypertension, hypertensive emergencies, hyperthyroidism, migraine, pheochromocytoma, menopause, and anxiety. [NIH] Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. [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] 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 protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [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 Kinase C: An enzyme that phosphorylates proteins on serine or threonine residues in the presence of physiological concentrations of calcium and membrane phospholipids. The additional presence of diacylglycerols markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by phorbol esters and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters. EC 2.7.1.-. [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]

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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] Proteoglycans: Glycoproteins which have a very high polysaccharide content. [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] 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] Protozoan: 1. Any individual of the protozoa; protozoon. 2. Of or pertaining to the protozoa; protozoal. [EU] Proxy: A person authorized to decide or act for another person, for example, a person having durable power of attorney. [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] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] 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] Psychotherapy: A generic term for the treatment of mental illness or emotional disturbances primarily by verbal or nonverbal communication. [NIH] Psychotropic: Exerting an effect upon the mind; capable of modifying mental activity; usually applied to drugs that effect the mental state. [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]

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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 Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [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]

Pyloroplasty: An operation to widen the opening between the stomach and the small intestine. This allows stomach contents to pass more freely from the stomach. [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] 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] 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] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radioactive iodine: A radioactive form of the chemical element iodine, often used for imaging tests or as a treatment for cancer. [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] Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Nonimmunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation. [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] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and

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interventional radiology or other planning and guiding medical radiology. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [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] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] 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] Receptor, Insulin: A cell surface receptor for insulin. It is comprised of a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precusor protein. The receptor contains an intrinsic tyrosine kinase domain that is located within the beta subunit. Activation of the receptor by insulin results in numerous metabolic changes including increased uptake of glucose into the liver, muscle, and adipose tissue. EC 2.7.11.-. [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] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Reconstitution: 1. A type of regeneration in which a new organ forms by the rearrangement of tissues rather than from new formation at an injured surface. 2. The restoration to original form of a substance previously altered for preservation and storage, as the restoration to a liquid state of blood serum or plasma that has been dried and stored. [EU] 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] 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

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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] 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] Reproduction Techniques: Methods pertaining to the generation of new individuals. [NIH] Reproductive History: An important aggregate factor in epidemiological studies of women's health. The concept usually includes the number and timing of pregnancies and their outcomes, the incidence of breast feeding, and may include age of menarche and menopause, regularity of menstruation, fertility, gynecological or obstetric problems, or contraceptive usage. [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] Resting metabolic rate: RMR accounts for 65 to 75 percent of daily energy expenditure and represents the minimum energy needed to maintain all physiological cell functions in the resting state. The principal determinant of RMR is lean body mass (LBM). Obese subjects have a higher RMR in absolute terms than lean individuals, an equivalent RMR when corrected for LBM and per unit surface area, and a lower RMR when expressed per kilogram of body weight. Obese persons require more energy for any given activity because of a larger mass, but they tend to be more sedentary than lean subjects. [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 Vein: Central retinal vein and its tributaries. It runs a short course within the optic nerve and then leaves and empties into the superior ophthalmic vein or cavernous sinus. [NIH]

Retinal Vein Occlusion: Occlusion of the retinal vein. Those at high risk for this condition include patients with hypertension, diabetes mellitus, arteriosclerosis, and other cardiovascular diseases. [NIH] Retinoid: Vitamin A or a vitamin A-like compound. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous

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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] Retroperitoneal: Having to do with the area outside or behind the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Ribonucleic acid: RNA. One of the two nucleic acids found in all cells. The other is deoxyribonucleic acid (DNA). Ribonucleic acid transfers genetic information from DNA to proteins produced by the cell. [NIH] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Risperidone: A selective blocker of dopamine D2 and serotonin-5-HT-2 receptors that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of schizophrenia. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rosiglitazone: A drug taken to help reduce the amount of sugar in the blood. Rosiglitazone helps make insulin more effective and improves regulation of blood sugar. It belongs to the family of drugs called thiazolidinediones. [NIH] Salicylate: Non-steroidal anti-inflammatory drugs. [NIH] Salicylic: A tuberculosis drug. [NIH] Salicylic Acids: Derivatives and salts of salicylic acid. [NIH] Saline: A solution of salt and water. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [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] Saturate: Means fatty acids without double bond. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed

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pictures of organs inside the body. MRI scans use a large magnet connected to a computer to create pictures of areas inside the body. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [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] Second Messenger Systems: Systems in which an intracellular signal is generated in response to an intercellular primary messenger such as a hormone or neurotransmitter. They are intermediate signals in cellular processes such as metabolism, secretion, contraction, phototransduction, and cell growth. Examples of second messenger systems are the adenyl cyclase-cyclic AMP system, the phosphatidylinositol diphosphate-inositol triphosphate system, and the cyclic GMP system. [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] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Self Care: Performance of activities or tasks traditionally performed by professional health care providers. The concept includes care of oneself or one's family and friends. [NIH] Sella Turcica: A bony prominence situated on the upper surface of the body of the sphenoid bone. It houses the pituitary gland. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senescence: The bodily and mental state associated with advancing age. [NIH] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [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] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [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] 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

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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] Shivering: Involuntary contraction or twitching of the muscles. It is a physiologic method of heat production in man and other mammals. [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] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [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] 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]

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] 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] 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 in contrast to the viscera. [EU] Somatostatin: A polypeptide hormone produced in the hypothalamus, and other tissues and organs. It inhibits the release of human growth hormone, and also modulates important physiological functions of the kidney, pancreas, and gastrointestinal tract. Somatostatin receptors are widely expressed throughout the body. Somatostatin also acts as a neurotransmitter in the central and peripheral nervous systems. [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

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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] 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] 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] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]

Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be expected to happen by chance alone. [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 instrumentation. [NIH] Stent: A device placed in a body structure (such as a blood vessel or the gastrointestinal tract) to provide support and keep the structure open. [NIH] Sterile: Unable to produce children. [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] Stillbirth: The birth of a dead fetus or baby. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]

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]

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Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [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] Stress management: A set of techniques used to help an individual cope more effectively with difficult situations in order to feel better emotionally, improve behavioral skills, and often to enhance feelings of control. Stress management may include relaxation exercises, assertiveness training, cognitive restructuring, time management, and social support. It can be delivered either on a one-to-one basis or in a group format. [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] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [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] Subiculum: A region of the hippocampus that projects to other areas of the brain. [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] 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 methionine. [NIH] Superantigens: Microbial antigens that have in common an extremely potent activating effect on T-cells that bear a specific variable region. Superantigens cross-link the variable region with class II MHC proteins regardless of the peptide binding in the T-cell receptor's pocket. The result is a transient expansion and subsequent death and anergy of the T-cells with the appropriate variable regions. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [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]

Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and

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followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Sweat Glands: Sweat-producing structures that are embedded in the dermis. Each gland consists of a single tube, a coiled body, and a superficial duct. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [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] Telomerase: Essential ribonucleoprotein reverse transcriptase that adds telomeric DNA to the ends of eukaryotic chromosomes. Telomerase appears to be repressed in normal human somatic tissues but reactivated in cancer, and thus may be necessary for malignant transformation. EC 2.7.7.-. [NIH] Telomere: A terminal section of a chromosome which has a specialized structure and which is involved in chromosomal replication and stability. Its length is believed to be a few hundred base pairs. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] 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] Tetany: 1. Hyperexcitability of nerves and muscles due to decrease in concentration of extracellular ionized calcium, which may be associated with such conditions as parathyroid hypofunction, vitamin D deficiency, and alkalosis or result from ingestion of alkaline salts; it is characterized by carpopedal spasm, muscular twitching and cramps, laryngospasm with inspiratory stridor, hyperreflexia and choreiform movements. 2. Tetanus. [EU] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH]

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Thermogenesis: The generation of heat in order to maintain body temperature. The uncoupled oxidation of fatty acids contained within brown adipose tissue and shivering are examples of thermogenesis in mammals. [NIH] 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] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [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] 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] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroid Hormones: Hormones secreted by the thyroid gland. [NIH] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [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 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 organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios. [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] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH]

Dictionary 209

Topical: On the surface of the body. [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] 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] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] 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 molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [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] Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [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] 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] 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]

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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] Trophoblast: The outer layer of cells of the blastocyst which works its way into the endometrium during ovum implantation and grows rapidly, later combining with mesoderm. [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] 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] 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] 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] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [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] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [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] 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] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi, protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [NIH]

Vagotomy: The interruption or removal of any part of the vagus (10th cranial) nerve. Vagotomy may be performed for research or for therapeutic purposes. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new

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blood vessel formation. [NIH] Vascular Resistance: An expression of the resistance offered by the systemic arterioles, and to a lesser extent by the capillaries, to the flow of blood. [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] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] 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] 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] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virilism: Development of masculine traits in the female. [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] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral fat: One of the three compartments of abdominal fat. Retroperitoneal and subcutaneous are the other two compartments. [NIH] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Vitamin U: A vitamin found in green vegetables. It is used in the treatment of peptic ulcers, colitis, and gastritis and has an effect on secretory, acid-forming, and enzymatic functions of the intestinal tract. [NIH] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Hemorrhage: Hemorrhage into the vitreous body. [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

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together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [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] 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] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [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] Zalcitabine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chainterminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy. [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]

213

INDEX A Abdominal, 8, 38, 46, 47, 50, 151, 152, 160, 181, 184, 191, 193, 202, 211 Abdominal fat, 8, 38, 47, 151, 211 Ablation, 38, 151 Abortion, 151, 190, 196 Acanthosis Nigricans, 60, 151 Acceptor, 151, 184, 191, 209 Acetylcholine, 44, 151, 162, 189 Acidosis, 114, 151, 182 Acitretin, 73, 151 Acne, 56, 87, 151 Activities of Daily Living, 24, 151 Acyl, 31, 151, 172 Adaptation, 7, 151 Adenosine, 152, 160, 194 Adipocytes, 19, 37, 55, 57, 108, 152, 183 Adipose Tissue, 13, 21, 27, 45, 55, 151, 152, 184, 200, 208 Adjustment, 6, 114, 151, 152 Adrenal Cortex, 152, 154, 166, 172, 179, 190, 196 Adrenal Glands, 116, 152 Adrenergic, 152, 156, 169, 170, 172, 197, 207 Adverse Effect, 49, 152, 204 Aerobic, 18, 24, 152, 191 Aerobic Exercise, 18, 152 Aerobic Metabolism, 152, 191 Aerobic Respiration, 152, 191 Afferent, 152, 183 Affinity, 152, 153, 168, 204 Age Groups, 98, 152 Age of Onset, 152, 210 Aged, 80 and Over, 152, 153 Agonist, 153, 160, 163, 169 Airway, 153, 204 Akathisia, 153, 156 Albumin, 119, 153, 194 Alertness, 153, 160 Algorithms, 50, 153, 158 Alimentary, 153, 192 Alkaline, 151, 153, 154, 160, 207 Alkaloid, 153, 160 Alleles, 12, 153, 178, 184 Alopecia, 58, 153 Alpha-1, 153, 170 Alternative medicine, 124, 153

Amenorrhea, 35, 153, 155, 160, 195 Amino Acid Sequence, 154, 155, 158 Ammonia, 154, 207, 210 Amnion, 154 Amniotic Fluid, 115, 154, 175 Anaemia, 90, 154 Anaesthesia, 154, 180 Anal, 154, 185, 188 Analgesic, 154, 171 Analog, 154, 183 Analogous, 57, 154, 209 Anaphylatoxins, 154, 164 Anatomical, 154, 162, 169, 180 Androgenic, 154 Androgens, 37, 55, 92, 152, 154, 166, 179 Androstenedione, 49, 100, 154 Anemia, 154, 185 Anergy, 154, 206 Aneurysm, 154, 211 Angina, 154, 197 Angina Pectoris, 154, 197 Angiotensin I, 34, 154 Angiotensinogen, 155, 201 Animal model, 6, 17, 22, 47, 155 Anions, 153, 155, 182, 204 Anorexia, 93, 99, 155 Anorexia Nervosa, 93, 99, 155 Anovulation, 7, 15, 36, 49, 54, 56, 155, 195 Antagonism, 155, 160, 169 Antecedent, 35, 155 Anthropometry, 27, 33, 155 Antibacterial, 155, 205 Antibiotic, 155, 205 Antibodies, 21, 59, 94, 118, 155, 157, 167, 185, 194 Antibody, 39, 59, 94, 152, 155, 156, 164, 167, 178, 180, 181, 182, 186, 187, 199, 200, 205, 212 Anticoagulant, 155, 197 Antidiabetic, 107, 155 Antiemetic, 155, 156 Antigen, 21, 152, 155, 156, 164, 178, 180, 181, 186, 199 Antigen-Antibody Complex, 156, 164 Anti-inflammatory, 156, 157, 166, 168, 175, 202 Anti-Inflammatory Agents, 156, 157, 166 Antioxidant, 64, 156, 191

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Antipsychotic, 47, 156, 188, 202 Antipyretic, 156 Anxiety, 17, 153, 156, 197 Apnea, 156 Apolipoproteins, 156, 184 Apoptosis, 33, 48, 156 Arginine, 17, 50, 154, 156 Arterial, 34, 53, 67, 86, 116, 156, 162, 179, 197, 207 Arteries, 156, 157, 159, 166, 185, 187, 188 Arterioles, 156, 157, 159, 160, 187, 188, 211 Arteriosclerosis, 156, 179, 188, 201 Artery, 11, 13, 53, 68, 81, 154, 156, 157, 166, 199, 207 Ascites, 157, 191 Aspirin, 37, 157 Assay, 15, 114, 157, 199 Asymptomatic, 10, 20, 157 Atherogenic, 46, 157, 211 Atrophy, 157, 184 Atypical, 47, 157, 202 Autoantibodies, 21, 93, 157 Autoantigens, 21, 157 Autonomic, 151, 156, 157, 189, 193 Axillary, 157, 159 Axillary Artery, 157, 159 B Bacteria, 151, 155, 157, 171, 187, 200, 205, 209, 210 Bacterial Physiology, 151, 157 Bactericidal, 157, 173 Bacteriophage, 157, 194, 209 Bacteriuria, 157, 210 Baroreflex, 34, 52, 157 Basal Ganglia, 156, 158, 163 Basement Membrane, 118, 158, 173, 183 Behavior Therapy, 158 Benzoic Acid, 125, 158 Beta-Endorphin, 97, 158 Bilateral, 158, 195 Bile, 158, 174, 182, 184, 205 Bilirubin, 116, 153, 158, 179 Bioavailability, 21, 158 Biochemical, 13, 26, 36, 48, 71, 85, 106, 119, 153, 158, 183, 203 Biogenesis, 26, 158 Biological therapy, 158, 177 Biomarkers, 22, 158 Biopsy, 23, 158, 192 Biosynthesis, 35, 158, 197, 203 Biotechnology, 60, 61, 124, 131, 158 Bladder, 158, 165, 197, 210

Blastocyst, 49, 159, 165, 171, 194, 210 Blood Coagulation, 159, 160, 208 Blood urea, 116, 159, 183 Blood vessel, 138, 157, 159, 160, 161, 162, 184, 193, 204, 205, 206, 208, 210, 211 Blot, 39, 159 Body Composition, 8, 9, 14, 17, 24, 25, 28, 38, 45, 46, 47, 48, 53, 72, 159 Body Fluids, 158, 159, 170, 204, 210 Body Image, 35, 159 Body Mass Index, 4, 5, 19, 21, 45, 78, 93, 118, 159, 191 Bone Density, 50, 159 Bone Marrow, 159, 175, 176, 185, 206 Bone Resorption, 8, 159 Bone scan, 159, 202 Brachial, 10, 159 Brachial Artery, 10, 159 Brachytherapy, 159, 181, 182, 199, 212 Breast Feeding, 159, 201 Breeding, 14, 52, 159 Bromocriptine, 98, 160 Buffers, 157, 160 Bulimia, 84, 160 C Caesarean section, 30, 160 Caffeine, 8, 67, 138, 160 Calcium, 79, 116, 160, 164, 169, 192, 197, 207 Capillary, 69, 72, 106, 118, 160, 184, 211 Carbohydrate, 5, 17, 43, 44, 46, 48, 73, 87, 109, 160, 166, 175, 176, 195 Carbon Dioxide, 160, 194 Carcinogen, 160, 173 Carcinogenesis, 22, 160, 162 Carcinogenic, 160, 181, 197, 205 Carcinoma, 56, 160 Cardiac, 14, 25, 82, 157, 160, 166, 167, 172, 188, 205 Cardiac catheterization, 15, 160 Cardiac Output, 157, 160 Cardiomyopathy, 14, 119, 161 Cardiorespiratory, 152, 161 Cardioselective, 161, 197 Cardiovascular disease, 10, 11, 12, 18, 34, 35, 40, 41, 44, 46, 51, 53, 60, 67, 93, 136, 161, 201 Carnitine, 31, 161 Carotene, 161, 201 Case-Control Studies, 28, 161 Catabolism, 44, 161 Cataract, 58, 161, 172

215

Catecholamine, 161, 169 Catheterization, 82, 161 Caudal, 161, 169, 179, 195 Causal, 54, 161 Cause of Death, 12, 136, 161 Cavernous Sinus, 161, 201 Cecum, 33, 161, 183 Cell Death, 156, 161, 188 Cell Differentiation, 49, 162 Cell Division, 157, 162, 177, 187, 194, 197, 203 Cell motility, 162, 178 Cell proliferation, 49, 157, 162 Cell Respiration, 152, 162, 191 Cell Survival, 162, 177 Central Nervous System, 151, 157, 160, 162, 174, 176, 177, 190, 203 Cerebral, 158, 162, 166, 168, 172, 173, 186 Cerebral Cortex, 162, 173 Cerebrospinal, 116, 162 Cerebrospinal fluid, 116, 162 Cerebrovascular, 161, 162 Chemoprevention, 22, 162 Chemopreventive, 22, 162 Chemoreceptor, 156, 162 Chemotactic Factors, 162, 164 Chin, 162, 187 Cholesterol, 5, 13, 46, 116, 118, 122, 137, 139, 158, 162, 163, 166, 170, 179, 184, 185, 205, 211 Cholesterol Esters, 162, 184 Cholinergic, 88, 156, 162 Chorea, 156, 163 Chromatin, 156, 163 Chromosomal, 27, 40, 41, 58, 163, 207 Chromosome, 27, 41, 163, 184, 203, 207 Chronic Disease, 11, 125, 163 Chronic renal, 163, 195 Chylomicrons, 163, 184 Circadian, 7, 68, 163 Circadian Rhythm, 7, 163 Cirrhosis, 17, 163, 177 CIS, 163, 201 Clamp, 14, 15, 17, 19, 23, 37, 43, 46, 69, 108, 163 Clinical study, 163, 166 Clinical trial, 4, 6, 29, 36, 59, 131, 163, 166, 170, 198, 200 Clomiphene, 56, 163 Cloning, 26, 158, 163 Cofactor, 163, 197, 208 Cognitive behavior therapy, 16, 163

Cognitive restructuring, 164, 206 Colitis, 164, 211 Collagen, 153, 158, 164, 174 Collapse, 164, 204 Colloidal, 153, 164, 203 Colon, 164, 183 Colonoscopy, 33, 164 Colorectal, 33, 164 Colorectal Cancer, 33, 164 Complement, 9, 154, 164, 165, 175, 185, 195 Complementary and alternative medicine, 53, 107, 110, 164 Complementary medicine, 107, 165 Compliance, 34, 47, 165 Computational Biology, 131, 165 Computed tomography, 40, 41, 46, 159, 165, 202 Computerized axial tomography, 165, 202 Computerized tomography, 165 Conception, 151, 165, 174, 196, 205 Concomitant, 47, 165 Cones, 165, 201 Confounding, 11, 45, 47, 165 Confusion, 165, 188, 210 Congestion, 156, 165 Conjugated, 158, 165 Connective Tissue, 159, 164, 165, 168, 174, 193, 206 Constipation, 156, 165 Consultation, 14, 165 Contraceptive, 165, 186, 201 Contraindications, ii, 165 Contralateral, 67, 166, 190 Control group, 9, 29, 166, 196, 200 Controlled clinical trial, 18, 35, 50, 51, 166 Convulsions, 166, 170, 196 Coronary, 15, 42, 81, 92, 105, 154, 161, 166, 187, 188 Coronary Disease, 92, 166 Coronary heart disease, 15, 42, 161, 166 Coronary Thrombosis, 166, 187, 188 Coronary Vessels, 166 Corpus, 166, 185, 196, 211 Corpus Luteum, 166, 185, 196 Cortex, 166, 172 Corticosteroid, 166, 196 Cortisol, 16, 63, 66, 153, 166 Cortisone, 87, 166, 168 Cost-benefit, 18, 51, 166 Cranial, 12, 167, 177, 190, 193, 210 Cranial Irradiation, 12, 167

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Creatine, 116, 167 Creatinine, 116, 167, 183 Criterion, 98, 167 Crossing-over, 167, 200 Cultured cells, 27, 56, 167 Curative, 167, 207 Cyclic, 55, 160, 167, 203 Cyst, 167, 191 Cytokine, 56, 167 Cytoplasm, 156, 167, 171, 177 D Daclizumab, 21, 167 Data Collection, 30, 38, 167 De novo, 43, 46, 167 Deamination, 167, 210 Decidua, 167, 194 Decompensation, 30, 167 Degenerative, 167, 202 Dehydroepiandrosterone, 100, 167 Deletion, 23, 37, 56, 156, 167 Delirium, 156, 167 Dementia, 156, 168 Density, 8, 19, 50, 81, 118, 139, 159, 168, 170, 184, 190 Dentate Gyrus, 168, 178 Deoxyribonucleic, 168, 202 Depressive Disorder, 16, 168, 184 Dermis, 168, 207 Desensitization, 168, 180 Desipramine, 16, 168 Dexamethasone, 82, 168 Diabetic Foot, 114, 119, 168 Diabetic Ketoacidosis, 114, 119, 168 Diabetic Retinopathy, 125, 169 Diagnostic procedure, 124, 169, 193 Dialyzer, 169, 177 Diastolic, 169, 179, 186 Diastolic pressure, 169, 179, 186 Diencephalon, 169, 179 Digestion, 153, 158, 169, 181, 184, 192, 205 Dilatation, Pathologic, 169, 211 Dilation, 169, 211 Diltiazem, 74, 169 Direct, iii, 27, 32, 33, 105, 169, 200, 207 Discrete, 55, 169 Disease Susceptibility, 12, 169 Disinfectant, 169, 173 Disparity, 32, 169 Disposition, 38, 44, 169 Distal, 34, 169 Diuresis, 160, 169 Dopamine, 70, 156, 160, 169, 189, 193, 202

Dose-dependent, 25, 45, 169 Double-blind, 21, 59, 170 Doxazosin, 74, 170 Drive, ii, vi, 36, 43, 55, 115, 118, 170, 183 Drug Interactions, 170 Drug Tolerance, 170, 208 Duct, 116, 161, 170, 173, 185, 202, 207 Duodenum, 158, 170, 175, 192, 205 Dyskinesia, 156, 170 Dyslipidemia, 32, 34, 37, 42, 46, 50, 114, 170 Dyspareunia, 170, 173 Dysphoric, 168, 170 Dyspnea, 167, 170 E Echocardiography, 14, 170 Eclampsia, 28, 170, 196 Edema, 167, 169, 170, 191, 196 Effector, 151, 164, 170 Effector cell, 170 Efficacy, 16, 18, 43, 50, 51, 59, 170 Elastic, 19, 170, 206 Elasticity, 11, 156, 170 Electrolyte, 166, 168, 170, 183, 195, 204 Electrons, 156, 171, 182, 191, 199, 200 Embryo, 49, 151, 154, 159, 162, 171, 180, 188, 190, 196, 205 Embryo Transfer, 171, 196 Embryology, 171, 174 Emollient, 171, 176 Encephalopathy, 47, 171 Endemic, 171, 185, 205 Endocrine Glands, 116, 171, 192 Endocrine System, 171, 188 Endocrinologist, 121, 171 Endocrinology, 63, 64, 66, 68, 84, 87, 89, 92, 93, 94, 97, 99, 100, 101, 105, 118, 119, 171 Endogenous, 22, 56, 64, 157, 158, 169, 171, 197 Endometrial, 21, 36, 56, 171 Endometrium, 22, 167, 171, 210 Endopeptidases, 171, 197 Endorphin, 66, 158, 171 Endotoxic, 171, 184 Endotoxins, 164, 171, 182 End-stage renal, 163, 172, 195 Energy balance, 14, 24, 45, 172, 183 Energy Intake, 9, 172 Enkephalin, 158, 172 Entorhinal Cortex, 172, 178 Environmental Health, 130, 132, 172

217

Enzymatic, 153, 160, 161, 164, 172, 178, 201, 211 Enzyme, 31, 57, 170, 172, 174, 175, 184, 187, 195, 197, 198, 201, 206, 208, 209, 211, 212 Epidemic, 12, 24, 34, 46, 172, 205 Epidemiological, 172, 201 Epigastric, 172, 191 Epinephrine, 75, 152, 169, 172, 189, 210 Epithelial, 167, 172, 173, 178, 183 Epithelial Cells, 172, 178, 183 Epithelium, 158, 172 Erectile, 125, 172 Erection, 172 Ergot, 160, 172 Erythrocytes, 154, 159, 172, 200 Esterification, 31, 172 Estradiol, 22, 23, 49, 55, 172, 173 Estrogen, 22, 56, 163, 172, 173, 197 Estrogen receptor, 23, 163, 172 Estrogen Replacement Therapy, 22, 173 Estrone, 21, 173 Ethanol, 108, 173, 174 Ethnic Groups, 13, 33, 38, 173 Etretinate, 151, 173 Evacuation, 165, 173, 175 Evoke, 7, 173, 205 Excitatory, 173, 176 Excrete, 173, 183 Exhaustion, 155, 173, 185 Exocrine, 116, 173, 191 Exogenous, 22, 108, 171, 173, 197, 210 External-beam radiation, 173, 182, 199, 212 Extracellular, 34, 165, 173, 174, 204, 207 Extracellular Matrix, 165, 173, 174 Extraction, 23, 173 Extrapyramidal, 153, 156, 169, 173 Extremity, 86, 173 F Facial, 42, 173 Family Planning, 131, 173 Fasting Blood Glucose Test, 137, 173 Fatigue, 122, 174 Fermentation, 108, 174 Fertilization in Vitro, 174, 196 Fetal Heart, 70, 174 Fetus, 30, 54, 151, 174, 194, 196, 205, 210 Fibroblasts, 58, 174 Fibrosis, 14, 71, 174 Fluoxetine, 16, 174 Fold, 139, 174

Follicular Fluid, 8, 174 Foot Ulcer, 168, 174 Forearm, 34, 77, 159, 174 Fractionation, 54, 174 Fructosamine, 72, 114, 119, 174 G Gallbladder, 151, 174 Ganglia, 151, 174, 188, 193 Gas, 154, 160, 174, 178, 189 Gastrectomy, 106, 174 Gastric, 92, 161, 174, 175, 178, 192 Gastric Emptying, 92, 175 Gastrin, 175, 178 Gastritis, 175, 211 Gastrointestinal, 172, 173, 175, 186, 203, 204, 205, 206, 210 Gastrointestinal tract, 173, 175, 203, 204, 205, 210 Gene, 17, 22, 26, 27, 28, 38, 42, 45, 47, 108, 153, 158, 175, 178, 179, 190, 203 Gene Expression, 22, 26, 108, 175 Gene Therapy, 42, 175 Genetic Engineering, 158, 163, 175 Genetics, 12, 41, 58, 76, 118, 175 Genotype, 26, 45, 48, 175, 193 Germ Cells, 175, 190, 191, 207 Gestation, 24, 28, 30, 43, 54, 57, 96, 175, 193, 194, 205 Gestational Age, 4, 29, 96, 175 Ginseng, 54, 175 Gland, 116, 152, 166, 175, 179, 191, 192, 194, 197, 203, 205, 207, 208 Glucocorticoid, 52, 168, 175, 196 Gluconeogenesis, 25, 32, 43, 46, 175 Glucose Clamp Technique, 23, 176 Glucose Intolerance, 12, 17, 20, 30, 42, 44, 58, 76, 104, 168, 176 Glucuronic Acid, 176, 177 Glutamate, 176 Glutamic Acid, 59, 176, 189 Glycerol, 25, 27, 87, 176, 194 Glycine, 153, 158, 176, 189, 203 Glycogen, 43, 176 Glycosuria, 63, 176 Gonad, 176 Gonadal, 46, 176, 205 Gonadotropic, 55, 176 Gonadotropin, 49, 55, 176 Governing Board, 176, 196 Graft, 42, 176, 188 Grafting, 176, 180 Graft-versus-host disease, 176, 188

218

Glucose Tolerance Test

Granulocytes, 177, 212 Growth factors, 33, 41, 177 H Half-Life, 151, 177 Haplotypes, 28, 177 Headache, 160, 177 Health Status, 13, 118, 177 Heart attack, 122, 137, 161, 177 Heartbeat, 177, 186 Hematology, 116, 177, 193 Heme, 158, 177, 195 Hemochromatosis, 17, 177 Hemodialysis, 109, 169, 177, 183 Hemoglobin, 21, 32, 77, 114, 115, 118, 139, 154, 172, 177, 183 Hemoglobin A, 77, 115, 177 Hemoglobinopathies, 175, 177 Hemorrhage, 177, 206, 211 Heparin, 22, 25, 177 Hepatic, 17, 23, 25, 31, 32, 43, 44, 46, 56, 60, 85, 153, 168, 176, 178, 184, 195 Hepatocyte, 42, 178 Hepatocyte Growth Factor, 42, 178 Hepatoma, 37, 178 Heredity, 125, 175, 178 Heterogeneity, 53, 81, 152, 178 Heterogenic, 178 Heterogenous, 118, 178 Heterozygotes, 45, 178 Hippocampus, 52, 168, 178, 206 Hirsutism, 35, 56, 178, 179 Histamine, 154, 156, 178 Homeostasis, 3, 39, 50, 54, 56, 178 Homogeneous, 45, 178 Homologous, 48, 153, 167, 175, 178, 203 Homozygotes, 17, 178 Hormonal, 35, 54, 118, 157, 166, 173, 178, 193 Hormone, 21, 35, 42, 48, 49, 50, 56, 57, 63, 66, 73, 75, 76, 83, 89, 91, 94, 97, 98, 158, 163, 166, 171, 172, 173, 175, 178, 181, 182, 183, 186, 190, 196, 197, 203, 204, 207, 208 Hydrogen, 151, 160, 178, 184, 187, 189, 191, 193, 212 Hydrolysis, 57, 178, 184, 195, 198 Hydrophobic, 179, 184 Hydroxyproline, 153, 164, 179 Hyperandrogenism, 7, 15, 49, 54, 56, 179 Hyperbilirubinemia, 28, 179, 182 Hypercholesterolemia, 46, 117, 170, 179

Hyperglycemia, 9, 29, 30, 37, 46, 48, 53, 54, 57, 91, 102, 179 Hyperlipidemia, 170, 179 Hyperlipoproteinemia, 179, 184 Hyperplasia, 21, 179 Hypertension, 10, 14, 42, 50, 56, 63, 68, 74, 83, 93, 99, 114, 117, 161, 170, 177, 179, 196, 197, 201 Hyperthyroidism, 179, 197 Hypertrichosis, 178, 179 Hypertriglyceridemia, 46, 170, 179 Hypertrophy, 179 Hypoglycemia, 3, 28, 30, 72, 101, 110, 114, 116, 119, 122, 125, 136, 138, 179 Hypoglycemic, 88, 108, 179 Hypoglycemic Agents, 88, 179 Hypotension, 156, 166, 179 Hypothalamic, 12, 33, 179 Hypothalamus, 12, 169, 172, 179, 194, 204 I Ileum, 161, 179 Imaging procedures, 179, 209 Immaturity, 82, 179 Immune response, 59, 154, 155, 157, 166, 179, 180, 185, 206, 211 Immune system, 32, 158, 170, 179, 180, 185, 212 Immunodeficiency, 139, 180 Immunogenic, 180, 184, 199 Immunoglobulin, 155, 180, 187 Immunologic, 162, 175, 180, 200 Immunology, 41, 57, 59, 152, 180 Immunoradiometric Assay, 89, 180 Immunosuppression, 29, 42, 180, 185 Immunosuppressive, 175, 180 Immunosuppressive Agents, 180 Impairment, 9, 38, 168, 170, 180, 198 Implant radiation, 180, 181, 182, 199, 212 Implantation, 81, 165, 180, 190, 210 Impotence, 172, 180 In vitro, 31, 39, 48, 49, 58, 92, 171, 175, 180 In vivo, 15, 29, 31, 39, 54, 55, 56, 57, 92, 175, 178, 180, 185 Incision, 160, 180, 182 Induction, 56, 154, 156, 180, 191, 197, 199 Infancy, 43, 180 Infant, Newborn, 152, 180 Infantile, 180, 184 Infarction, 180 Infection, 125, 157, 158, 162, 168, 180, 183, 185, 189, 206, 212 Infertility, 15, 49, 56, 160, 181, 191

219

Inflammation, 10, 151, 153, 156, 157, 164, 174, 175, 181, 195, 202 Infusion, 23, 70, 79, 176, 181, 209 Ingestion, 67, 176, 181, 207 Initiation, 46, 181 Inorganic, 67, 109, 181 Inositol, 15, 181, 203 Inotropic, 169, 181 Insight, 10, 25, 36, 49, 181 Insulin-dependent diabetes mellitus, 76, 139, 181 Insulin-like, 33, 57, 97, 181 Intermittent, 86, 181 Intermittent Claudication, 86, 181 Internal radiation, 181, 182, 199, 212 Interstitial, 86, 159, 181, 182, 212 Intestinal, 108, 161, 176, 181, 211 Intestine, 164, 181, 183 Intracellular, 27, 31, 34, 55, 57, 160, 181, 195, 203 Intramuscular, 26, 181, 192 Intraperitoneal, 39, 181 Intravascular, 81, 182, 191 Intravenous, 10, 16, 17, 23, 24, 25, 33, 35, 36, 40, 41, 46, 53, 59, 60, 62, 63, 64, 66, 67, 69, 72, 73, 75, 76, 77, 78, 79, 80, 81, 84, 86, 87, 88, 92, 94, 96, 97, 98, 99, 100, 101, 103, 115, 118, 181, 182, 192 Intrinsic, 152, 158, 182, 200 Invasive, 14, 182, 185 Iodine, 182, 199 Ion Channels, 182 Ions, 160, 170, 178, 182 Irradiation, 12, 182, 212 Islet, 21, 29, 38, 41, 44, 59, 83, 93, 94, 118, 182 J Jaundice, 179, 182 K Kb, 130, 182 Keto, 67, 182, 209 Ketoacidosis, 122, 182 Ketone Bodies, 168, 182 Ketosis, 102, 168, 182 Kidney Disease, 117, 130, 138, 182 Kidney Failure, 53, 172, 183 Kidney Failure, Acute, 183 Kidney Failure, Chronic, 183 Kidney stone, 183, 210 Kinetic, 48, 183 L Labile, 164, 183

Lactation, 183, 190, 197 Laminin, 158, 183 Lamivudine, 46, 183 Large Intestine, 161, 164, 181, 183, 200, 204 Latent, 183, 196 Lens, 161, 183 Leprosy, 80, 174, 183 Leptin, 17, 27, 42, 85, 183 Lesion, 174, 183, 184, 207 Leucine, 44, 158, 183 Leukemia, 167, 175, 183 Libido, 154, 183 Ligaments, 166, 184 Linkage, 27, 28, 40, 41, 184 Linkage Disequilibrium, 40, 41, 184 Lipid, 22, 25, 26, 31, 32, 34, 43, 45, 46, 47, 55, 57, 75, 85, 114, 118, 156, 176, 181, 182, 184, 191, 209, 211 Lipid A, 26, 31, 43, 45, 184 Lipid Peroxidation, 184, 191 Lipodystrophy, 27, 32, 42, 50, 184 Lipolysis, 19, 43, 46, 55, 184 Lipopolysaccharides, 184 Lipoprotein, 4, 13, 43, 45, 46, 57, 81, 118, 139, 170, 184, 185, 211 Lipoprotein Lipase, 45, 57, 184 Lithium, 101, 156, 184 Liver, 31, 37, 74, 80, 85, 90, 99, 151, 153, 158, 161, 163, 174, 176, 177, 178, 184, 195, 200, 202, 210, 211 Liver Cirrhosis, 74, 99, 184 Liver scan, 184, 202 Localization, 27, 57, 119, 184 Localized, 178, 179, 181, 183, 184, 194 Locomotion, 184, 185, 194 Locomotor, 7, 185 Longitudinal Studies, 36, 185 Longitudinal study, 13, 16, 42, 53, 185 Low-density lipoprotein, 139, 170, 184, 185 Lutein Cells, 185, 197 Lymphatic, 181, 185 Lymphocyte, 155, 180, 185, 186 Lymphocyte Depletion, 180, 185 Lymphoid, 155, 185 Lytic, 185, 203 M Magnetic Resonance Imaging, 27, 43, 53, 185, 202 Major Histocompatibility Complex, 177, 185 Malaria, 79, 185, 186

220

Glucose Tolerance Test

Malaria, Falciparum, 185, 186 Malaria, Vivax, 185, 186 Malignancy, 151, 186 Malignant, 186, 200, 207 Malnutrition, 153, 157, 186 Mammary, 116, 184, 186 Manic, 156, 184, 186, 198 Manifest, 20, 186 Mean blood pressure, 118, 186 Medial, 11, 157, 186, 190 Mediate, 19, 26, 169, 186 Mediator, 15, 37, 186, 203 Medical Records, 29, 186 MEDLINE, 131, 186 Medroxyprogesterone, 101, 186 Medroxyprogesterone Acetate, 101, 186 Melanin, 186, 193, 210 Melanosis, 151, 186 Membrane, 58, 154, 164, 169, 182, 183, 186, 188, 191, 192, 194, 195, 197, 201 Memory, 155, 168, 186 Menarche, 186, 201 Menopause, 45, 186, 190, 193, 195, 196, 197, 201 Menstruation, 153, 167, 186, 190, 201 Mental, iv, 6, 46, 71, 114, 130, 132, 162, 165, 167, 168, 169, 174, 186, 187, 198, 203, 210 Mental Health, iv, 6, 114, 130, 132, 187, 198 Mesolimbic, 156, 187 Metabolic acidosis, 168, 187 Metabolic disorder, 31, 187 Metabolite, 151, 173, 187 Methionine, 158, 187, 206 MI, 4, 5, 78, 103, 108, 118, 150, 187 Microbiology, 151, 157, 187 Microcirculation, 184, 187 Microorganism, 163, 187, 211 Milliliter, 159, 187 Mitosis, 156, 187 Modeling, 23, 64, 75, 92, 101, 106, 187 Modification, 88, 153, 175, 187, 199, 212 Modulator, 56, 187 Molecule, 155, 164, 170, 177, 178, 187, 191, 200, 209, 211 Monitor, 167, 187, 189 Monoclonal, 39, 167, 182, 187, 199, 212 Morphological, 171, 187 Morphology, 8, 38, 54, 161, 177, 188 Morula, 159, 188 Mucosa, 188, 197, 206

Multivariate Analysis, 16, 188 Mycophenolate mofetil, 21, 188 Myocardial infarction, 105, 166, 187, 188, 197 Myocardial Ischemia, 154, 166, 188 Myocardium, 154, 187, 188 N Natural selection, 158, 188 Nausea, 155, 156, 182, 188, 210 Necrosis, 156, 180, 187, 188 Neonatal, 5, 30, 80, 82, 188 Neoplasia, 33, 173, 188 Nephrology, 10, 188 Nephropathy, 14, 119, 122, 125, 183, 188 Nerve, 53, 119, 138, 152, 162, 186, 188, 190, 202, 205, 209, 210 Nervous System, 152, 162, 186, 188, 189, 193, 207 Neural, 152, 168, 188, 193 Neuroendocrine, 33, 188 Neuroleptic, 153, 156, 188 Neurologic, 18, 51, 189 Neuromuscular, 151, 189 Neuromuscular Junction, 151, 189 Neuronal, 48, 189, 193 Neurons, 168, 173, 174, 189, 207 Neuropathy, 114, 119, 122, 125, 189, 212 Neuropeptide, 12, 189 Neurotransmitter, 151, 152, 153, 169, 176, 178, 182, 189, 203, 204, 206 Neutrons, 182, 189, 199 Nitrogen, 116, 153, 154, 183, 189 Norepinephrine, 152, 168, 169, 189 Normotensive, 10, 68, 86, 189 Nuclear, 26, 158, 171, 188, 189, 199 Nuclei, 171, 175, 185, 187, 189, 190 Nucleic acid, 189, 202, 212 Nucleus, 156, 163, 167, 189, 197, 206 O Odds Ratio, 29, 189 Oestradiol, 92, 190 Oestrogen, 101, 190 Oligo, 35, 190 Oligomenorrhea, 190, 195 Oliguria, 183, 190 Oncogene, 178, 190 Oocytes, 49, 190 Opacity, 161, 168, 190 Ophthalmic, 114, 190, 201 Opiate, 158, 172, 190 Opsin, 190, 201, 202 Optic Chiasm, 179, 190

221

Optic Nerve, 190, 201 Orthostatic, 156, 190 Osmolality, 116, 190 Osmoles, 190, 191 Osmosis, 191 Osmotic, 14, 153, 190, 191, 204 Osteoporosis, 12, 173, 190, 191 Ovarian Follicle, 166, 174, 191 Ovarian Hyperstimulation Syndrome, 57, 191 Ovaries, 55, 92, 97, 116, 179, 191, 195, 204 Ovary, 8, 15, 49, 154, 166, 172, 176, 190, 191, 206 Overweight, 9, 18, 53, 122, 191 Ovulation, 15, 56, 155, 163, 191 Ovulation Induction, 56, 191 Ovum, 166, 167, 174, 175, 188, 191, 196, 197, 210, 212 Oxidation, 26, 31, 44, 45, 81, 151, 156, 168, 184, 191, 208 Oxidative metabolism, 26, 152, 191 Oxidative Stress, 13, 34, 191 P Palliative, 190, 191, 207 Pancreas, 39, 116, 119, 151, 158, 177, 181, 182, 191, 192, 204, 210 Pancreatic, 15, 20, 29, 41, 44, 87, 102, 161, 192 Pancreatic cancer, 20, 192 Parathyroid, 116, 192, 207 Parathyroid Glands, 116, 192 Parathyroid hormone, 192 Parenteral, 21, 56, 59, 172, 192 Parkinsonism, 156, 192 Partial remission, 192, 201 Particle, 192, 209 Parturition, 192, 197 Pathogenesis, 12, 42, 44, 47, 113, 119, 192 Pathologic, 14, 151, 156, 158, 166, 179, 192, 198 Pathologic Processes, 156, 192 Pathophysiology, 50, 60, 118, 192 Patient Care Team, 114, 192 Patient Education, 114, 136, 144, 146, 150, 192 Pedigree, 13, 192 Pelvis, 151, 183, 191, 192, 210 Peptic, 192, 211 Peptic Ulcer, 192, 211 Percutaneous, 105, 192 Perfusion, 176, 192, 208 Perimenopausal, 78, 193

Perinatal, 6, 11, 12, 28, 52, 70, 82, 91, 95, 193 Periodicity, 80, 193 Peripheral Nerves, 183, 193 Peripheral Nervous System, 189, 193, 204, 206 Peripheral Vascular Disease, 53, 119, 122, 193 Peritoneal, 157, 181, 193 Peritoneal Cavity, 157, 181, 193 PH, 71, 95, 97, 159, 193 Pharmacists, 115, 193 Pharmacologic, 4, 45, 155, 177, 193, 208, 209 Phenotype, 27, 31, 47, 48, 58, 193 Phenylalanine, 44, 193, 210 Phlebotomy, 13, 17, 193 Phorbol, 194, 197 Phorbol Esters, 194, 197 Phospholipids, 174, 181, 184, 194, 197 Phosphorus, 116, 160, 192, 194 Phosphorylate, 26, 194 Phosphorylation, 37, 55, 56, 57, 194 Physical Examination, 20, 60, 118, 175, 194 Physical Fitness, 25, 194 Physiologic, 15, 23, 24, 32, 35, 39, 50, 92, 153, 158, 177, 186, 194, 200, 204 Physiology, 14, 35, 39, 40, 44, 55, 67, 70, 86, 101, 107, 108, 171, 177, 188, 194 Pigment, 158, 194 Pilot study, 12, 53, 98, 194 Pituitary Gland, 116, 166, 194, 203 Placenta, 52, 172, 173, 194, 196 Plants, 153, 159, 160, 175, 188, 189, 194, 202, 209 Plaque, 157, 194 Plasma cells, 155, 194 Plasma protein, 153, 174, 194, 203 Plethysmography, 34, 195 Pneumonia, 166, 195 Polycystic, 7, 15, 35, 36, 49, 54, 56, 72, 74, 82, 92, 97, 101, 179, 195 Polycystic Ovary Syndrome, 35, 36, 56, 74, 82, 97, 179, 195 Polymorphism, 45, 92, 195 Polypeptide, 153, 154, 164, 195, 197, 204, 212 Polyposis, 164, 195 Polysaccharide, 155, 195, 198 Porphyria, 193, 195 Porphyria Cutanea Tarda, 193, 195 Posterior, 154, 191, 195

222

Glucose Tolerance Test

Postmenopausal, 18, 45, 66, 69, 173, 191, 195 Postnatal, 52, 55, 62, 195 Postoperative, 75, 96, 195 Postprandial, 5, 72, 195 Potassium, 195 Potentiates, 56, 168, 195 Practice Guidelines, 132, 195 Precancerous, 162, 196 Preclinical, 42, 196 Precursor, 154, 155, 169, 170, 172, 189, 193, 196, 210 Predisposition, 35, 45, 122, 196 Prednisolone, 75, 196 Preeclampsia, 6, 10, 28, 196 Pre-eclamptic, 170, 196 Pregnancy Complications, 103, 196 Pregnancy Outcome, 4, 5, 30, 49, 63, 78, 196 Pregnancy Tests, 175, 196 Premenopausal, 24, 68, 196 Prenatal, 4, 6, 7, 11, 52, 55, 74, 171, 196 Preoperative, 94, 119, 196 Pressoreceptors, 157, 196 Prevalence, 6, 12, 17, 21, 32, 45, 46, 53, 63, 94, 115, 118, 190, 196 Primary endpoint, 59, 196 Progeny, 52, 196 Progesterone, 49, 57, 196, 197, 205 Progestogen, 101, 196 Progression, 14, 26, 36, 38, 155, 197 Progressive, 9, 28, 162, 163, 168, 170, 173, 183, 188, 197 Prolactin, 101, 160, 197 Promoter, 56, 197 Prone, 24, 197 Prophase, 190, 197 Propranolol, 63, 197 Prospective Studies, 33, 197 Prospective study, 16, 185, 197 Prostate, 158, 190, 197, 210 Protease, 32, 46, 197 Protease Inhibitors, 32, 46, 197 Protein Binding, 197, 208 Protein C, 43, 153, 154, 156, 157, 184, 197, 210 Protein Kinase C, 26, 197 Protein S, 44, 158, 197 Proteinuria, 196, 198 Proteoglycans, 158, 198 Proteolytic, 153, 164, 198 Protocol, 17, 21, 24, 42, 198

Protozoan, 185, 198 Proxy, 19, 198 Psoriasis, 151, 173, 198 Psychiatric, 46, 198 Psychiatry, 8, 15, 16, 32, 46, 198 Psychic, 183, 187, 198 Psychosis, 156, 175, 198 Psychotherapy, 163, 198 Psychotropic, 47, 198 Psyllium, 108, 198 Puberty, 36, 38, 198 Public Health, 12, 46, 132, 198 Public Policy, 131, 198 Publishing, 60, 115, 125, 199 Pulmonary, 159, 183, 199, 206, 211 Pulmonary Artery, 159, 199, 211 Pulmonary Edema, 183, 199 Pulse, 34, 50, 187, 199 Pyloroplasty, 85, 199 Q Quality of Life, 18, 35, 51, 138, 199 R Race, 19, 24, 32, 52, 117, 199 Radiation, 154, 167, 173, 174, 180, 181, 182, 199, 200, 202, 212 Radiation therapy, 173, 174, 181, 182, 199, 212 Radioactive, 116, 159, 177, 178, 180, 181, 182, 184, 189, 199, 202, 212 Radioactive iodine, 116, 199 Radioactivity, 167, 199 Radiography, 175, 199 Radioimmunoassay, 180, 199 Radioisotope, 199, 209 Radiolabeled, 182, 199, 212 Radiological, 192, 199 Radiotherapy, 159, 182, 199, 200, 212 Random Allocation, 200 Randomization, 59, 200 Randomized, 8, 9, 16, 21, 24, 35, 43, 47, 53, 57, 59, 170, 200 Reactive Oxygen Species, 34, 200 Receptor, 23, 26, 27, 34, 38, 49, 56, 75, 151, 155, 162, 169, 178, 197, 199, 200, 203, 206 Receptor, Insulin, 49, 200 Recombinant, 14, 42, 56, 200, 211 Recombination, 48, 175, 200 Reconstitution, 32, 200 Rectum, 33, 164, 174, 183, 197, 200 Recur, 193, 200 Recurrence, 48, 162, 163, 193, 200 Red blood cells, 116, 172, 195, 200, 202

223

Refer, 1, 164, 184, 188, 189, 198, 200, 209 Refraction, 200, 205 Regeneration, 200, 201 Regimen, 46, 114, 170, 201 Remission, 16, 96, 105, 200, 201 Renin, 154, 155, 201 Reproduction Techniques, 196, 201 Reproductive History, 13, 201 Respiratory distress syndrome, 28, 201 Resting metabolic rate, 45, 201 Retina, 165, 169, 183, 190, 201, 202 Retinal, 67, 169, 190, 201, 202 Retinal Vein, 67, 201 Retinal Vein Occlusion, 67, 201 Retinoid, 22, 151, 173, 201 Retinol, 201, 202 Retinopathy, 119, 122, 169, 202 Retroperitoneal, 152, 202, 211 Retrospective, 94, 202 Retroviral vector, 175, 202 Rhodopsin, 190, 201, 202 Ribonucleic acid, 49, 202 Risperidone, 47, 202 Rod, 163, 202 Rosiglitazone, 22, 56, 202 S Salicylate, 202 Salicylic, 202 Salicylic Acids, 202 Saline, 25, 202 Saliva, 202 Salivary, 116, 192, 202 Salivary glands, 116, 202 Saponins, 202, 205 Saturate, 40, 41, 202 Scans, 14, 19, 45, 202 Schizophrenia, 47, 202, 203 Screening, 5, 20, 28, 33, 59, 63, 73, 85, 89, 93, 101, 115, 117, 119, 163, 203, 210 Sebaceous, 116, 168, 203 Sebaceous gland, 116, 168, 203 Sebum, 203 Second Messenger Systems, 203 Secretion, 15, 17, 23, 25, 28, 31, 32, 35, 38, 50, 53, 55, 56, 57, 59, 64, 65, 66, 73, 75, 82, 83, 90, 91, 94, 97, 100, 103, 104, 105, 106, 160, 163, 166, 178, 179, 181, 183, 203 Secretory, 53, 99, 203, 211 Sedentary, 44, 60, 122, 201, 203 Sediment, 203, 210 Segregation, 157, 200, 203 Self Care, 114, 138, 151, 203

Sella Turcica, 194, 203 Semisynthetic, 160, 203 Senescence, 58, 203 Senile, 191, 203 Sequencing, 27, 203 Serine, 171, 197, 203 Serologic, 21, 203 Serotonin, 156, 168, 174, 189, 202, 203 Serum Albumin, 106, 199, 203 Sex Characteristics, 154, 190, 198, 204, 207 Shivering, 204, 208 Side effect, 42, 47, 53, 152, 153, 156, 158, 204, 209, 212 Signs and Symptoms, 201, 204 Skeletal, 19, 23, 26, 108, 154, 163, 204 Skeleton, 204 Sleep apnea, 36, 204 Small intestine, 161, 163, 170, 178, 179, 181, 199, 204 Smooth muscle, 34, 154, 160, 178, 204, 206 Social Environment, 199, 204 Social Support, 114, 204, 206 Sodium, 104, 204, 207 Solvent, 173, 176, 190, 191, 204 Somatic, 187, 193, 204, 207 Somatostatin, 38, 204 Specialist, 114, 140, 169, 204 Species, 38, 52, 54, 172, 178, 185, 187, 199, 200, 204, 206, 209, 212 Specificity, 152, 171, 205, 208 Spectrum, 12, 25, 205 Sperm, 154, 163, 205 Spinal cord, 159, 162, 188, 189, 193, 205 Spontaneous Abortion, 196, 205 Sporadic, 20, 195, 205 Staging, 59, 202, 205 Statistically significant, 18, 51, 205 Steatosis, 31, 85, 205 Steel, 163, 205 Stent, 81, 82, 205 Sterile, 192, 205 Sterility, 68, 74, 101, 103, 181, 205 Steroid, 35, 42, 154, 166, 174, 190, 202, 205 Stillbirth, 122, 196, 205 Stimulant, 160, 178, 205 Stimulus, 170, 182, 205, 208 Stomach, 151, 174, 175, 176, 178, 182, 188, 192, 193, 199, 204, 205 Strand, 58, 206 Stress, 7, 34, 35, 52, 114, 116, 149, 161, 166, 188, 191, 196, 206 Stress management, 114, 206

224

Glucose Tolerance Test

Stroke, 53, 122, 130, 137, 160, 161, 206 Stromal, 36, 206 Stromal Cells, 36, 206 Subacute, 119, 181, 206 Subclinical, 11, 181, 206 Subcutaneous, 50, 152, 170, 184, 192, 206, 211 Subiculum, 178, 206 Subspecies, 205, 206 Substance P, 187, 196, 200, 203, 206 Substrate, 26, 206 Sulfur, 183, 187, 206 Superantigens, 118, 206 Support group, 114, 206 Suppression, 15, 19, 46, 76, 82, 100, 101, 166, 206 Surfactant, 52, 206 Survival Rate, 43, 206 Sweat, 116, 168, 207 Sweat Glands, 116, 168, 207 Sympathomimetic, 169, 172, 189, 207 Synapse, 152, 168, 189, 207, 209 Synergistic, 34, 54, 197, 207 Systemic, 39, 159, 168, 172, 181, 182, 196, 199, 207, 211, 212 Systolic, 5, 34, 179, 186, 207 Systolic blood pressure, 5, 207 Systolic pressure, 186, 207 T Tardive, 156, 207 Telomerase, 58, 207 Telomere, 58, 207 Temporal, 178, 207 Teratogenic, 169, 173, 207 Testis, 154, 172, 190, 207 Testosterone, 22, 57, 72, 101, 154, 207 Tetany, 192, 207 Therapeutics, 207 Thermogenesis, 25, 208 Thigh, 8, 19, 208 Thorax, 71, 151, 208 Threonine, 197, 203, 208 Threshold, 20, 179, 208 Thrombin, 197, 208 Thrombomodulin, 197, 208 Thrombosis, 50, 197, 206, 208 Thyroid, 63, 83, 99, 116, 179, 182, 192, 208, 210 Thyroid Gland, 116, 179, 192, 208 Thyroid Hormones, 208, 210 Thyrotropin, 83, 94, 103, 208 Thyroxine, 153, 193, 208

Tissue Distribution, 43, 208 Tomography, 208 Tone, 189, 208 Tooth Preparation, 151, 208 Topical, 173, 209 Toxaemia, 196, 209 Toxic, iv, 32, 189, 209, 212 Toxicity, 170, 209 Toxicology, 132, 209 Toxin, 171, 208, 209 Tracer, 43, 209 Trachea, 208, 209 Traction, 163, 209 Transaminases, 116, 209 Transcriptase, 183, 207, 209, 212 Transduction, 26, 56, 57, 181, 209 Transfection, 37, 158, 175, 209 Transfusion, 79, 209 Translation, 39, 153, 209 Transmitter, 151, 169, 182, 186, 189, 209 Transplantation, 29, 41, 83, 90, 119, 163, 171, 183, 185, 209 Tricyclic, 168, 209 Trigger zone, 156, 209 Triglyceride, 4, 13, 27, 31, 46, 179, 209 Troglitazone, 8, 210 Trophoblast, 159, 210 Tumor marker, 158, 210 Tyrosine, 56, 169, 200, 210 U Ultrasonography, 175, 210 Urea, 44, 159, 207, 210 Uremia, 67, 183, 210 Urethra, 197, 210 Uric, 116, 210 Urinalysis, 116, 210 Urinary, 75, 104, 157, 190, 210 Urine, 104, 114, 119, 125, 139, 157, 158, 167, 169, 173, 176, 182, 183, 190, 198, 210 Uterus, 90, 151, 166, 167, 171, 187, 191, 196, 210 V Vaccines, 210, 211 Vagotomy, 75, 85, 210 Vascular, 10, 34, 52, 74, 119, 157, 168, 180, 181, 184, 187, 191, 194, 196, 208, 210, 211 Vascular endothelial growth factor, 74, 210 Vascular Resistance, 34, 157, 211 Vasodilation, 44, 211 Vasodilator, 169, 178, 211 Vasomotor, 173, 211

225

Vector, 106, 209, 211 Vein, 154, 182, 189, 193, 201, 211 Venous, 34, 69, 106, 161, 167, 197, 211 Ventricle, 178, 179, 199, 207, 211 Venules, 159, 160, 187, 211 Very low-density lipoprotein, 31, 211 Vesicular, 174, 211 Veterinary Medicine, 131, 211 Viral, 24, 41, 46, 209, 211, 212 Virilism, 179, 211 Virus, 139, 157, 175, 194, 202, 209, 211 Visceral, 19, 38, 39, 40, 41, 42, 45, 50, 211 Visceral fat, 19, 38, 42, 45, 50, 211 Vitamin A, 181, 201, 211 Vitamin U, 13, 211 Vitreous, 169, 183, 201, 211 Vitreous Hemorrhage, 169, 211

Vitro, 31, 178, 211 Vivo, 10, 29, 47, 54, 58, 185, 212 W White blood cell, 116, 155, 185, 194, 212 Windpipe, 208, 212 Womb, 210, 212 X Xenograft, 155, 212 X-ray, 43, 46, 53, 159, 165, 182, 189, 199, 200, 202, 212 X-ray therapy, 182, 212 Y Yeasts, 193, 212 Z Zalcitabine, 183, 212 Zymogen, 197, 212

226

Glucose Tolerance Test

227

228

Glucose Tolerance Test