CHRONIC BRONCHITIS 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., 1960Chronic Bronchitis: 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: 0-497-00244-2 1. Chronic Bronchitis-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on chronic bronchitis. 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 CHRONIC BRONCHITIS ............................................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Chronic Bronchitis ........................................................................ 6 E-Journals: PubMed Central ....................................................................................................... 36 The National Library of Medicine: PubMed ................................................................................ 37 CHAPTER 2. NUTRITION AND CHRONIC BRONCHITIS ................................................................... 83 Overview...................................................................................................................................... 83 Finding Nutrition Studies on Chronic Bronchitis....................................................................... 83 Federal Resources on Nutrition ................................................................................................... 84 Additional Web Resources ........................................................................................................... 85 CHAPTER 3. ALTERNATIVE MEDICINE AND CHRONIC BRONCHITIS ............................................. 87 Overview...................................................................................................................................... 87 National Center for Complementary and Alternative Medicine.................................................. 87 Additional Web Resources ........................................................................................................... 91 General References ....................................................................................................................... 94 CHAPTER 4. PATENTS ON CHRONIC BRONCHITIS .......................................................................... 95 Overview...................................................................................................................................... 95 Patents on Chronic Bronchitis ..................................................................................................... 95 Patent Applications on Chronic Bronchitis ............................................................................... 101 Keeping Current ........................................................................................................................ 105 CHAPTER 5. BOOKS ON CHRONIC BRONCHITIS............................................................................ 107 Overview.................................................................................................................................... 107 Book Summaries: Federal Agencies............................................................................................ 107 Book Summaries: Online Booksellers......................................................................................... 108 Chapters on Chronic Bronchitis................................................................................................. 108 CHAPTER 6. MULTIMEDIA ON CHRONIC BRONCHITIS ................................................................. 111 Overview.................................................................................................................................... 111 Video Recordings ....................................................................................................................... 111 CHAPTER 7. PERIODICALS AND NEWS ON CHRONIC BRONCHITIS .............................................. 113 Overview.................................................................................................................................... 113 News Services and Press Releases.............................................................................................. 113 Academic Periodicals covering Chronic Bronchitis ................................................................... 115 CHAPTER 8. RESEARCHING MEDICATIONS .................................................................................. 117 Overview.................................................................................................................................... 117 U.S. Pharmacopeia..................................................................................................................... 117 Commercial Databases ............................................................................................................... 119 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 123 Overview.................................................................................................................................... 123 NIH Guidelines.......................................................................................................................... 123 NIH Databases........................................................................................................................... 125 Other Commercial Databases..................................................................................................... 127 APPENDIX B. PATIENT RESOURCES ............................................................................................... 129 Overview.................................................................................................................................... 129 Patient Guideline Sources.......................................................................................................... 129 Finding Associations.................................................................................................................. 132 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 135 Overview.................................................................................................................................... 135 Preparation................................................................................................................................. 135 Finding a Local Medical Library................................................................................................ 135
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Medical Libraries in the U.S. and Canada ................................................................................. 135 ONLINE GLOSSARIES................................................................................................................ 141 Online Dictionary Directories ................................................................................................... 143 CHRONIC BRONCHITIS DICTIONARY................................................................................ 145 INDEX .............................................................................................................................................. 205
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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 chronic bronchitis 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 chronic bronchitis, 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 chronic bronchitis, 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 chronic bronchitis. 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 chronic bronchitis, 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 chronic bronchitis. The Editors
1
From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON CHRONIC BRONCHITIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on chronic bronchitis.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and chronic bronchitis, 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 “chronic bronchitis” (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: •
Potential Associations Between Chronic Respiratory Disease and Periodontal Disease: Analysis of National Health and Nutrition Examination Survey III Source: Journal of Periodontology. 72(1): 50-56. January 2001. Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: Associations between poor oral health and chronic lung disease have recently been reported. This article reports on a study that evaluated these potential associations by analyzing data from the National Health and Nutrition Examination Survey III (NHANES III), which documents the general health and nutritional status of randomly selected United States subjects from 1988 to 1994. This cross sectional, retrospective
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Chronic Bronchitis
study of the NHANES III database included a study population of 13,792 subjects older than 20 years of age, with at least 6 natural teeth. A history of bronchitis or emphysema was recorded from the medical questionnaire, and a dichotomized variable combined those with either chronic bronchitis or emphysema, together considered as chronic obstructive pulmonary disease (COPD). Subject lung function and oral health status were assessed. Analyses adjusted for age, gender, race and ethnicity, education, income, frequency of dental visits, diabetes mellitus, smoking, and alcohol use. The mean age of all subjects was 44.4 years (plus or minus 17.8 years); the mean age of subjects with COPD was 51.2 years and subjects without COPD was 43.9 years. Subjects with a history of COPD had more periodontal attachment loss (a measure of periodontal disease) than subjects without COPD. A trend was noted in that lung function appeared to diminish with increasing periodontal attachment loss. The authors conclude that these findings support recently published reports that suggest an association between periodontal disease and COPD. 4 tables. 46 references. •
Managing the Patient with Severe Respiratory Problems Source: CDA Journal. Journal of the California Dental Association. 28(8): 585-586, 588589, 591-593, 595-598. August 2000. Contact: Available from California Dental Association (CDA). 1201 K Street, Sacramento, CA 95814. (916) 443-0505. Summary: The dental management of patients with severe respiratory problems continues to be a significant challenge to the dental health care practitioner. Chronic obstructive pulmonary diseases, such as chronic bronchitis and emphysema, are the fourth leading cause of death in the United States. Asthma has increased in prevalence during the past 20 years, and the rate of death from this chronic inflammatory disease of the airways has also risen despite recent advances in medical treatments. This article reviews the pathophysiology and medical treatment modalities for these chronic pulmonary diseases. The author also discusses the recognition and management of dental patients with these diseases, including how to avoid precipitating factors that could initiate an acute episode in the dental setting. The author notes that because dentists operate at the origin of the upper airway, and many dental procedures are deemed stressful, patients with chronic respiratory diseases are at special risk. The author provides detailed suggestions for preventing and managing respiratory distress in the dental setting. The entire dental team should be familiar with the signs, symptoms, and management of an emergent episode associated with asthma or chronic obstructive pulmonary diseases. 2 tables. 41 references.
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Uncovering Lesser-Known Symptoms of GERD Source: Digestive Health and Nutrition. 4(2):6. March-April 2002. Contact: Available from American Gastroenterological Association. 7910 Woodmont Avenue, 7th Floor, Bethesda, MD 20814. (877) DHN-4YOU or (301) 654-2055, ext. 650. Email:
[email protected]. Summary: This article describes some of the lesser known symptoms of gastroesophageal reflux disease (GERD), which are usually separated into three groups: pulmonary (asthma and chronic bronchitis); ear, nose and throat (cough, hoarseness, changing of the voice); and other, including chest pain. The author emphasizes that any chest pain indicates the need for a complete work up, to eliminate the possibility of heart disease. In addition to heartburn, the most common symptoms of GERD are chronic cough, hoarseness, sore throat, frequent clearing of the throat in the morning,
Studies
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and asthma. Some studies suggest that up to 80 percent of adult onset asthma that is not allergy related may be caused by acid reflux, especially if the episodes are frequent at night. The author also notes that an endoscopy performed on a patient with extraesophageal symptoms will usually come back normal, and more sophisticated testing will need to be done to prove a connection. 1 reference. •
Chronic Cough Source: American Family Physician. 56(5): 1395-1402. October 1, 1997. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237. Website: www.aafp.org. Summary: This article reviews chronic cough, defined as a cough that lasts for more than three weeks, and updates readers on the current thinking regarding treatment options. The author notes that more than 90 percent of cases of chronic cough result from five common causes: smoking, post-nasal drip, asthma, gastroesophageal reflux, and chronic bronchitis. Although in most patients chronic cough has a single cause, in up to one fourth of patients, multiple disorders contribute to the cough. A stepwise evaluation in patients with chronic cough can minimize the invasiveness and expense of the work up. Initial screening of patients with chronic cough should look for smoking, occupational exposure to an airway irritant, cough-inducing medications, airway hyperresponsiveness following upper respiratory infection, chronic bronchitis, or any systemic symptoms that may indicate serious disease. Patients who are not diagnosed after an initial screening are evaluated and empirically treated in a stepwise fashion for postnasal drip, asthma, and reflux. Bronchoscopy is reserved for use in the few patients still without a diagnosis after the previous steps have been completed. 1 figure. 2 tables. 32 references. (AA-M).
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Relation Between Morbidity and Cognitive Performance in a Normal Aging Population Source: Journal of Gerontology: Medical Sciences. 53A(2): M147-M154. 1998. Summary: This journal article describes a study of the association between morbidity and cognitive performance in an aging population of 1,360 community residents who were enrolled in the Maastricht Aging Study, the Netherlands. People with evidence of stroke, chronic neurological pathology, mental retardation, or chronic psychotropic drug use were excluded. Standard neuropsychological tests were used to assess memory, sensorimotor speed, and information processing speed/cognitive flexibility. Data concerning active and total (active plus inactive) health problems were obtained from a computerized patient database, and classified according to the International Classification of Primary Care. Multiple regression analyses adjusted for age, sex, and educational level revealed that both insulin-dependent and noninsulin-dependent diabetes were negatively associated with all cognitive measures. Negative associations also were found between chronic bronchitis and performance speed, and between presbyacusia and memory. The authors conclude that some specific, relatively common diseases of older age, such as diabetes and chronic bronchitis, may contribute to the age-related decline in cognitive ability. 3 tables, 30 references. (AA-M).
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Federally Funded Research on Chronic Bronchitis The U.S. Government supports a variety of research studies relating to chronic bronchitis. 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 chronic bronchitis. 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 chronic bronchitis. The following is typical of the type of information found when searching the CRISP database for chronic bronchitis: •
Project Title: AIR PARTICLES CAUSE DEATH IN ANIMALS WITH LUNG DISEASE Principal Investigator & Institution: Godleski, John J.; Associate Professor; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2002 Summary: This project will define the effects of concentrated air particles in an animal model of chromic bronchitis. It will determine the role of concentration vs composition in producing adverse effects. The project focuses upon discovery of mechanisms of death and morbidity caused by ambient air particles in animals with pre-existing pulmonary inflammation and airway hyperresponsiveness. Specific aims are: 1) To define the extent of mortality resulting from exposure to various levels of concentrated ambient air particles (CAPs) using normal adult rats and rats with chronic bronchitis; and 2) To determine the mechanisms by which inflammation contributes to mortality and morbidity from exposure to CAPs in the rat model of chronic bronchitis, and 3) To characterize the degree of airway obstruction and hypoventilation present in rats with chronic bronchitis that could lead to increased morbidity and mortality with exposure to CAPs. To assess effects of ambient air particles, animals will be exposed using the Harvard Ambient Particulate Concentration (HAPC), a newly developed device that can increase ambient particle concentrations up to thirty times ambient levels without changing the physical or chemical characteristics of the particles. The exposed animal populations will model human populations and adverse effects including increased mortality that have been identified epidemiologically. Concentrating airborne particles for use in exposures will permit the populations studied in the laboratory to be of a size to see the modeled effect and a size unable to test mechanistic hypotheses. Exposures will take place in Boston, MA, which has a typical fine particle urban aerosol ranging from 5-15 gu/m3 with transported sulfur-containing acidic particles during the summer and local combustion product particulate in winter. With Core support, extensive physical, chemical, andmicrobiologic analysis of the exposure aerosol will be carried out with correlation between these parameters and biologic responses of the animals.
2
Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Established physiologic methods will probe airway responses and their mechanisms. Cell and molecular biology methods will test mechanistic hypotheses on the role of proinflammatory mediators in the development of morbidity and mortality. The novel application of of sophisticated techniques in our proposed studies will offer new insights into mechanisms of toxicity of ambient air particles. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AIRWAY INFLAMMATION BRONCHITIS
&
MEDIATORS
IN
CHRONIC
Principal Investigator & Institution: Knowles, Michael R.; Professor; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 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 •
Project Title: AIRWAY REMODELING IN SEVERE ASTHMA Principal Investigator & Institution: Castro, Mario; Associate Professor; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 20-SEP-2001; Project End 30-JUN-2006 Summary: (provided by applicant): The overall goal of this proposal is to better understand the molecular basis for airway remodeling in children and adults with severe asthma and how it differs from mild-to-moderate asthma. In that context, we propose to study a well characterized cohort of subjects with severe asthma at baseline and two years later and contrast these findings to mild-moderate asthma, normal controls, and diseased controls (chronic bronchitis). We propose that individuals with severe asthma have more severe airway remodeling and inflammation than subjects with mild-to-moderate asthma and normal controls and that the remodeling is associated with less reversible airflow obstruction. Airway remodeling appears to develop in asthma due to a complex interaction between acute and chronic airway inflammation, insults to the airway (due to infections/toxins/environmental exposures), and underlying genetic susceptibility. Ongoing airway inflammation, epithelial desquamation/denudation (due to death or apoptosis), and repair processes, such as epithelial hyperplasia (cellular proliferation) and subepithelial fibrosis, result in abnormal structural changes in the airway. In subjects with severe asthma, this may manifest clinically as irreversible airflow obstruction and poor asthma control despite appropriate anti-inflammatory therapy. The mechanism behind this pathologic process in humans with asthma is unclear and will be better defined in this project. Furthermore, we hypothesize that a noninvasive measurement of airway wall thickness using high resolution computed tomography of the lung will correlate to the physiologic and pathologic measures of remodeling (on a segmental airway level). We will evaluate how these factors associated with remodeling are modified over time in the same individual. Accordingly, in order to better define the molecular basis for airway remodeling in severe asthma and how it differs from mild-to-moderate asthma, we propose to: (1) Define the relationship between airway remodeling and reversibility of airflow obstruction in a well characterized cohort of subjects with severe asthma; (2) Define the pro- and anti-apoptotic factors in airway epithelium associated with airway remodeling in subjects with severe asthma; and (3) Investigate whether radiologic measures of airway thickness correlate with pathologic and physiologic markers in subjects with severe asthma; and compare these findings to subjects with mild-to-
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moderate asthma and diseased and normal controls. The identification of the potential variables associated with remodeling and severe asthma will help identify individuals at risk who would benefit from specific targeted therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANALYSIS OF THE AIRWAY ANTIPROTEINASE DEFENSE SYSTEM Principal Investigator & Institution: Cataltepe, Sule U.; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 31-DEC-2006 Summary: (Adapted from applicant's abstract) Proteinases play a major role in the development of inflammatory lung diseases such as cystic fibrosis, asthma, chronic bronchitis, emphysema and chronic lung disease of prematurity. A better understanding of the regulation of proteinases by inhibitors synthesized by the lung itself could facilitate efforts to develop specific treatments for these diseases. Squamous cell carcinoma antigens (SCCA) 1 and 2 are members of the high molecular weight serine proteinase inhibitor (serpin) family. Although SCCA1 inhibits lysosomal cysteine proteinases, cathepsins (cat)L,S and K, whereas SCCA2 inhibits chymotrypsin-like serine proteinases, catG and mast cell chymase. SCCA1 and SCCA2 show a tissue restricted expression pattern and are co-localized in the tracheal, bronchial and bronchiolar epithelium. In addition, target proteinases of SCCA1, catS and catK, are expressed by the airway epithelial cells. Another source of these potent elastolytic cysteine proteinases in the lung is alveolar macrophages. Based on the in vitro inhibitory profiles and distribution patterns of SCCA1 and SCCA2 in the airways, the investigators hypothesize that these two serpins protect the airways against proteinase mediated injury. The objective of this proposal is to test this hypothesis using in vitro cell culture and in vivo transgenic animal models. The specific aims of the proposed project are to: 1) characterize the deleterious effects of exogenous and endogenous cysteine proteinases catS and catK on bronchial epithelial cells in vitro, 2) determine whether SCCA1 and/or SCCA2 can protect cultured bronchial epithelial cells from the proteinase-mediated injury and isolate the target proteinases, 3) determine whether targeted expression of SCCA1 and SCCA2 can protect the airways from proteinase-mediated injury. The experimental design involves use of cell cultures in conjunction with stable transfections to overexpress SCCA1 and SCCA2. Barrier function of the airway epithelium will be studied by permeability and transepithelial resistance measurements as well as structural analysis. Affinity chromatography and co-immunoprecipation will be used to identify the target proteinases of SCCA1 and SCCA2 in proteinase-mediated injury in vivo. The rat clara cell 10kD protein promoter (CC10) will be used to target expression of SCCA1 and SCCA2 genes to the lung. Animals will be examined to determine the extent of protection against proteinase-mediated lung injury following exposure to acrolein. These studies should enhance our understanding of the mechanisms of proteinase mediated injury and whether the locally synthesized inhibitors such as SCCA1 and SCCA2 can prevent this type of damage. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: APPROACHES TO THE GENETICS OF COPD Principal Investigator & Institution: Silverman, Edwin K.; Assistant Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 16-AUG-1999; Project End 30-JUN-2004
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Summary: Cigarette smoking is the major environmental risk factor for the development of chronic obstructive pulmonary disease (COPD); however, only a subset of smokers develop clinically significant COPD. In addition to the risk from smoking, subjects with severe alpha 1-antitrypsin deficiency have a major genetic predisposition to COPD; other genetic determinants of COPD have not been proven. The frequent development of COPD in individuals with alpha 1-antitrypsin deficiency has provided a foundation for the protease-antiprotease hypothesis for the pathogenesis of COPD. However, many subjects with severe, early-onset COPD are not alpha 1-antitrypsin deficient. To define the mechanisms responsible for the development of severe, early-onset COPD unrelated to alpha 1-antitrypsin deficiency, we propose a multidisciplinary study that combines field, laboratory, and analytical approaches. We will assemble a group of 140 pedigrees ascertained through probands with severe, early-onset COPD (without severe alpha 1antitrypsin deficiency) who are referred for lung transplant or lung volume reduction surgery evaluations. We will assess these probands and their relatives with spirometry (including bronchodilator response) and a questionnaire. We will obtain genotyping with highly polymorphic short tandem repeat (STR) markers at 10 cM intervals throughout the genome from the NHLBI Mammalian Genotyping Service; these genotypes will be used to assess for genetic linkage to phenotypes including FEV1, FEV1/FVC, chronic bronchitis, and bronchodilator responsiveness. In chromosomal regions with suggestive linkage from the genome screen, additional STR markers will be tested at 1 cM intervals; multipoint linkage analysis, family-based association studies, and haplotype analysis will be used to narrow the regions likely to contain genetic determinants of COPD-related phenotypes. mRNA levels of genes within these regions narrowed by fine mapping will be compared in lung tissue from early-onset COPD probands and control subjects. The results of this study could identify specific regions of the genome which are likely to contain COPD susceptibility genes and provide candidate susceptibility genes for COPD. Identification of such genetic determinants could provide insight into the biochemical mechanisms causing the variable development of COPD at all ages, allow identification of highly susceptible individuals, and lead to new therapeutic interventions for COPD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ASSESSING THE OCCUPATION BURDEN IN COPD Principal Investigator & Institution: Blanc, Paul D.; Professor of Medicine; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 01-SEP-2000; Project End 31-AUG-2004 Summary: (From applicant's abstract): The aims are to assess the population burden of occupational exposures in the prevalence of chronic obstructive pulmonary disease (COPD) and to estimate the impact of selected occupational risks on the severity of progression of COPD. COPD is common and costly. The contribution of occupational risk factors to its prevalence and progression have not been well characterized. Better delineation of these associations has been identified as a priority area for study in the NIOSH National Occupational Research Agenda. A population sample of the continental United States of those aged 55-75, supplemented by an enriched sample in geographic "hot spots" identified by NIOSH through respiratory diseases mapping, will yield 2120 subjects, of whom 400 will have COPD defined by report of chronic bronchitis or emphysema without asthma. Structured telephone interviews will assess demographics, health status, smoking exposures, and occupational histories. High risk jobs will later be coded using a job matrix system independent of subject report of specific exposures. Two hundred of those with COPD, with over-sampling of those with
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greater severity, will be followed at 12-14 months to assess health status and health services utilization, as well as decrements in quality of life. This study will provide statistically powerful estimates of the occupational association with COPD. We should be able to identify a work-related RR of 1.35 which, coupled with an exposure frequency of 20 percent, would reflect a PAR percent of 6.5 percent. In the longitudinal study component, we should be able to detect a RR>2.1 for selected occupational risk factors as predictors of outcomes occurring in at least 10 percent of the group. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BASIS HYPERPLASIA
OF
LONG-TERM
VIRUS-INDUCED
GOBLET
CELL
Principal Investigator & Institution: Holtzman, Michael J.; Professor; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2007 Summary: (provided by applicant): The long-term goal of this proposal is to understand how respiratory viral infections lead to chronic hypersecretory airway diseases like asthma. The present proposal focuses on new findings related to the role of respiratory viruses in fine development of long-term goblet cell hyperplasia. This focus derives from our studies of mice and mouse tracheal epithelial cells successively defining that paramyxoviral infection produces not only acute bronchiolitis but also triggers a chronic response with airway hyperreactivity and goblet cell hyperplasia lasting at least a year after viral clearance. This chronic response proceeds despite protection from acute airway infammation and hyperreactivity, and in contrast to allergen challenge, the chronic response persists indefinitely and is uninfluenced by IFN-gamma deficiency. Similar to allergen, the chronic response is at least partially prevented by glucocorticoid treatment. The virus-induced chronic response also exhibits genetic susceptibility allowing for the identification of candidate target genes by a combined genetic/microarray strategy. Memory for the chronic response appears to be contained in the adaptive immune system allowing for adoptive transfer in vivo and in vitro. In addition, we find similar phenotypic responses in human subjects with asthma. Thus, we propose that paramyxoviruses cause both acute airway inflammation/hyperreactivity and chronic airway remodeling/hyperreactivity phenotypes (the latter by a hit-and-ran strategy since viral effects persist after clearance). Further, each of these phenols (acute inflammation/hyperreactivity, chronic hyperreactivity, and chronic goblet cell hyperplasia) may be genetically segregated and therefore depend on distinct controls that appear critical for the development of lifelong airway diseases. Accordingly, we have the following specific aims: I. Use a mouse model of bronchiolitis to define how specific candidate genes control longterm virusinduced goblet cell hyperplasia and how immune cells mediate this response. Here, we develop a plan to identify and characterize our first candidate gene, i.e. mouse calciumactivated chloride channel (mCLCA3) as well as a specific immune cell subset, i.e., virus-specific CD8+ memory T cells. II. Use isolated airway epithelial cells to define the molecular basis for how specific candidate genes and immune cells cause goblet cell hyperplasia in coordination with Aim I. III Use healthy and asthmatic subjects in a glucocorticoid treatment-withdrawal model to define the relationship between goblet cell hyperplasia and the status of candidates from Aims I and II. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BIOLOGY OF SUBMUCOSAL GLAND STEM CELLS IN THE AIRWAY Principal Investigator & Institution: Engelhardt, John F.; Associate Professor; Anatomy and Cell Biology; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2002; Project Start 01-MAY-1990; Project End 30-APR-2005 Summary: The identification of airway stem cells is a critical aspect in the development of gene therapies for diseases such as cystic fibrosis (CF). Furthermore, the complexities of disease pathophysiology in CF have suggested that submucosal glands may be important therapeutic targets. One approach to target this region, which is inaccessible from the airway lumen, is to facilitate gene transfer to airway stem cells responsible for submucosal gland development in utero. However, at present little is known about the biology of these stem cell targets in the airway. To this end, we propose to characterize the cellular phenotype of airway stem cells using molecular approaches that evaluate critical aspects of gene regulation important in the formation of submucosal glands. Experiments will attempt to identify and characterize the developmental pathways leading to stem cell commitment in submucosal gland morphogenesis. Such developmental mechanisms likely also play important roles in other hypersecretory diseases such asthma and chronic bronchitis, where submucosal gland hyperplasia and/or hypertrophy occur. Previous studies by this laboratory using retroviral based lineage analysis in the airway have suggested that a pluripotent surface airway epithelial stem cell compartment also has the ability to form submucosal glands. However, relatively little is currently known about the molecular phenotype of these airway stem cells. We will evaluate in detail the regulation of one particular gene, lymphoid enhancing factor-1 (Lef-1), a transcription factor known to regulate cell-fate decisions in other tissues. Recently we showed that activation of Lef-1 gene expression defines an airway progenitor/stem cell compartment at the earliest stages of epithelial commitment to form submucosal glands (ie., epithelial condensation involved in gland bud formation). Using Lef-1 as a molecular marker for this stem cell compartment, we propose to delineate pathways and transcription factors involved in its regulation using ferret and transgenic mouse models of the airway. Detailed analysis of the Lef-1 promoter will be performed using novel in vivo based model systems that include both recombinant gutted adenoviral vectors, as well as more traditional approaches involving transgenic mice. Lastly, this proposal will also attempt to evaluate mechanisms of Lef-1 action in submucosal gland morphogenesis. Of specific interest is the pathway involving wnt activation of beta-catenin, which is known to be a co-factor for Lef-1 in some, but not all, tissues. We will evaluate a possible role for the wnt pathway and beta-catenin in submucosal gland development using a novel airway specific transgenic mouse model expressing Lef-1 mutants incapable of binding with beta-catenin. Ultimately, this project will increase our understanding of stem cell phenotypes in the airway that have pluripotent capacity for submucosal gland development. Such information will undoubtedly be useful in the development of gene therapies targeting airway stem cells and submucosal glands. Additionally, an increased understanding of submucosal gland developmental mechanisms may provide new therapeutic approaches for treating submucosal gland hyperplasia and hypertrophy in hypersecretory diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BTP1000 & THE CLEARANCE OF MUCUS FROM THE LUNGS Principal Investigator & Institution: Yeates, Donovan B.; Research Professor; Biotechplex Corporation 755 Nicholas Blvd Elk Grove Village, Il 60007
12
Chronic Bronchitis
Timing: Fiscal Year 2002; Project Start 15-JUL-2002; Project End 16-OCT-2003 Summary: (provided by applicant): Patients with chronic bronchitis, bronchiectasis, cystic fibrosis, asthmatic bronchitis and asthma have inspissated mucus and plugs of highly viscoelastic mucus. The inability to clear this mucus leads to impaired airway function and gas exchange and consequent morbidity and mortality. Present pharmacological therapies to treat such abnormalities, although widely applied in clinical practice, are inadequate and many have little or no scientific basis. BioTechPlex proposes to demonstrate the mechanisms of action and efficacy of a new therapeutic regime (BTP1000) to hydrate the airways and enhance mucociliary clearance. The specific aim of this Phase I project is to provide the preliminary data to support the novel intracellular mechanisms underlying the rationale for the use of BTP 1000 to increase airway hydration and ciliary beat frequency; factors that can be predicted to increase the clearance of secretions from the lungs. BioTechPlex will utilize its in-depth expertise in the mechanisms governing ion and water transport across epithelium and ciliary activity as well as its advanced technologies for the investigation of these airway epithelial functions. In the Phase II project the mechanisms of action of BTP1000 will be further expanded, validated and shown to substantially increase bronchial mucociliary clearance in dogs with minimal side effects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CD14 AND LPS-INDUCED INFLAMMATION IN CHRONIC BRONCHITIS Principal Investigator & Institution: Peden, David B.; Professor of Pediatrics and Center Direc; Pediatrics; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 29-SEP-2000; Project End 31-AUG-2004 Summary: (adapted from the applicants' abstract) Chronic bronchitis and COPD are characterized by chronic neutrophilic inflammation and is associated with both airway sepsis with gram-negative bacteria. Smoking is a major risk factor for development of these diseases, but only about 20 percent of smokers develop COPD. Endotoxin (ET) from gram- negative bacteria likely plays a significant role in this inflammation. Airway ET may come directly from gram-negative bacteria infecting the airway or from tobacco smoke as this is another rich source of ET. The investigators propose that responsiveness to ET also an important risk factor for development of COPD in smokers. One mechanism by which persons may be more sensitive to ET is by enhanced production of CD14, the primary receptor for ET. CD14 exists in both a cell bound form and as a soluble from in serum and airway secretions. Soluble CD14 in the airway is enhanced by acute allergic inflammation. Additionally, a C/T polymorphism has been identified at the - 159 position of the CD14 promoter gene (CD14 gene). Those persons homozygous for the T allele have been shown to have increased soluble CD14 in serum and CD14 expression on blood monocytes compared to those with CT or CC genotype. The investigators present preliminary data that demonstrates that levels of sCD14 in sputum and CD14 expression on alveolar macrophages prior to challenge with lipopolysacharride (LPS, a form of ET) correlates with neutrophil influx in sputum following inhaled LPS challenge. Also, in the nasal airway, allergen enhances granulocyte response to LPS in a fashion which correlates with local sCD14 levels. The investigators propose to examine the role that CD14 has in determining responsiveness to airway LPS and risk for COPD in smokers. First, the investigators will determine if the level of sCD14 and CD14 on macrophages is increased in volunteers with experimentally-induced and naturally occurring bronchitis and if they have increased
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neutrophil response to LPS. Second, the investigators determine if airway CD14 correlates with PMN response to LPS in normal volunteers. Third, the investigators will determine if airway CD14 levels and LPS response in healthy volunteers with the TT genotype for the CD14 gene is enhanced relative to that in those with the CC and CT genotype. Finally, the investigators will genotype cohorts of COPD patients and healthy smokers to determine if the T allele is a risk factor in development of COPD in those who smoke. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CD40 AND TGFB IN HUMAN LUNG TRANSPLANT CHRONIC REJECTION Principal Investigator & Institution: Mckee, Charlotte M.; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 16-JUL-2001; Project End 01-AUG-2002 Summary: Chronic rejection is the most important clinical problem in human lung transplantation. The underlying causes of this process (which is manifest as obliterative bronchiolitis (OB) in lung transplants) are not completely understood, but host antidonor cellular immunity has been shown to be a key factor. The CD40 costimulatory pathway is critical for optimal cellular immune responses, and evidence suggests that CD40 activity plays a major role in chronic rejection. However, the mechanism(s) by which CD40 facilitates chronic rejection are not known. CD40 signaling can induce the production of TGFbeta, a pro-fibrotic cytokine whose role in chronic rejection and organ fibrosis is well-established, in human B cells. We postulate that CD40-mediated induction of TGFbeta1 by alveolar macrophages (AM), which are important sources of this cytokine in pulmonary fibrosis, represents a mechanistic link between CD40 activity and chronic rejection. We therefore propose to study 1) indices of CD40 activity in tissues from lung transplant patients with OB and from patients with acute rejection (who are at increased risk of developing OB) and 2) the ability of CD40 signaling to induce TGFbeta1 in AM from lung transplant patients. The Principal Investigator has an extensive background in basic immunology and clinical lung transplantation. The research project outlined here will train her to integrate these elements of her background and to approach clinical problems such as chronic rejection with the combined tools of basic science and clinical research. This award will provide her with the training, resources and protected time she needs to establish a successful career as an independent investigator in lung transplant immunology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CHARACTERIZING A 5P-LINKED BHR SUSCEPTIBILITY LOCUS Principal Investigator & Institution: Ober, Carole; Professor; Human Genetics; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-AUG-2005 Summary: (Adapted from the applicant's abstract) Asthma is the most common chronic disease in industrialized nations, affecting >10 million people in the U.S. alone. Familial aggregation and concordance rates in monozygotic twins have suggested a genetic component to asthma. We have been conducting studies on the genetics of asthma and atopy in the Hutterites, a founder population of European origins that practices a communal lifestyle. A genome-wide screen with 564 markers (average spacing 6 cM) was completed in an extended pedigree of 717 Hutterites who were well characterized with respect to asthma, atopy, and related phenotypes. These individuals are
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Chronic Bronchitis
descendants of only 64 ancestors who lived in the early 1700's to the early 1800's. Evidence for linkage with bronchial hyperresponsiveness2 (BHR) by the likelihood ratio test extended over 30 cM on chromosome 5p, with P-values as small as 0.001. Additional evidence for linkage at this same location was evident by the transmission disequilibrium test (P=0.0061). Typing additional markers in this region identified a critical region of 2.4 cM, corresponding to 1.5 Mb of DNA, and a high risk haplotype that is over transmitted to affected individuals. In this application, we propose to characterize the 5p-linked BHR susceptibility locus in the Hutterites by positional cloning and to replicate these findings in outbred, ethnically diverse populations. We will examine single nucleotide polymorphisms (SNPs) spaced about 10 kb apart in each gene, and assess the evidence for over transmission to affected offspring with each SNP and SNP haplotypes. Associations in the Hutterites will be replicated in the outbred samples. The functional effects of associated variants will be assessed by in vitro assays as well as by genotype-phenotype studies in outbred samples that have been evaluated for asthma and atopy phenotypes. Identifying asthma or BHR susceptibility loci may identify novel pathways in asthma pathogenesis, thereby allowing for the development of new therapies and intervention strategies for these common diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHEMOKINE BIOLOGY IN BRONCHIOLITIS OBLITERANS SYNDROME Principal Investigator & Institution: Belperio, John A.; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 15-MAR-2001; Project End 28-FEB-2006 Summary: (Adapted from applicant's abstract) Chronic lung allograft rejection, Bronchiolitis Obliterans Syndrome (BOS) is a chronic process that demonstrates features of dysregulated and aberrant repair of airways. This process of fibroproliferation and deposition of extracellular matrix that ultimately leads to fibro-obliteration of airways, and impaired lung function. In this proposal, the investigators hypothesize that the persistent expression of monocyte chemoattractant protein-1 (MCP-1) during an allogeneic response and recruitment and activation of mononuclear phagocytes expression CC chemokine receptor 2 (CCR2) is a pivotal event that promotes the continuum of acute to chronic lung allograft rejection. Specifically, MCP-1 production, and the recruitment and activation of CCR2 expressing mononuclear phagocytes occurs during acute rejection. Moreover, the persistent presence of MCP-1 in the allograft maintains recruitment and activation of specific populations of mononuclear phagocytes expressing CCR2. These cells have a unique pro- fibrogenic phenotype that promotes fibrogenesis of chronic allograft rejection, BOS. Understanding the interaction between MCP-1 and CCR2 during the continuum of acute to chronic lung allograft rejection, will lead to novel therapies in the treatment and prevention of BOS. This proposal ,will test this hypothesis by performing the following experiments: I) determine the time-course, magnitude of expression, and cellular sources of MCP-1, as correlated to the recruitment of monocular cells expression CCR2 in an orthotopic rat model of acute lung allograft rejection. II) determine the specific contribution of MCP-1 to the pathogenesis of acute lung allograft rejection by a strategy of depletion of MCP-1. III) determine the timecourse of MCP-1 expression, as correlated to the recruitment of mononuclear cells expression CCR2 in a murine model of BOS. B) determine the specific contribution of MCP-1/CCR2 biology to the pathogenesis of BOS by using genetic approaches for deletion of the bioactivity of MCP-1 and/or CCR2. IV) determine if CCR2 expression mononuclear phagocytes are phenotypically profibrogenic (i.e., produce higher levels of
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TGF-beta and PDGF) and promote fibrogenesis during the pathogenesis of BOS. By successfully completing these objectives, the applicants hope to have gained significant insight into the persistence of MCP-1/CCR2 biology that impacts on the continuum and transition of acute lung allograft rejection to BOS. The understanding of this pathobiology will lead to novel therapies in the treatment and prevention of chronic lung allograft rejection, BOS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHEMOKINES IN LUNG TRANSPLANTATION Principal Investigator & Institution: Medoff, Benjamin D.; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2003; Project Start 04-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): With the proposed Mentored Clinical Scientist Development Award the applicant will continue his investigations into basic mechanisms of lung inflammation. After two productive years in this laboratory the applicant remains firmly committed to a career in academic pulmonary medicine. The proposed research will allow the applicant to master a broad range of laboratory techniques in immunology, cell, and molecular biology. The research experience will be supplemented by a program of study of immunology and medical science. The project focuses on the development of inflammation and fibrosis following lung transplantation and the role of chemokines in these processes. After a lung is transplanted there may be several types of injury to the graft, including ischemia-reperfusion injury, acute rejection, and chronic rejection. These immune mediated injuries contribute to the development of scarring of the airways, so called bronchiolitis obliterans (BO). Over 50% of all lung transplants will develop BO after transplantation, and this remains the major cause of morbidity and mortality after lung transplantation. Neutrophils have been shown to be a prominent component of ischemia-reperfusion injury while T lymphocytes are the primary mediators of both acute and chronic rejection. The proposed project will determine which chemokines are produced after transplantation and their contribution to the development of graft injury and subsequent BO. Further experiments will manipulate chemokine or chemokine receptor expression in animal models of lung transplantation to investigate their role in the development of graft injury and BO. The applicant specifically proposes to: (1) investigate the expression of chemokines and chemokine receptors in the lung following transplantation in patients with and without acute rejection and BO; (2) investigate the role of chemokines in the development of ischemia-reperfusion injury in the airways using the murine tracheal heterotopic model of lung transplantation; (3) investigate the role of chemokines in the development of acute airway rejection and the development of BO in the murine tracheal heterotopic model of lung transplantation; (4) develop a novel murine model of airway rejection and BO. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CHRONIC LOCALIZATION
OBSTRUCTIVE
PULMONARY
DISEASE
GENE
Principal Investigator & Institution: Hasstedt, Sandra J.; Associate Professor; Human Genetics; University of Utah Salt Lake City, Ut 84102 Timing: Fiscal Year 2002; Project Start 01-APR-2001; Project End 31-MAR-2004 Summary: (Applicant's Abstract): Chronic obstructive pulmonary disease (COPD) is a slowly progressive disorder characterized by airways obstruction that lasts for at least
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several months. The two major causes of COPD are chronic bronchitis and emphysema. Either disorder may occur with or without airways obstruction, but airways obstruction causes impairment of lung function leading to disability and death. COPD is a major health problem in the United States and throughout the world, consistently ranking among the most common causes of death in the United States. Cigarette smoking is the primary environmental factor that increases the risk of COPD, but other environmental factors have also been implicated. However, despite a well-established role, environmental factors alone do not cause COPD. Symptomatic COPD develops in only 10-20 percent of heavy cigarette smokers, probably those with a genetic susceptibility, although common COPD susceptibility genes have yet to be identified. This project proposes a single specific aim: to localize, within the genome, a COPD susceptibility gene. The strategy proposed is to apply statistical linkage analysis to family data. Pulmonary measurements have already been collected on 159 members of 16 pedigrees and evidence supporting a COPD susceptibility gene in these pedigrees has been obtained from segregation analysis. Each of 11,995 genetic markers, which have already been genotyped on pedigree members, will be tested for evidence of linkage to the inferred COPD susceptibility gene. Evidence of linkage to one or more genetic markers will identify genomic locations of COPD susceptibility genes. The high density of markers will allow fine-mapping of the gene. Successful completion of this gene localization project is the necessary prerequisite for a project to identify and characterize a COPD susceptibility gene. Identifying a gene that when mutated increases the risk of COPD may increase understanding of pulmonary function, as well as allowing genecarriers to be identified and made aware of their susceptibility. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE--EXPOSURE FACILITY Principal Investigator & Institution: Spengler, John; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2002 Summary: The Exposures Facility Core has seven components: 1) Organic chemistry laboratory, 2) Inorganic chemistry laboratory, 3) Microbiology laboratory Particle measurements (aerosol properties) laboratory, 4) Metal analysis laboratory, 5) Radiation laboratory, 6) Inhalation laboratory. The aims of this core are to maintain the analytical equipment, to facilitate quality control/quality assurance programs, to provide staff and Center faculty with flexibility to develop/adopt analytical methods, and to provide training and supervision to students, postdoctoral fellows, and visiting scientists. All laboratories have written standard operating procedures and quality assurance programs, many of which include interlaboratory testing. The organic chemistry laboratory has analyzed breast milk and cord blood samples for PCBs as part of a study of the effect of low levels of PCBs on reproductive outcomes in New Bedford, and this work will be extended to examine reproductive effects of PCBs in a Russian city contaminated by PCBs. They have also participated in several interlaboratory studies. The inorganic chemistry laboratory has developed an annular denuder system and methods for studying acidic aerosols and gases, ammonia, and passive and active ozone samplers. The environmental microbiology laboratory has developed methods for assessing fungi, bacteria, endotoxin and allergens in bulk dust and air samples. The aerosol properties laboratory specializes in the generation and characterization of particles. The laboratory has developed an ambient particle concentrator for use in animal and human exposure studies. Work is currently in progress on determining the partitioning between gas and particle phase of semi-volatile organic compounds. The
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metals/aquatic laboratory has studied samples of metal exposures of workers, in sediments and biota of Boston and New Bedford harbors, and in water along the USMexican border, and arsenic in the toenails of Taiwanese as part of a study of bladder and skin cancer. A future project will study the bioavailability of heavy metals in contaminated marine sediments. The radiation biology laboratory has several unique radiation sources, including an X-ray generator, an high intensity cobalt source, and an irradiation chamber for animals. Members of the Biochemical and Environmental Toxicology and the Radiobiology and Environmental Carcinogenesis Cores have used these devices to produce "feed layers" of cells for studies of the growth of differentiated cells an tissues in vitro and in studies of DNA damage and repair. The inhalation laboratory provides researchers with the facilities and technical expertise to expose animals to various types of air pollutants, including ozone, sulfur dioxide, particles, fly ash, ethylene oxide, and cigarette smoke, and to monitor their pulmonary responses, including ventilatory parameters and pulmonary mechanics, to these exposures. Studies conducted include the examination of various mechanisms or markers of ozone induced lung injury, the role of adhesion molecules and ctytokines in epithelial injury and repair, the role of sensory neuropeptides found in C-fibers in ozone-induced lung injury and altered airway responsiveness, and the use of SO2 exposure to generate animal models of chronic bronchitis. The mechanisms of mortality and morbidity associated with urban exposure to particles is being studies by exposing dogs and rats to concentrated ambient particles. Future plans include evaluation of the role of adhesion molecules in the airway hyper-responsiveness characteristic of ozone exposure, and further work on the development of biomarkers of ozone exposure. Physiologic responses, e.g., measures of ventilation, to inhaled gases or particles can be monitored. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TOXICOLOGY
CORE--RESPIRATORY
BIOLOGY
AND
INHALATION
Principal Investigator & Institution: Brain, Joseph D.; Professor; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2002 Summary: The Respiratory Biology and Inhalation Toxicology (RBIT) Core has as its objective "to understand how breathing results in environmental and occupational lung disease." The core seeks to develop prevention strategies and more effective treatments for pulmonary diseases including lung cancer, asthma, pulmonary fibrosis, and emphysema. The RBIT Core is primarily concerned with the effects of inhaled environmental toxicants on the mammalian pulmonary system. The Respiratory Biology and Inhalation Toxicology Core is involved with five primary lines of investigation. First, they have investigated the mechanisms of particle binding to alveolar macrophages and epithelial cell lines. Their data suggest that the macrophage scavenger receptor system is responsible for the binding of charged particles such as latex beads and titanium dioxide as well as quartz, fly ash and urban air particulates. This system did not appear to be operative in A549 epithelial cell lines. They now wish to pursue studies of the calcium concentration dependency of this binding and inhibition of this binding by scavenger receptor ligands. They have determined that appropriately-raised polyclonal antibodies block particle binding. Thus, they would like to investigate the molecular biology of this further using scavenger receptor knock out mice and expression cloning of blocking antibodies. Lastly , they plan to study the effects of mitochondrial oxidant production on cytokine release upon exposure to quartz versus titanium. The second line of investigation seeks to elucidate the mechanism of the
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epidemiologic finding that mortality of cardiovascular etiology is elevated about 24 hours after peaks in the concentration of urban air particulates (PM10). To carry out these studies they have used the ambient air particle concentrator (a series of virtual impactors) built by Sioutas and Koutrakis, et al. to generate concentrated urban air aerosols from Boston ambient air. Animal models (dogs, rats, and mice) are used that attempt to recreate the susceptibility factors that are associated with mortality during urban air inversions. Included are a chronic bronchitis model, various knock out mice, and dogs with induced cardiac ischemia. The third research interest concerns the physiology and biology of airway hyper-responsiveness. This group has worked extensively with a technique that measures the stiffness of smooth muscle cell cytoskeleton by manipulating and measuring the effects of cytoskeleton-bound ferromagnetic spheres on magnetic fields. This technique allows Respiratory Biology and Inhalation Toxicology Core investigators to test the effects of cytokines or pharmacologic agents on the contractility of airway smooth muscle cells. They are also interested in developing mouse models for allergic inflammation and airway hyperresponsiveness. They describe their fourth area of research interest as the development and application of bioassays for lung injury. For the most part this appears to be an effort to bring published assays into the laboratory s repertoire. Assays include lavage cytokines, enzymes, proteins, and message for several mediators. The last area of investigation described for the Respiratory Biology and Inhalation Toxicology Core is studies of the molecular mechanisms of pulmonary inflammation. In this work the investigators are considering signal transduction pathways for lung cell adhesion and the dynamics of neutrophil migration into the lung. They are also investigating the cells and chemokines that trigger the release of reactive oxygen species. In particular, they have studied rat MIP-1 alpha and MIP-2, a neutrophil chemotactic chemokine. Within these research studies is evidence of collaboration between the Respiratory Biology and Inhalation Toxicology Core and several other cores and facilities within the Center. Most notable are the Environmental Epidemiology Research Core and the Toxicology Research Core although there is reference to the Occupational Health Core and the Environmental Sciences and Engineering Core as well. The Respiratory Biology and Inhalation Toxicology Core investigators rely on a number of facilities for equipment and expertise. A central molecular biology laboratory provides nucleic acid and protein sequencing, PCR, in site hybridization and immunocytochemistry. Tissue and cell culture facilities are maintained within the Physiology Program. The Bioimaging Core provides laser scanning, confocal microscopy and morphometrics capabilities. The two electron microscopy laboratories offer scanning and transmission electron microscopy with electron specrtoscope imaging capabilities. An inhalation toxicology laboratory has three 1m3 Lucite chambers and two 100 l Lucite chambers. They are primarily set-up for the generation of gases (ozone and So2) and for concentrated Boston ambient air particles. The Respiratory Biology and Inhalation Toxicology Core is equipped with devices for blood and gaseous phase gas analysis and devices for respiratory mechanics and electrophysiology. Lastly, the core has developed a device for magnetometry in order to study changes in cytoskeletal stiffness. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EPIDEMIOLOGIC STUDIES OF LUNG CANCER RISKS IN NSAID USERS Principal Investigator & Institution: Zheng, Wei; Professor; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2002
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Summary: (provided by applicant): Cumulative evidence from in vitro and animal studies suggests that the enzyme cyclooxygenase-2 (COX-2) is important in the development and progression of lung cancer. Epidemiologic studies evaluating the association between the use of aspirin (an inhibitor of COX-2) and the risk of lung cancer have been conflicting, and no study has been conducted to evaluate non-aspirin nonsteroidal anti-inflammatory drugs (NSAIDs). Using pre-recorded drug prescription databases of the Tennessee Medicaid program and North Jutland County of Denmark, we propose to conduct two studies in these populations to examine the effect of NSAID use on the risk of lung cancer. The first is a retrospective cohort study of over 10,000 enrollees of the Tennessee Medicaid Program who were diagnosed with chronic obstructive pulmonary diseases (COPD) during the period of 1980 to 2002. The second is a population-based, retrospective cohort study of over 150,000 users of NSAIDs in the general population of North Jutland County during the period of 1991 to 2002. Within the Danish cohort will be a nested case-control study of 350 cases and 700 controls, in which relevant information will be obtained on over the counter (OTC) analgesic use, as well as cigarette smoking and other potential confounding factors. The two studies proposed here complement each other and provide for an international comparison of NSAIDs as possible lung cancer chemoprevention agents. Because the data on NSAID use have already been collected, the studies will be very cost-efficient. More importantly, the use of pre-recorded pharmacy records minimizes potential errors in exposure assessment and provides a major advantage over existing cohort studies in evaluating the potential chemopreventive effect of NSAIDs. Given the high incidence and mortality of lung cancer and high prevalence of NSAID use, the results from our studies may have important public health implications in lung cancer prevention, and could set the stage for future randomized trials of COX-2 inhibitors in cancer prevention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EPITHELIAL CELL RESPONSE TO H.INFLUENZAE IN THE AIRWAY Principal Investigator & Institution: Look, Dwight C.; Professor; Internal Medicine; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2002; Project Start 20-SEP-2000; Project End 31-JUL-2004 Summary: (adapted from the application): Inflammation of the airway epithelium is often required for effective innate defense against microbes, and epithelial cells provide critical biochemical signals that regulate this response. One major mechanism that epithelial cells in the airway use to participate in the inflammatory response is through regulation of leukocyte trafficking and/or activation by expression of intercellular adhesion molecule-1 (ICAM-1). ICAM-1 serves as a ligand for leukocyte beta2-integrins and thereby mediates epithelial-leukocyte interactions that may allow for "appropriate" inflammatory responses (e.g., to a respiratory bacterial infection) or "inappropriate" responses (e.g., airway inflammation in cystic fibrosis). This proposal focuses on Haemophilus influenzae, which frequently colonizes human respiratory mucosa and often produces respiratory tract disease, particularly in patients with chronic bronchitis, bronchiectasis, and cystic fibrosis. The specific aims of this proposal are based on four observations regarding airway epithelial cell ICAM-1 expression in response to H. influenzae: 1) H. influenzae induces airway epithelial cell ICAM-1 expression in vivo and in vitro; 2) ICAM-1 expression is required for efficient bacterial clearance in a murine model of airway infection with H. influenzae; 3) increased ICAM-1 expression can be initiated by epithelial cell interaction with a constitutive molecule on the bacterial cell surface; and 4) airway epithelial cell interaction with H. influezae results in
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generation of soluble ICAM-1 inducing activity containing a novel mediator(s) of ICAM1 expression. Based on these observations, they hypothesize that direct induction of specific epithelial genes (such as ICAM-l) allow for rapid targeting and/or activation of neutrophils and other leukocytes at sites of H. influenzae infection, resulting in efficient innate defense in the airway. Accordingly, there are two specific aims. 1) Define mechanisms for induction of epithelial cell ICAM-1 expression by H. influenzae. This aim will take advantage of in vitro coculture models of epithelial cell interaction with bacteria. Definition of mechanisms for ICAM-1 gene activation in response to H influenzae will be accomplished by analysis of ICAM-1 promoter function and identification of mediator molecules. This latter refers to the observation that airway epithelial cells challenged with H. influenzae release a novel soluble factor into the medium capable of eliciting ICAM-1 in naive epithelial cells. 2) Determine functions of ICAM-1 in defense against H. influenzae infection. This aim will take advantage of in vivo murine models of airway infection by bacteria. The functions of ICAM-1 will be determined by examining ICAM-1 expression, leukocyte recruitment and function, and bacteria clearance under conditions that allow for manipulation of airway defense factors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FUEL OIL ASH AND HUMAN HEALTH Principal Investigator & Institution: Christiani, David C.; Professor; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02115 Timing: Fiscal Year 2002 Summary: Population-based epidemiologic studies of communities in the United States have revealed a consistent association between ambient particulate air pollution and increases in morbidity and mortality. The observed increases result from both respiratory and cardiovascular diseases for subjects over age 65. These ambient exposures are to levels of particulates many times lower than occupational exposures faced by workers in a variety of industries, including manufacturing, construction, transportation and electric-power generation. The objective of this proposal is to investigate the role of occupational exposure to particulates in the development of respiratory and cardiac responses in boilermakers with and without chronic bronchitis. We will employ a detailed continuous-exposure assessment to PM2.5 with repeated measures of biologic and physiologic markers of response. Specific hypotheses to be tested will include: (1) occupational exposure to fuel-oil ash particulates and associated metals induce airway inflammation as reflected in decreases in peak flow (PEFR) and FEV1; (2) particulate exposure and associated metals will result in acute changes in cardiovascular function, as reflected in changes in heart rate, heart-rate variability and blood pressure; (3) particulate metal exposure will result in increased serum fibrinogen levels, a known risk factor for cardiovascular disease; and (4) chronic bronchitis predisposes exposed workers to changes in cardiac function. The experimental approach will be an epidemiologic study employing a prospective, repeated measures design assessing several biologic parameters in relation to exposure. The expected results will clarify the relationship between exposure to oil-combustion ash metals and human cardiopulmonary responses in both normal and chronic bronchitic populations. Clarification of such exposure-response relationships will have important implications for preventive efforts aimed at reducing morbidity and mortality form exposure to respirable particulates and their associated metals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IL-12 P80 MEDIATED AIRWAY INFLAMMATION Principal Investigator & Institution: Walter, Michael J.; Assistant Professor; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2006 Summary: (provided by applicant): Asthma is characterized by an inappropriate immune response manifested as enhanced accumulation of immune cells in the airway. In general, the immune response has been divided into innate and adaptive components, and recent evidence indicates the innate immune response generates inflammatory mediators that provide critical immunomodulatory signals to the adaptive immune system. In the particular context of the inflammatory response to inhaled materials, we have proposed the airway epithelial cells represent an ideal candidate to act as a primary sentinel site in innate immunity. This possibility was derived from observations that these cells express a network of immune-response genes that provide critical immunomodulatory and biochemical signals for immune cell influx, activation, and retention in the airway. The current proposal is based on several novel findings related to a member of the interleukin (IL)-12 family, called IL-12 p80 (p80). We identified the airway epithelial cell as a novel cellular source for p80 production following cytokine administration, infection with Sendai virus, and in subjects with asthma. Furthermore, Sendai viral infection of mice that lacked another IL-12 family member (IL-12 p35) overproduced p80 and displayed inappropriate inflammation characterized by enhanced accumulation of macrophages in the airway. Interestingly, in asthma subjects, but not normal or chronic bronchitis patients, we again found p80 overproduction that correlated with enhanced macrophage accumulation. Further studies demonstrated p80 functions as a macrophage chemoattractant and the IL-12 receptor beta 1 chain (IL-12Rbeta1) is necessary and sufficient to generate this p80dependent chemotactic response. Taken together, our results associate p80 overproduction with excessive viral and asthmatic inflammation, new functional consequences of p80 production in vivo, and p80-dependent immunomodulatory properties, such as macrophage chemotaxis, that are mediated through IL-12Rbeta1 signaling. Accordingly, the aims of this proposal are to define p80-dependent macrophage accumulation following SdV infection and characterize the proteins that mediate this response. In addition, we will define the structural components of IL12Rbeta1 that mediate p80-dependent chemotaxis. These studies will provide insight into the pathogenesis of inappropriate viral and asthmatic airway inflammation, and exploitation of this knowledge will provide the framework to develop selective regulators of p80 function in order to modulate this inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IMMUNE MECHANISMS OF REJECTION IN HUMAN LUNG ALLOGRAFTS Principal Investigator & Institution: Mohanakumar, Thalachallour; Professor; Surgery; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 01-AUG-1996; Project End 31-JUL-2004 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INFLUENCE OF CRANBERRY ON PLAQUE-RELATED DISEASES Principal Investigator & Institution: Koo, Hyun; Eastman Dentistry; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627
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Chronic Bronchitis
Timing: Fiscal Year 2004; Project Start 01-JAN-2004; Project End 30-NOV-2006 Summary: (provided by applicant): Dental caries is the most common oral infectious disease that afflicts humans. More than 95% of all adults have experienced this disease. It is more common than asthma, hay fever or chronic bronchitis in 5-17 year old children. The American public spends close to $40 billion per year to treat this disease or its consequences. Dental caries results from the interaction of specific bacteria with constituents of the diet on a susceptible tooth surface. Dental plaque accumulation is the first clinical evidence of this interaction; dental plaque is a biofilm which is comprised of a population of bacteria growing on the tooth surface enmeshed in a polysaccharide matrix. Acid can be formed rapidly by acidogenic bacteria, such as Streptococcus mutans, within the matrix and its persistence results in dissolution of the tooth. Furthermore, plaque is also the major aetiological factor in gingivitis. Cranberries, like other natural products, harbor a plethora of biological compounds such as flavonoids (e.g. quercetin and myricetin), phenolic acids (benzoic acid), anthocyanins, condensed tannins, and others. We have shown that many of these substances can: (i) inhibit enzymes associated with the formation of the plaque polysaccharide matrix, (ii) block adherence of bacteria to surfaces, (iii) prevent acid formation, and (iv) reduce acid tolerance of cariogenic organisms. For example, quercetin and myricetin are effective inhibitors of glucosyltransferases (GTFs), enzymes responsible for the synthesis of glucans; glucans synthesized by GTFs mediate the adherence and accumulation of cariogenic streptococci on the tooth surface. Weak acids, such as benzoate (benzoic acid), affect the acid production by S. mutans and have been shown to reduce dental caries in rats. We propose a comprehensive plan to explore the influence of cranberry on many of the biological aspects involved in the pathogenesis of dental plaque formation and caries. We also propose to examine the ability of cranberry to prevent or reduce caries in our well-proven rodent model and to investigate the effects of cranberry on plaque formation and gingivitis in vivo. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INHALED PARTICLE CHARACTERISTICS AND EARLY LUNG EFFECTS Principal Investigator & Institution: Beckett, William S.; Professor; Environmental Medicine; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 01-JUN-2000; Project End 31-MAY-2004 Summary: (Adapted from the Investigator's Abstract) Chronic obstructive pulmonary disease (COPD) is a disabling condition produced by chronic bronchitis (airway inflammation and mucus hypersecretion) and emphysema (loss of alveolar surface area). Epidemiologic studies of the workplace have consistently shown an excess of COPD associated with dusty work environments, yet only a few substances (coal, silica, cadmium) causing COPD in the workplace have been characterized based on chemical composition and respirable particle size. These findings suggest that the much broader range of workplace dusts may in certain conditions contribute to COPD based on characteristics other than chemical composition alone. Pulmonary inflammation plays a role in early events leading to COPD. Particles less than 10 micron aerodynamic diameter are considered to be able to penetrate the upper airways and reach the respiratory tract, and are thus designated as being in the respirable range. Ambient fine particles (<2.5um) consist of two fractions: ultrafines (0.01 to 0.1 um) and accumulation mode particles (0.1 to 1.0 um). Recent studies of ambient particulates indicate that ultrafine particles may be more harmful than other fine particles on an equal mass exposure basis. In animal models, ultrafine particles have a higher alveolar deposition
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fraction, translocate more easily from the airways to the interstitium, induce greater activation of macrophages and cytokine release, and cause greater impairment of macrophage clearance function.One reason for the greater toxicity of equal masses of these smaller particles is their much greater surface area. We hypothesize that the size of inhaled fine particles, in addition to their chemical and other physical characteristics, plays a critical role in determining occupational health effects. To test this we will study early lung and systemic inflammatory responses as well as cardiac effects in adults after carefully controlled inhalation exposure to ultrafine and accumulation mode zinc oxide, a particle we have previously characterized for the dose-response relationship of its short term pulmonary and systemic inflammatory effects. Studies will be conducted in the Environmental Exposure Facility of the Adult General Clinical Research Center. We will compare ultrafine to larger, accumulation mode particles (on an equal mass exposure basis) in their ability to produce symptoms, fever, markers of airway inflammation, antioxidants, systemic acute phase proteins, and alterations in the blood clotting cascade, cytokine release, heart rate, rhythm, and repolarization. We anticipate that the results will help to determine whether there are differential effects for equal mass exposures to fine particles of different size fractions in the pathogenesis of COPD Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INHIBITION OF MUCIN SECRETION IN MURINE MODEL OF ASTHMA Principal Investigator & Institution: Parikh, Indu; Biomarck Pharmaceuticals, Ltd 4364 S Alston Ave Durham, Nc 27713 Timing: Fiscal Year 2003; Project Start 29-SEP-2003; Project End 28-FEB-2004 Summary: (provided by applicant): Hypersecretion of mucus into the respiratory airways is a major factor in several lung diseases, including chronic bronchitis, asthma, cystic fibrosis, and bronchiectasis. Despite the obvious medical importance, mechanisms that regulate production and secretion of airway mucus have not been elucidated fully, and, relatedly, there presently are no effective therapies to control excess mucus secretion in disease, and very few potential therapeutic targets. In previous NIH-funded research from the laboratories of the scientific consultants, a key molecule in the secretory pathway in human airway goblet cells was described. This molecule, MARCKS protein (Myristoylated Alanine-Rich C Kinase Substrate) plays a major role in regulating secretion of mucus in well-differentiated human airway epithelial cells in vitro. In the course of these studies, we developed a peptide to inhibit the function of MARCKS. The peptide corresponds to the N-terminal region of the MARCKS molecule. The peptide, named the MANS peptide, inhibits secretion of mucus by normal human bronchial epithelial (NHBE) cells in tissue culture in response to exogenous stimulation. A control peptide, consisting of the same N-terminal amino acids, but arranged in random order, has no effect. In the present application, we wish to determine if this peptide, instilled intratracheally into asthmatic mice that secrete excessive amounts of mucus can, similar to its effects in vitro, inhibit mucus secretion in vivo. If successful, these studies will be expanded in Phase II to include additional species, efficacy and toxicity studies, and research to optimize peptide solubility and stability; steps necessary for commercial development. The long-term goal is to develop a novel treatment that reduces mucus hypersecretion in the respiratory tract by directly blocking a step in the intracellular secretory pathway. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INHIBITORS OF PROTEOLYTIC ENZYMES Principal Investigator & Institution: Groutas, William C.; Distinguished Professor; Chemistry; Wichita State University Wichita, Ks 672600007 Timing: Fiscal Year 2002; Project Start 10-DEC-1997; Project End 30-NOV-2005 Summary: (provided by applicant): Chronic obstructive pulmonary disease (COPD), a disease characterized by airflow obstruction due to chronic bronchitis and emphysema, affects more than 16 million Americans and is currently the fourth most common cause of death. COPD is continuing to increase in both prevalence and mortality, with the cost of care estimated to be approximately $24 billion/yr. It is generally accepted that COPD is a multifactorial disease the pathophysiology of which is associated with in influx of neutrophils and other phagocytic cells to the lungs, and the subsequent release of an array of proteases, leading to an imbalance between the levels of the proteases and their endogenous protein inhibitors. This imbalance results in poor regulation of the activity of these enzymes, which then degrade the major components of the extracellular matrix, ultimately leading to the onset of disease. It is hypothesized herein that agents capable of regulating selectively the activity of the renegade enzymes, thereby re-establishing a protease-antiprotease balance, are of value as probes for delineating the precise role of a particular protease in COPD, and as potential therapeutic agents. Thus, the specific aims of the proposed research are (a) structure-based design and synthesis of selective inhibitors of various proteases implicated in COPD based on an array of heterocyclic scaffolds. This aim includes the formulation and validation of a general strategy related to the design of selective inhibitors of (chymo)trypsin-like mammalian, viral and bacterial proteases; (b) structure-based design and synthesis of two novel and general classes of inhibitors of serine, cysteine and metallo-proteases; (c) design of a novel class of mechanism-based inhibitors of serine proteases that are postulated to inactivate a target enzyme via an unprecedented enzyme-induced 3-aza Grob fragmentation process and, (d) biochemical and structural studies aimed at determining the inhibitory activity, enzyme selectivity and mechanism of action of the inhibitors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OF OXIDANT-INDUCED CHRONIC BRONCHITIS Principal Investigator & Institution: Forteza, Rosanna M.; Assistant Professor; Medicine; University of Miami-Medical Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2007 Summary: (provided by applicant): Mucus hypersecretion, goblet celt hyperplasia and metaplasia as well as submucosal gland hypertrophy are pathophysiological and histological hallmarks of chronic bronchitis. The activation of epidermal growth factor (EGF) signaling is believed to be responsible for many of these morphological changes of the airway epithelium. Cigarette smoke, the major cause of chronic bronchitis in human subjects, has also been demonstrated to induce mucin secretion and mucous cell hyperplasia, at least in part, via oxidative stress and EGF signaling. EGF is expressed in the airways, stimulates the EGF receptor (EGFR) and, as shown by us, is made from proEGF through cleavage by tissue kaltikreJn (TK). We have also shown that TK is secreted by submucosal glands together with hyaluronan, which inhibits the activity of TK. Hyaluronan also immobilizes bronchial TK at the epithelial surface, creating a pool of readily available, yet inactive TK at the airway surface. Reactive oxygen species (ROS) can cleave hyaturonan, thereby releasing activateded TK. In chronic bronchitis, ROS and active TK are elevated in the airway compared to normal subjects, possibly due to continued degradation of hyaluronan by ROS. We hypothesize that the increased
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availability of active TK in these conditions is a critical link between oxidative stress and EGF-mediated airway mucous cell hyperplasia. This proposal will test the hypothesis that ROS-mediated goblet cell metaplasia and submucosai gland celt hyperplasia occurs through a multi-step cascade beginning with hyaturonan degradation (initiation step) that results in sustained release of activated TK (priming step) and thereby increased availability of mature EGF (activation step) that in turn activates EGFR (signaling step). The specific aims are: 1) to confirm and extend our preliminary in vitro observations that ROS degrade epithelialbound hyaluronan and thereby release active TK that in turn cleaves pro-EGF to activate EGFR (proof of concept in culture); 2) to evaluate hyaluronan degradation, TK activation and pro-EGF processing in airways obtained from patients with chronic bronchitis (proof of concept in human disease); and 3) to examine whether TK-mediated pro-EGF cleavage regulates submucosal gland cell proliferation (relevance of concept). The proposed experiments will thus examine a new link between oxidative stress and chronic bronchitis and may identify new approaches to prevent or even reverse such changes in the airway mucosa. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MESENCHYMAL STEM CELL HOMING TO THE LUNG IN EMPHYSEMA Principal Investigator & Institution: Welsh, David A.; Medicine; Louisiana State Univ Hsc New Orleans New Orleans, La 70112 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 30-JUN-2007 Summary: (provided by applicant): Chronic Obstructive Pulmonary Disease (Chronic Bronchitis & Emphysema) is a leading cause of morbidity & mortality in the United States. Emphysema is histologically defined as the destruction of alveolar walls without significant fibrosis. Regeneration of alveoli in the emphysematous lung should improve pulmonary function and lessen the burden of this common disease. Marrow Stromal Cells (MSCs) are pluripotent cells that can be harvested from adult bone marrow and can potentially be used in tissue repair. The currently achievable, low levels of engraftment in the lung are unlikely to result in clinically significant improvements in pulmonary function. Therefore this proposal focuses on enhancing recruitment and engraftment of MSCs to the lung. This proposal will test the hypothesis that population of "stem sites" in the alveolar wall with bone marrow-derived stromal cells will allow "neo-alveolarization" to occur in the emphysematous lung with restoration of alveolar morphology and function. The 1st specific aim of the project will confirm the hypothesis that homing of MSCs to the lung is increased in the elastase-induced rat model of emphysema. Administration techniques will be optimized. These interventions will be assessed by transplanting MSCs harvested from male rats into female rats previously treated with intratracheal elastase and quantitating engraftment by chimerism of the X& Y-chromosomes. Engraftment will be confirmed by fluorescent microscopy (of EGFPtransgenic MSCs), immunohistochemistry & FACS analysis. The 2nd specific aim investigates the expression of chemokine receptors on MSCs and chemokine ligands by the injured lung. Specific aim 3 will expand on this by exploring the effects of chemokines on MSC migration in vitro and lung recruitment in vivo by over expression of ligand through tetracycline-regulated gene therapy techniques. Finally, in Specific Aim 4 the benefits of enhancing recruitment to the lung will be defined by assessing the morphologic and functional impact of MSC transplantation. These studies will expand our understanding of the biology of MSCs & methods to improve recruitment to the lung, hopefully leading to novel therapies for emphysema. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MUC4 MUCIN AND AIRWAY EPITHELIAL REGENERATION IN COPD Principal Investigator & Institution: Voynow, Judith A.; Associate Professor; Pediatrics; Duke University Durham, Nc 27710 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): In chronic obstructive pulmonary diseases such as chronic bronchitis, and in cystic fibrosis, the airway epithelium is constantly exposed to neutrophil elastase (NE), an inflammatory protease. The cellular response to NE dictates the balance between epithelial injury and repair. A critical factor in this balance is the activation of the epidermal growth factor receptor (EGFR), a member of the ErbB receptor tyrosine kinase family. Activation of EGFR requires homo- or heterodimerization of the receptor. A major EGFR heterodimerization partner in airway epithelial cells is ErbB2. To date, the only ligand known to activate ErbB2 is MUC4. MUC4 is a major membrane-tethered, respiratory tract mucin with epidermal growth factor (EGF)-like domains. We have made four key observations supporting a critical role for MUC4 in activating the airway epithelial response to NE: (1) NE acts on airway epithelial cells to enhance MUC4 mRNA stability and increase MUC4 protein levels. (2) NE induces tyrosine phosphorylation of EGFR. (3) NE stimulates proliferation of normal human bronchial epithelial cells in serum-free and EGF-free media. 4. MUC4, ErbB2 and EGFR colocalize in injured superficial airway epithelial cells in vivo. These observations support the hypotheses that NE triggers a molecular cascade of events in airway epithelial cells by inducing the production of MUC4, a key regulatory molecule in the cascade, activating ErbB2, and thereby promoting the heterodimerization/activation of EGFR. EGFR activation is a critical prerequisite for epithelial proliferation. The Specific Aims to be tested in this proposal are: (1) To determine whether NE induces MUC4activation of the ErbB2/EGFR receptor tyrosine kinase cascade, resulting in epithelial cell proliferation. (2) To identify the RNA stability domains and RNA-binding proteins regulating NE-induced expression of MUC4, a key molecule in this signaling cascade. (3) To determine the relevance of these signaling pathways in mediating epithelial proliferation in vivo in chronic bronchitis and cystic fibrosis. Our ultimate goal is to use information from this project to identify new biologic targets for rational therapies to induce normal airway epithelial proliferation and differentiation following injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NKP608 CAPSULES IN ADULT PATIENTS WITH CHRONIC BRONCHITIS Principal Investigator & Institution: Mcfadden, Edward R.; 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: Specific Aims and Hypothesis: The purpose of this study is to identify if the administration of NKP 608 decreases sputum production and improves the clinical symptoms of chronic bronchitis. The primary experimental objective is to compare the effects of placebo and four daily doses (0.1mg, 1mg, 5mg, 20mg) of NKP 608 upon the amount of sputum that can be induced by hypertonic saline. The secondary experimental objectives are to evaluate the effect of NKP 608 on: health related quality of life and clinical signs and symptoms of chronic bronchitis, the safety and tolerability compared to placebo, and population pharmacokinetics in a sample trial population. This study will employ a multiple-center, randomized, double-blind, placebo-controlled, parallel group design. Patients will make 6 visits to the investigation site. Subjects must
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have been taking all allowed concomitant medications without change for at least 2 weeks prior to screening. Subjects with chronic bronchitis that have a forced expiratory flow rate (FEV1) is greater than or equal to 35% of predicted and whom have no other unstable disease will be screened for inclusion in the study. Approximately 10-20 ml of blood will be drawn at each visit. Each subject will also undergo a physical exam. The ECG will be repeated on Visit 4 and Visit 6. Lung function will be evaluated by spirometry. Bronchodilator medications will be withheld for a minimum of 6 hrs. prior to testing. Daily diaries will be completed. The study has been closed by the sponsor. 15 subjects were screened, 10 enrolled and 8 completed the study at the site. Data is being compiled by the sponsor and results are not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NOVEL PA1-INHIBITORS OF NEUTROPHIL PROTEINASES Principal Investigator & Institution: Day, Duane E.; Molecular Innovations, Inc. 21315 Hilltop St Southfield, Mi 48304 Timing: Fiscal Year 2003; Project Start 19-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant): Neutrophil elastase and cathepsin G are serine proteases stored within the primary granules of neutrophils. The activation and degranulation of neutrophils at inflammatory sites result in the release of these proteases where they encounter inhibitors that regulate their activity in certain inflammatory conditions. These proteases have been implicated in the pathogenesis of a variety of diseases. One example of an inflammatory disease associated with neutrophil recruitment is Chronic Obstructive Pulmonary Disease (COPD). COPD is a slowly progressive and incurable disease of the airways, characterized by a gradual loss of lung function. An estimated 20.9 million Americans are currently affected by COPD; of which 18.3 million suffer from chronic bronchitis and 2.7 million suffer from emphysema. Our Phase I study involved the development of two rationally designed mutants of Plasminogen Activator Inhibitor One (PAI-1). The normal targets for PAl-1 are the plasminogen activators tPA and uPA. The gene for PAl-1 has been altered to produce mutants with altered protease specificity. These two new mutant inhibitors now target neutrophil elastase and cathepsin G. Due to the unique properties of PAl-1, these mutants actually exhibit properties superior to the natural inhibitors Alpha One Proteinase Inhibitor and Antichymotrypsin. Specifically, these mutants both inactivate and facilitate the cellular endocytosis and degradation of the neutrophil proteinases in the presence of polyanionic surfaces such as heparin and DNA, which sequester these very basic enzymes. The DNA that codes for these mutants has been cloned into a E. coli bacterial construct for expression at very high levels, and a patent pending method for the purification of PAl-1 will be scaled up in our Phase II study. The Phase II proposal extends and expands our studies to include: improving the properties of the mutants for therapeutic use, further characterization of the performance of the mutants compared with commercially available and endogenous inhibitors in a number of animal models, development of sensitive and specific immunoassays for neutrophil elastase and cathepsin G and, a study to examine the large scale production of the PAl-1 mutants using a rapid patent pending purification process. Destructive lung diseases are a major cause of morbidity in the U.S. We believe that these mutants can be developed into therapeutic agents for the treatment of a variety of inflammatory diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ORAL LY333013 AND METHOTREXATE DRUG INTERACTIONS STUDY Principal Investigator & Institution: Branch, Robert A.; Professor and Director; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002 Summary: This is a two-part study (A&B) designed to evaluate the safety and tolerability of commitant LY333013 and methotrexate administration in rheumatoid arthritis patients. Each part of this multicenter study will be conducted independently and will consist of a single blind, placebo controlled, randomized two period crossover. LY333013 is a prodrug of LY315920 which is a potent inhibitor of human non-pancreatic secretory phospholipase A2 (sPLA2). LY333013 is being developed for oral administration in patients with chronic inflammatory conditions such as rheumatoid arthritis, osteoarthritis, asthma and chronic bronchitis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PHARMACOKINETICS OF GREPAFLOXACIN & CIPROFLOXACIN IN LUNG Principal Investigator & Institution: Bascom, Rebecca; Professor; Pennsylvania State Univ Hershey Med Ctr 500 University Drive Hershey, Pa 170332390 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2002 Summary: The purpose of this study is to determine the concentration of the antibiotic Grepafloxacin (Raxar) or Ciprofloxacin (Cipro) in the lung after taking a single dose. Both drugs are used for treating lung infections such as pneumonia and acute exacerbations of chronic bronchitis caused by bacteria that are resistant to many antibiotics. The greater the amount of antibiotic that is deposited at the site of the infection, the faster the bacteria is eliminated and the course of treatment is shorter. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PRENATAL TOBACCO SMOKE AND EXPRESSION IN AIRWAYS Principal Investigator & Institution: Van Winkle, Laura S.; Vet Anatomy/Physiol/Cell Biol; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 956165200 Timing: Fiscal Year 2004; Project Start 01-MAY-2004; Project End 31-MAR-2007 Summary: (provided by applicant): Metabolism is a key step in eliminating xenobiotics from the body. Despite the fundamental importance of metabolism in determining the potency of contaminants and carcinogens, little is known about the influence of exposures early in life on the adult expression of these systems, particularly in females. Environmental tobacco smoke (ETS) is one of the most ubiquitous sources of pulmonary exposure to known human carcinogens. Widespread exposure of children to ETS is supported by the fact that as many as 85% of children have detectable levels of cotinine in their blood. Yet the effect of early life exposure on adult onset lung diseases such as cancer has received limited attention. We propose to investigate the effect of pre and post-natal ETS exposures on the expression of genes for metabolism and detoxification enzymes in the target organ for airborne carcinogens, the lung. ETS toxicity is of interest in the female population because women develop lung cancer earlier and after less cigarette exposure than men. We propose to investigate female specific alterations in gene expression in the airways. We will examine the effects of ETS exposures on the lung by comparing the gene expression profiles and histopathology of samples obtained
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from female mice exposed to well characterized aged and diluted side stream tobacco smoke with those from filtered air control mice. The proposed studies will use microarray approaches to define, at the cellular level, the occurrence and persistence of altered gene expression in mice exposed either prenatally or both pre and postnatally to side stream cigarette smoke. We will use an experimental approach that identifies changes in genes as well as pathobiology specific to conducting airways, the site of many changes associated with both smoke exposure and adult onset diseases such as asthma, chronic bronchitis and lung cancer. The central hypothesis is that adult onset lung diseases in females, such as lung cancer and asthma, are related to the ability of the lung to metabolically activate compounds and this is profoundly influenced by the history of prior exposure to such compounds, particularly in utero. We will address the central hypothesis through 3 Specific Aims that will define: 1) the effect of pre and postnatal ETS exposure on gene expression in adult airways, 2) the effect of prenatal ETS exposure on gene expression in infant airways and 3) which changes in infant gene expression persist into adulthood. These studies will thus address the fetal basis of adult diseases of the lung caused by exposure in utero to environmental tobacco smoke. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSPORT
PROTEASE
REGULATION
OF
AIRWAY
CELL
SODIUM
Principal Investigator & Institution: Bridges, Robert J.; Professor; Cell Biology and Physiology; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 30-APR-2006 Summary: (provided by applicant): Electrogenic transepithelial Na+ transport is mediated by an apical membrane, amiloride sensitive Na+ channel (ENaC) and plays an important role in the physiology of a number of organs including the kidney, colon, sa1ivary, and sweat glands as well as the lungs. Sodium transport in the lungs has an important impact on mucociliary clearance, which is impaired in a number respiratory diseases including cystic fibrosis, chronic obstructive pulmonary disease, asthma and acute and chronic bronchitis. Pharmacological modulation of Na+ transport is expected to improve mucociliary clearance in these diseases. In this application, we present results that demonstrate 70 percent of Na+ transport, in primary cultures of human bronchial epithelial cells (HBE), is regulated by a novel extracellular protease-mediated mechanism. We will show that HBE cells express an endogenous protease, prostasin, that we hypothesize is the ENaC channel activating protease (CAP). In addition, we will show that an endogenous protease inhibitor, bikunin, inhibits Na+ transport and this inhibitory effect can be reversed upon washout of the inhibitor or by the addition of exogenous protease. We are convinced this protease/protease inhibitor mediated mechanism represents a paradigm shift in how we view the regulation of ENaC with important basic science and therapeutic implications. Our specific aims are designed to test several hypothesis predicated on a model we have proposed to explain the mechanism of protease/protease inhibitor mediated regulation of ENaC in the airways. The hypotheses we will test include: (i) prostasin is the HBE CAP, (ii) that prostasin directly binds to ENaC and proteolysis one or more of the subunits to cause ENaC activation, (iii) that inactive ENaC is inserted into the apical membrane where it is activated by prostasin and has a short half-life as an active channel before being retrieved and degraded, (iv) that bikunin inhibits prostasin via its Kunitz' domains and (v) that the binding site on ENaC for prostasin is at the Kunitz-like domain in the second cysteine rich domain of the channel. We will use short circuit current measurements,
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fluctuation analysis, site directed mutagenesis protein biochemical and high resolution field emission scanning electron microscopy methods to test our hypotheses. The successful completion of our proposed studies is certain to provide new an important insight about how ENaC is regulated by this novel extracellular mechanism. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF AIRWAY GOBLET CELL MUCIN SECRETION Principal Investigator & Institution: Davis, C William.; Cellular/Molecular Physiology; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2004; Project Start 15-FEB-2000; Project End 31-MAR-2008 Summary: The obstructive pulmonary diseases (OPD), cystic fibrosis, chronic bronchitis, bronchiectasis, emphysema, and asthma, are inflammatory diseases with very different inflammatory cell profiles, cytokine responses, etc; mucin hypersecretion from airway surface goblet cells and submucosal mucous cells represents a singular, shared characteristic. Conceptually, mucin hypersecretion may result from inflammation-driven goblet cell meta/hyperplasia and/or elevated rates of mucin secretion. Although the best long-term treatment for OPDs will likely target the individual causes of inflammation, it is notable that acute relief to OPD patients, generally, could be achieved by selectively inhibiting mucin secretion. Possibly more important, such an inhibitor would help to open mucus-clogged airways to enable efficient, inhalation-based treatment of the underlying disease. Hence, our long-range goal is to study the molecular mechanisms by which mucin granule exocytosis in airway goblet cells is regulated, to identify molecular targets for selective drug therapies. It is well known that goblet cell mucin secretion is regulated by extracellular ATP and UTP acting through the P2Y2 receptor (P2Y2-R), and that the subsequent secretory response is mediated by the phospholipase C pathway through PKC and Ca2+. Yet, our knowledge of the signaling pathways involved in goblet cell regulation is incomplete. For instance, the effects of muscarinic agonists are highly controversial, there are no data relevant to the mechanisms and pathways underlying the regulation of basal mucin secretion from airway goblet cells, and the effects of agents signaling through receptors acting via tyrosine kinase pathways are uknown, though many of them do have metaplastic effects on the airways epithelium. At the molecular level, we know very little of the effectors regulating exocytosis beyond the identities of the intracellular messengers. Hence, we propose a broadly based approach using the primary cultures of human bronchial epithelial cells, airways epithelium from human lungs and genetically manipulated mice rendered metaplastic for goblet cells, and SPOC1 goblet cells to further delineate the intracellular molecular regulation of mucin granule exocytosis from airway goblet cells, and to extend our knowledge of the signaling pathways regulating goblet cell function into new areas involving basal mucin secretion, type I receptor and involvement, and mechanical shear effects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FUNCTIONS
REGULATION
OF
CHEMOKINE
MEDIATED
LEUKOCYTE
Principal Investigator & Institution: Richardson, Micheler R.; Associate Professor; Biochemistry; Meharry Medical College 1005-D B Todd Blvd Nashville, Tn 37208 Timing: Fiscal Year 2002; Project Start 01-JUN-1996; Project End 31-JAN-2007
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Summary: (provided by the applicant): Chemokines are inflammatory mediators of the chemotactic and cytotoxic functions of a large variety of cells including neutrophils, monocytes, eosinophils, basophils and lymphocytes. These functions are initiated through interaction with specific cell surface G-protein coupled receptors (GPCRs). Most chemokines activate more than one receptor on leukocytes. The hypothesis that underlies this application is that since multiple chemokines are present at sites of inflammation, the chemokine receptors activities must be tightly regulated to prevent tissue damage. We have developed a cellular model, a rat basophilic leukemia cell line (RBL-2H3), in which chemokine receptors can be singly or multiply expressed to display many leukocytes activities. These studies have provided striking evidence that these receptors cross-regulate each other?s function at multiple steps. Signal duration and protein kinase C (PKC) activation have been shown to be critical for receptor crossregulation. Studies in phagocytes and mouse models of peritoneal and skin inflammation have shown a complexity of cross-regulation among interleukin-8 (IL-8) and RANTES. This complexity likely reflects the ability of these chemokines to activate multiple receptors in leukocytes. The overall objective of this application is to elucidate the mechanism(s) of cross-regulation among the receptors for IL-8 (CXCR1 and CXCR2) and RANTES (CCR1 and CCR5) and to identify specific molecular targets in the signaling pathways, which modulate their ability to mediate and undergo crossdesensitization. Mechanisms of cross-desensitization will be investigated by determining the role of different protein kinase C (PKC) isozymes in receptor crossphosphorylation. The hypothesis that arrestin-mediated receptor internalization modulate signal duration will also be tested in beta arrestin deficient mice. Chemokines are involved in many acute and chronic inflammatory diseases such as rheumatoid arthritis, emphysema, cystic fibrosis, chronic bronchitis and bronchiectasis and proliferation of tumor malignant melanoma cells. Understanding the molecular mechanisms governing the regulation of chemokine will aid in understanding the control of inflammation as well as the etiology of many inflammatory disorders. These studies will also identify specific targets for the development of therapeutic drugs for the modulation of inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF MUCOUS CELL METAPLASIA IN ASTHMA Principal Investigator & Institution: Tesfaigzi, Yohannes; Staff Scientist; Lovelace Biomedical & Environmental Res Albuquerque, Nm 87108 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2007 Summary: (provided by applicant): Clinical manifestations of asthma result in part from chronic inflammation that leads to mucous cell metaplasia (MCM), the appearance of mucous cells in peripheral airways that are normally devoid of these cells. In a mouse model of asthma, systemic immunization with ovalbumin (OVA) followed by repeated exposures to OVA aerosols initially induces inflammation and MCM, while prolonged exposures cause increase of IFNgamma levels and resolution of MCM. Instillation of IFNgamma in allergen-exposed mice induces expression of Bax, a pro-apoptotic protein, and accelerates the resolution of MCM by causing apoptosis. Mice deficient in Bax or Stat 1, an obligatory signaling molecule for IFNgamma, do not resolve MCM during prolonged exposures to allergen. IL-13 inhibits IFNgamma-induced Bax expression and apoptosis in mucous cells of mice and in normal human bronchial epithelial cells (HBEs). Our guiding hypothesis is that IL-13 induces MCM and counteracts the role of IFNgamma to activate Stat 1 and induce apoptosis through a Bax-mediated pathway in metaplastic mucous cells. In Aim 1, we will determine the pathway by which IL-13
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Chronic Bronchitis
inhibits IFNgamma signaling and Bax mediated resolution of MCM. We will determine whether IL-13 directly inhibits Bax expression or activates Stat 3, which is known to cause expression of anti-apoptotic proteins, Bcl-2 and BcI-lxL. Furthermore, we will determine whether IL-13 requires signaling through IL-4Ralpha and Stat 6 to inhibit IFNgamma-induced Bax expression. In Aim 2, we will determine the pathway by which IFNgamma induces Bax expression in allergen-induced MCM and whether the Baxmediated pathway is essential to resolve MCM. We will investigate whether IFNgamma signals through IFN(R and Stat 1 to induce Bax in allergen-induced MCM and whether IFN( induces surface expression of IL-13Ralpha2 to inhibit IL-13 signaling through Stat 6. We will determine the requirement of Bax in decreasing MCM by instilling IFNgamma in Bax-deficient mice that have allergen-induced MCM. Our preliminary results with human autopsy tissues and bronchial brushings show that Bax is expressed in mucous cells from non-asthmatics and is absent in asthmatics. Therefore, in Aim 3, we will determine whether inflammatory mediators from asthmatics suppress expression of Bax and enhance mucous cell survival. The difference in the percentages of Bax-expressing cells among subjects with asthma, chronic bronchitis, and controls without respiratory diseases will be investigated using autopsy tissues and bronchial brushings. Furthermore, we will determine the effect of bronchoalveolar lavage fluid in inducing MCM and Bax expression in HBEs. These studies will provide new strategies to reduce mucous cell numbers in asthmatic patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF THE STIMULATION OF MUCIN GENE EXPRESSION A Principal Investigator & Institution: Koo, Ja S.; Thoracic Head/Neck Med Oncol; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2002; Project Start 25-SEP-2001; Project End 31-JUL-2004 Summary: (Taken from the Candidate's Abstract) Acute or chronic exposure of environmental insults and toxicants trigger inflammatory pulmonary conditions, resulting in infiltration of inflammatory cells and elevation of inflammatory mediators, and alteration of the integrity and function of the airway epithelium. Hypersecreted visco-elastic mucus causes obstruction of central and peripheral airways in many inflammatory airway diseases such as asthma, cystic fibrosis, chronic bronchitis, and bronchiectasis. Inhibition of over expressed pathophysiologic mucus is one of the major targets for treatments of airway inflammatory disorders. Previously, the candidate has shown that tetinoic acid (RA), a key element required for mucous cell differentiation, mucin production, and mucin gene expression is mediated through retinoic acid receptor alpha. Based on these findings, the candidate hypothesizes that repressing receptor alpha activity will inhibit over expression of mucin gene mRNAs and mucin hypersecretion induced by inflammatory mediators. The specific aims are to clarify: 1) the biochemical mechanisms by which inflammatory mediators increase the expression of mucin gene mRNAs and mucin secretion; 2) the molecular mechanisms by which receptor alpha signaling pathway regulate inflammatory mediators-increased mucin production; and, 3) the molecular mechanisms of a cross-talk between receptor alpha and IL-1 beta signaling pathways. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RESPONSE OF INFLAMMATION PRIMED LUNG CELLS TO PARTICLES Principal Investigator & Institution: Kobzik, Lester; Associate Professor; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2002 Summary: The Problem: Particulates within air pollution are associated with significant morbidity and mortality at commonly encountered ambient concentrations. The biologic basis for their health effects is unknown, but the same epidemiologic studies which reveal particle effects also offer an important clue. Harmful health effects occur most notably among individuals with pre-existing respiratory disease, e.g. chronic bronchitis and asthma, indicating a heightened sensitivity to particle effects within inflammed lungs. Experimentally, we have found that inhalation exposure of animals to "realworld" concentrated ambient particulates (CAPs) prepared via a novel technology causes toxic effects--but only in animals with pre-existing pulmonary inflammation (asthma, SO2, bronchitis), and not in healthy controls. Hypothesis: The central thesis of this proposal is that pre-existing pulmonary disease alters or "primes" the lung's response to inhaled ambient particles, resulting in increased inflammation and health effects. We further postulate that oxidative stress mediated by particulate components is a central mechanism for increased production of inflammatory mediators by "primed" lung cells. Experimental Plan: In specific Aim #1 we will measure in vitro the production of reactive oxygen species, nitric oxide and cyrokines in response to uptake of CAPs by lung marcophages or epithelial cells with or without "priming" by inflammatory mediators (LPS, TNF). We will test our hypothesis regarding oxidant mechanisms of CAPs effects by: 1) measuring oxidant stress in primed and normal lung cells after uptake of CAPs (oxidation of intracellular reporter DCFH; lipid peroxidation); 2) analyzing oxidant components (e.g. SiO2, Fe) in samples of CAPs that vary in inflammatory effects; 3) testing the ability of antioxidants to block cellular responses. In specific Aim #2 we will characterize in vivo the effects of inhaled concentrated ambient particulates (CAPs) on pre-existing inflammatory lung disease using a mouse asthma model. We will test our hypotheses by inhalation exposure of normal and "asthmatic" mice to CAPs, measuring both lung lavage markers of cellular inflammation (total cells, number of eosinophils, cytokine levels) and physiologic tests of airway bronchoconstriction. To complete our study of mechanisms in vivo, we will also measure the effects of antioxidant intervention, both pharmacologic and through use of genetically altered mice. Significance: The proposed studies will determine mechanisms for the effect of air pollution particulates. Such informaiton is critical to public health management of this problem. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF A NEUTROPHIL INTEGRIN IN LUNG INFLAMMATION Principal Investigator & Institution: Sheppard, Dean C.; Professor and Director; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 01-FEB-2000; Project End 30-NOV-2003 Summary: Neutrophils contribute to the tissue injury central to a number of common lung diseases, including acute lung injury, cystic fibrosis and chronic bronchitis. A key step in the development of neutrophil-mediated tissue injury is the recruitment of neutrophils to sites of extravascular injury. Although several of the critical receptors involved in the recruitment of neutrophils have been identified, considerable evidence
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Chronic Bronchitis
suggests that unidentified receptors must participate in neutrophil recruitment, especially recruitment into the lung. Recently, we have identified the integrin alpha9beta1 on human neutrophils, and have found that this integrin together with its close structural relative, alpha4beta1, is critical for neutrophil migration across activated endothelial monolayers in vitro. The central issues addressed in this application are the mechanisms by which alpha9beta1 in the distinct steps of rolling, stable adhesion and endothelial transmigration, we will utilize blocking monoclonal antibodies and neutrophils derived from the bone marrow of alpha9 null chimeric mice. To determine the in vivo significance of alpha9beta1 on neutrophils we will examine neutrophil sequestration, extra-vascular emigration and neutrophil-mediated tissue injury in the lungs and peritoneal cavity in guinea pigs treated with alpha9beta1 blocking antibody and in chimeric mice with alpha9 null neutrophils. We will then utilize cell lines stably transfected with a variety of deletion and chimeric mutant versions of alpha9 to determine the role of specific sequences in the alpha9 and alpha4 cytoplasmic domains in adhesion, migration and endothelial transmigration. Finally we will utilize ch8imeric and mutant forms of alpha9 with defined functional properties to determine the roles of rapid spatial redistribution of integrins and cytoskeletal associations in integrinmediated migration, both in leukocyte and non-leukocyte model systems. These studies should provide insight into key steps in neutrophil recruitment and could lead to the development of novel interventions for the treatment of diseases characterized by neutrophil-mediated tissue injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SMOKE INDUCED MUCIN TRANSCRIPTION AND MITOGENESIS Principal Investigator & Institution: Basbaum, Carol B.; Professor; Anatomy; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 01-AUG-1990; Project End 31-JUL-2003 Summary: The mechanisms by which tobacco smoke cause chronic bronchitis and lung cancer are unknown. Clues are provided, however, by our recent findings showing that smoke directly induces mucin mRNA and mitogenesis in lung epithelial cells and that this is preceded by activation of Src kinase and phosphorylation of the EGF receptor (EGFr). Src kinase inhibitors abrogate smoke-induced EGFr phosphorylation, mucin transcription induction and mitogenesis. EGFr kinase inhibitors abrogate smokeinduced EGFr phosphorylation and mitogenesis but only partially block mucin transcriptional upregulation. This leads us to hypothesize that smoke activates a branched signaling pathway emanating from Src kinase. One arm of the pathway is EGFr-dependent and is sufficient to account for smoke-induced mitogenesis; the other is EGFr-independent and its effects summate with those of the other branch to mediate mucin transcription. The experiments described in this proposal will provide information regarding both the EGFr-dependent and -independent signaling pathways. In experiments described under Specific Aim I, we will identify EGFr-interacting elements of the smoke-signaling pathway leading to (a) mucin induction and (b) mitogenesis. In experiments described under Specific Aim II, we will identify Srcinteracting elements of the smoke signaling pathway leading to (a) mucin induction and (b) mitogenesis. In experiments described under Specific Aim III, we will identify components of smoke responsible for activating (a) mucin induction and (b) mitogenesis. The results of these studies should reveal control points amenable to inhibition by pharmacological agents. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: T CELL CONTROL OF AIRWAY MUCUS PRODUCTION Principal Investigator & Institution: Cohn, Lauren E.; Associate Professor; Internal Medicine; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2004 Summary: Mucus hyperproduction contributes to morbidity and mortality in patients with chronic airway diseases. In asthma, chronic bronchitis and cystic fibrosis, inflammation is believed to stimulate mucus production, despite their different characteristic airway pathologies. We have defined two inflammatory pathways that lead to mucus production, using a murine system we developed to study the inflammatory effects of Th1 and Th2 cells in the respiratory tract. Th2 cells activated in the airways of mice stimulate airway eosinophilia, airway hyperresponsiveness and mucus production; features found in asthmatic patients. We show that mucus induction by Th2 cells does not require IL-4, IL-5, eosinophils or mast cells, but depends on signaling through IL-4Ralpha, the common chain in IL-13 and IL-4 receptors. Thus, it appears that IL-13 stimulates mucus production induced by Th2 cells. We also show that mucus can be induced by a mechanism that is Th2-independent and associated with airway neutrophilia, suggesting some of the features in chronic bronchitis and cystic fibrosis. We present novel studies showing that Th1 cells, through the production of IFNgamma, inhibit mucus production induced by both Th1 and Th2 cells. Furthermore, IFNgamma produced by Th1 cells has the potential to reduce airway pathology in immunotherapy of asthma. Our goals in this proposal are to gain a more complete understanding of the cellular and molecular mechanisms that regulate mucus production. Our aims are to 1) determine the mechanism by which CD4 Th cells stimulate mucus production; 2) determine how airway epithelial mucus production is inhibited by IFNgamma 3) determine the extent of inhibitory effects of IFNgamma on mucus production. Using our established adoptive transfer system in which Th1 and Th2 cells and recipient mice can be independently genetically manipulated, the precise factors important in the control of mucus production will be determined. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THE VASCULAR BIOLOGY OF LUNG PRESERVATION Principal Investigator & Institution: Pinsky, David J.; Professor and Scientific Director; Medicine; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2002; Project Start 01-AUG-1996; Project End 31-JUL-2003 Summary: Nitric oxide (NO) levels plummet precipitously after lung transplantation (LTX), due to quenching by superoxide (O2-) in the reperfusion milieu. This can lead to graft thrombosis, leukostasis, and primary graft failure. In biological systems, however, alternative pathways are often activated when a primary homeostatic pathway fails, to contain the damage. Using a novel porphyrinic sensor capable of specifically detecting carbon monoxide (CO), we show that this diatomic gas which, like NO, binds to and activates heme-containing proteins, is produced at high levels in lungs subjected to ischemic stress at a time when NO levels plummet. CO given to rat LTX donors prior to lung harvest markedly improves posttransplant graft function and recipient survival. Heme oxygenase (HO) type 1, which catabolizes heme to liberate CO in vivo, is induced by ischemic stress. Mice null for the HO-1 gene exhibit exaggerated lung injury in response to ischemia but are rescued from ischemic lung injury by CO inhalation. Mechanistically, CO appears to restore vascular homeostasis by suppressing endothelial cell apoptosis in response to oxidant stress and by preventing ischemic induction of plasminogen activator inhibitor-1(PAI-1), thereby potentiating lysis of thrombus in
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Chronic Bronchitis
postischemic microvessels. These data lead us to hypothesize that lung ischemia or preservation triggers expression of HO-1, which drives CO production to reestablish protective vascular homeostasis. The aims of the current proposal are (1) to elucidate the functional role of endogenous HO-1 and CO in lung ischemia and transplantation; (2) to elucidate the mechanism(s) by which CO protects the ischemic lungs; and (3) to determine whether early HO-1/CO induction may limit the late development of obliterative after LTX. Studies will use orthotopic rat LTX and murine tracheal allograft models, HO-1 and PAI-1 gene-deleted mice (and endothelial cells derived therefrom) with or without reconstitution with CO, and unique CO/NO/O2- porphyrinic sensor technology to describe a novel HO- 1/CO mediated axis of ischemic pulmonary protection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANS-MEMBRANE WATER AND ION MEASUREMENT SYSTEM (TWIMS) Principal Investigator & Institution: Wong, Lid B.; Chief Scientific Officer; Biotechplex Corporation 755 Nicholas Blvd Elk Grove Village, Il 60007 Timing: Fiscal Year 2003; Project Start 30-SEP-2000; Project End 30-JUN-2005 Summary: (provided by applicant): BioTechPlex proposes to develop a Transmembrane Water and Ion Measurement System (TWIMS) to measure miniscule water fluxes across biological membranes in conjunction with their electro-physiological properties. BioTechPlex has accomplished all the objectives proposed in Phase I. A) Developed a novel light source and associated optics for fluorescence photon detection and analysis. B) Integrated the bench optics into a measurement system, tested the system and demonstrated its markedly increased sensitivity for the measurement of transmembrane water fluxes. In this Phase II project, BioTechPlex will integrate the principle and concepts of the electro-optics developed in this Phase I to build an 8-tissue chamber system. To develop a manufacturability prototype of the TWIMS, we will proceed with the development of further innovative technologies. These include: 1) fluorescence detection technology; 2) prototyping of the chambers and tissue holders to accommodate both native epithelia and confluent tissue cultures; and 3) a virtual instrumentation platform for the measurement of luminal to basolateral and basolateral to luminal waters fluxes, potential difference and short circuit current. This multichamber system will be designed to suit the needs of physiologists and pharmacologists, in academia, government and industry. It will be designed for scientific research experiments as well as for use in the drug discovery industry. BioTechPlex plans to market the TWIMS for scientific investigations and drug discovery in fields including but not limited to, 1) respiratory disease such as chronic bronchitis, asthma bronchiectasis and cystic fibrosis; 2) gastrointestinal disease such as diarrhea, cholera infection and severe dehydration; 3) kidney disease such as renal failure; and 4) eye diseases such as dry eye syndrome. 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 3
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
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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 “chronic bronchitis” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for chronic bronchitis in the PubMed Central database: •
Contributions of Loss of Lung Recoil and of Enhanced Airways Collapsibility to the Airflow Obstruction of Chronic Bronchitis and Emphysema. by Leaver DG, Tattersfield AE, Pride NB.; 1973 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=333012
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Pharmacokinetics of [18F]fleroxacin in patients with acute exacerbations of chronic bronchitis and complicated urinary tract infection studied by positron emission tomography. by Fischman AJ, Livni E, Babich JW, Alpert NM, Bonab A, Chodosh S, McGovern F, Kamitsuka P, Liu YY, Cleeland R, Prosser BL, Correia JA, Rubin RH.; 1996 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=163176
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The circulation in patients with chronic bronchitis and emphysema at rest and during exercise, with special reference to the influence of changes in blood viscosity and blood volume on the pulmonary circulation. by Segel N, Bishop JM.; 1966 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=292837
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 chronic bronchitis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “chronic bronchitis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for chronic bronchitis (hyperlinks lead to article summaries):
4
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. 6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A comparative study of clarithromycin modified release and amoxicillin/clavulanic acid in the treatment of acute exacerbation of chronic bronchitis. Author(s): Martinot JB, Carr WD, Cullen S, Heredia Budo JL, Bauer K, MacLeod C, Sanguinetti CM, van Veldhuizen WC; Clarithromycin Once-a-Day Study Group. Source: Adv Ther. 2001 January-February; 18(1): 1-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11512528
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A comparison of gemifloxacin and clarithromycin in acute exacerbations of chronic bronchitis and long-term clinical outcomes. Author(s): Wilson R, Schentag JJ, Ball P, Mandell L; 068 Study Group. Source: Clinical Therapeutics. 2002 April; 24(4): 639-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12017408
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A multinational, multicentre, non-blinded, randomized study of moxifloxacin oral tablets compared with co-amoxiclav oral tablets in the treatment of acute exacerbation of chronic bronchitis. Author(s): Schaberg T, Ballin I, Huchon G, Bassaris H, Hampel B, Reimnitz P; AECB Study Group. Source: J Int Med Res. 2001 July-August; 29(4): 314-28. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11675905
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Acute exacerbation of chronic bronchitis: disease-specific issues that influence the cost-effectiveness of antimicrobial therapy. Author(s): Saint S, Flaherty KR, Abrahamse P, Martinez FJ, Fendrick AM. Source: Clinical Therapeutics. 2001 March; 23(3): 499-512. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11318083
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Acute exacerbation of chronic bronchitis: what is the clinical significance of pathogenic bacteria in sputum cultures? Author(s): Watanakunakorn C. Source: Chest. 2000 December; 118(6): 1523-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11115428
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Acute exacerbations of chronic bronchitis: a pharmacoeconomic review of antibacterial use. Author(s): Morris S, Anderson P, Irwin DE. Source: Pharmacoeconomics. 2002; 20(3): 153-68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11929346
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Acute exacerbations of chronic bronchitis: what role for the new fluoroquinolones? Author(s): Obaji A, Sethi S. Source: Drugs & Aging. 2001; 18(1): 1-11. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11232735
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Airway eosinophilia and expression of interleukin-5 protein in asthma and in exacerbations of chronic bronchitis. Author(s): Saetta M, Di Stefano A, Maestrelli P, Turato G, Mapp CE, Pieno M, Zanguochi G, Del Prete G, Fabbri LM. Source: Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology. 1996 July; 26(7): 766-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8842549
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Airway inflammation and etiology of acute exacerbations of chronic bronchitis. Author(s): Sethi S, Muscarella K, Evans N, Klingman KL, Grant BJ, Murphy TF. Source: Chest. 2000 December; 118(6): 1557-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11115440
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Airway inflammation in nonobstructive and obstructive chronic bronchitis with chronic haemophilus influenzae airway infection. Comparison with noninfected patients with chronic obstructive pulmonary disease. Author(s): Bresser P, Out TA, van Alphen L, Jansen HM, Lutter R. Source: American Journal of Respiratory and Critical Care Medicine. 2000 September; 162(3 Pt 1): 947-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10988111
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Airways inflammation in asthma and chronic bronchitis. Author(s): Humbert M. Source: Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology. 1996 July; 26(7): 735-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8842545
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An open-label, randomized, multicenter, comparative study of the efficacy and safety of 7 days of treatment with clarithromycin extended-release tablets versus clarithromycin immediate-release tablets for the treatment of patients with acute bacterial exacerbation of chronic bronchitis. Author(s): Weiss K, Vanjaka A; Canadian Clarithromycin Study Group on Bronchitis. Source: Clinical Therapeutics. 2002 December; 24(12): 2105-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12581548
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Animal models of chronic bronchitis and their relevance to studies of particleinduced disease. Author(s): Nikula KJ, Green FH. Source: Inhalation Toxicology. 2000; 12 Suppl 4: 123-53. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12881890
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Antibiotic therapy in acute exacerbations of chronic bronchitis. Author(s): Adams SG, Anzueto A. Source: Seminars in Respiratory Infections. 2000 September; 15(3): 234-47. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11052424
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Antibiotic treatment and baseline severity of disease in acute exacerbations of chronic bronchitis: a re-evaluation of previously published data of a placebo-controlled randomized study. Author(s): Allegra L, Blasi F, de Bernardi B, Cosentini R, Tarsia P. Source: Pulmonary Pharmacology & Therapeutics. 2001; 14(2): 149-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11273797
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Antibiotics in the treatment of acute exacerbations of chronic bronchitis. Author(s): Dever LL, Shashikumar K, Johanson WG Jr. Source: Expert Opinion on Investigational Drugs. 2002 July; 11(7): 911-25. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12084002
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Assessing patient outcomes in acute exacerbations of chronic bronchitis: the measure your medical outcome profile (MYMOP), medical outcomes study 6-item general health survey (MOS-6A) and EuroQol (EQ-5D). Author(s): Paterson C, Langan CE, McKaig GA, Anderson PM, Maclaine GD, Rose LB, Walker SJ, Campbell MJ. Source: Quality of Life Research : an International Journal of Quality of Life Aspects of Treatment, Care and Rehabilitation. 2000; 9(5): 521-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11190007
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Association between airway bacterial load and markers of airway inflammation in patients with stable chronic bronchitis. Author(s): Hill AT, Campbell EJ, Hill SL, Bayley DL, Stockley RA. Source: The American Journal of Medicine. 2000 September; 109(4): 288-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10996579
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Asthma, chronic bronchitis and respiratory symptoms among adults in Estonia according to a postal questionnaire. Author(s): Meren M, Jannus-Pruljan L, Loit HM, Polluste J, Jonsson E, Kiviloog J, Lundback B. Source: Respiratory Medicine. 2001 December; 95(12): 954-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11778792
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Azithromycin is effective in patients with chronic bronchitis. Author(s): Kopjar B. Source: The Journal of Antimicrobial Chemotherapy. 2002 September; 50(3): 433-4; Author Reply 434. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12205072
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Bacteria-induced IgE-mediated histamine release: examination of patients with chronic bronchitis (CB) during acute exacerbations. Author(s): Norn S, Jensen L, Kjaergaard LL, Permin H, Skov PS, Espersen F. Source: Agents Actions. 1994 June; 41 Spec No: C22-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7526646
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Bacterial adhesion to oropharyngeal and bronchial epithelial cells in smokers with chronic bronchitis and in healthy nonsmokers. Author(s): Riise GC, Larsson S, Andersson BA. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1994 October; 7(10): 1759-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7828681
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Bacterial colonisation of the respiratory tract in chronic bronchitis. Author(s): Butt HL, Clancy RL, Cripps AW, Murree-Allen K, Saunders NA, Sutherland DC, Hensley MJ. Source: Aust N Z J Med. 1990 February; 20(1): 35-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2322199
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Bacterial isolates and cigarette smoking in patients with chronic bronchitis: results from an Italian multicenter survey. Author(s): Cazzola M, Ariano R, Gioia V, Mancini V, Rimoldi R, Scala G, Scoccia S, Girbino G. Source: Clinical Therapeutics. 1990 March-April; 12(2): 105-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2112984
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Bacteriological eradication of Streptococcus pneumoniae from patients with acute exacerbations of chronic bronchitis: cefuroxime axetil versus cefixime. Author(s): Zuck P, Petitpretz P, Geslin P, Rio Y, Leblanc F. Source: Int J Clin Pract. 1999 September; 53(6): 437-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10622071
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Bacteriological findings in the transtracheal aspirate from patients with acute exacerbation of chronic bronchitis. Author(s): Schreiner A, Bjerkestrand G, Digranes A, Halvorsen FJ, Kommedal TM. Source: Infection. 1978; 6(2): 54-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=25845
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Bacteriology and beta-lactamase activity in acute exacerbation of chronic bronchitis. Author(s): Brook I, Frazier EH. Source: International Journal of Infectious Diseases : Ijid : Official Publication of the International Society for Infectious Diseases. 2001; 5(2): 74-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11468101
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Basophil-bound IgE and serum IgE directed against Haemophilus influenzae and Streptococcus pneumoniae in patients with chronic bronchitis during acute exacerbations. Author(s): Kjaergard LL, Larsen FO, Norn S, Clementsen P, Skov PS, Permin H. Source: Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica. 1996 January; 104(1): 61-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8645460
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Biotypes of Haemophilus parainfluenzae from the respiratory secretions in chronic bronchitis. Author(s): Taylor DC, Cripps AW, Clancy RL, Murree-Allen K, Hensley MJ, Saunders NA, Sutherland DC. Source: Journal of Medical Microbiology. 1992 April; 36(4): 279-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1560450
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Body position, membrane diffusing capacity and pulmonary capillary blood volume in chronic bronchitis and pulmonary emphysema. Author(s): Chou KC, Chang SC, Chang HI, Shiao GM. Source: Zhonghua Yi Xue Za Zhi (Taipei). 1999 April; 62(4): 209-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10367481
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Bombesin enhances monocyte and macrophage activities: possible role in the modulation of local pulmonary defenses in chronic bronchitis. Author(s): Meloni F, Ballabio P, Bianchi L, Mangiarotti P, Grassi G, Bignamini A, Grassi GG. Source: Respiration; International Review of Thoracic Diseases. 1996; 63(1): 28-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8833990
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Bombesin/gastrin releasing peptide levels of peripheral mononuclear cells, monocytes and alveolar macrophages in chronic bronchitis. Author(s): Meloni F, Bertoletti R, Corsico A, Di Fazio P, Cecchettin M, Gialdroni-Grassi G. Source: Int J Tissue React. 1992; 14(4): 195-201. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1478797
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Breathlessness, chronic bronchitis and reduced pulmonary function as predictors of cardiovascular disease mortality among men in England, Scotland and the United States. Author(s): Ebi-Kryston KL, Hawthorne VM, Rose G, Shipley MJ, Gillis CR, Hole DJ, Carmen W, Eshleman S, Higgins MW. Source: International Journal of Epidemiology. 1989 March; 18(1): 84-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2722386
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Bronchial brush biopsies for studies of epithelial inflammation in stable asthma and nonobstructive chronic bronchitis. Author(s): Riise GC, Andersson B, Ahlstedt S, Enander I, Soderberg M, Lowhagen O, Larsson S. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1996 August; 9(8): 1665-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8866592
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Bronchial cartilage atrophy in chronic bronchitis: observations on chondrolytic processes. Author(s): Tetlow LC, Freemont AJ, Woolley DE. Source: Pathobiology : Journal of Immunopathology, Molecular and Cellular Biology. 1999 July-August; 67(4): 196-201. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10738181
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Bronchial inflammation in acute bacterial exacerbations of chronic bronchitis: the role of leukotriene B4. Author(s): Crooks SW, Bayley DL, Hill SL, Stockley RA. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2000 February; 15(2): 274-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10706491
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Bronchial inflammation in chronic bronchitis assessed by measurement of cell products in bronchial lavage fluid. Author(s): Riise GC, Ahlstedt S, Larsson S, Enander I, Jones I, Larsson P, Andersson B. Source: Thorax. 1995 April; 50(4): 360-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7785007
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Bronchodilator treatment in moderate asthma or chronic bronchitis: continuous or on demand? A randomised controlled study. Author(s): van Schayck CP, Dompeling E, van Herwaarden CL, Folgering H, Verbeek AL, van der Hoogen HJ, van Weel C. Source: Bmj (Clinical Research Ed.). 1991 December 7; 303(6815): 1426-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1837744
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Broncho-vaxom therapy for children with chronic bronchitis. Author(s): Marialigeti T, Szekely E, Kereki E. Source: Ther Hung. 1989; 37(1): 28-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2756512
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Budgerigar breeders' hypersensitivity pneumonitis presenting as chronic bronchitis with purulent sputum. Author(s): Tanaka H, Honda Y, Hirasawa M, Fujishima T, Abe S. Source: Intern Med. 1995 July; 34(7): 676-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7496084
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Canadian guidelines for the management of acute exacerbations of chronic bronchitis. Author(s): Balter MS, La Forge J, Low DE, Mandell L, Grossman RF; Canadian Thoracic Society; Canadian Infectious Disease Society. Source: Can Respir J. 2003 July-August; 10 Suppl B: 3B-32B. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12944998
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Canadian guidelines for the management of acute exacerbations of chronic bronchitis: executive summary. Author(s): Balter MS, La Forge J, Low DE, Mandell L, Grossman RF; Chronic Bronchitis Working Group; Canadian Thoracic Society; Canadian Infectious Disease Society. Source: Can Respir J. 2003 July-August; 10(5): 248-58. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12945001
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Cause of death in older patients with anatomo-pathological evidence of chronic bronchitis or emphysema: a case-control study based on autopsy findings. Author(s): Janssens JP, Herrmann F, MacGee W, Michel JP. Source: Journal of the American Geriatrics Society. 2001 May; 49(5): 571-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11380749
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Cefaclor AF vs Clarithromycin in acute exacerbation of chronic bronchitis (B3M-PKAJBG). Author(s): Khan S, Javaid A, Ghori RA, Mahmood K, Anwer N, Khan SU, Iqbal ZH, Rahman F, Ullah S, Imran K, Akhter N, Khan MK, Siddqui SJ, Fareed A, Khan MH. Source: J Pak Med Assoc. 2003 August; 53(8): 338-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14558738
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Changes in bronchial inflammation during acute exacerbations of chronic bronchitis. Author(s): Gompertz S, O'Brien C, Bayley DL, Hill SL, Stockley RA. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2001 June; 17(6): 1112-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11491152
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Chlamydia pneumoniae and chronic bronchitis: association with severity and bacterial clearance following treatment. Author(s): Blasi F, Damato S, Cosentini R, Tarsia P, Raccanelli R, Centanni S, Allegra L; Chlamydia InterAction with COPD (CIAC) Study Group. Source: Thorax. 2002 August; 57(8): 672-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12149525
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Chronic bronchitis among French adults: high prevalence and underdiagnosis. Author(s): Huchon GJ, Vergnenegre A, Neukirch F, Brami G, Roche N, Preux PM. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 October; 20(4): 806-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12412668
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Chronic bronchitis and emphysema: clearing the air. Author(s): Wisniewski A. Source: Nursing. 2003 May; 33(5): 46-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12792571
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Chronic bronchitis and risk of coronary heart disease. Author(s): Sjogren B. Source: Lancet. 1996 November 16; 348(9038): 1389. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8918306
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Chronic bronchitis and risk of coronary heart disease. Author(s): Simons L, Simons J, Friedlander Y, McCallum J. Source: Lancet. 1996 November 16; 348(9038): 1388-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8918305
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Chronic bronchitis in an elderly population. Author(s): Lange P, Parner J, Prescott E, Vestbo J. Source: Age and Ageing. 2003 November; 32(6): 636-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14600005
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Chronic bronchitis in immunocompromised patients: association with a novel Mycoplasma species. Author(s): Webster D, Windsor H, Ling C, Windsor D, Pitcher D. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2003 September; 22(9): 530-4. Epub 2003 August 26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12942342
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Chronic bronchitis: an old man's enemy? Author(s): Connolly MJ. Source: Age and Ageing. 2003 November; 32(6): 561-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14599993
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Clinical outcomes of ambulatory acute exacerbations of chronic bronchitis with older versus newer antimicrobials. Author(s): Madaras-Kelly KJ, Magdanz SB, Johnson CK, Jue SG. Source: The Annals of Pharmacotherapy. 2002 June; 36(6): 975-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12022895
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Comparative study of cefaclor AF vs. cefuroxime axetil in acute exacerbations of chronic bronchitis. Author(s): Haczynski J, Chyczewska E, Grzelewska-Rzymowska I, Malolepszy J, Marcinkowska-Suchowierska E, Milanowski J, Oklek K, Plusa T, Slominski J, Szmygin K, Rek M. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2002 January; 8(1): Pi1-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11782685
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Comparison of azithromycin and co-amoxiclav in the treatment of acute tracheobronchitis and acute infectious exacerbations of chronic bronchitis in adults. Azithromycin Study Group. Author(s): Biebuyck XA. Source: J Int Med Res. 1996 September-October; 24(5): 407-18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8895044
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Comparison of chest X-ray findings and other parameters in acute exacerbation of chronic bronchitis in Japan and the West. Author(s): Watanabe A, Kohno S, Niki Y, Saito A. Source: Journal of Infection and Chemotherapy : Official Journal of the Japan Society of Chemotherapy. 2001 March; 7(1): 37-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11406755
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Costs of broad-spectrum antibiotic use for acute sinusitis, chronic bronchitis, and pneumonia in a managed care population. Author(s): Coughlin CM, Nelson M, Merchant S, Gondek K. Source: Manag Care Interface. 2003 June; 16(6): 34-40, 55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12841074
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Costs of chronic bronchitis and COPD: a 1-year follow-up study. Author(s): Miravitlles M, Murio C, Guerrero T, Gisbert R. Source: Chest. 2003 March; 123(3): 784-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12628879
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Decreased C4 complement component serum levels correlate with the degree of emphysema in patients with chronic bronchitis. Author(s): Kosmas EN, Zorpidou D, Vassilareas V, Roussou T, Michaelides S. Source: Chest. 1997 August; 112(2): 341-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9266867
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Defining subsets of patients with chronic bronchitis. Author(s): Wilson R, Wilson CB. Source: Chest. 1997 December; 112(6 Suppl): 303S-309S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9400893
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Delta F508 mutation of cystic fibrosis gene is not found in chronic bronchitis with severe obstruction in Japan. Author(s): Akai S, Okayama H, Shimura S, Tanno Y, Sasaki H, Takishima T. Source: Am Rev Respir Dis. 1992 September; 146(3): 781-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1519863
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Deposition and clearance in large and small airways in chronic bronchitis. Author(s): Svartengren K, Ericsson CH, Svartengren M, Mossberg B, Philipson K, Camner P. Source: Experimental Lung Research. 1996 September-October; 22(5): 555-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8886759
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Detection of CFTR gene mutations in patients suffering from chronic bronchitis. Author(s): Kostuch M, Semczuk A, Szarewicz-Adamczyk W, Gasowska-Giszczak U, Wojcierowski J, Kulczycki L. Source: Archives of Medical Research. 2000 January-February; 31(1): 97-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10767489
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Determinants of chronic bronchitis prevalence in an elderly sample from south-west of France. Author(s): Nejjari C, Tessier JF, Letenneur L, Lafont S, Dartigues JF, Salamon R. Source: Monaldi Arch Chest Dis. 1996 October; 51(5): 373-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9009624
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Diagnosing chronic obstructive pulmonary disease. The importance of differentiating asthma, emphysema, and chronic bronchitis. Author(s): Martinez FJ. Source: Postgraduate Medicine. 1998 April; 103(4): 112-7, 121-2, 125. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9553591
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Diagnosis of emphysema in patients with chronic bronchitis: a new approach. Author(s): Kohlhaufl M, Brand P, Selzer T, Scheuch G, Meyer T, Weber N, Schulz H, Haussinger K, Heyder J. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1998 October; 12(4): 793-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9817147
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Differences in airway responsiveness to acetaldehyde and methacholine in asthma and chronic bronchitis. Author(s): Sanchez-Toril F, Prieto L, Peris R, Perez JA, Millan M, Marin J. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2000 February; 15(2): 260-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10706489
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Different cytokine patterns in bronchial biopsies in asthma and chronic bronchitis. Author(s): Mueller R, Chanez P, Campbell AM, Bousquet J, Heusser C, Bullock GR. Source: Respiratory Medicine. 1996 February; 90(2): 79-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8730325
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Direct medical costs of chronic obstructive pulmonary disease: chronic bronchitis and emphysema. Author(s): Cochrane Database Syst Rev. 2003;(2):CD001287 Source: Respiratory Medicine. 2000 March; 94(3): 204-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12804402
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Dirithromycin versus amoxiclav in the treatment of acute exacerbations of chronic bronchitis. Author(s): Van Royen P, Betz W, Heyrman J, Taziaux P, Van den Haute M, Poelman M. Source: J Int Med Res. 1997 January-February; 25(1): 33-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9027671
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Does the continuous use of bronchodilators mask the progression of asthma or chronic bronchitis? Author(s): van Schayck CP, Folgering H, den Otter JJ, Tirimanna P, van Weel C. Source: Family Practice. 1992 December; 9(4): 397-404. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1490530
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Does the presence of antibodies justify the use of antibiotics in exacerbations of chronic bronchitis? Author(s): Niederman MS. Source: American Journal of Respiratory and Critical Care Medicine. 2004 February 15; 169(4): 434-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14766657
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Domestic biomass fuel combustion and chronic bronchitis in two rural Bolivian villages. Author(s): Albalak R, Frisancho AR, Keeler GJ. Source: Thorax. 1999 November; 54(11): 1004-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10525559
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Domestic smoke pollution and prevalence of chronic bronchitis/asthma in a rural area of Kashmir. Author(s): Qureshi KA. Source: Indian J Chest Dis Allied Sci. 1994 April-June; 36(2): 61-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7851950
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Dornase in treatment of chronic bronchitis. Author(s): Hudson TJ. Source: The Annals of Pharmacotherapy. 1996 June; 30(6): 674-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8792955
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Double-blind comparative study of ofloxacin (Hoe 280) and trimethoprimsulfamethoxazole in the treatment of patients with acute exacerbations of chronic bronchitis and chronic obstructive lung disease. Author(s): Boye NP, Gaustad P. Source: Infection. 1991; 19 Suppl 7: S388-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1804789
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Double-blind randomized study comparing the efficacies and safeties of a short (3day) course of azithromycin and a 5-day course of amoxicillin in patients with acute exacerbations of chronic bronchitis. Author(s): Mertens JC, van Barneveld PW, Asin HR, Ligtvoet E, Visser MR, Branger T, Hoepelman AI. Source: Antimicrobial Agents and Chemotherapy. 1992 July; 36(7): 1456-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1324645
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Double-blind, comparative study of rufloxacin once daily versus amoxicillin three times a day in treatment of outpatients with exacerbations of chronic bronchitis. Author(s): Klietmann W, Cesana M, Rondel RK, Focht J. Source: Antimicrobial Agents and Chemotherapy. 1993 November; 37(11): 2298-306. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8285609
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Economic evaluation of ciprofloxacin compared with usual antibacterial care for the treatment of acute exacerbations of chronic bronchitis in patients followed for 1 year. Author(s): Torrance G, Walker V, Grossman R, Mukherjee J, Vaughan D, La Forge J, Lampron N. Source: Pharmacoeconomics. 1999 November; 16(5 Pt 1): 499-520. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10662396
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Effect of aerosolized uridine 5'-triphosphate on mucociliary clearance in mild chronic bronchitis. Author(s): Bennett WD, Zeman KL, Foy C, Shaffer CL, Johnson FL, Regnis JA, Sannuti A, Johnson J. Source: American Journal of Respiratory and Critical Care Medicine. 2001 July 15; 164(2): 302-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11463605
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Effect of sputum processing with dithiothreitol on the detection of inflammatory mediators in chronic bronchitis and bronchiectasis. Author(s): Woolhouse IS, Bayley DL, Stockley RA. Source: Thorax. 2002 August; 57(8): 667-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12149524
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Effectiveness of short-course therapy (5 days) with grepafloxacin in the treatment of acute bacterial exacerbations of chronic bronchitis. Author(s): DeAbate CA, Bettis R, Munk ZM, Fleming H, Munn NJ, Riffer E, Bagby B, Giguere G, Collins JJ. Source: Clinical Therapeutics. 1999 January; 21(1): 172-88. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10090434
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Efficacy and safety of a 10-day course of 400 or 600 milligrams of grepafloxacin once daily for treatment of acute bacterial exacerbations of chronic bronchitis: comparison with a 10-day course of 500 milligrams of ciprofloxacin twice daily. Author(s): Chodosh S, Lakshminarayan S, Swarz H, Breisch S. Source: Antimicrobial Agents and Chemotherapy. 1998 January; 42(1): 114-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9449270
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Efficacy and safety of azithromycin vs levofloxacin in the outpatient treatment of acute bacterial exacerbations of chronic bronchitis. Author(s): Amsden GW, Baird IM, Simon S, Treadway G. Source: Chest. 2003 March; 123(3): 772-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12628877
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Efficacy and safety of short course (5-day) moxifloxacin vs 7-day ceftriaxone in the treatment of acute exacerbations of chronic bronchitis (AECB). Author(s): Grassi C, Casali L, Curti E, Tellarini M, Lazzaro C, Schito G; SMART Study Group. Studio Multicentrico con Moxifloxacina nel Trattamento delle Riacutizzazioni de Bronchite Cronica. Source: J Chemother. 2002 December; 14(6): 597-608. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12583552
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Efficacy and tolerability of gatifloxacin in community treatment of acute exacerbations of chronic bronchitis. Author(s): Anzueto A, Gotfried M, Wikler MA, Russo R, Nicholson SC. Source: Clinical Therapeutics. 2002 June; 24(6): 906-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12117081
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Efficacy and tolerability of myrtol standardized in long-term treatment of chronic bronchitis. A double-blind, placebo-controlled study. Study Group Investigators. Author(s): Meister R, Wittig T, Beuscher N, de Mey C. Source: Arzneimittel-Forschung. 1999 April; 49(4): 351-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10337455
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Efficacy and tolerability of twice-daily ciprofloxacin 750 mg in the treatment of patients with acute exacerbations of chronic bronchitis and pneumonia. Author(s): Pryka R, Kowalsky S, Haverstock D. Source: Clinical Therapeutics. 1998 January-February; 20(1): 141-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9522111
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Efficacy of ciprofloxacin and clarithromycin in acute bacterial exacerbations of complicated chronic bronchitis: interim analysis. Bronchitis Study Group. Author(s): Anzueto A, Niederman MS, Haverstock DC, Tillotson GS. Source: Clinical Therapeutics. 1997 September-October; 19(5): 989-1001. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9385486
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Efficacy of gemifloxacin in acute exacerbations of chronic bronchitis: a randomised, double-blind comparison with trovafloxacin. Author(s): Ball P, Wilson R, Mandell L, Brown J, Henkel T; 069 Clinical Study Group. Source: J Chemother. 2001 June; 13(3): 288-98. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11450888
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Efficacy of oral ciprofloxacin vs. clarithromycin for treatment of acute bacterial exacerbations of chronic bronchitis. The Bronchitis Study Group. Author(s): Chodosh S, Schreurs A, Siami G, Barkman HW Jr, Anzueto A, Shan M, Moesker H, Stack T, Kowalsky S. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1998 October; 27(4): 730-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9798025
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Eotaxin and CCR3 are up-regulated in exacerbations of chronic bronchitis. Author(s): Bocchino V, Bertorelli G, Bertrand CP, Ponath PD, Newman W, Franco C, Marruchella A, Merlini S, Del Donno M, Zhuo X, Olivieri D. Source: Allergy. 2002 January; 57(1): 17-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11991282
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Equal effectiveness of older traditional antibiotics and newer broad-spectrum antibiotics in treating patients with acute exacerbations of chronic bronchitis. Author(s): Peng CC, Aspinall SL, Good CB, Atwood CW Jr, Chang CC. Source: Southern Medical Journal. 2003 October; 96(10): 986-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14570342
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Etiology, susceptibility, and treatment of acute bacterial exacerbations of complicated chronic bronchitis in the primary care setting: ciprofloxacin 750 mg b.i.d. versus clarithromycin 500 mg b.i.d. Bronchitis Study Group. Author(s): Anzueto A, Niederman MS, Tillotson GS. Source: Clinical Therapeutics. 1998 September-October; 20(5): 885-900. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9829441
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Evaluation of apoptosis of eosinophils, macrophages, and T lymphocytes in mucosal biopsy specimens of patients with asthma and chronic bronchitis. Author(s): Vignola AM, Chanez P, Chiappara G, Siena L, Merendino A, Reina C, Gagliardo R, Profita M, Bousquet J, Bonsignore G. Source: The Journal of Allergy and Clinical Immunology. 1999 April; 103(4): 563-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10200002
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Evidence of bacterial infection in acute exacerbations of chronic bronchitis. Author(s): Wilson R. Source: Seminars in Respiratory Infections. 2000 September; 15(3): 208-15. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11052421
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FAB-MS characterization of sialyl Lewis x determinants on polylactosamine chains of human airway mucins secreted by patients suffering from cystic fibrosis or chronic bronchitis. Author(s): Morelle W, Sutton-Smith M, Morris HR, Davril M, Roussel P, Dell A. Source: Glycoconjugate Journal. 2001 September; 18(9): 699-708. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12386455
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Factors affecting the decline of FEV1 in chronic bronchitis. Author(s): Barter CE, Campbell AH, Tandon MK. Source: Aust N Z J Med. 1974 August; 4(4): 339-45. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4529408
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Failure of an antagonist of histamine--chlorpheniramine--to modify the pulmonary vascular response to hypoxia in chronic bronchitis. Author(s): Stark RD, Joshi RC, Bishop JM. Source: Cardiovascular Research. 1977 May; 11(3): 219-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=872161
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Familial related risk-factors in the development of chronic bronchitis/emphysema as compared to asthma assessed in a postal survey. Author(s): Montnemery P, Lanke J, Lindholm LH, Lundback B, Nyberg P, Adelroth E, Lofdahl CG. Source: European Journal of Epidemiology. 2000; 16(11): 1003-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11421467
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Five day moxifloxacin therapy compared with 7 day clarithromycin therapy for the treatment of acute exacerbations of chronic bronchitis. Author(s): Wilson R, Kubin R, Ballin I, Deppermann KM, Bassaris HP, Leophonte P, Schreurs AJ, Torres A, Sommerauer B. Source: The Journal of Antimicrobial Chemotherapy. 1999 October; 44(4): 501-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10588312
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Five days of cefprozil versus 10 days of clarithromycin in the treatment of an acute exacerbation of chronic bronchitis. Author(s): McCarty JM, Pierce PF. Source: Annals of Allergy, Asthma & Immunology : Official Publication of the American College of Allergy, Asthma, & Immunology. 2001 October; 87(4): 327-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11686426
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Five-day dirithromycin therapy is as effective as seven-day erythromycin therapy for acute exacerbations of chronic bronchitis. Author(s): Wasilewski MM, Johns D, Sides GD. Source: The Journal of Antimicrobial Chemotherapy. 1999 April; 43(4): 541-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10350384
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Five-day moxifloxacin therapy compared with 7-day co-amoxiclav therapy for the treatment of acute exacerbation of chronic bronchitis. Author(s): Starakis I, Gogos CA, Bassaris H. Source: International Journal of Antimicrobial Agents. 2004 February; 23(2): 129-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15013037
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Five-year winter chemoprophylaxis for chronic bronchitis. Author(s): Johnston RN, McNeill RS, Smith DH, Dempster MB, Nairn JR, Purvis MS, Watson JM, Ward FG. Source: British Medical Journal. 1969 November 1; 4(678): 265-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4899454
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Follow-up evaluation of a prevalence study for chronic bronchitis and chronic airway obstruction. Author(s): Petty TL, Pierson DJ, Dick NP, Hudson LD, Walker SH. Source: Am Rev Respir Dis. 1976 November; 114(5): 881-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1086621
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Follow-up study of disability among elderly patients discharged from hospital with exacerbations of chronic bronchitis. Author(s): Peach H, Pathy MS. Source: Thorax. 1981 August; 36(8): 585-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7314032
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Food allergy--its role in the symptoms of obstructive emphysema and chronic bronchitis. Author(s): Rowe AH, Rowe A Jr, Sinclair C. Source: J Asthma Res. 1967 September; 5(1): 11-20. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6066422
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Foreign-body aspiration, asthma and chronic bronchitis. Author(s): Deshpande KS, Haramati LB, Aldrich TK, Edelman M, Villanueva E. Source: American Family Physician. 2000 October 1; 62(7): 1513, 1517, 1519. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11037072
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Formulary decision making and acute exacerbations of chronic bronchitis. Author(s): Penna P. Source: Manag Care Interface. 2001 February; 14(2): 50-1. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11228816
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Frequency dependence of compliance and resistance in chronic bronchitis. Author(s): Grimby G. Source: Bull Physiopathol Respir (Nancy). 1970 October-December; 6(4): 881-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5522026
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Frequency of common cystic fibrosis gene mutations in chronic bronchitis patients. Author(s): Entzian P, Muller E, Boysen A, Artlich A, Schwinger E, Schlaak M. Source: Scandinavian Journal of Clinical and Laboratory Investigation. 1995 May; 55(3): 263-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7638561
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Gastroesophageal reflux in patients with asthma and chronic bronchitis. Author(s): Ducolone A, Vandevenne A, Jouin H, Grob JC, Coumaros D, Meyer C, Burghard G, Methlin G, Hollender L. Source: Am Rev Respir Dis. 1987 February; 135(2): 327-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3813193
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Gemifloxacin versus amoxicillin/clavulanate in the treatment of acute exacerbations of chronic bronchitis. The 070 Clinical Study group. Author(s): File T, Schlemmer B, Garau J, Lode H, Lynch S, Young C. Source: J Chemother. 2000 August; 12(4): 314-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10949981
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Gene expression and immunolocalization of 15-lipoxygenase isozymes in the airway mucosa of smokers with chronic bronchitis. Author(s): Zhu J, Kilty I, Granger H, Gamble E, Qiu YS, Hattotuwa K, Elston W, Liu WL, Oliva A, Pauwels RA, Kips JC, De Rose V, Barnes N, Yeadon M, Jenkinson S, Jeffery PK. Source: American Journal of Respiratory Cell and Molecular Biology. 2002 December; 27(6): 666-77. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12444026
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Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis. Author(s): Silverman EK, Chapman HA, Drazen JM, Weiss ST, Rosner B, Campbell EJ, O'DONNELL WJ, Reilly JJ, Ginns L, Mentzer S, Wain J, Speizer FE. Source: American Journal of Respiratory and Critical Care Medicine. 1998 June; 157(6 Pt 1): 1770-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9620904
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Genetic markers for chronic bronchitis and peak expiratory flow in the Copenhagen Male Study. Author(s): Vestbo J, Hein HO, Suadicani P, Sorensen H, Gyntelberg F. Source: Dan Med Bull. 1993 June; 40(3): 378-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8339607
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Geographic distribution of chronic bronchitis. Author(s): Ferris BG Jr. Source: Bull Physiopathol Respir (Nancy). 1973 July-August; 9(4): 1121-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4770753
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Glycoprotein secretion in vitro by human airway: normal and chronic bronchitis. Author(s): Coles SJ, Reid L. Source: Experimental and Molecular Pathology. 1978 December; 29(3): 326-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=720544
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Glycosaminoglycans in the bronchial mucus of patients with chronic bronchitis and mucoid impaction of the bronchus. Author(s): Theocharis DA. Source: Life Sciences. 1985 June 17; 36(24): 2287-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4010457
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Goblet cell hyperplasia and epithelial inflammation in peripheral airways of smokers with both symptoms of chronic bronchitis and chronic airflow limitation. Author(s): Saetta M, Turato G, Baraldo S, Zanin A, Braccioni F, Mapp CE, Maestrelli P, Cavallesco G, Papi A, Fabbri LM. Source: American Journal of Respiratory and Critical Care Medicine. 2000 March; 161(3 Pt 1): 1016-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10712357
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Goblet cells in the peripheral airways in chronic bronchitis. Author(s): Thurlbeck WM, Malaka D, Murphy K. Source: Am Rev Respir Dis. 1975 July; 112(1): 65-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1147385
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Goblet-cell density in human bronchus in chronic bronchitis. Author(s): Tos M, Moller K. Source: Arch Otolaryngol. 1983 October; 109(10): 673-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6615319
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Gram stain and culture of morning and 24 h sputum in the diagnosis of bacterial exacerbation of chronic bronchitis: a dogma disputed. Author(s): Medici TC, von Graevenitz A, Shang H, Bohni E, Wall M. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1988 December; 1(10): 923-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2465180
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Guidelines for the treatment of acute exacerbations of chronic bronchitis. Author(s): Grossman RF. Source: Chest. 1997 December; 112(6 Suppl): 310S-313S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9400894
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Haemophilus influenzae release histamine and enhance histamine release from human bronchoalveolar cells. Examination of patients with chronic bronchitis and controls. Author(s): Clementsen P, Larsen FO, Milman N, Skov PS, Norn S. Source: Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica. 1995 November; 103(11): 806-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8546845
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Health-based selection for asthma, but not for chronic bronchitis, in pig farmers: an evidence-based hypothesis. Author(s): Vogelzang PF, van der Gulden JW, Tielen MJ, Folgering H, van Schayck CP. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1999 January; 13(1): 187-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10836346
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Healthy worker effect in cohort studies on chronic bronchitis. Author(s): Radon K, Goldberg M, Becklake M. Source: Scand J Work Environ Health. 2002 October; 28(5): 328-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12432986
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Helicobacter pylori and chronic bronchitis. Author(s): Caselli M, Zaffoni E, Ruina M, Sartori S, Trevisani L, Ciaccia A, Alvisi V, Fabbri L, Papi A. Source: Scandinavian Journal of Gastroenterology. 1999 August; 34(8): 828-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10499486
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Hemophilus influenzae biotypes and chronic bronchitis. Author(s): Kilbourn JP, Haas H, Morris JF, Samson S. Source: Am Rev Respir Dis. 1983 December; 128(6): 1093-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6606372
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High dose salbutamol in chronic bronchitis: comparison of 400 micrograms, 1 mg, 1.6 mg, 2 mg and placebo delivered by Rotahaler. Author(s): Jenkins SC, Moxham J. Source: Br J Dis Chest. 1987 July; 81(3): 242-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3311117
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High plasma calcitonin concentrations in chronic bronchitis. Author(s): Galan FG, Hurtado J, Cano RP, Peralta MG. Source: British Medical Journal (Clinical Research Ed.). 1982 September 25; 285(6345): 850-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6811038
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Histamine content of sputum from patients with asthma and chronic bronchitis. Author(s): Bryant DH, Pui A. Source: Clin Allergy. 1982 January; 12(1): 19-27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6175438
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HLA-A and -B antigens in chronic bronchitis. Author(s): Anagnostopoulou U, Toumbis M, Konstantopoulos K, Kotsovoulou-Fouskaki V, Zervas J. Source: Journal of Clinical Epidemiology. 1993 December; 46(12): 1413-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8263568
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HLA-DR and ICAM-1 expression on bronchial epithelial cells in asthma and chronic bronchitis. Author(s): Vignola AM, Campbell AM, Chanez P, Bousquet J, Paul-Lacoste P, Michel FB, Godard P. Source: Am Rev Respir Dis. 1993 September; 148(3): 689-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8103654
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How accurate is the self-reported diagnosis of chronic bronchitis? Author(s): Bobadilla A, Guerra S, Sherrill D, Barbee R. Source: Chest. 2002 October; 122(4): 1234-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12377847
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How to prevent the progression of chronic bronchitis: the role of smoking cessation prevention. Author(s): Fiore MC. Source: Monaldi Arch Chest Dis. 1994 June; 49(3 Suppl 1): 13-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8087133
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Human immune response to nontypeable Haemophilus influenzae in chronic bronchitis. Author(s): Yi K, Sethi S, Murphy TF. Source: The Journal of Infectious Diseases. 1997 November; 176(5): 1247-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9359725
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Hypothalamic digoxin, hemispheric chemical dominance, and chronic bronchitis emphysema. Author(s): Kurup RK, Kurup PA. Source: The International Journal of Neuroscience. 2003 September; 113(9): 1241-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12959742
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Hypoxemia in chronic bronchitis and pulmonary emphysema. Author(s): Manicatide MA, Teculescu DB, Racoveanu CL. Source: Med Interne. 1977 January-March; 15(1): 41-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=841252
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IgG antibodies, chronic bronchitis, and pulmonary function values in farmer's lung patients and matched controls. Author(s): Erkinjuntti-Pekkanen R, Reiman M, Kokkarinen JI, Tukiainen HO, Terho EO. Source: Allergy. 1999 November; 54(11): 1181-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10604554
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IgG subclasses in smokers with chronic bronchitis and recurrent exacerbations. Author(s): Qvarfordt I, Riise GC, Andersson BA, Larsson S. Source: Thorax. 2001 June; 56(6): 445-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11359959
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Immune response to Fusobacterium nucleatum and Prevotella intermedia in the sputum of patients with acute exacerbation of chronic bronchitis. Author(s): Brook I, Frazier EH. Source: Chest. 2003 September; 124(3): 832-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12970005
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Improved sputum expectoration following a single dose of INS316 in patients with chronic bronchitis. Author(s): Johnson FL, Donohue JF, Shaffer CL. Source: Chest. 2002 December; 122(6): 2021-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12475842
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In patients with chronic bronchitis a four week trial with inhaled steroids does not attenuate airway inflammation. Author(s): Loppow D, Schleiss MB, Kanniess F, Taube C, Jorres RA, Magnussen H. Source: Respiratory Medicine. 2001 February; 95(2): 115-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11217907
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Incidence and prevalence of asthma among adult Finnish men and women of the Finnish Twin Cohort from 1975 to 1990, and their relation to hay fever and chronic bronchitis. Author(s): Huovinen E, Kaprio J, Laitinen LA, Koskenvuo M. Source: Chest. 1999 April; 115(4): 928-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10208188
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Increased exhaled nitric oxide in chronic bronchitis: comparison with asthma and COPD. Author(s): Delen FM, Sippel JM, Osborne ML, Law S, Thukkani N, Holden WE. Source: Chest. 2000 March; 117(3): 695-701. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10712993
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Increasing prevalence of asthma but not of chronic bronchitis in Finland? Report from the FinEsS-Helsinki Study. Author(s): Pallasaho P, Lundback B, Laspa SL, Jonsson E, Kotaniemi J, Sovijarvi AR, Laitinen LA. Source: Respiratory Medicine. 1999 November; 93(11): 798-809. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10603629
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Infection in acute exacerbations of chronic bronchitis: a clinical perspective. Author(s): Read RC. Source: Respiratory Medicine. 1999 December; 93(12): 845-50. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10653044
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Infectious etiology of acute exacerbations of chronic bronchitis. Author(s): Sethi S. Source: Chest. 2000 May; 117(5 Suppl 2): 380S-5S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10843981
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Infectious exacerbations of chronic bronchitis. ORIONE Board. Author(s): Donner CF. Source: Monaldi Arch Chest Dis. 1999 February; 54(1): 43-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10218370
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Infectious exacerbations of chronic bronchitis: diagnosis and management. Author(s): Sethi S. Source: The Journal of Antimicrobial Chemotherapy. 1999 March; 43 Suppl A: 97-105. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10225579
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Inflammation and acute exacerbations of chronic bronchitis. Author(s): Stockley RA. Source: Chest. 2001 October; 120(4): 1422-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11591596
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Interleukin 8 in bronchoalveolar lavage of asthmatic and chronic bronchitis patients. Author(s): Chanez P, Enander I, Jones I, Godard P, Bousquet J. Source: International Archives of Allergy and Immunology. 1996 September; 111(1): 838. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8753849
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Interleukin-13 and -4 expression in the central airways of smokers with chronic bronchitis. Author(s): Miotto D, Ruggieri MP, Boschetto P, Cavallesco G, Papi A, Bononi I, Piola C, Murer B, Fabbri LM, Mapp CE. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 October; 22(4): 602-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14582911
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Interleukin-4 and interleukin-5 gene expression and inflammation in the mucussecreting glands and subepithelial tissue of smokers with chronic bronchitis. Lack of relationship with CD8(+) cells. Author(s): Zhu J, Majumdar S, Qiu Y, Ansari T, Oliva A, Kips JC, Pauwels RA, De Rose V, Jeffery PK. Source: American Journal of Respiratory and Critical Care Medicine. 2001 December 15; 164(12): 2220-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11751191
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International study comparing cefdinir and cefuroxime axetil in the treatment of patients with acute exacerbation of chronic bronchitis. Author(s): Van Herwaarden CL, Langan CE, Siemon G, Rudolph C, Keyserling CH, Nemeth MA, Tack KJ. Source: International Journal of Infectious Diseases : Ijid : Official Publication of the International Society for Infectious Diseases. 2000; 4(1): 26-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10689211
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Interrelationship between pharmacokinetics and pharmacodynamics in choosing the appropriate antibiotic and the dosage regimen for treating acute exacerbations of chronic bronchitis. Author(s): Cazzola M, Matera MG. Source: Respiratory Medicine. 1998 July; 92(7): 895-901. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10070561
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Interrelationship between the pharmacokinetics and pharmacodynamics of cefaclor advanced formulation in patients with acute exacerbation of chronic bronchitis. Author(s): Cazzola M, Di Perna F, Boveri B, Di Marco F, Diamare F, Centanni S. Source: J Chemother. 2000 June; 12(3): 216-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10877516
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Introduction: the role of bacterial infection in chronic bronchitis. Author(s): Wilson R, Grossman R. Source: Seminars in Respiratory Infections. 2000 March; 15(1): 1-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10749544
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Kinin generation in acute pneumonia and chronic bronchitis. Author(s): Zhang M, Peng B, Niehus J, Baumgarten CR, Brunnee T, Thalhofer S, Dorow P, Kunkel G. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1997 August; 10(8): 1747-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9272914
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Latamoxef (moxalactam) in acute exacerbations of chronic bronchitis. Author(s): Maesen FP, Davies BI, Brouwers J, Salemans T, Nelissen-Wamper M, Debruyne H. Source: The Journal of Antimicrobial Chemotherapy. 1983 February; 11(2): 115-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6219980
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Latent alpha1-antichymotrypsin. A molecular explanation for the inactivation of alpha1-antichymotrypsin in chronic bronchitis and emphysema. Author(s): Chang WS, Lomas DA. Source: The Journal of Biological Chemistry. 1998 February 6; 273(6): 3695-701. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9452500
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Leisure time physical activity and disease-specific mortality among men with chronic bronchitis: evidence from the Whitehall study. Author(s): Batty GD, Shipley MJ, Marmot MG, Smith GD. Source: American Journal of Public Health. 2003 May; 93(5): 817-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12721150
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Leukocyte function and chronic bronchitis. Author(s): McCusker KT, Hoidal J. Source: Seminars in Respiratory Infections. 1988 March; 3(1): 5-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3283881
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Levofloxacin versus cefuroxime axetil in the treatment of acute exacerbation of chronic bronchitis: results of a randomized, double-blind study. Author(s): Shah PM, Maesen FP, Dolmann A, Vetter N, Fiss E, Wesch R. Source: The Journal of Antimicrobial Chemotherapy. 1999 April; 43(4): 529-39. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10350383
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Linking Helicobacter pylori and chronic bronchitis: fact or fancy? Author(s): Shiotani A. Source: Journal of Gastroenterology. 2002; 37(5): 402-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12051543
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Lipid peroxidation--antioxidant activity system in erythrocytes of patients with chronic bronchitis inhaling and not inhaling ozone. Author(s): Abdrashitova NF, Romanov YA. Source: Bulletin of Experimental Biology and Medicine. 2001 September; 132(3): 884-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11740585
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Local airways immune modifications induced by oral bacterial extracts in chronic bronchitis. Author(s): Lusuardi M, Capelli A, Carli S, Spada EL, Spinazzi A, Donner CF. Source: Chest. 1993 June; 103(6): 1783-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8404101
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Local immunity in patients with chronic bronchitis and the effects of a bacterial extract, Broncho-Vaxom, on T lymphocytes, macrophages, gamma-interferon and secretory immunoglobulin A in bronchoalveolar lavage fluid and other variables. Author(s): Emmerich B, Emslander HP, Pachmann K, Hallek M, Milatovic D, Busch R. Source: Respiration; International Review of Thoracic Diseases. 1990; 57(2): 90-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2122507
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Lomefloxacin versus amoxicillin in the treatment of acute exacerbations of chronic bronchitis: an Italian multicenter study. Author(s): Grassi C, Albera C, Pozzi E. Source: The American Journal of Medicine. 1992 April 6; 92(4A): 103S-107S. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1316058
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Long-lasting effects on rheology and clearance of bronchial mucus after short-term administration of high doses of carbocysteine-lysine to patients with chronic bronchitis. Author(s): Braga PC, Allegra L, Rampoldi C, Ornaghi A, Beghi G. Source: Respiration; International Review of Thoracic Diseases. 1990; 57(6): 353-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2099568
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Long-term oral carbocisteine therapy in patients with chronic bronchitis. A double blind trial with placebo control. Author(s): Grillage M, Barnard-Jones K. Source: Br J Clin Pract. 1985 October; 39(10): 395-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3907681
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Loracarbef (LY163892) in the treatment of acute exacerbations of chronic bronchitis: results of U.S. and European comparative clinical trials. Author(s): Zeckel ML. Source: The American Journal of Medicine. 1992 June 22; 92(6A): 58S-64S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1621746
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Loracarbef (LY163892) versus amoxicillin/clavulanate in the treatment of acute bacterial exacerbations of chronic bronchitis. Author(s): Zeckel ML, Jacobson KD, Guerra FJ, Therasse DG, Farlow D. Source: Clinical Therapeutics. 1992 March-April; 14(2): 214-29. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1611645
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Lower airway bacterial colonization in asymptomatic smokers and smokers with chronic bronchitis and recurrent exacerbations. Author(s): Qvarfordt I, Riise GC, Andersson BA, Larsson S. Source: Respiratory Medicine. 2000 September; 94(9): 881-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11001080
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Lower respiratory tract inflammation in chronic bronchitis. Evaluation by bronchoalveolar lavage and changes associated with treatment with Immucytal, a biological response modifier. Author(s): Balbi B, Aufiero A, Pesci A, Oddera S, Zanon P, Rossi GA, Olivieri D. Source: Chest. 1994 September; 106(3): 819-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8082365
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Lower respiratory tract lactoferrin and lysozyme arise primarily in the airways and are elevated in association with chronic bronchitis. Author(s): Thompson AB, Bohling T, Payvandi F, Rennard SI. Source: The Journal of Laboratory and Clinical Medicine. 1990 February; 115(2): 148-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2299262
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Lung function profiles in farmer's lung, asthma, chronic bronchitis and emphysema. Author(s): Sovijarvi AR. Source: Eur J Respir Dis Suppl. 1987; 154: 94-100. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3480836
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Lymphocytes, chronic bronchitis and chronic obstructive pulmonary disease. Author(s): Jeffery PK. Source: Novartis Found Symp. 2001; 234: 149-61; Discussion 161-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11199094
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Management of a patient in respiratory failure due to chronic bronchitis. Author(s): Ledger SD. Source: Intensive Care Nurs. 1986; 2(1): 30-43. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3639113
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Management of acute exacerbation of chronic bronchitis. Author(s): Grossman RF. Source: Can Respir J. 1999 January-February; 6 Suppl A: 40A-5A. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10202233
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Managing patients with chronic bronchitis: from primary prevention to advance directives. Author(s): Schaberg DR. Source: Hosp Pract (Off Ed). 2000 November 15; 35(11): 1-2. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11108002
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Marked up-regulation of T lymphocytes and expression of interleukin-9 in bronchial biopsies from patients With chronic bronchitis with obstruction. Author(s): Panzner P, Lafitte JJ, Tsicopoulos A, Hamid Q, Tulic MK. Source: Chest. 2003 November; 124(5): 1909-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14605067
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Mast cells in the airway lumen and bronchial mucosa of patients with chronic bronchitis. Author(s): Pesci A, Rossi GA, Bertorelli G, Aufiero A, Zanon P, Olivieri D. Source: American Journal of Respiratory and Critical Care Medicine. 1994 May; 149(5): 1311-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8173772
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Maximal oxygen consumption and pulmonary circulation in patients with chronic bronchitis. Author(s): Henriquez A, Schrijen F, Poincelot F, Gimenez M, Polu JM, Sadoul P. Source: European Journal of Clinical Investigation. 1986 December; 16(6): 526-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3104053
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Measurement of psychophysiologic response variables in chronic bronchitis and emphysema. Author(s): Moody LE. Source: Applied Nursing Research : Anr. 1990 February; 3(1): 36-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2317055
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Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema. Author(s): Catterall JR, Calverley PM, MacNee W, Warren PM, Shapiro CM, Douglas NJ, Flenley DC. Source: Journal of Applied Physiology (Bethesda, Md. : 1985). 1985 December; 59(6): 1698-703. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4077777
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Mediator release from human lung mast cell subtypes in chronic bronchitis and emphysema. Author(s): van Overveld FJ. Source: Agents Actions. 1989 April; 27(1-2): 97-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2473645
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Monocyte chemotactic and activating factor/monocyte chemoattractant protein (MCAF/MCP-1) in bronchoalveolar lavage fluid from patients with atopic asthma and chronic bronchitis. Author(s): Jahnz-Rozyk KM, Kuna P, Pirozynska E. Source: J Investig Allergol Clin Immunol. 1997 July-August; 7(4): 254-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9330191
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Monocyte chemotactic and activating factor/monocyte chemoattractant protein in bronchoalveolar lavage fluid from patients with atopic asthma and chronic bronchitis. Relationship to lung function tests, bronchial hyper-responsiveness and cytology of bronchoalveolar lavage fluid. Author(s): Rozyk KJ, Plusa T, Kuna P, Pirozynska E. Source: Immunology Letters. 1997 June; 58(1): 47-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9436469
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Mortality from asthma and chronic bronchitis associated with changes in sulfur oxides air pollution. Author(s): Imai M, Yoshida K, Kitabatake M. Source: Archives of Environmental Health. 1986 January-February; 41(1): 29-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3963884
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Moxifloxacin in acute exacerbations of chronic bronchitis: clinical evaluation and assessment by patients. Author(s): Lorenz J, Busch W, Thate-Waschke IM; BRONCHIMOX Study Group. Source: J Int Med Res. 2001 March-April; 29(2): 61-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11393350
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Mucociliary clearance in early simple chronic bronchitis. Author(s): Dirksen H, Hermansen F, Groth S, Molgaard F. Source: Eur J Respir Dis Suppl. 1987; 153: 145-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3322859
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Mucociliary clearance in patients with chronic bronchitis and bronchial carcinoma. Author(s): Matthys H, Vastag E, Kohler D, Daikeler G, Fischer J. Source: Respiration; International Review of Thoracic Diseases. 1983; 44(5): 329-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6312521
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Mucolytic agents for chronic bronchitis or chronic obstructive pulmonary disease. Author(s): Poole PJ, Black PN. Source: Cochrane Database Syst Rev. 2003; (2): Cd001287. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12804402
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Mucolytic agents for chronic bronchitis or chronic obstructive pulmonary disease. Author(s): Poole PJ, Black PN. Source: Cochrane Database Syst Rev. 2000; (2): Cd001287. Review. Update In: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10796634
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Multidimensional analysis of the symptoms of chronic bronchitis and emphysema. Author(s): Kinsman RA, Fernandez E, Schocket M, Dirks JF, Covino NA. Source: Journal of Behavioral Medicine. 1983 December; 6(4): 339-57. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6668602
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N-acetylcysteine by metered dose inhaler in the treatment of chronic bronchitis: a multi-centre study. Author(s): Dueholm M, Nielsen C, Thorshauge H, Evald T, Hansen NC, Madsen HD, Maltbaek N. Source: Respiratory Medicine. 1992 March; 86(2): 89-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1615189
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Nebulized ipratropium bromide in ventilator-assisted patients with chronic bronchitis. Author(s): Yang SC, Yang SP, Lee TS. Source: Chest. 1994 May; 105(5): 1511-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8181345
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Nifedipine and impaired oxygenation in patients with chronic bronchitis and cor pulmonale. Author(s): Kalra L, Bone MF. Source: Lancet. 1989 May 20; 1(8647): 1135-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2566071
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Nimesulide in the treatment of chronic bronchitis. Author(s): Sofia M, Molino A, Mormile M, Stanziola A, Scaricabarozzi I, Carratu L. Source: Drugs. 1993; 46 Suppl 1: 111-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7506147
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N-isobutyrylcysteine, a donor of systemic thiols, does not reduce the exacerbation rate in chronic bronchitis. Author(s): Ekberg-Jansson A, Larson M, MacNee W, Tunek A, Wahlgren L, Wouters EF, Larsson S. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1999 April; 13(4): 829-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10362048
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Non specific immunity in aged healthy subjects and in patients with chronic bronchitis. Author(s): Fietta A, Merlini C, De Bernardi PM, Gandola L, Piccioni PD, Grassi C. Source: Aging (Milano). 1993 October; 5(5): 357-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8123696
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Nontypeable Haemophilus influenzae in the lower respiratory tract of patients with chronic bronchitis. Author(s): Bandi V, Apicella MA, Mason E, Murphy TF, Siddiqi A, Atmar RL, Greenberg SB. Source: American Journal of Respiratory and Critical Care Medicine. 2001 December 1; 164(11): 2114-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11739144
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Novel mechanistic targets for the treatment of sub-acute and chronic bronchitis. Author(s): Wegner CD. Source: Current Pharmaceutical Design. 2001 February; 7(3): 199-212. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11311113
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Nucleolar silver staining patterns and HLA-DR antigen expression in bronchial epithelial cells in chronic bronchitis. Author(s): Popp W, Braun O, Wachtler F, Mosgoller W, Holzner JH. Source: Pathology, Research and Practice. 1992 October; 188(7): 852-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1448375
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Obstructive sleep apnoea syndrome is common in subjects with chronic bronchitis. Report from the Obstructive Lung Disease in Northern Sweden studies. Author(s): Larsson LG, Lindberg A, Franklin KA, Lundback B; Obstructive Lung Disease in Northern Sweden Studies. Source: Respiration; International Review of Thoracic Diseases. 2001; 68(3): 250-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11416244
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Ofloxacin once daily versus twice daily in community-acquired pneumonia and acute exacerbation of chronic bronchitis. A randomized multicenter study. Author(s): Rayman J, Krchnavy M, Balciar P, Duchon J, Fortunik J, Faith L, Manduchova H, Drgona L, Koren P, Kraszko I, Krcmery V Jr. Source: Chemotherapy. 1996 May-June; 42(3): 227-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8983892
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Ofloxacin versus trimethoprim-sulfamethoxazole in the treatment of patients with acute exacerbation of chronic bronchitis. Study of Ofloxacin in Lower Respiratory Tract Infections Research Group. Author(s): Perez-Gonzalvo ME, Mosquera-Pestana JA, Ramos D, Apilanez J, Borja J, Arnau C, Garcia-Barbal J, Marin-Pardo J. Source: Clinical Therapeutics. 1996 May-June; 18(3): 440-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8829019
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Open-label, randomized comparison of the efficacy and tolerability of clarithromycin, levofloxacin, and cefuroxime axetil in the treatment of adults with acute bacterial exacerbations of chronic bronchitis. Author(s): Weiss LR. Source: Clinical Therapeutics. 2002 September; 24(9): 1414-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12380633
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Optimal treatment strategies for acute exacerbations of chronic bronchitis: high-risk patients. Author(s): Norrby SR. Source: Chemotherapy. 2001; 47 Suppl 4: 47-52; Discussion 53-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11586005
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Optimizing ceftazidime pharmacodynamics in patients with acute exacerbation of severe chronic bronchitis. Author(s): Lubasch A, Luck S, Lode H, Mauch H, Lorenz J, Bolcskei P, Welte T; COPD Study Group. Source: The Journal of Antimicrobial Chemotherapy. 2003 March; 51(3): 659-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12615868
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Optimizing economic outcomes in acute exacerbations of chronic bronchitis. Author(s): Destache CJ. Source: Pharmacotherapy. 2002 January; 22(1 Pt 2): 12S-17S; Discussion 30S-32S. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11791624
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Oral gemifloxacin once daily for 5 days compared with sequential therapy with i.v. ceftriaxone/oral cefuroxime (maximum of 10 days) in the treatment of hospitalized patients with acute exacerbations of chronic bronchitis. Author(s): Wilson R, Langan C, Ball P, Bateman K, Pypstra R; Gemifloxacin 207 Clinical Study Group. Source: Respiratory Medicine. 2003 March; 97(3): 242-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12645831
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Oral telithromycin 800 mg once daily for 5 days versus cefuroxime axetil 500 mg twice daily for 10 days in adults with acute exacerbations of chronic bronchitis. Author(s): Zervos MJ, Heyder AM, Leroy B. Source: J Int Med Res. 2003 May-June; 31(3): 157-69. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12870368
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Oxygen cost of breathing in patients with emphysema or chronic bronchitis in acute respiratory failure. Author(s): Sridhar MK. Source: American Journal of Respiratory and Critical Care Medicine. 1996 June; 153(6 Pt 1): 1988-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8665067
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Passive smoking exposure: a risk factor for chronic bronchitis and asthma in adults? Author(s): Radon K, Busching K, Heinrich J, Wichmann HE, Jorres RA, Magnussen H, Nowak D. Source: Chest. 2002 September; 122(3): 1086-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12226059
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Periodicity of asthma, emphysema, and chronic bronchitis in a northwest health maintenance organization. Author(s): Osborne ML, Vollmer WM, Buist AS. Source: Chest. 1996 December; 110(6): 1458-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8989061
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Pharmacoeconomic evaluation of acute exacerbations of chronic bronchitis and COPD. Author(s): Miravitlles M, Murio C, Guerrero T, Gisbert R; DAFNE Study Group. Decisiones sobre Antibioticoterapia y Farmacoeconomia en la EPOC. Source: Chest. 2002 May; 121(5): 1449-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12006427
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Prevalence and risk factors for asthma and chronic bronchitis in the capitals Helsinki, Stockholm, and Tallinn. Author(s): Pallasaho P, Lundback B, Meren M, Kiviloog J, Loit HM, Larsson K, Laitinen LA. Source: Respiratory Medicine. 2002 October; 96(10): 759-69. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12412974
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Prevalence of nasal symptoms and their relation to self-reported asthma and chronic bronchitis/emphysema. Author(s): Bousquet J, Leynaert B, Neukirch F. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 January; 19(1): 202-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11843322
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Preventing exacerbations of chronic bronchitis and COPD: therapeutic potential of mucolytic agents. Author(s): Poole PJ, Black PN. Source: American Journal of Respiratory Medicine : Drugs, Devices, and Other Interventions. 2003; 2(5): 367-70. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14719989
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Prophylactic antibiotic therapy for chronic bronchitis. Author(s): Black P, Staykova T, Chacko E, Ram FS, Poole P. Source: Cochrane Database Syst Rev. 2003; (1): Cd004105. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12535510
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Prophylaxis for acute exacerbations of chronic bronchitis using an antibacterial sublingual vaccine obtained through mechanical lysis: a clinical and pharmacoeconomic study. Author(s): Cogo R, Ramponi A, Scivoletto G, Rippoli R. Source: Acta Biomed Ateneo Parmense. 2003 August; 74(2): 81-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14509916
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Psychological distress and depressed mood in employees with asthma, chronic bronchitis or emphysema: a population-based observational study on prevalence and the relationship with smoking cigarettes. Author(s): Wagena EJ, Kant I, Huibers MJ, van Amelsvoort LG, Swaen GM, Wouters EF, van Schayck CP. Source: European Journal of Epidemiology. 2004; 19(2): 147-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15080082
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Pulmonary strongyloidiasis presenting as chronic bronchitis leading to interlobular septal fibrosis and cured by treatment. Author(s): Mukerjee CM, Carrick J, Walker JC, Woods RL. Source: Respirology (Carlton, Vic.). 2003 December; 8(4): 536-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14708557
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Quality of life in acute exacerbation of chronic bronchitis: results from a German population study. Author(s): Doll H, Grey-Amante P, Duprat-Lomon I, Sagnier PP, Thate-Waschke I, Lorenz J, Rychlik R, Pfeil T. Source: Respiratory Medicine. 2002 January; 96(1): 39-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11863209
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Quality of life, distress and self-esteem: a focus group study of people with chronic bronchitis. Author(s): Nicolson P, Anderson P. Source: British Journal of Health Psychology. 2003 September; 8(Pt 3): 251-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606972
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Quantified pathology of emphysema, pneumoconiosis, and chronic bronchitis in coal workers. Author(s): Leigh J, Outhred KG, McKenzie HI, Glick M, Wiles AN. Source: Br J Ind Med. 1983 August; 40(3): 258-63. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6871115
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Quantitation of tissue components in the bronchi in chronic bronchitis and emphysema. Author(s): Massarella GR. Source: Journal of Clinical Pathology. 1971 July; 24(5): 480-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5571851
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Quantitative evaluation of aerosol deposition pattern in the lung in patients with chronic bronchitis. Author(s): Olseni L, Palmer J, Wollmer P. Source: Physiological Measurement. 1994 February; 15(1): 41-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8161959
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Quantitative immunoelectrophoretic analysis of the plasma proteins in the sol phase of sputum from patients with chronic bronchitis. Author(s): Ryley HC, Brogan TD. Source: Journal of Clinical Pathology. 1973 November; 26(11): 852-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4128930
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Quantitative study of the bronchial bacterial flora in acute exacerbations of chronic bronchitis. Author(s): Martinez JA, Rodriguez E, Bastida T, Buges J, Torres M. Source: Chest. 1994 March; 105(3): 976. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8131595
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Questionnaire of the European Community for Coal and Steel (ECSC) on respiratory symptoms. 1987--updating of the 1962 and 1967 questionnaires for studying chronic bronchitis and emphysema. Author(s): Minette A. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1989 February; 2(2): 165-77. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2703044
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Quinolone antimicrobial agents in acute exacerbations of chronic bronchitis. Author(s): Maesen FP, Davies BI, Teengs JP, Baur C. Source: Eur J Respir Dis Suppl. 1986; 146: 585-90. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3465584
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Randomised double-blind comparison of oral gatifloxacin and co-amoxiclav for acute exacerbation of chronic Bronchitis. Author(s): Soler M, Lode H, Baldwin R, Levine JH, Schreurs AJ, van Noord JA, Maesen FP, Zehrer M; European Gatifloxacin Study group. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2003 March; 22(3): 144-50. Epub 2003 March 05. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12649711
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Randomized comparison of once-daily ceftibuten and twice-daily clarithromycin in the treatment of acute exacerbation of chronic bronchitis. Author(s): Ziering W, McElvaine P. Source: Infection. 1998 January-February; 26(1): 68-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9505188
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Randomized, double-blind study comparing 5- and 7-day regimens of oral levofloxacin in patients with acute exacerbation of chronic bronchitis. Author(s): Masterton RG, Burley CJ. Source: International Journal of Antimicrobial Agents. 2001 December; 18(6): 503-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11738336
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Randomized, double-blind study of ciprofloxacin and cefuroxime axetil for treatment of acute bacterial exacerbations of chronic bronchitis. The Bronchitis Study Group. Author(s): Chodosh S, McCarty J, Farkas S, Drehobl M, Tosiello R, Shan M, Aneiro L, Kowalsky S. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1998 October; 27(4): 722-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9798024
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Randomized, double-blind study of prulifloxacin versus ciprofloxacin in patients with acute exacerbations of chronic bronchitis. Author(s): Grassi C, Salvatori E, Rosignoli MT, Dionisio P; Prulifloxacin Study Group. Source: Respiration; International Review of Thoracic Diseases. 2002; 69(3): 217-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12097764
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Randomized, double-blind study of short-course (5 day) grepafloxacin versus 10 day clarithromycin in patients with acute bacterial exacerbations of chronic bronchitis. Author(s): Langan CE, Zuck P, Vogel F, McIvor A, Peirzchala W, Smakal M, Staley H, Marr C. Source: The Journal of Antimicrobial Chemotherapy. 1999 October; 44(4): 515-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10588313
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Randomized, double-blind, double-dummy study comparing the efficacy and safety of amoxycillin 1 g bd with amoxycillin 500 mg tds in the treatment of acute exacerbations of chronic bronchitis. Author(s): Georgopoulos A, Borek M, Ridl W; Amoxycillin Bronchitis Study Group. Source: The Journal of Antimicrobial Chemotherapy. 2001 January; 47(1): 67-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11152433
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Recent advances in diagnosis and management of chronic bronchitis and emphysema. Author(s): Chitkara RK, Sarinas PS. Source: Current Opinion in Pulmonary Medicine. 2002 March; 8(2): 126-36. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11845008
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Resolution of bronchial inflammation is related to bacterial eradication following treatment of exacerbations of chronic bronchitis. Author(s): White AJ, Gompertz S, Bayley DL, Hill SL, O'Brien C, Unsal I, Stockley RA. Source: Thorax. 2003 August; 58(8): 680-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12885984
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Risk factors for lower airway bacterial colonization in chronic bronchitis. Author(s): Monso E, Rosell A, Bonet G, Manterola J, Cardona PJ, Ruiz J, Morera J. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1999 February; 13(2): 338-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10065678
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Safety and effectiveness of lomefloxacin in patients with acute exacerbation of chronic bronchitis (AECB) chronically treated with oral theophyllines. Author(s): Melani AS, Pirrelli M, Sarlo F, Cantoni V; Lo-Theo Study Group. Source: J Chemother. 2001 December; 13(6): 628-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11806624
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Selection of clinical, patient-reported, and economic end points in acute exacerbation of chronic bronchitis. Author(s): Perfetto EM, Mullins CD, Subedi P, Li-McLeod J. Source: Clinical Therapeutics. 2001 October; 23(10): 1747-72. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11726009
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Short-course therapy of acute bacterial exacerbation of chronic bronchitis: a doubleblind, randomized, multicenter comparison of extended-release versus immediaterelease clarithromycin. Author(s): Nalepa P, Dobryniewska M, Busman T, Notario G. Source: Current Medical Research and Opinion. 2003; 19(5): 411-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13678478
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Short-term and long-term outcomes of moxifloxacin compared to standard antibiotic treatment in acute exacerbations of chronic bronchitis. Author(s): Wilson R, Allegra L, Huchon G, Izquierdo JL, Jones P, Schaberg T, Sagnier PP; MOSAIC Study Group. Source: Chest. 2004 March; 125(3): 953-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15006954
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Solutions for difficult diagnostic cases of acute exacerbations of chronic bronchitis. Author(s): Tsang KW. Source: Chemotherapy. 2001; 47 Suppl 4: 28-38; Discussion 53-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11586003
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Spirometric abnormalities associated with chronic bronchitis, asthma, and airway hyperresponsiveness among boilermaker construction workers. Author(s): Hauser R, Eisen EA, Pothier L, Lewis D, Bledsoe T, Christiani DC. Source: Chest. 2002 June; 121(6): 2052-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12065377
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Sulfated oligosaccharides isolated from the respiratory mucins of a secretor patient suffering from chronic bronchitis. Author(s): Degroote S, Maes E, Humbert P, Delmotte P, Lamblin G, Roussel P. Source: Biochimie. 2003 March-April; 85(3-4): 369-79. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12770775
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Symptom resolution assessed using a patient directed diary card during treatment of acute exacerbations of chronic bronchitis. Author(s): Woolhouse IS, Hill SL, Stockley RA. Source: Thorax. 2001 December; 56(12): 947-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11713358
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Symptoms of chronic bronchitis and the risk of coronary disease. Author(s): Jousilahti P, Vartiainen E, Tuomilehto J, Puska P. Source: Lancet. 1996 August 31; 348(9027): 567-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8774568
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Symptoms related to obstructive sleep apnoea are common in subjects with asthma, chronic bronchitis and rhinitis in a general population. Author(s): Larsson LG, Lindberg A, Franklin KA, Lundback B. Source: Respiratory Medicine. 2001 May; 95(5): 423-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11392586
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Telithromycin is as effective as amoxicillin/clavulanate in acute exacerbations of chronic bronchitis. Author(s): Aubier M, Aldons PM, Leak A, McKeith DD, Leroy B, Rangaraju M, BienfaitBeuzon C. Source: Respiratory Medicine. 2002 November; 96(11): 862-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12418583
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The economic impact of acute exacerbations of chronic bronchitis in the United States and Canada: a literature review. Author(s): Halpern MT, Higashi MK, Bakst AW, Schmier JK. Source: J Manag Care Pharm. 2003 July-August; 9(4): 353-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14613454
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The efficacy of moxifloxacin in acute exacerbations of chronic bronchitis: a Spanish physician and patient experience. Author(s): Miravitlles M, Ros F, Cobos A, Kubin R, Tillotson G. Source: Int J Clin Pract. 2001 September; 55(7): 437-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11594251
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The excess cost of acute exacerbations of chronic bronchitis in patients aged 45 and older in England and Wales. Author(s): McGuire A, Irwin DE, Fenn P, Gray A, Anderson P, Lovering A, MacGowan A. Source: Value in Health : the Journal of the International Society for Pharmacoeconomics and Outcomes Research. 2001 September-October; 4(5): 370-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11705127
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The place of antibiotic therapy in the management of chronic acute exacerbations of chronic bronchitis. Author(s): Akalin HE. Source: International Journal of Antimicrobial Agents. 2001; 18 Suppl 1: S49-55. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11574196
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The relation of body mass index to asthma, chronic bronchitis, and emphysema. Author(s): Guerra S, Sherrill DL, Bobadilla A, Martinez FD, Barbee RA. Source: Chest. 2002 October; 122(4): 1256-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12377850
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The safety and efficacy of short course (5-day) moxifloxacin vs. azithromycin in the treatment of patients with acute exacerbation of chronic bronchitis. Author(s): DeAbate CA, Mathew CP, Warner JH, Heyd A, Church D. Source: Respiratory Medicine. 2000 November; 94(11): 1029-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11127487
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Thromboxane antagonism and cough in chronic bronchitis. Author(s): Ishiura Y, Fujimura M, Yamamori C, Nobata K, Myou S, Kurashima K, Takegoshi T. Source: Annals of Medicine. 2003; 35(2): 135-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12795341
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Time course of recovery of health status following an infective exacerbation of chronic bronchitis. Author(s): Spencer S, Jones PW; GLOBE Study Group. Source: Thorax. 2003 July; 58(7): 589-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12832673
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Treatment outcomes in acute exacerbations of chronic bronchitis: comparison of macrolides and moxifloxacin from the patient perspective. Author(s): Lorenz J, Thate-Waschke IM, Mast O, Kubin R, Rychlik R, Pfeil T, Daniel D, Tillotson GS. Source: J Int Med Res. 2001 March-April; 29(2): 74-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11393351
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Ultrastructural changes of ciliated columnar epithelium and goblet cells in chronic bronchitis biopsy material. Author(s): Miskovits G, Appel J, Szule P. Source: Acta Morphol Acad Sci Hung. 1974; 22(1): 91-103. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4455047
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Ultrastructural characteristics of the alveolar phagocytic cells from patients with various forms of chronic bronchitis. Author(s): Polosukhin VV. Source: Ultrastructural Pathology. 2001 November-December; 25(6): 419-29. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11783906
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Ultrastructural heterogeneity of the alveolar macrophages from tobacco smokers with chronic bronchitis. Author(s): Polosukhin VV, Manouilova LS, Romberger DJ, Matthews KI, Pirruccello SJ, West W, Daughton DM, Millatmal T, Umino T, Rennard SI. Source: Ultrastructural Pathology. 2001 January-February; 25(1): 5-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11297319
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Use of oxygen driven nebulizer delivery systems for beta-2 agonists in chronic bronchitis. Author(s): O'Donnell D, Kelly CP, Cotter P, Clancy L. Source: Ir J Med Sci. 1985 May; 154(5): 198-200. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4030280
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Use of quinolones for the treatment of acute exacerbations of chronic bronchitis. Author(s): Chodosh S. Source: The American Journal of Medicine. 1991 December 30; 91(6A): 93S-100S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1662900
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Validity of the St George's respiratory questionnaire at acute exacerbation of chronic bronchitis: comparison with the Nottingham health profile. Author(s): Doll H, Duprat-Lomon I, Ammerman E, Sagnier PP. Source: Quality of Life Research : an International Journal of Quality of Life Aspects of Treatment, Care and Rehabilitation. 2003 March; 12(2): 117-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12639059
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Variability of plethysmographic measurements of airway resistance during the day in normal subjects and in patients with bronchial asthma and chronic bronchitis. Author(s): Zedda S, Sartorelli E. Source: Respiration; International Review of Thoracic Diseases. 1971; 28(2): 158-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5089793
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Variability of the pulmonary vascular response to acute hypoxia in chronic bronchitis. Author(s): Weitzenblum E, Schrijen F, Mohan-Kumar T, Colas des Francs V, Lockhart A. Source: Chest. 1988 October; 94(4): 772-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3139371
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Variation of CD8+ T-lymphocytes around the bronchial internal perimeter in chronic bronchitis. Author(s): Gamble E, Burns W, Zhu J, Ansari T, De Rose V, Kips J, Barnes NC, Jeffery PK. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 December; 22(6): 992-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14680091
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Variations in the prevalence across countries of chronic bronchitis and smoking habits in young adults. Author(s): Cerveri I, Accordini S, Verlato G, Corsico A, Zoia MC, Casali L, Burney P, de Marco R; European Community Respiratory Health Survey (ECRHS) Study Group. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2001 July; 18(1): 85-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11510810
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Ventilatory and pulmonary hemodynamic response to the respiratory stimulant doxapram in chronic bronchitis. Author(s): Conti F, Bertoli L, Bertoli M, Mantero O. Source: Pharmacol Res Commun. 1976 June; 8(3): 243-51. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=800260
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Ventilatory capacity, working capacity and exercise-induced bronchoconstriction in a population sample of subjects with bronchial asthma or chronic bronchitis. Author(s): Kiviloog J, Irnell L, Eklund G. Source: Scand J Respir Dis. 1975 August; 56(2): 73-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1166292
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Ventilatory limitation of exercise in patients with chronic bronchitis and/or emphysema. Author(s): Smidt U, Worth H, Petro W. Source: Bull Eur Physiopathol Respir. 1979 January-February; 15(1): 95-104. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=465826
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Viral antibody levels and clinical status in acute exacerbations of chronic bronchitis: a controlled prospective study. Author(s): Stenhouse AC. Source: British Medical Journal. 1968 August 3; 3(613): 287-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4299087
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Viscoelasticity, protein content and ciliary transport rate of sputum in patients with recurrent and chronic bronchitis. Author(s): Puchelle E, Zahm JM, Aug F. Source: Biorheology. 1981; 18(3-6): 659-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7326401
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Will falling death rates from acute and chronic bronchitis continue? Author(s): Wiggins J, Lyster W. Source: Lancet. 1988 July 30; 2(8605): 286. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2899282
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Workplace costs associated with acute exacerbation of chronic bronchitis: a comparison of moxifloxacin and levofloxacin. Author(s): Li-McLeod J, Perfetto EM. Source: Manag Care Interface. 2001 February; 14(2): 52-9. Erratum In: Manag Care Interface 2001 May; 14(5): 39. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11228817
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CHAPTER 2. NUTRITION AND CHRONIC BRONCHITIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and chronic bronchitis.
Finding Nutrition Studies on Chronic Bronchitis The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “chronic bronchitis” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7
Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following information is typical of that found when using the “Full IBIDS Database” to search for “chronic bronchitis” (or a synonym): •
A survey of chronic bronchitis among brassware workers. Author(s): Epidemiology Division, Industrial Toxicology Research Centre, Lucknow, India. Source: Rastogi, S K Gupta, B N Mathur, N Husain, T Mahendra, P N Pangtey, B S Srivastava, S Ann-Occup-Hyg. 1992 June; 36(3): 283-94 0003-4878
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Effect of four-week treatment with oxitropium bromide on lung mucociliary clearance in patients with chronic bronchitis or asthma. Author(s): Department of Thoracic Medicine, Royal Free Hospital and Bracknell, Berkshire, UK. Source: Pavia, D Lopez Vidriero, M T Agnew, J E Taylor, R G Eyre Brook, A Lawton, W A Pellow, P G Clarke, S W Respiration. 1989; 55(1): 33-43 0025-7931
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Effects of captopril combined with oxygen therapy at rest and on exercise in patients with chronic bronchitis and pulmonary hypertension. Author(s): Department of Medecine, Hopital A. Michallon, Joseph Fourier University, Grenoble, France. Source: Pison, C M Wolf, J E Levy, P A Dubois, F Brambilla, C G Paramelle, B Respiration. 1991; 58(1): 9-14 0025-7931
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Respiratory tract inflammation during the induction of chronic bronchitis in rats: role of C-fibres. Author(s): Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA. Source: Long, N C Abraham, J Kobzik, L Weller, E A Krishna Murthy, G G Shore, S A Eur-Respir-J. 1999 July; 14(1): 46-56 0903-1936
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Some aspects of “deep lung” cellular immunity in chronic bronchitis before and after therapy with tiopronin. Source: Fraschini, F Scaglione, F Coppi, G Piazza, G Marchi, E Montoli, C C Scarpazza, G Int-J-Clin-Pharmacol-Res. 1987; 7(2): 129-33 0251-1649
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
The following is a specific Web list relating to chronic bronchitis; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Vitamin A Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10066,00.html
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Minerals Carnitine Source: Prima Communications, Inc.www.personalhealthzone.com
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Food and Diet Garlic Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca
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CHAPTER 3. ALTERNATIVE MEDICINE AND CHRONIC BRONCHITIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to chronic bronchitis. 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 chronic bronchitis 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 “chronic bronchitis” (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 chronic bronchitis: •
Alternative therapies for chronic bronchitis. Author(s): Jones KL, Robbins RA. Source: The American Journal of the Medical Sciences. 1999 August; 318(2): 96-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10452567
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An investigation of renal function in chronic bronchitis. Author(s): Daggett P. Source: Postgraduate Medical Journal. 1977 January; 53(615): 24-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=17853
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Binding and diffusion characteristics of 14C EDTA and 99mTc DTPA in respiratory tract mucus glycoprotein from patients with chronic bronchitis. Author(s): Cheema MS, Groth S, Marriott C. Source: Thorax. 1988 September; 43(9): 669-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3143162
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Care for emphysema and chronic bronchitis. Author(s): Petty TL, Neff TA. Source: Annals of Internal Medicine. 1970 March; 72(3): 435-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5415427
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Chest physical therapy in patients with acute exacerbation of chronic bronchitis: effectiveness of three methods. Author(s): Bellone A, Lascioli R, Raschi S, Guzzi L, Adone R. Source: Archives of Physical Medicine and Rehabilitation. 2000 May; 81(5): 558-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10807091
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Chronic bronchitis and emphysema. Author(s): Webster JR Jr, Addington WW. Source: Postgraduate Medicine. 1971 December; 50(6): 113-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5128034
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Chronic bronchitis in the 1990s: up-to-date treatment. Author(s): Clarke SW. Source: Respiration; International Review of Thoracic Diseases. 1991; 58 Suppl 1: 43-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1925078
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Clinical observation in 31 cases of chronic bronchitis at remission stage treated with bufei keli. Author(s): Liu Y, Wang N, Wang N, Liu G, Yan H. Source: J Tradit Chin Med. 2003 December; 23(4): 246-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14719287
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Editorial: Does treatment for severe emphysema and chronic bronchitis really help? (A response). Author(s): Petty TL. Source: Chest. 1974 February; 65(2): 124-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4810668
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Effect of chest wall vibrations on pulmonary function in chronic bronchitis. Author(s): Rivington-Law BA, Epstein SW, Thompson GL, Corey PN.
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Source: Chest. 1984 March; 85(3): 378-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6697796 •
Effects of guided imagery in patients with chronic bronchitis and emphysema. Author(s): Moody LE, Fraser M, Yarandi H. Source: Clinical Nursing Research. 1993 November; 2(4): 478-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8220200
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Esberitox N as supportive therapy when providing standard antibiotic treatment in subjects with a severe bacterial infection (acute exacerbation of chronic bronchitis). A multicentric, prospective, double-blind, placebo-controlled study. Author(s): Hauke W, Kohler G, Henneicke-Von Zepelin HH, Freudenstein J. Source: Chemotherapy. 2002 December; 48(5): 259-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12476043
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History of the treatment of chronic bronchitis. Author(s): Ziment I. Source: Respiration; International Review of Thoracic Diseases. 1991; 58 Suppl 1: 37-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1925077
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Long-term treatment of chronic bronchitis with positive expiratory pressure mask and chest physiotherapy. Author(s): Christensen EF, Nedergaard T, Dahl R. Source: Chest. 1990 March; 97(3): 645-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2106412
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Measurement of tracheobronchial clearance after sauna in subjects with chronic bronchitis. Author(s): van Hengstum M, Festen J, Corstens F. Source: Thorax. 1991 October; 46(10): 732-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1750021
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No effect of oral high frequency oscillation combined with forced expiration manoeuvres on tracheobronchial clearance in chronic bronchitis. Author(s): van Hengstum M, Festen J, Beurskens C, Hankel M, van den Broek W, Corstens F. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1990 January; 3(1): 14-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2311725
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Oxygen therapy in hypoxic chronic bronchitis. Feasibility of nocturnal oxygen supplementation at home after hospital-induced improvement. Author(s): Mays EE.
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Source: J Chronic Dis. 1969 December; 22(6): 421-30. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5370514 •
Psychophysiologic predictors of weaning from mechanical ventilation in chronic bronchitis and emphysema. Author(s): Moody LE, Lowry L, Yarandi H, Voss A. Source: Clinical Nursing Research. 1997 November; 6(4): 311-30; Discussion 330-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9384053
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Regular balloon inflation for patients with chronic bronchitis: a randomised controlled trial. Author(s): Chauhan AJ, McLindon JP, Dillon P, Sawyer JP, Gray L, Leahy BC. Source: Bmj (Clinical Research Ed.). 1992 June 27; 304(6843): 1668-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1633520
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Rehabilitation in chronic bronchitis and bronchial asthma. Author(s): Trendelenburg F, Reinert M. Source: Scand J Respir Dis Suppl. 1974; 89: 41-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4528710
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Respiratory physical therapy in the treatment of chronic bronchitis. Author(s): Burford JG, George RB. Source: Seminars in Respiratory Infections. 1988 March; 3(1): 55-60. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3283882
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Solanum xanthocarpum (Kantakari) in chronic bronchitis, bronchial asthma and nonspecific unproductive cough. (An experimental and clinical co-relation). Author(s): Bector NP, Puri AS. Source: J Assoc Physicians India. 1971 October; 19(10): 741-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5132261
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Studies on the use of warming kidney regime in senile chronic bronchitis. Author(s): Shen ZY, Jiang XH, Zha LL, Chen WH, Chen SZ, Zhang RJ, Chen JQ, Chen XZ, Shi SZ, Zhou XX. Source: J Tradit Chin Med. 1983 December; 3(4): 295-302. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6562303
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The circulation in patients with chronic bronchitis and emphysema at rest and during exercise, with special reference to the influence of changes in blood viscosity and blood volume on the pulmonary circulation. Author(s): Segel N, Bishop JM.
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Source: The Journal of Clinical Investigation. 1966 October; 45(10): 1555-68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5925514 •
The efficiency of thermoregulation in adult patients with bronchial asthma and chronic bronchitis after climatic treatment at the Baltic seaside. Author(s): Maczynski B. Source: Pol Med Sci Hist Bull. 1970 October; 13(4): 179-81. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5489792
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Treatment of chronic bronchitis with modified ma xing shi gan tang and er chen tang. Author(s): Zhu Y, Liu X. Source: J Tradit Chin Med. 2004 March; 24(1): 12-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15119160
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Yoga therapy in chronic bronchitis. Author(s): Behera D. Source: J Assoc Physicians India. 1998 February; 46(2): 207-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11273114
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
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The following is a specific Web list relating to chronic bronchitis; 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 Bronchitis Source: Healthnotes, Inc.; www.healthnotes.com Bronchitis Source: Integrative Medicine Communications; www.drkoop.com Chronic Obstructive Pulmonary Disease Source: Healthnotes, Inc.; www.healthnotes.com Chronic Obstructive Pulmonary Disease Source: Integrative Medicine Communications; www.drkoop.com Emphysema Source: Integrative Medicine Communications; www.drkoop.com Immune Function Source: Healthnotes, Inc.; www.healthnotes.com
•
Chinese Medicine Beiling Jiaonang Alternative names: Beiling Capsules Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Manshanhong Alternative names: Dahurian Rhododendron Leaf; Folium Rhododendri Daurici Source: Chinese Materia Medica Manshanhongyou Alternative names: Daurian Rhododendron Oil; Oleum Rhododendri Daurici Source: Chinese Materia Medica Mujingye Alternative names: Hempleaf Negundo Chastetree Leaf; Folium Viticis Negundo Source: Chinese Materia Medica Mujingyou Alternative names: Negundo Chastetree Oil; Oleum Viticis Negundo Source: Chinese Materia Medica Yanbaicaisu Alternative names: ergenin; Yanbaicaisu (Yan Bai Cai Su); Bergeninu Source: Chinese Materia Medica
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•
Herbs and Supplements Blood Root Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Bromelain Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,760,00.html Cinnamomum Alternative names: Cinnamon; Cinnamomum zeylanicum Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Cysteine Source: Integrative Medicine Communications; www.drkoop.com Echinacea Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,775,00.html Elecampane Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca English Lavendar Source: Integrative Medicine Communications; www.drkoop.com French Lavendar Source: Integrative Medicine Communications; www.drkoop.com Indian Tobacco Source: Integrative Medicine Communications; www.drkoop.com Ivy Leaf Alternative names: Hedera helix Source: Healthnotes, Inc.; www.healthnotes.com Lavandula Alternative names: Lavender; Lavandula sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Lavandula Angustifolia Source: Integrative Medicine Communications; www.drkoop.com Lavender Alternative names: Lavandula angustifolia, English Lavendar, French Lavendar Source: Integrative Medicine Communications; www.drkoop.com
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Lobelia Alternative names: Lobelia inflata, Indian Tobacco Source: Integrative Medicine Communications; www.drkoop.com Lobelia Inflata Source: Integrative Medicine Communications; www.drkoop.com NAC (N-Acetyl Cysteine) Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,809,00.html N-Acetyl Cysteine Source: Healthnotes, Inc.; www.healthnotes.com Plantain Alternative names: Plantago lanceolata, Plantago major Source: Healthnotes, Inc.; www.healthnotes.com Thymus Extracts Source: Healthnotes, Inc.; www.healthnotes.com Wild Cherry Bark Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. PATENTS ON CHRONIC BRONCHITIS Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.8 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “chronic bronchitis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on chronic bronchitis, we have not necessarily excluded nonmedical patents in this bibliography.
Patents on Chronic Bronchitis By performing a patent search focusing on chronic bronchitis, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. 8Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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The following is an example of the type of information that you can expect to obtain from a patent search on chronic bronchitis: •
Certain dinucleotides and their use as modulators of mucociliary clearance and ciliary beat frequency Inventor(s): Pendergast; William (Durham, NC), Rideout; Janet L. (Raleigh, NC), Siddiqi; Suhaib M. (Raleigh, NC), Yerxa; Benjamin R. (Raleigh, NC) Assignee(s): Inspire Pharmaceuticals, Inc. (Durham, NC) Patent Number: 6,348,589 Date filed: July 10, 1998 Abstract: The present invention relates to certain novel dinucleotides and formulations thereof which are highly selective agonists of the P2Y.sub.2 and/or P2Y.sub.4 purinergic receptor. They are useful in the treatment of chronic obstructive pulmonary diseases such as chronic bronchitis, PCD, cystic fibrosis, as well as prevention of pneumonia due to immobility. Furthermore, because of their general ability to clear retained mucus secretions and stimulate ciliary beat frequency, the compounds of the present invention are also useful in the treatment of sinusitis, otitis media and nasolacrimal duct obstruction. They are also useful for treatment of dry eye disease and retinal detachment. Excerpt(s): This invention relates to certain dinucleotides which increase the hydration of retained mucus secretions, stimulate the production of mucins and increase ciliary beat frequency to increase clearance of retained secretions. Chronic obstructive pulmonary disease (COPD) affects 15 million patients in the U.S. and is the sixth leading cause of death. It is characterized by the retention of mucus secretions in the lungs. Many patients diagnosed with COPD have a disorder called chronic bronchitis (CB), and 600,000 patients are hospitalized each year due to an acute exacerbation of CB. Cystic fibrosis and Primary Ciliary Dyskinesia (PCD) are other examples of lung disorders which assume a clinical profile similar to COPD. Ciliary dyskinesia, whether primary or secondary, results in retained secretions that can only be cleared by coughing. Another disease state characterized by the accumulation of retained mucous secretions is sinusitis. Sinusitis is an inflammation of the paranasal sinuses typically associated with an upper respiratory infection. It is this country's most common healthcare complaint, affecting an estimated 31 million people. (A. Moss and V. Parsons, National Center for Health Statistics, 1986: 66-7, DHHS Publication No. (PHS)86-1588 (1985)). Web site: http://www.delphion.com/details?pn=US06348589__
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Compositions and methods for the inhibition of MUC-5 mucin gene expression Inventor(s): Basbaum; Carol (San Francisco, CA), Gallup; Marianne (Greenbrae, CA), Gebremichael; Assefa (Berkeley, CA), Gensch; Erin (San Francisco, CA), Li; Daizong (San Francisco, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,136,539 Date filed: February 11, 1999
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Abstract: The invention relates to methods for identifying inhibitors of mucin production, methods for inhibiting mucin production and methods for treating airway diseases, such as cystic fibrosis, chronic bronchitis, bronchial pneumonia and asthma. Compositions are provided for use in the method comprising reporter gene constructs which are inducible by mucomones. Excerpt(s): The present invention provides for methods of identifying compounds for treating medical conditions related to the inappropriate production of mucin, such as Pseudomonas infections of cystic fibrosis patients, bronchial pneumonia, chronic bronchitis and bronchial asthma. Mucins are a family of glycoproteins secreted from epithelial cells at many body surfaces, including the eyes, pancreatic ducts, gallbladder, prostate and mainly, respiratory, gastrointestinal and female reproductive tracts. Mucins are responsible for the viscoelastic properties of mucus. In the airways, mucin interacts with cilia to trap and clear pathogens and irritants. Bacterial infection of the airway epithelium is often accompanied by mucin overproduction. In addition, airway diseases such as chronic bronchitis, cystic fibrosis and asthma are characterized by mucus hypersecretion. Hypersecretion can overwhelm the ability of the cilia to function properly. Mucociliary impairment leads to airway mucus plugging which promotes chronic infection, airflow obstruction, and sometimes death. Nine mucin genes are known to be expressed in man: MUC 1, MUC 2, MUC 3, MUC 4, MUC 5AC, MUC 5B, MUC 6, MUC 7 and MUC 8 (Bobek, et al. (1993) J. Biol. Chem. 268:20563-9; Dusseyn, et al., (1997), J. Biol. Chem. 272:3168-78; Gendler, et al. (1991) Am. Rev.Resp. Dis. 144:S42S47; Gum, et al. (1989) J. Biol. Chem. 264:6480-6487; Gum, et al. (1990) Biochemical and Biophysical Research Communications 171:407-415; Lesuffleur, et al. (1995) J. Biol. Chem., 270:13665-13673; Meerzaman, et al. (1994) J. Biol. Chem. 269:12932-12939; Porchet, et al. (1991) Biochem. Biophys. Res. Comm. 175(2):414-422; Shankar, et al. (1994) Biochem. J., 300:295-298; Toribara, et al. (1997) J. Biol. Chem. 272:16398-403). Cysteinerich domains are considered to be typical of mucin sequences, having been reported in many mucins including MUC 2(Gum, et al. (1992), J. Biol. Chem. 267:21375-21383; Gum, et al. (1994), J. Biol. Chem. 269:2440-2446), MUC 5AC (Meerzaman, et al. (1994), J. Biol. Chem. 269:12932-12939), MUC 5B (Desseyn, et al. (1997) J. Biol. Chem. 272:3168-3178) and MUC 6 (Toribara, et al. (1997) J. Biol. Chem. 272:16398-16403) as well as in rat (Ohmori, et al. (1994) J. Biol. Chem. 269:17833-17840), pig (Eckhardt, et al. (1991) The Journal of Biological Chemistry, 266(15):9678-9686), cow (Bhargava, et al. (1990) Proc. Nat. Acad. Sci. U.S.A. 97:6798-6802) and frog (Probst, et al. (1990) Biochemistry 29:62406244) mucins. The cysteine-rich domains in mucins show varying degrees of similarity to the D-domains of von Willebrand factor (vWF). Web site: http://www.delphion.com/details?pn=US06136539__ •
Decongestant/expectorant compositions Inventor(s): D'Addio; Alexander D. (Piscataway, NJ), Dang; Phuong Grace (West Windsor, NJ) Assignee(s): Medpointe Healthcare Inc. (Somerset, NJ) Patent Number: 6,462,094 Date filed: August 22, 2001 Abstract: Compositions consisting essentially of phenylephrine tannate and guaifenesin which are effective when administered orally for the symptomatic relief of cough associated with respiratory tract conditions such as the common cold, bronchial asthma, acute and chronic bronchitis are disclosed.
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Excerpt(s): The invention relates to novel decongestant/expectorant compositions containing two essential ingredients phenylephrine tannate and guaifenesin. A considerable number of tannic acids occur in nature. Chemically, these acids are described as polymers of different hydroxybenzoic acids. Generally, when the term tannic acid is employed, as in the present case, the acid referred to is gallotannic acid. The internal ester of gallic acid also frequently referred to as tannin. Tannic acid consists of an amorphous powder, glistening scales, or spongy masses varying in color from yellowish-white to light brown. Tannic acid is very soluble in water or alcohol. Web site: http://www.delphion.com/details?pn=US06462094__ •
Method for the treatment of severe chronic bronchitis (bronchietasis) with an aerosolized antibiotic Inventor(s): Baker; William R. (Bellevue, WA), Montgomery; Alan B. (Medina, WA) Assignee(s): Chiron Corporation (Emeryville, CA) Patent Number: 6,387,886 Date filed: November 28, 2001 Abstract: The present invention is directed to a method for the treatment of severe chronic bronchitis, i.e., bronchiectasis, using a concentrated aminoglycoside antibiotic formulation delivering the antibiotic to the lung endobronchial space, including alveoli, in an aerosol or dry powder having a mass medium diameter predominately between 1 to 5 microns. Excerpt(s): The invention relates to methods and compositions for the treatment of severe chronic bronchitis or bronchiectasis by endobronchial delivery of aminoglycoside antibiotic compounds, such as tobramycin. In particular, the invention concerns formulations including aminoglycoside powders or concentrated solutions having pH between 5.5 and 7.0. The formulations permit delivery of aminoglycoside antibiotic compounds to the lung endobronchial space of airways in dry powder form or as an aerosol having mass medium average diameter predominantly between 1 to 5.mu. The formulated and delivered efficacious amount of aminoglycoside antibiotic compound, such as tobramycin, is sufficient for treatment and prophylaxis of acute and chronic endobronchial infections, particularly those caused by the bacterium Pseudomonas aeruginosa. In other aspects, the invention relates to the endobronchial delivery of effective amounts of an aminoglycoside antibiotic, such as tobramycin, to patients with bronchiectasis with P. aeruginosa to cause substantially complete eradication of the organism. The novel formulations have small volume yet deliver effective doses of aminoglycoside antibiotic compounds to the site of the infection. Bronchiectasis is defined as irreversible abnormal dilatation of the airways. Bronchiectasis can be caused by either acquired or congenital mechanisms that disrupt the normal processes of airway clearance and/or host defense. These causes may include ciliary motility disorders and cystic fibrosis (CF), or processes that cause persistent damage, such as a bacterial or viral pneumonia. Defects in host defense such as agammaglobulinemia, or mechanical processes such as foreign bodies that cause post-obstructive infection can also result in bronchiectasis (Barker, A. F. et al., "Bronchiectasis: update of an orphan disease," Am Rev Respir Dis; 137(4):969-78(1988)). Morbidity from bronchiectasis is caused by persistent airway infection. Treatment of infection may reduce morbidity. The microbiology of lung infections in CF has been well characterized, with Staphylococcus aureus, Haemophilus influenzae, and Pseudomonas aeruginosa colonizing in an age-related sequence. P. aeruginosa infects 60% of all
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patients with CF (Cystic Fibrosis Foundation, Cystic Fibrosis Foundation Patient Registry, Annual Data Report 1992, (1993)). However, the microbiology of bronchiectasis in patients without CF has not been well-characterized. One retrospective study of bronchiectasis found the most frequently isolated organisms to be P. aeruginosa (30.9% of patients), Haemophilus influenzae (30.1%), mycobacteria (22.8%), Mycobacterium avium-intracelluare (17.1%), other Gram-negative bacilli (13%), and Streptococcus pneumoniae (10.6%) (Nicotra, M. B. et al., "Clinical, pathophysiologic, and microbiologic characterization of bronchiectasis in an aging cohort," Chest 108(4):955-61 (1995)). Clinically, bronchiectasis is characterized by chronic airway infection, associated with intermittent exacerbations. Infection may manifest by expectoration of purulent sputum, fever, malaise, and weight loss. The density of P. aeruginosa in sputum in patients with exacerbations of bronchiectasis has been estimated at 10.sup.7 cfu/mL (Currie D. C. et al., "Simple method of monitoring colonizing microbial load in chronic bronchial sepsis: pilot comparison of reduction in colonizing microbial load with antibiotics given intermittently and continuously," J Clin Pathol 40:830-836 (1987)). Exacerbations may be treated with oral or parenteral antibiotics, but the options for treatment of P. aeruginosa are limited. One common regimen, a 14-21 day course of parenteral aminoglycoside in combination with a third-generation cephalosporin, is widely used but has several disadvantages. The penetration of parenterallyadministered aminoglycosides into bronchial secretions is poor and thus hill doses must be given in order to achieve high sputum concentrations (Pennington J. E., "Penetration of antibiotics into respiratory secretions," Rev Infect Dis 3(1):67-73 (1981)). High doses and multiple courses of therapy lead to high serum concentrations and increase the risk of serious adverse effects, such as ototoxicity and nephrotoxicity. Treatment of patients with bronchiectasis with P. aeruginosa seldom, if ever, eradicates the organisms--most of the treatment benefit from either oral or IV antibiotics just suppresses growth, with regrowth occurring after discontinuation of antibiotic therapy. Therefore, any method that can eradicate infection for any period of time would be useful, novel and an advance in the art. Web site: http://www.delphion.com/details?pn=US06387886__ •
Method for treatment of chronic bronchitis using indole compounds Inventor(s): Macias; William Louis (Indianapolis, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,972,988 Date filed: March 12, 1998 Abstract: A method is disclosed for the treatment of chronic bronchitis by administering to a mammal in need thereof a therapeutically effective amount of a 1Hindole-3-glyoxylamide compound. Excerpt(s): This invention relates to the use of 1H-indole-3-glyoxylamide compounds for the treatment of chronic bronchitis. Respiratory diseases represent an increasingly important category of illness. The incidence of such diseases is expected to steadily increase with world industrialization and the rise of atmospheric pollutants. Among respiratory diseases of concern is chronic bronchitis. In man, the lower conductive airway system begins with the trachea which divides into a series of inverted "Y" air conducting passages. The parts of the system of lower conducting airways in man comprise the two stem bronchi, the smaller bronchi, and the bronchioles. If the trachea is regarded as the starting branch, then the bronchi represent 1 to 3 stage branching and
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the bronchioles are 4 to 16 stage branching. These airway branches are the site of chronic bronchitis. Web site: http://www.delphion.com/details?pn=US05972988__ •
Treatment of viscous mucous-associated diseases Inventor(s): Babior; Bernard M. (San Diego, CA), Gottlieb; Roberta A. (San Diego, CA) Assignee(s): The Scripps Research Institute (La Jolla, CA) Patent Number: 5,908,611 Date filed: May 5, 1995 Abstract: The present invention relates to therapeutic methods for treating diseases characterized by an accumulation of high molecular weight DNA in mucous, thereby contributing to the viscosity of the mucous. Such diseases include cystic fibrosis and chronic bronchitis. Treatment includes administration of weak organic acids to promote acidification of cells and consequently apoptosis-induced DNA fragmentation. The invention also relates to therapeutic apparatus for administering the acid compositions. Excerpt(s): The present invention relates to therapeutic methods for treating diseases characterized by an accumulation of DNA in mucous thereby creating viscous mucous. More particularly, the invention relates to the treatment of viscous mucous-associated diseases such as cystic fibrosis (CF) and chronic bronchitis (CB). The therapeutic methods are directed to decreasing the amount of high molecular weight DNA that contributes to the mucous viscosity. Acidifying compositions including weak organic acids and other chemicals are used to promote acidification in DNA-generating cells thereby inducing fragmentation of DNA. The invention also relates to therapeutic apparatus for delivery of the therapeutic composition formulations. In healthy individuals whose lungs are uninfected, lung secretions are complex non-homogeneous materials that form a viscous hydrophilic whitish gel. Mucous glycoproteins in the uninfected lung secretions contribute to the viscosity. However, in infected or purulent yellowish or greenish lung secretions as seen in cystic fibrosis, chronic bronchitis and pneumonia, both mucous glycoproteins and DNA are responsible for increasing the viscosity of the secretions. Cystic fibrosis patients who do not have concurrent bacterial or viral infections also exhibit increased mucous viscosity. Investigators have determined that DNA, absent from healthy lung secretions, is present in large amounts from 3-14 milligrams/milliliters in purulent lung secretions. See, Chernick et al., Pediatrics, 24:739-745 (1959) and Potter et al., Am. J. Dis. Child, 100:493-495 (1960). While the viscosity of uninfected as well as infected mucous secretions in individuals with cystic fibrosis, chronic bronchitis or pneumonia was originally thought to be the result of a network of entangled glycoproteins, more recent data suggests that DNA present in the secretions contributes to the entanglement of the network. See, Shak et al., Proc. Natl. Acad. Sci., USA, 87:9188-9192 (1990). Moreover, addition of DNA to a sputum sample has been shown to increase the viscosity of DNA as described by Picot et al., Thorax, 33:235-242 (1978). Web site: http://www.delphion.com/details?pn=US05908611__
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Patent Applications on Chronic Bronchitis As of December 2000, U.S. patent applications are open to public viewing.9 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to chronic bronchitis: •
Antitussive/expectorant compositions Inventor(s): D'Addio, Alexander D.; (Piscataway, NJ), Dang, Phuong Grace; (West Windsor, NJ) Correspondence: Carella, Byrne, Bain, Gilfillan, Cecchi,; Stewart & Olstein; 6 Becker Farm Road; Roseland; NJ; 07068; US Patent Application Number: 20030044461 Date filed: August 22, 2001 Abstract: Compositions consisting essentially of carbetapentane tannate and guaifenesin which are effective when administered orally for the symptomatic relief of cough associated with respiratory tract conditions such as the common cold, bronchial asthma, acute and chronic bronchitis are disclosed. Excerpt(s): A considerable number of tannic acids occur in nature. Chemically, these acids are described as polymers of different hydroxybenzoic acids. Generally, when the term tannic acid is employed, as in the present case, the acid referred to is gallotannic acid. The internal ester of gallic acid also frequently referred to as tannin. Tannic acid consists of an amorphous powder, glistening scales, or spongy masses varying in color from yellowish-white to light brown. Tannic acid is very soluble in water or alcohol. Tannic acids are usually obtained from glycosides which consist of several molecules of a tannic acid in combination with glucose. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Devices for creating collateral channels in the lungs Inventor(s): Laufer, Michael D.; (Menlo Park, CA), Roschak, Ed; (Mountain View, CA), Tanaka, Don; (Saratoga, CA) Correspondence: Morrison & Foerster Llp; 755 Page Mill RD; Palo Alto; CA; 94304-1018; US Patent Application Number: 20020049370 Date filed: July 18, 2001 Abstract: The devices and methods disclosed herein are directed to altering gaseous flow within a lung to improve the expiration cycle of, for instance, an individual having Chronic Obstructive Pulmonary Disease. More particularly, these devices and methods produce and to maintain collateral openings or channels through the airway wall so that expired air is able to pass directly out of the lung tissue to facilitate both the exchange of oxygen ultimately into the blood and/or to decompress hyper-inflated lungs. The devices and methods also disclose locating and selecting a site for creation of a collateral opening.The invention is directed to methods and devices to altering gaseous flow within a lung to improve the expiration cycle of an individual, particularly individuals
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This has been a common practice outside the United States prior to December 2000.
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having Chronic Obstructive Pulmonary Disease (COPD). More particularly, methods and devices are disclosed to produce and to maintain collateral openings or channels th rough the airway wall so that expired air is able to pass directly out of the lung tissue to facilitate both the exchange of oxygen ultimately into the blood and/or to decompress hyper-inflated lungs.The term "Chronic Obstructive Pulmonary Disease" (COPD) is generally used to describe the disorders of emphysema and chronic bronchitis. Previously, COPD was also known as Chronic Obstructive Lung Disease (COLD), Chronic Airflow Obstruction (CAO), or Chronic Airflow Limitation (CAL). Some also consider certain types of asthma to fall under the definition of COPD. Emphysema is characterized by an enlargement of air spaces inside the lung. Hence, Emphysema is an anatomic definition and it can only be presumed in a living patient. Chronic bronchitis is characterized by excessive mucus production in the bronchial tree. Chronic bronchitis is a clinical definition and denotes those individuals who meet criteria defining the disease. It is not uncommon for an individual to suffer from both disorders. Excerpt(s): In 1995, the American Lung Association (ALA) estimated that between 15-16 million Americans suffered from COPD. The ALA estimated that COPD was the fourthranking cause of death in the U.S. The ALA estimates that the rates of emphysema is 7.6 per thousand population, and the rate for chronic bronchitis is 55.7 per thousand population. Those inflicted with COPD face disabilities due to the limited pulmonary functions. Usually, individuals afflicted by COPD also face loss in muscle strength and an inability to perform common daily activities. Often, those patients desiring treatment for COPD seek a physician at a point where the disease is advanced. Since the damage to the lungs is irreversible, there is little hope of recovery. Most times, the physician cannot reverse the effects of the disease but can only offer treatment and advice to halt the progression of the disease. To understand the detrimental effects of COPD, the workings of the lungs requires a cursory discussion. The primary function of the lungs is to permit the exchange of two gasses by removing carbon dioxide from venous blood and replacing it with oxygen. Thus, to facilitate this exchange, the lungs provide a blood gas interface. The oxygen and carbon dioxide move between the gas (air) and blood by diffusion. This diffusion is possible since the blood is delivered to one side of the bloodgas interface via small blood vessels (capillaries). The capillaries are wrapped around numerous air sacs called alveoli which function as the blood-gas interface. A typical human lung contains about 300 million alveoli. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of treatment Inventor(s): Henkel, Timothy John; (King of Prussia, PA) Correspondence: Glaxosmithkline; Corporate Intellectual Property - Uw2220; P.O. Box 1539; King OF Prussia; PA; 19406-0939; US Patent Application Number: 20020137751 Date filed: September 17, 2001 Abstract: A method of reducing the recurrences of acute exacerbations of chronic bronchitis (AECB) in a patient in need thereof comprising administering a therapeutically effective amount of gemifloxacin, or a pharmaceutically acceptable salt thereof. Excerpt(s): The present invention relates to the use of gemifloxacin for reducing the recurrences and/or reducing the severity of recurrences of acute exacerbations of
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chronic bronchitis (AECB). Patients with chronic bronchitis frequently experience episodes of exacerbation, characterised by increased cough, increased sputum volume and purulence, and respiratory distress. Annual death rates from chronic bronchitis and its exacerbations in various countries, range from approximately 20 to 80 deaths per 100,000 males aged from 55 to 65 years. The total direct medical costs of treating AECB have been estimated as at least.English Pound.396 million in the United Kingdom (UK) (1992/3) and up to $2.3 billion in the USA (1995/6). Patients who are hospitalised account for at least 67% of all costs. AECB is also responsible for a significant loss of working days, 1.54 million, and restricted activity days, 3.63 million, in the USA (1994). Patient well-being and quality of life may also be expected to be affected by AECB. The social, medical and economic consequences of AECB are thus considerable. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods for treating chronic obstructive pulmonary disease (COPD) Inventor(s): Bell, Gregory; (Tiburon, CA), Gladue, Ronald P.; (Stonington, CT), Kudlacz, Elizabeth M.; (Groton, CT), Showell, Henry J.; (Westbrook, CT), Yang, Xiao-dong; (Palo Alto, CA) Correspondence: Knobbe Martens Olson & Bear Llp; 2040 Main Street; Fourteenth Floor; Irvine; CA; 92614; US Patent Application Number: 20030232048 Date filed: March 18, 2003 Abstract: The present disclosure relates to methods of treating Chronic Obstructive Pulmonary Disease (COPD) and its various indications, particularly including chronic bronchitis, emphysema, and irreversible asthma. Treatment regimens generally include the administration of anti-interleukin-8 antibodies to the patient to reduce the severity of an inflammatory response by the patient's immune system. Excerpt(s): Anti-interleukin-8 antibodies are described for use in the treatment of chronic obstructive pulmonary disease (COPD). Chronic Obstructive Pulmonary Disease (COPD) is one of the most common chronic conditions and the fourth leading cause of death in the United States. COPD includes several related disorders that restrict the patient's ability to exhale. Accordingly, patients frequently experience dyspnea, or shortness of breath. Dyspnea typically causes patient discomfort, limits the patient's ability to engage in physical activity, and can induce further adverse health effects due to a diminished supply of oxygen. The two most common disorders associated with COPD are chronic bronchitis and emphysema, though patients suffering from COPD may also have chronic asthma, bronchiectasis, immunoglobulin deficiency, and cystic fibrosis. Although various environmental toxins are believed to contribute to COPD, cigarette smoking is the most common cause. Cigarette smoke is believed to be the cause of more than 80% of all COPD cases. Cigarette smoke contains harmful irritants that inflame the airways and the lungs. In turn, this inflammation triggers a series of biochemical events in the body's immune system which cause substantial damage of the lungs and airways. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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USE OF AEROSOLIZED CYCLOSPORINE FOR PREVENTION AND TREATMENT OF PULMONARY DISEASE Inventor(s): IACONO, ALDO T.; (PITTSBURGH, PA) Correspondence: Baker & Botts; 30 Rockefeller Plaza; New York; NY; 10112 Patent Application Number: 20020006901 Date filed: February 5, 1999 Excerpt(s): The present invention relates to methods and compositions for prevention of graft rejection in lung transplant recipients and for treatment of subjects with pulmonary disorders. Specifically, the methods and compositions of the invention provide a means for inhibiting immune response mediated inflammatory processes in the lungs. The method of the invention comprises the administration of aerosolized cyclosporine for prevention of acute and/or chronic refractory rejection in lung transplant patients. The invention is based on the observation that when aerosolized cyclosporine is administered shortly after lung transplantation, the preparation is well tolerated and the rate of acute rejection is substantially reduced, compared to controls that receive conventional oral or intravenous immunosuppression only. The invention further provides for the use of aerosolized cyclosporine to treat subjects having immunologically mediated inflammatory pulmonary disorders including, but not limited to, asthma, cystic fibrosis, idiopathic pulmonary fibrosis, chronic bronchitis and allergic rhinitis. The present invention, by enabling a method for the use of aerosolized cyclosporine for inhibiting pulmonary inflammation leading to prevention of graft rejection and treatment of pulmonary disorders, provides a safer and less toxic treatment than those methods that utilize systemic administration of cyclosporine. The long-term success of lung transplantation is currently limited by the high incidence of transplant-related lung disease (Glanville, A. R., et al., 1987, Ann Intern Med 107:300306; Trulock, E. P., 1993, Chest 103:1566-1576; Kesten, S., 1995, 152: 1321-1324; Paradis, I. et al., 1993, 14:751-763). This complication is related to the transplant recipients' ongoing immune response against donor major histocompatability antigens. Such an immune response generally leads to persistent acute rejection of the lung allograft which is a predominant risk factor for the subsequent development of chronic rejection and permanent allograft dysfunction and failure resulting in excessive morbidity and mortality. This is a tragic consequence of lung transplantation and for this reason, is a leading area of research in this field. Although the rates of short-term survival after lung transplantation have improved compared to most other solid organ transplants, the therapeutic benefit of lung transplantation is still limited by poor longer-term outcomes principally due to chronic rejection of the transplanted lung. Patients, whose lung allografts are in acute and/or chronic rejection, are currently treated by a variety of potent immunosuppressive agents, such as azathioprine, tacrolimus, mycophenolate mofetil and cyclosporine, generally given by the intravenous or oral route, that profoundly inhibit the T cell response to donor antigen within the transplanted allograft. Unfortunately, these immunosuppressive agents diminish the patient's ability to mount an effective response to viral, fungal and bacterial pathogens thereby predisposing the patient to life threatening opportunistic infections and other toxic events such as kidney toxicity. Despite usage of conventional systemic (oral or intravenous) immunosuppressive drugs, about 50% of the treated patients develop refractory chronic rejection, characterized histologically by bronchiolitis obliterans, followed by a progressive decline in pulmonary function and eventually respiratory failure and death. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Keeping Current In order to stay informed about patents and patent applications dealing with chronic bronchitis, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “chronic bronchitis” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on chronic bronchitis. You can also use this procedure to view pending patent applications concerning chronic bronchitis. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 5. BOOKS ON CHRONIC BRONCHITIS Overview This chapter provides bibliographic book references relating to chronic bronchitis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on chronic bronchitis 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 “chronic bronchitis” (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 chronic bronchitis: •
Complete Bedside Companion: No-Nonsense Advice on Caring for the Seriously Ill Source: New York, NY: Simon and Schuster Consumer Group. 1998. 544 p. Contact: Available from Simon and Schuster Consumer Group. 1633 Broadway, New York, NY 10019-6785. (212) 654-8232. Fax (212) 654-4758. PRICE: $27.00. ISBN: 0684801434. Summary: This book for caregivers traces the sequences of events common to a lifethreatening illness and examines the concerns and crises that arise on the journey from diagnosis to death and beyond. The first eleven chapters cover the hospital and medical team, working with the doctors, essential nursing skills (preventing infection, skin care, hygiene, wound care, toileting, preventing falls, measuring vital signs, administering medications, and managing pain), emotional considerations, support services (mustering family and friends, utilizing social support and nursing care services),
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consumer activism (including drug and treatment trials), caring for the caregivers (respite care, caring for oneself, caring for other loved ones), paying the bills and other financial concerns, preparing for death (legal issues, advanced medical directives, withholding treatment), death and dying, and the aftermath of death (grieving, funeral arrangements). The second section consists of eight chapters focusing on specific illnesses: cancer, cardiovascular disease, cerebrovascular stroke or traumatic brain injury (TBI), chronic obstructive pulmonary disease (emphysema and chronic bronchitis), diabetes, AIDS, liver disease, kidney disease, and progressive neurological disease (Alzheimer's, Parkinsons, amyotrophic lateral sclerosis). Each chapter outlines initial symptoms, diagnostic tests and procedures, treatment methods and their side effects, tips on preventing and managing common complications, how the illness typically progresses, and medical terms related to the illness. The text concludes with a lengthy resource list, a bibliography, and a detailed subject index.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “chronic bronchitis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “chronic bronchitis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “chronic bronchitis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Pathology of chronic bronchitis and emphysema; by Brian Edyvean Heard; ISBN: 0700014195; http://www.amazon.com/exec/obidos/ASIN/0700014195/icongroupinterna
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The chemotherapy of chronic bronchitis and allied disorders by John Robert May; ISBN: 0340049669; http://www.amazon.com/exec/obidos/ASIN/0340049669/icongroupinterna
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The Natural history of chronic bronchitis and emphysema: An eight-year study of early chronic obstructive lung disease in working men in London; ISBN: 0192611194; http://www.amazon.com/exec/obidos/ASIN/0192611194/icongroupinterna
Chapters on Chronic Bronchitis In order to find chapters that specifically relate to chronic bronchitis, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and chronic bronchitis 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 “chronic bronchitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on chronic bronchitis:
Books
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Pulmonary Disease Source: in Little, J.W., et al. Dental Management of the Medically Compromised Patient. 5th ed. St. Louis, MO: Mosby, Inc. 1997. p. 241-259. Contact: Available from Harcourt Health Sciences. 11830 Westline Industrial Drive, St. Louis, MO 63146. (800) 325-4177. Fax (800) 874-6418. Website: www.harcourthealth.com. PRICE: $48.00 plus shipping and handling. ISBN: 0815156340. Summary: A working knowledge of the multitude of compromised health states is essential for dental professionals, as the majority of medically compromised patients need or want oral health care. This chapter on pulmonary (lung) disease is from a text that provides the dental practitioner with an up to date reference work describing the dental management of patients with selected medical problems. The authors focus on some of the more commonly encountered pulmonary conditions, including chronic obstructive pulmonary disease (COPD, including chronic bronchitis and emphysema), asthma, and tuberculosis. The authors discuss incidence and prevalence of each condition, its etiology (including genetic and lifestyle causes), pathophysiology and complications, signs and symptoms (clinical presentation and laboratory findings), the medical management of patients with pulmonary diseases, and the dental management of this population. 7 figures. 8 tables. 45 references.
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Infection and 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. 485-499. 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 infection and diabetes is from a compilation and assessment of data on diabetes and its complications in the United States. The authors characterize infections related to diabetes as 'probable' (the data support the presence of the association), 'possible' (presence or absence of an association cannot be established from current data) and 'doubtful' (data argue for no association). People with diabetes probably have a higher risk of the following infections: asymptomatic bacteriuria, lower extremity infections, reactivation tuberculosis in American Indians, infections in surgical wounds after sternotomy and total hip replacement, and group B streptococcal. Support for these associations comes from controlled observational studies in all cases, except for lower extremity infections, where the magnitude of the association between foot and ankle infection and diabetes from hospital-based data appears too great to be explained by detection, selection, or other potential biases. Local and systemic immunologic defects probably account for higher infection rates in patients with diabetes. Autonomic and sensory neuropathy probably account for higher bacteriuria and lower extremity infection rates, while systemic immunologic effects of diabetes may be responsible for the increased risk of surgical wound infection and tuberculosis reinfection. Populationbased data also support a probable higher influenza and pneumonia mortality rate in patients with diabetes. There is a possible association between diabetes and prevalence of the following infections: cystitis, pyelonephritis, candida vulvovaginitis and cystitis, pneumonia, influenza, chronic bronchitis, bacteremia, primary tuberculosis, reactivation tuberculosis in non-American Indians, mucormycosis, malignant otitis
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externa, and Fournier's gangrene. Doubtful associations exist between diabetes and prevalence of chronic sinusitis or S. aureus colonization (staph infection). 6 tables. 103 references. (AA-M). •
Respiratory Disorders Source: in Grundy, M.C.; Shaw, L.; and Hamilton, D.V. Illustrated Guide to Dental Care for the Medically Compromised Patient. St. Louis, MO: Mosby-Year Book, Inc. 1993. p. 37-40. Contact: Available from Mosby-Year Book, Inc. 11830 Westline Industrial Drive, St. Louis, MO 63146-9934. (800) 426-4545 or (314) 872-8370; Fax (800) 535-9935 or (314) 4321380; E-mail:
[email protected]; http://www.mosby.com. PRICE: $24.95 plus shipping and handling. ISBN: 0815140223. Summary: This chapter, from an illustrated guide to dental care for medically compromised patients, discusses respiratory disorders. Disorders covered include chronic obstructive pulmonary disease (chronic bronchitis); bronchiectasis; cystic fibrosis; and asthma. For each condition, the authors provide a brief description, the components of medical management, and suggestions for dental care. Illustrations, including photographs, are included. 3 figures.
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CHAPTER 6. MULTIMEDIA ON CHRONIC BRONCHITIS Overview In this chapter, we show you how to keep current on multimedia sources of information on chronic bronchitis. 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 chronic bronchitis is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “chronic bronchitis” 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 “chronic bronchitis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on chronic bronchitis: •
Diagnosing Alpha 1 Antitrypsin Deficiency Source: Minneapolis, MN: Alpha 1 Association. 199x. (videocassette). Contact: Available from Alpha 1 Association. 8120 Penn Avenue, South, Suite 549, Minneapolis, MN 55431-1326. (800) 521-3025 or (612) 703-9979. Fax (612) 703-9977. Email:
[email protected]. Website: www.alpha1.org. PRICE: $3.00 plus shipping and handling. Summary: This videotape program, narrated by Sandra Brandley, the Executive Director of the Alpha 1 National Association, reminds physicians of the symptoms and differential diagnosis of alpha 1 antitrypsin deficiency (A1AD or Alpha 1). The program features Dr. James Stoller, who describes the typical underdiagnosis of A1AD which is typical: the mean time until diagnosis is 7 years (from onset of symptoms) and the mean number of doctors consulted before diagnosis is 3.5. Alpha 1 is a relatively common genetic disorder that affects infants, children, and adults. It is the most common
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metabolic disorder that causes liver disease in infants and children; the disorder also causes cirrhosis and cancer of the liver in adults. Symptoms of A1AD deficiency in children include prolonged obstructive jaundice, low birth weight, mildly elevated liver enzymes, cholestasis, enlarged liver, abnormal bleeding, feeding difficulties, poor growth (or failure to thrive), and ascites (abnormal accumulation of fluids). In adults, the spectrum of liver disease associated with A1AD deficiency varies from mild to severe. Symptoms include chronic active hepatitis, cryptogenic cirrhosis (liver scarring of unknown cause), portal hypertension (high blood pressure in the portal vein of the liver), and hepatocellular carcinoma (liver cancer). A rare but telling symptom is panniculitis, a chronic inflammation of subcutaneous fat featuring ulcerated skin lesions on the torso. Dr. Stoller reminds viewers of the indications for A1AD screening: premature onset of moderate to severe chronic obstructive pulmonary disease (COPD) before age 50; predominant basilar emphysema; chronic bronchitis with airflow obstruction in a nonsmoker; bronchiectasis (irreversible dilation and destruction of the bronchial walls) without clear risk factors; development of unremitting asthma; family history of A1AD; cirrhosis without apparent risk factors; and family history of panniculitis. The program includes a chart of laboratory values and the risk of development of A1AD, and a series of interviews with patients about the interplay of early diagnosis and good quality of life. The program concludes with the contact information for the Alpha 1 National Association (800-521-3025).
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CHAPTER 7. PERIODICALS AND NEWS ON CHRONIC BRONCHITIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover chronic bronchitis.
News Services and Press Releases One of the simplest ways of tracking press releases on chronic bronchitis 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 “chronic bronchitis” (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 chronic bronchitis. 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 “chronic bronchitis” (or synonyms). The following was recently listed in this archive for chronic bronchitis: •
Colonization with C. pneumoniae tied to chronic bronchitis flare-ups Source: Reuters Medical News Date: August 07, 2002
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Phase II Results On Effectiveness Of Oral Mucosal Vaccine For Chronic Bronchitis Released Source: Reuters Medical News Date: September 12, 1997 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 “chronic bronchitis” (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 “chronic bronchitis” (or synonyms). If you know the name of a company that is relevant to chronic bronchitis, 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 “chronic bronchitis” (or synonyms).
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Academic Periodicals covering Chronic Bronchitis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to chronic bronchitis. In addition to these sources, you can search for articles covering chronic bronchitis that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 8. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for chronic bronchitis. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a non-profit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with chronic bronchitis. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.).
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The following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to chronic bronchitis: Bronchodilators, Adrenergic •
Inhalation - U.S. Brands: Adrenalin Chloride; Airet; Alupent; Arm-a-Med Isoetharine; Arm-a-Med Metaproterenol; Asthmahaler Mist; AsthmaNefrin; Beta2; Brethaire; Bronkaid Mist; Bronkaid Suspension Mist; Bronkometer; Bronkosol; Dey-Lute Isoetharine; Dey-Lute Metaproterenol; Foradil; Isuprel; Isuprel Mistometer; Maxair; Maxair Autohaler; Medihaler-Iso; microNefrin; Nephron; Primatene Mist; Proventil; Proventil HFA; S-2; Serevent Diskus; Vaponefrin; Ventolin; Ventolin HFA; Ventolin Nebules; Ventolin Rotacaps http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202095.html
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Oral/Injection - U.S. Brands: Adrenalin; Alupent; Ana-Guard; Brethine; Bricanyl; EpiPen Auto-Injector; EpiPen Jr. Auto-Injector; Isuprel; Proventil; Proventil Repetabs; Ventolin; Volmax http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202096.html
Bronchodilators, Theophylline •
Systemic - U.S. Brands: Aerolate Sr; Asmalix; Choledyl; Choledyl SA; Elixophyllin; Lanophyllin; Phyllocontin; Quibron-T Dividose; Quibron-T/SR Dividose; Respbid; Slo-Bid Gyrocaps; Slo-Phyllin; Theo-24; Theobid Duracaps; Theochron; Theo-Dur; Theolair; Theolair-SR; Theo-Time; Theovent Long-Acting; Theo-X; T-Phyl; Truphylline; Truxophyllin; Uni-Dur; Uniphyl http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/201945.html
Corticosteroids •
Dental - U.S. Brands: Kenalog in Orabase; Orabase-HCA; Oracort; Oralone http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202010.html
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Inhalation - U.S. Brands: AeroBid; AeroBid-M; Azmacort; Beclovent; Pulmicort Respules; Pulmicort Turbuhaler; Qvar; Vanceril; Vanceril 84 mcg Double Strength http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202011.html
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Nasal - U.S. Brands: Beconase; Beconase AQ; Dexacort Turbinaire; Flonase; Nasacort; Nasacort AQ; Nasalide; Nasarel; Nasonex; Rhinocort; Vancenase; Vancenase AQ 84 mcg; Vancenase pockethaler http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202012.html
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Ophthalmic - U.S. Brands: AK-Dex; AK-Pred; AK-Tate; Baldex; Decadron; Dexair; Dexotic; Econopred; Econopred Plus; Eflone; Flarex; Fluor-Op; FML Forte; FML Liquifilm; FML S.O.P.; HMS Liquifilm; Inflamase Forte; Inflamase Mild; I-Pred; Lite Pred; Maxidex; Ocu-Dex; Ocu-Pred; Ocu-Pred Forte; Ocu-PredA; Pred Forte; Pred Mild; Predair; Predair A; Predair Forte; Storz-Dexa; Ultra Pred http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202013.html
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Otic - U.S. Brands: Decadron http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202014.html
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Rectal - U.S. Brands: Anucort-HC; Anu-Med HC; Anuprep HC; Anusol-HC; Anutone-HC; Anuzone-HC; Cort-Dome; Cortenema; Cortifoam; Hemorrhoidal HC; Hemril-HC Uniserts; Proctocort; Proctosol-HC; Rectasol-HC http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203366.html
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Dyphylline •
Systemic - U.S. Brands: Dilor; Dilor-400; Lufyllin; Lufyllin-400 http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202752.html
Formoterol •
Inhalation-Local - U.S. Brands: Foradil http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500269.html
Ipratropium •
Inhalation - U.S. Brands: Atrovent http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202304.html
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Nasal - U.S. Brands: Atrovent http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202713.html
Ipratropium and Albuterol •
Inhalation-Local - U.S. Brands: Combivent; DuoNeb http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203487.html
Oxtriphylline and Guaifenesin •
Systemic - U.S. Brands: Brondelate http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202430.html
Theophylline and Guaifenesin •
Systemic - U.S. Brands: Bronchial; Broncomar GG; Ed-Bron G; Elixophyllin-GG; Equibron G; Glyceryl-T; Quibron; Quibron-300; Slo-Phyllin GG; Theocon; Theolate http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202557.html
Theophylline, Ephedrine, and Hydroxyzine •
Systemic - U.S. Brands: Marax; Marax-DF http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202555.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.
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PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute10: •
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
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
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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.11 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:12 •
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/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
•
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
•
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/
•
Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
•
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
•
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
11
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). 12 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 Gateway13 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.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “chronic bronchitis” (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 9613 119 802 46 200 10780
HSTAT15 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.16 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.17 Simply search by “chronic bronchitis” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
13
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
14
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). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17
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 Biologists18 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.19 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.20 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/.
18 Adapted 19
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. 20 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 chronic bronchitis can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internetbased 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 chronic bronchitis. 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 chronic bronchitis. 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 “chronic bronchitis”:
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Bronchitis http://www.nlm.nih.gov/medlineplus/bronchitis.html COPD http://www.nlm.nih.gov/medlineplus/copdchronicobstructivepulmonarydisease.t ml Emphysema http://www.nlm.nih.gov/medlineplus/emphysema.html Respiratory Diseases http://www.nlm.nih.gov/medlineplus/respiratorydiseases.html
Within the health topic page dedicated to chronic bronchitis, the following was listed: •
Diagnosis/Symptoms Blood Gas Tests Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/blood_gases/test.html Spirometry Source: National Lung Health Education Program http://www.nlhep.org/spirom1.html Understanding PFT's (Pulmonary Function Testing) Source: Alpha 1 Association http://www.alpha1.org/what/lunginfo_pfts.htm
•
Children Bronchiolitis and Your Child Source: American Academy of Family Physicians http://familydoctor.org/020.xml
•
From the National Institutes of Health Lungs in Health and Disease Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/lung/other/lungs_hd.pdf
•
Organizations American Lung Association http://www.lungusa.org/ National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/ National Lung Health Education Program http://www.nlhep.org/
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Research AHRQ Report Says Doctors Commonly Treat Bronchiolitis with Medicines that May Be Ineffective Source: Agency for Healthcare Research and Quality http://www.ahrq.gov/news/press/pr2003/bronchpr.htm
•
Statistics FASTATS: Bronchitis Source: National Center for Health Statistics http://www.cdc.gov/nchs/fastats/brnchtis.htm
•
Teenagers Bronchitis Source: Nemours Foundation http://kidshealth.org/teen/infections/common/bronchitis.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 chronic bronchitis. 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: •
Cigars: More Dangerous Than You Think Source: South Deerfield, MA: Channing L. Bete Co., Inc. 1999. 15 p. Contact: Available from Channing L. Bete Co., Inc. 200 State Road, South Deerfield, MA 01373. (800) 628-7733. Fax (800) 499-6464. E-mail:
[email protected]. Website: www.channing-bete.com. PRICE: $1.05 for 1-99 copies; bulk copies available. Item number 73958B-01-99. Summary: This booklet describes the health hazards associated with smoking cigars. Contrary to a popular myth that cigar smoking is a harmless habit, the booklet explains that cigars can be addictive because of their nicotine content. The booklet explores why people start smoking cigars; the publicity and imaging that surrounds cigars and cigar users; how smoking causes cancer of the mouth, larynx, esophagus, and lungs; other risks associated with smoking cigars, including emphysema and chronic bronchitis, heart disease, and nicotine addiction; the problem of secondhand cigar smoke; and the
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impact of cigar smoking on one's breath, teeth, hair, clothes, and home. The booklet includes a section of ideas on how to handle a variety of situations where smoking may be encountered; and another section on tips for quitting cigar smoking. One sidebar lists the telephone numbers for some organizations through which readers can get more information. The brochure is illustrated with line drawings of a variety of people, depicted in everyday settings. 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 chronic bronchitis. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or 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. PEDBASE Similar to NORD, PEDBASE covers relatively rare disorders, limited mainly to pediatric conditions. PEDBASE was designed by Dr. Alan Gandy. To access the database, which is more oriented to researchers than patients, you can view the current list of health topics covered at the following Web site: http://www.icondata.com/health/pedbase/pedlynx.htm. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMDHealth: http://my.webmd.com/health_topics
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to chronic bronchitis. By consulting all of associations
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listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with chronic bronchitis. 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 chronic bronchitis. 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 “chronic bronchitis” (or a synonym), and you will receive information on all relevant organizations listed in the database. 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 “chronic bronchitis”. 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 “chronic bronchitis” (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 “chronic bronchitis” (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.21
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
21
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)22: •
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
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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
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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/
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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/
22
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
•
Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
•
Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
•
Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
•
Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
•
Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
•
Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
•
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
•
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
•
Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
•
Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
•
Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
•
Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
•
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
•
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
•
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
•
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
•
Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
•
Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
•
Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
•
Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
•
Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
•
Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
•
Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
•
Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
•
Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
•
Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
•
Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
•
Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
•
Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
•
Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
•
Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
•
National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
•
National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
•
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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•
Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
•
New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
•
New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
•
New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
•
New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
•
New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
•
New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
•
New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
•
Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
•
Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
•
Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
•
Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
•
Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
•
Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
•
Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
•
Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
•
Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
•
Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
•
Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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•
South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
•
Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
•
Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
•
Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
•
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
•
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 chronic bronchitis: •
Basic Guidelines for Chronic Bronchitis Chronic bronchitis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000119.htm
•
Signs & Symptoms for Chronic Bronchitis Ankle, feet, and leg swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003104.htm Cough Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003072.htm Coughing up blood Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003073.htm Fatigue Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm
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Headaches Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003024.htm Leg swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003104.htm Rales Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003323.htm Shortness of breath Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003075.htm Stress Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Vision abnormalities Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003029.htm Wheezing Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003070.htm •
Diagnostics and Tests for Chronic Bronchitis Arterial blood gas Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003855.htm Chest X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003804.htm Pulmonary function tests Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003853.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm
•
Background Topics for Chronic Bronchitis Aggravated by Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002227.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Cigarette smoking Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002032.htm Exercise Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm
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Lung disease - support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002158.htm Respiratory Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002290.htm Smoking Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002032.htm Support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002150.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/
•
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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CHRONIC BRONCHITIS 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] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abscess: A localized, circumscribed collection of pus. [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] Acetaldehyde: A colorless, flammable liquid used in the manufacture of acetic acid, perfumes, and flavors. It is also an intermediate in the metabolism of alcohol. It has a general narcotic action and also causes irritation of mucous membranes. Large doses may cause death from respiratory paralysis. [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] Acetylcysteine: The N-acetyl derivative of cysteine. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adoptive Transfer: Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (immunotherapy, adoptive). [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] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]
Agammaglobulinemia: An immunologic deficiency state characterized by an extremely low level of generally all classes of gamma-globulin in the blood. [NIH] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making
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emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [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] Air Pollutants: Substances which pollute the air. [NIH] Air Sacs: Thin-walled sacs or spaces which function as a part of the respiratory system in birds, fishes, insects, and mammals. [NIH] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Airway Obstruction: Any hindrance to the passage of air into and out of the lungs. [NIH] Airway Resistance: Physiologically, the opposition to flow of air caused by the forces of friction. As a part of pulmonary function testing, it is the ratio of driving pressure to the rate of air flow. [NIH] 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] 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] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allergic Rhinitis: Inflammation of the nasal mucous membrane associated with hay fever; fits may be provoked by substances in the working environment. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Alpha 1-Antichymotrypsin: Glycoprotein found in alpha(1)-globulin region in human serum. It inhibits chymotrypsin-like proteinases in vivo and has cytotoxic killer-cell activity in vitro. The protein also has a role as an acute-phase protein and is active in the control of immunologic and inflammatory processes, and as a tumor marker. It is a member of the serpin superfamily. [NIH] Alpha 1-Antitrypsin: Plasma glycoprotein member of the serpin superfamily which inhibits trypsin, neutrophil elastase, and other proteolytic enzymes. Commonly referred to as alpha 1-proteinase inhibitor (A1PI), it exists in over 30 different biochemical variant forms known collectively as the PI (protease inhibitor) system. Hereditary A1PI deficiency is associated with pulmonary emphysema. [NIH] Alpha 1-Antitrypsin Deficiency: A disease caused by single gene defects. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons,
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i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] 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] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to ampicillin except that its resistance to gastric acid permits higher serum levels with oral administration. [NIH] Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broadspectrum antibiotic. [NIH] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [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] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH]
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Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [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] Ankle: That part of the lower limb directly above the foot. [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] Anthocyanins: Glycosidic pigments in blue, red, and purple flowers and also found as metabolic byproducts in blood and urine. [NIH] Antiarrhythmic: An agent that prevents or alleviates cardiac arrhythmia. [EU] 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] Antidepressant: A drug used to treat depression. [NIH] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Anti-infective: An agent that so acts. [EU]
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Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiplasmin: A member of the serpin superfamily found in human plasma that inhibits the lysis of fibrin clots which are induced by plasminogen activator. It is a glycoprotein, molecular weight approximately 70,000 that migrates in the alpha 2 region in immunoelectrophoresis. It is the principal plasmin inactivator in blood, rapidly forming a very stable complex with plasmin. [NIH] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antiviral: Destroying viruses or suppressing their replication. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Aphakia: Absence of crystalline lens totally or partially from field of vision, from any cause except after cataract extraction. Aphakia is mainly congenital or as result of lens dislocation and subluxation. [NIH] Apnoea: Cessation of breathing. [EU] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Aqueous: Having to do with water. [NIH] Archaea: One of the three domains of life (the others being bacteria and Eucarya), formerly called Archaebacteria under the taxon Bacteria, but now considered separate and distinct. They are characterized by: 1) the presence of characteristic tRNAs and ribosomal RNAs; 2) the absence of peptidoglycan cell walls; 3) the presence of ether-linked lipids built from branched-chain subunits; and 4) their occurrence in unusual habitats. While archaea resemble bacteria in morphology and genomic organization, they resemble eukarya in their method of genomic replication. The domain contains at least three kingdoms: crenarchaeota, euryarchaeota, and korarchaeota. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arrestin: A 48-Kd protein of the outer segment of the retinal rods and a component of the phototransduction cascade. Arrestin quenches G-protein activation by binding to phosphorylated photolyzed rhodopsin. Arrestin causes experimental autoimmune uveitis when injected into laboratory animals. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU]
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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] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Articular: Of or pertaining to a joint. [EU] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Aspirate: Fluid withdrawn from a lump, often a cyst, or a nipple. [NIH] Aspiration: The act of inhaling. [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] Astringent: Causing contraction, usually locally after topical application. [EU] Asymptomatic: Having no signs or symptoms of disease. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] Atrial: Pertaining to an atrium. [EU] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] 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] Atropine: A toxic alkaloid, originally from Atropa belladonna, but found in other plants, mainly Solanaceae. [NIH] Autopsy: Postmortem examination of the body. [NIH] Azithromycin: A semi-synthetic macrolide antibiotic structurally related to erythromycin. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis. [NIH] Bacteremia: The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion. [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 Infections: Infections by bacteria, general or unspecified. [NIH] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Bacteriuria: The presence of bacteria in the urine with or without consequent urinary tract infection. Since bacteriuria is a clinical entity, the term does not preclude the use of urine/microbiology for technical discussions on the isolation and segregation of bacteria in the urine. [NIH]
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Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophil: A type of white blood cell. Basophils are granulocytes. [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-Lactamases: Enzymes found in many bacteria which catalyze the hydrolysis of the amide bond in the beta-lactam ring. Well known antibiotics destroyed by these enzymes are penicillins and cephalosporins. EC 3.5.2.6. [NIH] Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Bioassays: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [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] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological Transport: The movement of materials (including biochemical substances and drugs) across cell membranes and epithelial layers, usually by passive diffusion. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biomass: Total mass of all the organisms of a given type and/or in a given area. (From Concise Dictionary of Biology, 1990) It includes the yield of vegetative mass produced from any given crop. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of
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tissue from the living body. [NIH] Biopsy specimen: Tissue removed from the body and examined under a microscope to determine whether disease is present. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Biotypes: Causes septicemic and pneumonic pasteurellosis in cattle and sheep, usually in conjunction with a virus infection such as parainfluenza 3. Also recorded as a cause of acute mastitis in cattle. [NIH] Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [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 vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Viscosity: The internal resistance of the blood to shear forces. The in vitro measure of whole blood viscosity is of limited clinical utility because it bears little relationship to the actual viscosity within the circulation, but an increase in the viscosity of circulating blood can contribute to morbidity in patients suffering from disorders such as sickle cell anemia and polycythemia. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] 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
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with marrow cells. [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] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchiectasis: Persistent abnormal dilatation of the bronchi. [NIH] Bronchioles: The tiny branches of air tubes in the lungs. [NIH] Bronchiolitis: Inflammation of the bronchioles. [NIH] Bronchiolitis Obliterans: Inflammation of the bronchioles with obstruction by fibrous granulation tissue or bronchial exudate. It may follow inhalation of irritating gases or foreign bodies and it complicates pneumonia. [NIH] Bronchitis: Inflammation (swelling and reddening) of the bronchi. [NIH] Bronchoalveolar Lavage: Washing out of the lungs with saline or mucolytic agents for diagnostic or therapeutic purposes. It is very useful in the diagnosis of diffuse pulmonary infiltrates in immunosuppressed patients. [NIH] Bronchoalveolar Lavage Fluid: Fluid obtained by washout of the alveolar compartment of the lung. It is used to assess biochemical and inflammatory changes in and effects of therapy on the interstitial lung tissue. [NIH] Bronchoconstriction: Diminution of the caliber of a bronchus physiologically or as a result of pharmacological intervention. [NIH] Bronchodilator: A drug that relaxes the smooth muscles in the constricted airway. [NIH] Bronchus: A large air passage that leads from the trachea (windpipe) to the lung. [NIH] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [NIH] Calcitonin: A peptide hormone that lowers calcium concentration in the blood. In humans, it is released by thyroid cells and acts to decrease the formation and absorptive activity of osteoclasts. Its role in regulating plasma calcium is much greater in children and in certain diseases than in normal adults. [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
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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] Captopril: A potent and specific inhibitor of peptidyl-dipeptidase A. It blocks the conversion of angiotensin I to angiotensin II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the renin-angiotensin system and inhibits pressure responses to exogenous angiotensin. [NIH] Carbocysteine: A compound formed when iodoacetic acid reacts with sulfhydryl groups in proteins. It has been used as an anti-infective nasal spray with mucolytic and expectorant action. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] 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] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiotonic: 1. Having a tonic effect on the heart. 2. An agent that has a tonic effect on the heart. [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] 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] Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes. [NIH] 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] Cathepsins: A group of lysosomal proteinases or endopeptidases found in aqueous extracts of a variety of animal tissue. They function optimally within an acidic pH range. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU]
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Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cefixime: A third-generation cephalosporin antibiotic that is stable to hydrolysis by betalactamases. [NIH] Ceftazidime: Semisynthetic, broad-spectrum antibacterial derived from cephaloridine and used especially for Pseudomonas and other gram-negative infections in debilitated patients. [NIH]
Ceftriaxone: Broad-spectrum cephalosporin antibiotic with a very long half-life and high penetrability to usually inaccessible infections, including those involving the meninges, eyes, inner ears, and urinary tract. [NIH] Cefuroxime: Broad-spectrum cephalosporin antibiotic resistant to beta-lactamase. It has been proposed for infections with gram-negative and gram-positive organisms, gonorrhea, and haemophilus. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [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] Cephaloridine: A cephalosporin antibiotic. [NIH] Cephalosporins: A group of broad-spectrum antibiotics first isolated from the Mediterranean fungus Acremonium (Cephalosporium acremonium). They contain the betalactam moiety thia-azabicyclo-octenecarboxylic acid also called 7-aminocephalosporanic acid. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH]
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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] 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] Chemotaxis: The movement of cells or organisms toward or away from a substance in response to its concentration gradient. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chest Pain: Pressure, burning, or numbness in the chest. [NIH] Chest wall: The ribs and muscles, bones, and joints that make up the area of the body between the neck and the abdomen. [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] Chlorpheniramine: A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than promethazine. [NIH] Cholera: An acute diarrheal disease endemic in India and Southeast Asia whose causative agent is vibrio cholerae. This condition can lead to severe dehydration in a matter of hours unless quickly treated. [NIH] Cholestasis: Impairment of biliary flow at any level from the hepatocyte to Vater's ampulla. [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] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] 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] Chromic: Catgut sterilized and impregnated with chromium trioxide. [NIH] Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic Obstructive Pulmonary Disease: Collective term for chronic bronchitis and
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emphysema. [NIH] Chymotrypsin: A serine endopeptidase secreted by the pancreas as its zymogen, chymotrypsinogen and carried in the pancreatic juice to the duodenum where it is activated by trypsin. It selectively cleaves aromatic amino acids on the carboxyl side. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciliary Motility Disorders: Disorders characterized by abnormal ciliary movement in the nose, paranasal sinuses, respiratory tract, and spermatozoa. Electron microscopy of the cilia shows that dynein arms are missing. The disorders manifest as Kartagener triad (Kartagener's syndrome), chronic respiratory disorders, chronic sinusitis, and/or chronic otitis. [NIH] Ciprofloxacin: A carboxyfluoroquinoline antimicrobial agent that is effective against a wide range of microorganisms. It has been successfully and safely used in the treatment of resistant respiratory, skin, bone, joint, gastrointestinal, urinary, and genital infections. [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] Clarithromycin: A semisynthetic macrolide antibiotic derived from erythromycin that is active against a variety of microorganisms. It can inhibit protein synthesis in bacteria by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation. [NIH] Clavulanic Acid: Clavulanic acid (C8H9O5N) and its salts and esters. The acid is a suicide inhibitor of bacterial beta-lactamase enzymes from Streptomyces clavuligerus. Administered alone, it has only weak antibacterial activity against most organisms, but given in combination with beta-lactam antibiotics prevents antibiotic inactivation by microbial lactamase. [NIH] Clear cell carcinoma: A rare type of tumor of the female genital tract in which the inside of the cells looks clear when viewed under a microscope. [NIH] Cleave: A double-stranded cut in DNA with a restriction endonuclease. [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis. [NIH] Coculture: The culturing of normal cells or tissues with infected or latently infected cells or
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tissues of the same kind (From Dorland, 28th ed, entry for cocultivation). It also includes culturing of normal cells or tissues with other normal cells or tissues. [NIH] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] 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] 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] Complement 1: The first complement component to act in the cytolysis reaction. It is a trimolecular complex held together with Ca ions and, when activated, has esterase activity which initiates the next step in the sequence. [NIH] Complement 1 Inactivators: Compounds which inhibit, antagonize, or inactivate complement 1. A well-known inhibitor is a serum glycoprotein believed to be alpha-2neuroaminoglycoprotein. It inhibits the activated (esterase) form of complement 1 as well as kinin-forming, coagulation, and fibrinolytic systems. Deficiency of this inactivator has been found in patients with hereditary angioneurotic edema. These compounds are members of the serpin superfamily. [NIH] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as
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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] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [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] 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] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Conjunctivitis: Inflammation of the conjunctiva, generally consisting of conjunctival hyperaemia associated with a discharge. [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] Consciousness: Sense of awareness of self and of the environment. [NIH] Constriction: The act of constricting. [NIH] Continuum: An area over which the vegetation or animal population is of constantly changing composition so that homogeneous, separate communities cannot be distinguished. [NIH]
Contractility: Capacity for becoming short in response to a suitable stimulus. [EU]
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Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]
Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] Cor pulmonale: Heart disease that results from resistance to the passage of blood through the lungs; it often leads to right heart failure. [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 Vessels: The veins and arteries of the heart. [NIH] Corticosteroids: Hormones that have antitumor activity in lymphomas and lymphoid leukemias; in addition, corticosteroids (steroids) may be used for hormone replacement and for the management of some of the complications of cancer and its treatment. [NIH] Cotinine: 1-Methyl-5-(3-pyridyl)-2-pyrrolidinone antidepressant. Synonym: Scotine. [NIH]
fumarate.
Stimulant
proposed
as
Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Cryptosporidiosis: Parasitic intestinal infection with severe diarrhea caused by a protozoan,
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Cryptosporidium. It occurs in both animals and humans. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cyst: A sac or capsule filled with fluid. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
Cystitis: Inflammation of the urinary bladder. [EU] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decongestant: An agent that reduces congestion or swelling. [EU] Decubitus: An act of lying down; also the position assumed in lying down. [EU] Decubitus Ulcer: An ulceration caused by prolonged pressure in patients permitted to lie too still for a long period of time. The bony prominences of the body are the most frequently affected sites. The ulcer is caused by ischemia of the underlying structures of the skin, fat, and muscles as a result of the sustained and constant pressure. [NIH] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydration: The condition that results from excessive loss of body water. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Dental Care: The total of dental diagnostic, preventive, and restorative services provided to meet the needs of a patient (from Illustrated Dictionary of Dentistry, 1982). [NIH] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel
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protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
Dental Plaque: A film that attaches to teeth, often causing dental caries and gingivitis. It is composed of mucins, secreted from salivary glands, and microorganisms. [NIH] Dentists: Individuals licensed to practice dentistry. [NIH] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] 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] DES: Diethylstilbestrol. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Desquamation: The shedding of epithelial elements, chiefly of the skin, in scales or small sheets; exfoliation. [EU] Detergents: Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action that depends on possessing both hydrophilic and hydrophobic properties. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diaphragm: The musculofibrous partition that separates the thoracic cavity from the abdominal cavity. Contraction of the diaphragm increases the volume of the thoracic cavity aiding inspiration. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] 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] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [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] Disulphides: A covalent bridge formed by the oxidation of two cysteine residues to a cystine residue. The-S-S-bond is very strong and its presence confers additional stability. [NIH]
Dithiothreitol: A reagent commonly used in biochemical studies as a protective agent to prevent the oxidation of SH (thiol) groups and for reducing disulphides to dithiols. [NIH]
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Dominance: In genetics, the full phenotypic expression of a gene in both heterozygotes and homozygotes. [EU] 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] Drip: The continuous slow introduction of a fluid containing nutrients or drugs. [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] Dry Eye Syndrome: A common condition that occurs when the eyes do not produce enough tears to keep the eye moist and comfortable. Common symptoms of dry eye include pain, stinging, burning, scratchiness, and intermittent blurring of vision. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dynein: A transport protein that normally binds proteins to the microtubule. [NIH] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dyspnea: Difficult or labored breathing. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [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] Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles
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or microvesicles. Endosomes play a central role in endocytosis. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endoscopy: Endoscopic examination, therapy or surgery performed on interior parts of the body. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] Enteropeptidase: A specialized proteolytic enzyme secreted by intestinal cells. It converts trypsinogen into its active form trypsin by removing the N-terminal peptide. EC 3.4.21.9. [NIH]
Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Environmental Microbiology: The study of microorganisms living in a variety of environments (air, soil, water, etc.) and their pathogenic relationship to other organisms including man. [NIH] Environmental tobacco smoke: ETS. Smoke that comes from the burning of a tobacco product and smoke that is exhaled by smokers (second-hand smoke). Inhaling ETS is called involuntary or passive smoking. [NIH] Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Eosinophil: A polymorphonuclear leucocyte with large eosinophilic granules in its cytoplasm, which plays a role in hypersensitivity reactions. [NIH] Eosinophilia: Abnormal increase in eosinophils in the blood, tissues or organs. [NIH] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermal Growth Factor: A 6 kD polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and epithelial cells. [NIH]
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Epidermal growth factor receptor: EGFR. The protein found on the surface of some cells and to which epidermal growth factor binds, causing the cells to divide. It is found at abnormally high levels on the surface of many types of cancer cells, so these cells may divide excessively in the presence of epidermal growth factor. Also known as ErbB1 or HER1. [NIH] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] 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] Erythrocyte Volume: Volume of circulating erythrocytes. It is usually measured by radioisotope dilution technique. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythromycin: A bacteriostatic antibiotic substance produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophagitis: Inflammation, acute or chronic, of the esophagus caused by bacteria, chemicals, or trauma. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Ethmoid: An unpaired cranial bone which helps form the medial walls of the orbits and contains the themoidal air cells which drain into the nose. [NIH] Exfoliation: A falling off in scales or layers. [EU] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Expectorant: 1. Promoting the ejection, by spitting, of mucus or other fluids from the lungs and trachea. 2. An agent that promotes the ejection of mucus or exudate from the lungs, bronchi, and trachea; sometimes extended to all remedies that quiet cough (antitussives). [EU]
Expiration: The act of breathing out, or expelling air from the lungs. [EU] Expiratory: The volume of air which leaves the breathing organs in each expiration. [NIH] External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at
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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] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Extravascular: Situated or occurring outside a vessel or the vessels. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Exudate: Material, such as fluid, cells, or cellular debris, which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces, usually as a result of inflammation. An exudate, in contrast to a transudate, is characterized by a high content of protein, cells, or solid materials derived from cells. [EU] Failure to Thrive: A condition in which an infant or child's weight gain and growth are far below usual levels for age. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] 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] Flatus: Gas passed through the rectum. [NIH] Fleroxacin: A third-generation fluoroquinolone derivative with a broad antimicrobial spectrum. The drug strongly inhibits the DNA-supercoiling activity of DNA gyrase which may account for its antibacterial activity. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Foramen: A natural hole of perforation, especially one in a bone. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention
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of free radical damage is being actively investigated. [NIH] Friction: Surface resistance to the relative motion of one body against the rubbing, sliding, rolling, or flowing of another with which it is in contact. [NIH] Fungistatic: Inhibiting the growth of fungi. [EU] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallic Acid: A colorless or slightly yellow crystalline compound obtained from nutgalls. It is used in photography, pharmaceuticals, and as an analytical reagent. [NIH] Gamma-interferon: Interferon produced by T-lymphocytes in response to various mitogens and antigens. Gamma interferon appears to have potent antineoplastic, immunoregulatory and antiviral activity. [NIH] Gangrene: Death and putrefaction of tissue usually due to a loss of blood supply. [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] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastroesophageal Reflux: Reflux of gastric juice and/or duodenal contents (bile acids, pancreatic juice) into the distal esophagus, commonly due to incompetence of the lower esophageal sphincter. Gastric regurgitation is an extension of this process with entry of fluid into the pharynx or mouth. [NIH] Gastroesophageal Reflux Disease: Flow of the stomach's contents back up into the esophagus. Happens when the muscle between the esophagus and the stomach (the lower esophageal sphincter) is weak or relaxes when it shouldn't. May cause esophagitis. Also called esophageal reflux or reflux esophagitis. [NIH] Gastrointestinal: Refers to 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] Generator: Any system incorporating a fixed parent radionuclide from which is produced a daughter radionuclide which is to be removed by elution or by any other method and used in a radiopharmaceutical. [NIH]
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Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic Markers: A phenotypically recognizable genetic trait which can be used to identify a genetic locus, a linkage group, or a recombination event. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gingivitis: Inflammation of the gingivae. Gingivitis associated with bony changes is referred to as periodontitis. Called also oulitis and ulitis. [EU] 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] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomeruli: Plural of glomerulus. [NIH] Glucans: Polysaccharides composed of repeating glucose units. They can consist of branched or unbranched chains in any linkages. [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] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucosyltransferases: Enzymes that catalyze the transfer of glucose from a nucleoside diphosphate glucose to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.-. [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] 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] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosidic: Formed by elimination of water between the anomeric hydroxyl of one sugar and a hydroxyl of another sugar molecule. [NIH]
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Goblet Cells: Cells of the epithelial lining that produce and secrete mucins. [NIH] Gonorrhea: Acute infectious disease characterized by primary invasion of the urogenital tract. The etiologic agent, Neisseria gonorrhoeae, was isolated by Neisser in 1879. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Gp120: 120-kD HIV envelope glycoprotein which is involved in the binding of the virus to its membrane receptor, the CD4 molecule, found on the surface of certain cells in the body. [NIH]
Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Graft-versus-host disease: GVHD. A reaction of donated bone marrow or peripheral stem cells against a person's tissue. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Granulation Tissue: A vascular connective tissue formed on the surface of a healing wound, ulcer, or inflamed tissue. It consists of new capillaries and an infiltrate containing lymphoid cells, macrophages, and plasma cells. [NIH] Granule: A small pill made from sucrose. [EU] Granulocyte: A type of white blood cell that fights bacterial infection. Neutrophils, eosinophils, and basophils are granulocytes. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Gyrase: An enzyme that causes negative supercoiling of E. coli DNA during replication. [NIH]
Haemophilus influenzae: A species of Haemophilus found on the mucous membranes of humans and a variety of animals. The species is further divided into biotypes I through VIII. [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] Hay Fever: A seasonal variety of allergic rhinitis, marked by acute conjunctivitis with lacrimation and itching, regarded as an allergic condition triggered by specific allergens. [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
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disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [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] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartburn: Substernal pain or burning sensation, usually associated with regurgitation of gastric juice into the esophagus. [NIH] Hematopoiesis: The development and formation of various types of blood cells. [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] 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] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]
Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocellular: Pertaining to or affecting liver cells. [EU] Hepatocellular carcinoma: A type of adenocarcinoma, the most common type of liver tumor. [NIH] Hepatocyte: A liver cell. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Heterodimers: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterozygotes: Having unlike alleles at one or more corresponding loci on homologous chromosomes. [NIH]
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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] Histamine Release: The secretion of histamine from mast cell and basophil granules by exocytosis. This can be initiated by a number of factors, all of which involve binding of IgE, cross-linked by antigen, to the mast cell or basophil's Fc receptors. Once released, histamine binds to a number of different target cell receptors and exerts a wide variety of effects. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Hoarseness: An unnaturally deep or rough quality of voice. [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] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hydration: Combining with water. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrogenation: Specific method of reduction in which hydrogen is added to a substance by the direct use of gaseous hydrogen. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophilic: Readily absorbing moisture; hygroscopic; having strongly polar groups that readily interact with water. [EU] Hydroxybenzoic Acids: Benzoic acid substituted by one or more hydroxy groups in any position on the benzene ring. [NIH]
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Hygienic: Pertaining to hygiene, or conducive to health. [EU] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [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] Hypersecretion: Excessive secretion. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] 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] Hypoventilation: A reduction in the amount of air entering the pulmonary alveoli. [NIH] Hypoxemia: Deficient oxygenation of the blood; hypoxia. [EU] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hypoxic: Having too little oxygen. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immune-response: The production of antibodies or particular types of cytotoxic lymphoid cells on challenge with an antigen. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunoglobulins: Glycoproteins present in the blood (antibodies) and in other tissue. They are classified by structure and activity into five classes (IgA, IgD, IgE, IgG, IgM). [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [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]
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Immunosuppressant: An agent capable of suppressing immune responses. [EU] 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] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Impaction: The trapping of an object in a body passage. Examples are stones in the bile duct or hardened stool in the colon. [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] 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] Incompetence: Physical or mental inadequacy or insufficiency. [EU] 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] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical
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signs of pain, heat, redness, swelling, and loss of function. [NIH] Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Inhalation Exposure: The exposure to potentially harmful chemical, physical, or biological agents by inhaling them. [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inner ear: The labyrinth, comprising the vestibule, cochlea, and semicircular canals. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] 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] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] Intercellular Adhesion Molecule-1: A cell-surface ligand with a role in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interleukin-5: Factor promoting eosinophil differentiation and activation in hematopoiesis. It also triggers activated B-cells for a terminal differentiation into Ig-secreting cells. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus.
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IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Interleukin-9: Factor that is thought to be a regulator of hematopoiesis. It has been shown to enhance the growth of human mast cells and megakaryoblastic leukemic cells as well as murine helper t-cell clones. IL-9 is a glycoprotein with a molecular weight of 32-39 that is derived from T-cells, and maps to human chromosome 5. [NIH] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] 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] 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] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Iodoacetic Acid: Iodoacetic acid and its salts and derivatives. Iodoacetic acid reacts with cysteine (-SH) groups to form a carboxymethylated protein and is used as an enzyme inhibitor in biochemical research. [NIH] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ipratropium: A muscarinic antagonist structurally related to atropine but often considered safer and more effective for inhalation use. It is used for various bronchial disorders, in rhinitis, and as an antiarrhythmic. [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] Irritants: Drugs that act locally on cutaneous or mucosal surfaces to produce inflammation; those that cause redness due to hyperemia are rubefacients; those that raise blisters are vesicants and those that penetrate sebaceous glands and cause abscesses are pustulants; tear gases and mustard gases are also irritants. [NIH]
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Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Isozymes: The multiple forms of a single enzyme. [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] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Keratolytic: An agent that promotes keratolysis. [EU] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lacrimal: Pertaining to the tears. [EU] Lacrimal Apparatus: The tear-forming and tear-conducting system which includes the lacrimal glands, eyelid margins, conjunctival sac, and the tear drainage system. [NIH] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lesion: An area of abnormal tissue change. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukemic Infiltration: A pathologic change in leukemia in which leukemic cells permeate various organs at any stage of the disease. All types of leukemia show various degrees of infiltration, depending upon the type of leukemia. The degree of infiltration may vary from site to site. The liver and spleen are common sites of infiltration, the greatest appearing in myelocytic leukemia, but infiltration is seen also in the granulocytic and lymphocytic types. The kidney is also a common site and of the gastrointestinal system, the stomach and ileum are commonly involved. In lymphocytic leukemia the skin is often infiltrated. The central nervous system too is a common site. [NIH] Leukostasis: Abnormal intravascular leukocyte aggregation and clumping often seen in leukemia patients. The brain and lungs are the two most commonly affected organs. This acute syndrome requires aggressive cytoreductive modalities including chemotherapy and/or leukophoresis. It is differentiated from leukemic infiltration which is a neoplastic process where leukemic cells invade organs. [NIH] Levofloxacin: A substance used to treat bacterial infections. It belongs to the family of drugs called quinolone antibiotics. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and
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strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver cancer: A disease in which malignant (cancer) cells are found in the tissues of the liver. [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] 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] Lower Esophageal Sphincter: The muscle between the esophagus and stomach. When a person swallows, this muscle relaxes to let food pass from the esophagus to the stomach. It stays closed at other times to keep stomach contents from flowing back into the esophagus. [NIH]
Lung Transplantation: The transference of either one or both of the lungs from one human or animal to another. [NIH] Lung volume: The amount of air the lungs hold. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [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 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] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale
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blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each); those with characteristics of neither major class are called null cells. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Macrolides: A group of organic compounds that contain a macrocyclic lactone ring linked glycosidically to one or more sugar moieties. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] 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] Malaise: A vague feeling of bodily discomfort. [EU] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mastitis: Inflammatory disease of the breast, or mammary gland. [NIH] Maxillary: Pertaining to the maxilla : the irregularly shaped bone that with its fellow forms the upper jaw. [EU] Mechanical ventilation: Use of a machine called a ventilator or respirator to improve the exchange of air between the lungs and the atmosphere. [NIH] Mechanoreceptors: Cells specialized to transduce mechanical stimuli and relay that information centrally in the nervous system. Mechanoreceptors include hair cells, which mediate hearing and balance, and the various somatosensory receptors, often with nonneural accessory structures. [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] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger
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cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH]
Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesenteric: Pertaining to the mesentery : a membranous fold attaching various organs to the body wall. [EU] 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] Metaplasia: A condition in which there is a change of one adult cell type to another similar adult cell type. [NIH] Methotrexate: An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of dihydrofolate reductase and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] 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] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei
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normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] 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] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocular: Diplopia identified with one eye only; it may be induced with a double prism, or it may occur either as a result of double imagery due to an optical defect in the eye, or as a result of simultaneous use of normal and anomalous retinal correspondence. [NIH] Monocyte: A type of white blood cell. [NIH] Monocyte Chemoattractant Protein-1: A chemokine that is a chemoattractant for human monocytes and may also cause cellular activation of specific functions related to host defense. It is produced by leukocytes of both monocyte and lymphocyte lineage and by fibroblasts during tissue injury. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphogenesis: The development of the form of an organ, part of the body, or organism. [NIH]
Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Moxalactam: Broad- spectrum beta-lactam antibiotic similar in structure to the cephalosporins except for the substitution of an oxaazabicyclo moiety for the thiaazabicyclo moiety of certain cephalosporins. It has been proposed especially for the meningitides because it passes the blood-brain barrier and for anaerobic infections. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucociliary: Pertaining to or affecting the mucus membrane and hairs (including eyelashes, nose hair, .): mucociliary clearing: the clearance of mucus by ciliary movement ( particularly in the respiratory system). [EU] Mucociliary Clearance: Rate of ciliary and secretory activity of the respiratory submucosal glands. It is a non-specific host defense mechanism, measurable in vivo by mucus transfer, ciliary beat frequency, and clearance of radioactive tracers. [NIH] Mucolytic: Destroying or dissolving mucin; an agent that so acts : a mucopolysaccharide or
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glycoprotein, the chief constituent of mucus. [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]
Muscarinic Agonists: Drugs that bind to and activate muscarinic cholinergic receptors (receptors, muscarinic). Muscarinic agonists are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder and the eye. They may also be used to reduce heart rate. [NIH] Mustard Gas: Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed). [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myalgia: Pain in a muscle or muscles. [EU] Mycophenolate mofetil: A drug that is being studied for its effectiveness in preventing graft-versus-host disease and autoimmune disorders. [NIH] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] 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] Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing myocardial reperfusion injury. [NIH] Myocardial Reperfusion Injury: Functional, metabolic, or structural changes in ischemic heart muscle thought to result from reperfusion to the ischemic areas. Changes can be fatal to muscle cells and may include edema with explosive cell swelling and disintegration, sarcolemma disruption, fragmentation of mitochondria, contraction band necrosis, enzyme washout, and calcium overload. Other damage may include hemorrhage and ventricular arrhythmias. One possible mechanism of damage is thought to be oxygen free radicals. Treatment currently includes the introduction of scavengers of oxygen free radicals, and injury is thought to be prevented by warm blood cardioplegic infusion prior to reperfusion. [NIH]
Myopia: That error of refraction in which rays of light entering the eye parallel to the optic axis are brought to a focus in front of the retina, as a result of the eyeball being too long from
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front to back (axial m.) or of an increased strength in refractive power of the media of the eye (index m.). Called also nearsightedness, because the near point is less distant than it is in emmetropia with an equal amplitude of accommodation. [EU] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Nasal Cavity: The proximal portion of the respiratory passages on either side of the nasal septum, lined with ciliated mucosa, extending from the nares to the pharynx. [NIH] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Nasolacrimal: Pertaining to the nose and lacrimal apparatus. [EU] Nebramycin: A complex of antibiotic substances produced by Streptomyces tenebrarius. [NIH]
Nebulizer: A device used to turn liquid into a fine spray. [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] Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms. [NIH] Nephropathy: Disease of the kidneys. [EU] 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] 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] Neuropeptides: Peptides released by neurons as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells. [NIH] Neuropsychological Tests: Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury. [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]
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Neutrophil: A type of white blood cell. [NIH] Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
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] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nursing Care: Care given to patients by nursing service personnel. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] Observational study: An epidemiologic study that does not involve any intervention, experimental or otherwise. Such a study may be one in which nature is allowed to take its course, with changes in one characteristic being studied in relation to changes in other characteristics. Analytical epidemiologic methods, such as case-control and cohort study designs, are properly called observational epidemiology because the investigator is observing without intervention other than to record, classify, count, and statistically analyze results. [NIH] Occupational Exposure: The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation. [NIH] Occupational Health: The promotion and maintenance of physical and mental health in the work environment. [NIH] Ofloxacin: An orally administered broad-spectrum quinolone antibacterial drug active against most gram-negative and gram-positive bacteria. [NIH] Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH] Oligosaccharides: Carbohydrates consisting of between two and ten monosaccharides
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connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteoclasts: A large multinuclear cell associated with the absorption and removal of bone. An odontoclast, also called cementoclast, is cytomorphologically the same as an osteoclast and is involved in cementum resorption. [NIH] Otitis: Inflammation of the ear, which may be marked by pain, fever, abnormalities of hearing, hearing loss, tinnitus, and vertigo. [EU] Otitis Media: Inflammation of the middle ear. [NIH] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxides: Binary compounds of oxygen containing the anion O(2-). The anion combines with metals to form alkaline oxides and non-metals to form acidic oxides. [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 -
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oxygenation the process of supplying, treating, or mixing with oxygen. [EU] 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] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic Ducts: Ducts that collect pancreatic juice from the pancreas and supply it to the duodenum. [NIH] Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum. [NIH] Panniculitis: General term for inflammation of adipose tissue, usually of the skin, characterized by reddened subcutaneous nodules. [NIH] Paranasal Sinuses: Air-filled extensions of the respiratory part of the nasal cavity into the frontal, ethmoid, sphenoid, and maxillary cranial bones. They vary in size and form in different individuals and are lined by the ciliated mucous membranes of the nasal cavity. [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] 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] 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] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Peak flow: The maximum amount of air breathed out; the power needed to produce this amount. [EU] 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] Pelvic: Pertaining to the pelvis. [EU] Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Chain Elongation: The process whereby an amino acid is joined through a substituted amide linkage to a chain of peptides. [NIH] Peptide T: N-(N-(N(2)-(N-(N-(N-(N-D-Alanyl L-seryl)-L-threonyl)-L-threonyl) L-threonyl)L-asparaginyl)-L-tyrosyl) L-threonine. Octapeptide sharing sequence homology with HIV
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envelope protein gp120. It is potentially useful as antiviral agent in AIDS therapy. The core pentapeptide sequence, TTNYT, consisting of amino acids 4-8 in peptide T, is the HIV envelope sequence required for attachment to the CD4 receptor. [NIH] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Periodontal Attachment Loss: Loss or destruction of periodontal tissue caused by periodontitis or other destructive periodontal diseases or by injury during instrumentation. Attachment refers to the periodontal ligament which attaches to the alveolar bone. It has been hypothesized that treatment of the underlying periodontal disease and the seeding of periodontal ligament cells enable the creating of new attachment. [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontal Ligament: Fibrous connective tissue surrounding the root of a tooth that separates it from and attaches it to the alveolar bone. [NIH] Periodontitis: Inflammation of the periodontal membrane; also called periodontitis simplex. [NIH]
Peripheral blood: Blood circulating throughout the body. [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] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] 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] Pharmacodynamics: The study of the biochemical and physiological effects of drugs and the mechanisms of their actions, including the correlation of actions and effects of drugs with their chemical structure; also, such effects on the actions of a particular drug or drugs. [EU] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] 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]
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Phenylephrine: An alpha-adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylated: Attached to a phosphate group. [NIH] 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 Therapy: The restoration of function and the prevention of disability following disease or injury with the use of light, heat, cold, water, electricity, ultrasound, and exercise. [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] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasma Volume: Volume of plasma in the circulation. It is usually measured by indicator dilution techniques. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH]
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Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Plasminogen Inactivators: Important modulators of the activity of plasminogen activators. Four inhibitors, all belonging to the serpin family of proteins, have been implicated in plasminogen activation inhibition. They are PAI-1, PAI-2, protease-nexin, and protein C inhibitor (PAI-3). All inhibit both the tissue-type and urokinase-type plasminogen activators. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelet Factor 4: A high-molecular-weight proteoglycan-platelet factor complex which is released from blood platelets by thrombin. It acts as a mediator in the heparin-neutralizing capacity of the blood and plays a role in platelet aggregation. At high ionic strength (I=0.75), the complex dissociates into the active component (molecular weight 29,000) and the proteoglycan carrier (chondroitin 4-sulfate, molecular weight 350,000). The molecule exists in the form of a dimer consisting of 8 moles of platelet factor 4 and 2 moles of proteoglycan. [NIH]
Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pneumoconiosis: Condition characterized by permanent deposition of substantial amounts of particulate matter in the lungs, usually of occupational or environmental origin, and by the tissue reaction to its presence. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Pneumonitis: A disease caused by inhaling a wide variety of substances such as dusts and molds. Also called "farmer's disease". [NIH] Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] 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] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Portal Hypertension: High blood pressure in the portal vein. This vein carries blood into the liver. Portal hypertension is caused by a blood clot. This is a common complication of
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cirrhosis. [NIH] Portal Vein: A short thick vein formed by union of the superior mesenteric vein and the splenic vein. [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potentiating: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Precipitating Factors: Factors associated with the definitive onset of a disease, illness, accident, behavioral response, or course of action. Usually one factor is more important or more obviously recognizable than others, if several are involved, and one may often be regarded as "necessary". Examples include exposure to specific disease; amount or level of an infectious organism, drug, or noxious agent, etc. [NIH] 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] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary Prevention: Prevention of disease or mental disorders in susceptible individuals or populations through promotion of health, including mental health, and specific protection, as in immunization, as distinguished from the prevention of complications or after-effects of existing disease. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] 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] Promethazine: A phenothiazine derivative with histamine H1-blocking, antimuscarinic, and sedative properties. It is used as an antiallergic, in pruritus, for motion sickness and sedation, and also in animals. [NIH]
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Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prophylaxis: An attempt to prevent disease. [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] 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 S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] 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] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [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] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Psychotropic: Exerting an effect upon the mind; capable of modifying mental activity; usually applied to drugs that effect the mental state. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Alveoli: Small polyhedral outpouchings along the walls of the alveolar sacs, alveolar ducts and terminal bronchioles through the walls of which gas exchange between
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alveolar air and pulmonary capillary blood takes place. [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 Circulation: The circulation of blood through the lungs. [NIH] Pulmonary Emphysema: Condition of the lungs characterized by increase beyond normal in the size of air spaces distal to the terminal bronchioles, either from dilatation of the alveoli or from destruction of their walls. [NIH] Pulmonary Fibrosis: Chronic inflammation and progressive fibrosis of the pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from oxygen lack or right heart failure. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Putrefaction: The process of decomposition of animal and vegetable matter by living organisms. [NIH] Pyelonephritis: Inflammation of the kidney and its pelvis, beginning in the interstitium and rapidly extending to involve the tubules, glomeruli, and blood vessels; due to bacterial infection. [EU] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and uracil) and form the basic structure of the barbiturates. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quercetin: Aglucon of quercetrin, rutin, and other glycosides. It is widely distributed in the plant kingdom, especially in rinds and barks, clover blossoms, and ragweed pollen. [NIH] Quinolones: Quinolines which are substituted in any position by one or more oxo groups. These compounds can have any degree of hydrogenation, any substituents, and fused ring systems. [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
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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] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiopharmaceutical: Any medicinal product which, when ready for use, contains one or more radionuclides (radioactive isotopes) included for a medicinal purpose. [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] 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] Reactivation: The restoration of activity to something that has been inactivated. [EU] 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] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Muscarinic: One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for muscarine over nicotine. There are several subtypes (usually M1, M2, M3.) that are characterized by their cellular actions, pharmacology, and molecular biology. [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] Rectum: The last 8 to 10 inches of the large intestine. [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] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflex: An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord. [NIH] Reflux: The term used when liquid backs up into the esophagus from the stomach. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU]
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Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regurgitation: A backward flowing, as the casting up of undigested food, or the backward flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] Reinfection: A second infection by the same pathogenic agent, or a second infection of an organ such as the kidney by a different pathogenic agent. [EU] Relapse: The return of signs and symptoms of cancer after a period of improvement. [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] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [NIH] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH] Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Respirable: Dust particles smaller than 0. 005 mm, which are deposited in the respiratory region of the lungs. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respirator: A mechanical device that helps a patient breathe; a mechanical ventilator. [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [NIH] Respiratory Mechanics: The physical or mechanical action of the lungs, diaphragm, ribs, and chest wall during respiration. It includes airflow, lung volume, neural and reflex controls, mechanoreceptors, breathing patterns, etc. [NIH] Respiratory Paralysis: Complete or severe weakness of the muscles of respiration. This condition may be associated with motor neuron diseases; peripheral nerve disorders; neuromuscular junction diseases; spinal cord diseases; injury to the phrenic nerve; and other
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disorders. [NIH] Respiratory Physiology: Functions and activities of the respiratory tract as a whole or of any of its parts. [NIH] Respiratory System: The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought about. [NIH] Respite Care: Patient care provided in the home or institution intermittently in order to provide temporary relief to the family home care giver. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Detachment: Separation of the inner layers of the retina (neural retina) from the pigment epithelium. Retinal detachment occurs more commonly in men than in women, in eyes with degenerative myopia, in aging and in aphakia. It may occur after an uncomplicated cataract extraction, but it is seen more often if vitreous humor has been lost during surgery. (Dorland, 27th ed; Newell, Ophthalmology: Principles and Concepts, 7th ed, p310-12). [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Rheology: The study of the deformation and flow of matter, usually liquids or fluids, and of the plastic flow of solids. The concept covers consistency, dilatancy, liquefaction, resistance to flow, shearing, thixotrophy, and viscosity. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [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] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of
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developing a disease. [NIH] Risk patient: Patient who is at risk, because of his/her behaviour or because of the type of person he/she is. [EU] Rod: A reception for vision, located in the retina. [NIH] Rutin: 3-((6-O-(6-Deoxy-alpha-L-mannopyranosyl)-beta-D-glucopyranosyl)oxy)-2-(3,4dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one. Found in many plants, including buckwheat, tobacco, forsythia, hydrangea, pansies, etc. It has been used therapeutically to decrease capillary fragility. [NIH] Saline: A solution of salt and water. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Sebaceous gland: Gland that secretes sebum. [NIH] 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] Segmental: Describing or pertaining to a structure which is repeated in similar form in successive segments of an organism, or which is undergoing segmentation. [NIH] Segmentation: The process by which muscles in the intestines move food and wastes through the body. [NIH] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH]
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Septal: An abscess occurring at the root of the tooth on the proximal surface. [NIH] Sequence Homology: The degree of similarity between sequences. Studies of amino acid and nucleotide sequences provide useful information about the genetic relatedness of certain species. [NIH] Sequester: A portion of dead bone which has become detached from the healthy bone tissue, as occurs in necrosis. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serine Endopeptidases: Any member of the group of endopeptidases containing at the active site a serine residue involved in catalysis. EC 3.4.21. [NIH] Serine Proteinase Inhibitors: Exogenous or endogenous compounds which inhibit serine endopeptidases. [NIH] Serpins: A family of serine proteinase inhibitors which are similar in amino acid sequence and mechanism of inhibition, but differ in their specificity toward proteolytic enzymes. This family includes alpha 1-antitrypsin, angiotensinogen, ovalbumin, antiplasmin, alpha 1antichymotrypsin, thyroxine-binding protein, complement 1 inactivators, antithrombin III, heparin cofactor II, plasminogen inactivators, gene Y protein, placental plasminogen activator inhibitor, and barley Z protein. Some members of the serpin family may be substrates rather than inhibitors of serine endopeptidases, and some serpins occur in plants where their function is not known. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Silver Staining: The use of silver, usually silver nitrate, as a reagent for producing contrast or coloration in tissue specimens. [NIH] Sinusitis: An inflammatory process of the mucous membranes of the paranasal sinuses that
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occurs in three stages: acute, subacute, and chronic. Sinusitis results from any condition causing ostial obstruction or from pathophysiologic changes in the mucociliary transport mechanism. [NIH] Skin Care: Maintenance of the hygienic state of the skin under optimal conditions of cleanliness and comfort. Effective in skin care are proper washing, bathing, cleansing, and the use of soaps, detergents, oils, etc. In various disease states, therapeutic and protective solutions and ointments are useful. The care of the skin is particularly important in various occupations, in exposure to sunlight, in neonates, and in decubitus ulcer. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smoking Cessation: Discontinuation of the habit of smoking, the inhaling and exhaling of tobacco smoke. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Soaps: Sodium or potassium salts of long chain fatty acids. These detergent substances are obtained by boiling natural oils or fats with caustic alkali. Sodium soaps are harder and are used as topical anti-infectives and vehicles in pills and liniments; potassium soaps are soft, used as vehicles for ointments and also as topical antimicrobials. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] 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] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] 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] Spermatozoa: Mature male germ cells that develop in the seminiferous tubules of the testes.
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Each consists of a head, a body, and a tail that provides propulsion. The head consists mainly of chromatin. [NIH] Sphenoid: An unpaired cranial bone with a body containing the sphenoid sinus and forming the posterior part of the medial walls of the orbits. [NIH] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spirometry: Measurement of volume of air inhaled or exhaled by the lung. [NIH] Splenic Vein: Vein formed by the union (at the hilus of the spleen) of several small veins from the stomach, pancreas, spleen and mesentery. [NIH] Sputum: The material expelled from the respiratory passages by coughing or clearing the throat. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Steroids: Drugs used to relieve swelling and inflammation. [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] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococci: A genus of spherical Gram-positive bacteria occurring in chains or pairs. They are widely distributed in nature, being important pathogens but often found as normal commensals in the mouth, skin, and intestine of humans and other animals. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] 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] Strongyloidiasis: Infection with nematodes of the genus Strongyloides. The presence of larvae may produce pneumonitis and the presence of adult worms in the intestine could lead to moderate to severe diarrhea. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU]
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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] Sublingual: Located beneath the tongue. [EU] Submaxillary: Four to six lymph glands, located between the lower jaw and the submandibular salivary gland. [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]
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] Sulfur Dioxide: A highly toxic, colorless, nonflammable gas. It is used as a pharmaceutical aid and antioxidant. It is also an environmental air pollutant. [NIH] Sulfur Oxides: Inorganic oxides of sulfur. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Surgical Wound Infection: Infection occurring at the site of a surgical incision. [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] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Systemic: Affecting the entire body. [NIH] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above
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100 beats per minute. [NIH] Tachypnea: Rapid breathing. [NIH] Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro. [NIH] Tear Gases: Gases that irritate the eyes, throat, or skin. Severe lacrimation develops upon irritation of the eyes. [NIH] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermoregulation: Heat regulation. [EU] 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] 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] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tobramycin: An aminoglycoside, broad-spectrum antibiotic produced by Streptomyces tenebrarius. It is effective against gram-negative bacteria, especially the Pseudomonas species. It is a 10% component of the antibiotic complex, nebramycin, produced by the same species. [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]
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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] Topical: On the surface of the body. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicokinetics: Study of the absorption, distribution, metabolism, and excretion of test substances. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] 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] Toxoplasmosis: The acquired form of infection by Toxoplasma gondii in animals and man. [NIH]
Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [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] Translocate: The attachment of a fragment of one chromosome to a non-homologous chromosome. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH]
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Triad: Trivalent. [NIH] Tricuspid Atresia: Absence of the orifice between the right atrium and ventricle, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy because the right ventricle is absent or not functional. [NIH] Trimethoprim-sulfamethoxazole: An antibiotic drug used to treat infection and prevent pneumocystis carinii pneumonia. [NIH] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [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] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [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] 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] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [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] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uveitis: An inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (the sclera and cornea, and the retina). [EU] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond
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to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasodilator: An agent that widens blood vessels. [NIH] Vegetative: 1. Concerned with growth and with nutrition. 2. Functioning involuntarily or unconsciously, as the vegetative nervous system. 3. Resting; denoting the portion of a cell cycle during which the cell is not involved in replication. 4. Of, pertaining to, or characteristic of plants. [EU] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertigo: An illusion of movement; a sensation as if the external world were revolving around the patient (objective vertigo) or as if he himself were revolving in space (subjective vertigo). The term is sometimes erroneously used to mean any form of dizziness. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Vibrio: A genus of Vibrionaceae, made up of short, slightly curved, motile, gram-negative rods. Various species produce cholera and other gastrointestinal disorders as well as abortion in sheep and cattle. [NIH] Vibrio cholerae: The etiologic agent of cholera. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU]
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Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Humor: The transparent, colorless mass of gel that lies behind the lens and in front of the retina and fills the center of the eyeball. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Vulva: The external female genital organs, including the clitoris, vaginal lips, and the opening to the vagina. [NIH] Vulvovaginitis: Inflammation of the vulva and vagina, or of the vulvovaginal glands. [EU] 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] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenobiotics: Chemical substances that are foreign to the biological system. They include naturally occurring compounds, drugs, environmental agents, carcinogens, insecticides, etc. [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] Zinc Oxide: A mild astringent and topical protectant with some antiseptic action. It is also used in bandages, pastes, ointments, dental cements, and as a sunblock. [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]
205
INDEX A Abdominal, 145, 162, 185, 186 Aberrant, 14, 145 Abscess, 145, 196 Acceptor, 145, 168, 177, 184 Acetaldehyde, 48, 145 Acetylcholine, 145, 156, 182, 183 Acetylcysteine, 69, 145 Adaptability, 145, 155 Adenocarcinoma, 145, 170 Adipose Tissue, 145, 185 Adoptive Transfer, 10, 35, 145 Adrenergic, 118, 145, 165, 187 Adverse Effect, 6, 99, 145, 196 Aerosol, 6, 16, 74, 98, 145 Agammaglobulinemia, 98, 145 Agar, 145, 187 Agonist, 146, 183, 187 Air Pollutants, 17, 146 Air Sacs, 102, 146, 147 Airway Obstruction, 6, 55, 146 Airway Resistance, 80, 146 Albumin, 146, 184, 187 Algorithms, 146, 152 Alimentary, 146, 185 Alkaline, 146, 147, 153, 184 Alkaloid, 146, 150, 183 Allergen, 10, 12, 31, 146, 162 Allergic Rhinitis, 104, 146, 169 Allogeneic, 14, 146, 169 Allograft, 14, 36, 104, 146 Alpha 1-Antichymotrypsin, 146, 196 Alpha 1-Antitrypsin, 9, 146, 196 Alpha 1-Antitrypsin Deficiency, 9, 146 Alpha Particles, 146, 191 Alternative medicine, 114, 147 Alveoli, 25, 98, 102, 147, 191, 203 Amine, 147, 171 Amino Acid Sequence, 147, 148, 168, 196 Amino Acids, 23, 147, 148, 157, 165, 168, 185, 186, 188, 190, 196, 199, 201, 202 Ammonia, 16, 147, 199, 202 Amoxicillin, 38, 49, 50, 55, 56, 65, 66, 78, 147 Ampicillin, 147 Ampulla, 147, 156 Anaerobic, 147, 180 Anaesthesia, 147, 173
Anal, 147, 164, 177 Analgesic, 19, 147 Analytes, 130, 147 Anaphylatoxins, 147, 158 Anatomical, 148, 150, 156, 163, 173, 195 Anemia, 148, 152, 153, 157 Anesthesia, 146, 148 Angiotensinogen, 148, 193, 196 Animal model, 6, 8, 15, 17, 18, 22, 27, 39, 148 Ankle, 109, 141, 148 Antagonism, 79, 148 Anthocyanins, 22, 148 Antiarrhythmic, 148, 175 Antibacterial, 38, 50, 73, 148, 155, 157, 166, 183, 197 Antibodies, 17, 49, 61, 103, 148, 172, 180, 187 Antibody, 34, 82, 148, 158, 171, 172, 173, 175, 178, 180, 192, 197, 204 Anticoagulant, 148, 190 Antidepressant, 148, 160 Antigen, 70, 104, 148, 158, 171, 172, 173, 174, 178 Antigen-Antibody Complex, 148, 158 Anti-infective, 148, 154, 171, 197 Anti-inflammatory, 7, 19, 149, 150, 168 Anti-Inflammatory Agents, 149, 150 Antimetabolite, 149, 179 Antimicrobial, 38, 41, 49, 50, 54, 62, 64, 71, 75, 76, 79, 149, 157, 162, 166 Antineoplastic, 149, 167, 179 Antioxidant, 33, 65, 149, 184, 199 Antiplasmin, 149, 196 Antiseptic, 149, 204 Antiviral, 145, 149, 167, 186 Anus, 147, 149, 158 Aphakia, 149, 194 Apnoea, 70, 78, 149 Apoptosis, 7, 31, 35, 52, 100, 149 Aqueous, 149, 151, 154, 161, 171 Archaea, 149, 179 Arginine, 147, 149, 183, 202 Arrestin, 31, 149 Arterial, 142, 149, 154, 160, 172, 190 Arteries, 149, 150, 152, 160, 181, 191 Arterioles, 150, 152, 153, 179, 181 Artery, 149, 150, 181, 191, 193
206
Chronic Bronchitis
Articular, 150, 184 Ascites, 112, 150 Aspirate, 41, 150 Aspiration, 55, 150 Aspirin, 19, 150 Astringent, 150, 204 Asymptomatic, 66, 109, 150 Atopic, 68, 150 Atrial, 150, 160, 202 Atrioventricular, 150, 160 Atrium, 150, 160, 202, 203 Atrophy, 43, 150 Atropine, 150, 175 Autopsy, 32, 44, 150 Azithromycin, 41, 46, 49, 51, 79, 150 B Bacteremia, 109, 150 Bacterial Infections, 150, 176 Bacteriostatic, 150, 165 Bacterium, 98, 150 Bacteriuria, 109, 150 Base, 151, 168, 176 Basement Membrane, 151, 166 Basophil, 42, 151, 171 Benzoic Acid, 22, 151 Beta-Lactamases, 151, 155 Beta-Thromboglobulin, 151, 175 Bile, 151, 167, 173, 176, 177 Bile Acids, 151, 167 Bile duct, 151, 173 Bile Pigments, 151, 176 Biliary, 151, 156 Bioassays, 18, 151 Bioavailability, 17, 151 Biochemical, 9, 17, 19, 21, 24, 30, 32, 97, 103, 146, 149, 151, 153, 162, 175, 184, 186 Biological response modifier, 66, 151, 174 Biological Transport, 151, 162 Biomarkers, 17, 151 Biomass, 49, 151 Biopsy, 52, 80, 151, 152 Biopsy specimen, 52, 152 Biosynthesis, 152, 196 Biotechnology, 36, 37, 114, 125, 152 Biotransformation, 152 Biotypes, 42, 59, 152, 169 Bladder, 17, 152, 159, 161, 181, 190, 202 Blood Coagulation, 152, 153, 200 Blood pressure, 20, 112, 152, 154, 172, 180, 188, 191, 197
Blood vessel, 102, 152, 154, 155, 156, 160, 164, 166, 176, 179, 186, 191, 197, 198, 200, 203 Blood Viscosity, 37, 90, 152 Blood Volume, 37, 42, 90, 152 Blood-Brain Barrier, 152, 180 Body Fluids, 151, 152, 163, 197, 202 Body Mass Index, 79, 152 Bone Marrow, 25, 34, 152, 161, 167, 169, 172, 177, 198 Brachytherapy, 153, 175, 192, 204 Bradykinin, 153, 183, 187 Broad-spectrum, 46, 52, 147, 153, 155, 183, 200 Bronchi, 74, 99, 153, 165, 201 Bronchiectasis, 12, 19, 23, 30, 31, 32, 36, 50, 98, 103, 110, 112, 153 Bronchioles, 99, 147, 153, 190, 191 Bronchiolitis, 10, 13, 14, 15, 104, 130, 131, 153 Bronchiolitis Obliterans, 14, 15, 104, 153 Bronchoalveolar Lavage, 32, 62, 65, 66, 68, 153 Bronchoalveolar Lavage Fluid, 32, 65, 68, 153 Bronchoconstriction, 33, 81, 153 Bronchodilator, 9, 27, 43, 153 Bronchus, 57, 153 C Cadmium, 22, 153 Cadmium Poisoning, 153 Calcitonin, 59, 153 Calcium, 10, 17, 153, 158, 181, 196 Capillary, 42, 153, 191, 195, 203 Captopril, 84, 154 Carbocysteine, 65, 154 Carbohydrate, 154, 168, 188 Carbon Dioxide, 102, 154, 161, 167, 193, 203 Carcinogenesis, 17, 154, 156 Carcinogenic, 154, 174, 184, 190 Carcinogens, 28, 154, 156, 181, 204 Carcinoma, 8, 68, 154 Cardiac, 18, 20, 23, 148, 154, 160, 165, 181 Cardiopulmonary, 20, 154 Cardiotonic, 154, 187 Cardiovascular, 18, 20, 43, 53, 108, 154 Cardiovascular disease, 20, 43, 108, 154 Carotene, 154, 194 Carrier Proteins, 154, 187 Cataract, 149, 154, 194 Cathepsins, 8, 154
207
Causal, 154, 164 Cause of Death, 4, 24, 96, 102, 103, 155 Cefixime, 41, 155 Ceftazidime, 71, 155 Ceftriaxone, 51, 72, 155 Cefuroxime, 41, 46, 63, 64, 71, 72, 76, 155 Cell Adhesion, 18, 155, 174 Cell Death, 149, 155, 182 Cell Differentiation, 32, 155, 196 Cell Division, 150, 155, 179, 187, 195 Cell membrane, 151, 154, 155, 162, 165, 187 Cell proliferation, 25, 26, 155, 175, 196 Cell Survival, 32, 155 Central Nervous System, 145, 155, 169, 176, 182 Cephaloridine, 155 Cephalosporins, 151, 155, 180 Cerebrovascular, 108, 154, 155 Cerebrum, 155 Chemokines, 15, 18, 25, 31, 155 Chemoprevention, 19, 156 Chemopreventive, 19, 156 Chemotactic Factors, 156, 158 Chemotaxis, 21, 156 Chemotherapy, 41, 46, 49, 50, 54, 62, 64, 71, 76, 77, 89, 108, 156, 176 Chest Pain, 4, 156 Chest wall, 88, 156, 193 Chin, 88, 90, 91, 156, 179 Chlorpheniramine, 53, 156 Cholera, 36, 156, 203 Cholestasis, 112, 156 Cholesterol, 151, 156, 160, 177 Cholinergic, 156, 181, 183, 192 Chromatin, 149, 156, 177, 198 Chromic, 6, 156 Chromium, 156 Chromosomal, 9, 156 Chromosome, 14, 156, 175, 177, 195, 201 Chronic Disease, 13, 156 Chymotrypsin, 8, 146, 157 Ciliary, 12, 82, 96, 98, 157, 180 Ciliary Motility Disorders, 98, 157 Ciprofloxacin, 28, 50, 51, 52, 76, 157 Cirrhosis, 112, 157, 189 CIS, 157, 194 Clarithromycin, 38, 39, 44, 51, 52, 54, 71, 75, 76, 77, 157 Clavulanic Acid, 38, 157 Clear cell carcinoma, 157, 162 Cleave, 24, 157
Clinical trial, 6, 65, 125, 157, 160, 161, 163, 181, 192 Cloning, 14, 17, 152, 157 Coagulation, 152, 157, 158, 170, 187 Cobalt, 17, 157 Coculture, 20, 157 Cofactor, 158, 190, 196, 200 Cohort Studies, 19, 58, 158, 164 Colon, 29, 158, 173 Complement, 19, 47, 147, 158, 159, 168, 174, 178, 187, 196 Complement 1, 158, 196 Complement 1 Inactivators, 158, 196 Complementary and alternative medicine, 87, 94, 158 Complementary medicine, 87, 158 Complete remission, 159, 193 Compliance, 55, 159 Computational Biology, 125, 159 Computed tomography, 7, 159 Computerized axial tomography, 159 Computerized tomography, 159 Concomitant, 27, 159 Cones, 159, 194 Confounding, 19, 159 Congestion, 159, 161 Conjugated, 151, 159 Conjunctiva, 159, 174 Conjunctivitis, 159, 169 Connective Tissue, 152, 159, 162, 166, 169, 179, 186, 198 Consciousness, 147, 159, 190 Constriction, 159, 176 Continuum, 14, 159 Contractility, 18, 159 Contraindications, ii, 160 Controlled study, 43, 51, 89, 160 Coordination, 10, 160 Cor, 69, 160 Cor pulmonale, 69, 160 Coronary, 45, 78, 154, 160, 181 Coronary Disease, 78, 160 Coronary heart disease, 45, 154, 160 Coronary Vessels, 160 Corticosteroids, 118, 160, 168 Cotinine, 28, 160 Cranial, 160, 165, 169, 185, 198 Cross-Sectional Studies, 160, 164 Cryptosporidiosis, 150, 160 Curative, 161, 200 Cutaneous, 161, 175 Cyclic, 161, 169, 183
208
Chronic Bronchitis
Cyclosporine, 104, 161 Cyst, 150, 161 Cysteine, 8, 24, 29, 93, 94, 97, 145, 155, 161, 162, 175, 199 Cystine, 161, 162 Cystitis, 109, 161 Cytokine, 13, 17, 21, 23, 30, 33, 48, 161, 174 Cytoplasm, 149, 155, 161, 164, 177 Cytoskeleton, 18, 161, 174 Cytotoxic, 31, 146, 161, 172, 173, 192, 196 D Decarboxylation, 161, 171 Decongestant, 97, 98, 161, 187 Decubitus, 161, 197 Decubitus Ulcer, 161, 197 Defense Mechanisms, 161, 174 Degenerative, 161, 170, 184, 194 Dehydration, 36, 156, 161 Deletion, 14, 34, 149, 161 Dental Care, 110, 161 Dental Caries, 22, 161, 162 Dental Plaque, 22, 162 Dentists, 4, 162 Depolarization, 162, 196 Dermis, 162, 199 DES, 81, 147, 162 Desensitization, 31, 162, 173 Desquamation, 7, 162 Detergents, 162, 197 Detoxification, 28, 162 Diabetes Mellitus, 4, 162, 168, 170 Diagnostic procedure, 95, 114, 162 Diaphragm, 162, 193 Diarrhea, 36, 160, 162, 198 Diffusion, 88, 102, 151, 162, 173 Digestion, 146, 151, 162, 175, 177, 198, 203 Dilation, 112, 153, 162 Direct, iii, 20, 48, 103, 117, 162, 171, 192 Distal, 162, 167, 190, 191 Disulphides, 162 Dithiothreitol, 50, 162 Dominance, 60, 163 Double-blind, 26, 49, 50, 51, 64, 75, 76, 77, 89, 163 Drip, 5, 163 Drug Interactions, 119, 120, 163 Drug Tolerance, 163, 200 Dry Eye Syndrome, 36, 163 Duct, 96, 147, 163, 177, 195, 199 Duodenum, 151, 157, 163, 185, 198 Dyes, 163 Dynein, 157, 163
Dyskinesia, 96, 163 Dyspnea, 103, 163, 191 E Effector, 145, 158, 163 Efficacy, 12, 23, 39, 50, 51, 52, 71, 76, 78, 79, 163 Elastic, 32, 163 Electrons, 149, 151, 163, 175, 184, 191, 192 Embryo, 155, 163, 173, 188 Enamel, 161, 163 Endemic, 156, 163 Endocytosis, 27, 163 Endogenous, 8, 24, 27, 29, 36, 164, 196, 201 Endoscopy, 5, 164 Endothelial cell, 35, 152, 164, 174, 200 Endothelium, 164, 183, 188 Endothelium-derived, 164, 183 Endotoxin, 12, 16, 164 Enteropeptidase, 164, 202 Environmental Exposure, 7, 23, 164 Environmental Health, 68, 124, 126, 164 Environmental Microbiology, 16, 164 Environmental tobacco smoke, 28, 164 Enzymatic, 153, 154, 158, 161, 164, 171, 194 Enzyme, 19, 24, 163, 164, 167, 169, 175, 176, 179, 181, 184, 187, 190, 192, 193, 196, 200, 204 Enzyme Inhibitors, 164, 187 Eosinophil, 164, 174 Eosinophilia, 35, 39, 164 Epidemiologic Studies, 20, 33, 164 Epidemiological, 53, 164 Epidermal, 24, 26, 164, 165, 176, 178 Epidermal Growth Factor, 24, 26, 164, 165 Epidermal growth factor receptor, 26, 165 Epidermis, 162, 164, 165, 176 Epinephrine, 145, 165, 182, 202 Epithelial Cells, 8, 10, 19, 21, 23, 26, 29, 30, 31, 33, 34, 41, 60, 70, 97, 164, 165 Epithelium, 7, 8, 12, 19, 24, 26, 30, 32, 80, 97, 151, 164, 165, 194 Erythrocyte Volume, 152, 165 Erythrocytes, 65, 148, 152, 165, 192 Erythromycin, 54, 150, 157, 165 Esophageal, 165, 167 Esophagitis, 165, 167 Esophagus, 131, 165, 167, 170, 177, 186, 192, 198 Ethmoid, 165, 185 Exfoliation, 162, 165 Exhaustion, 148, 165 Exocytosis, 30, 165, 171
209
Exogenous, 8, 23, 29, 152, 154, 164, 165, 196 Expectorant, 97, 98, 101, 154, 165 Expiration, 89, 101, 165, 193 Expiratory, 27, 56, 89, 165 External-beam radiation, 165, 175, 191, 204 Extracellular, 14, 24, 29, 30, 159, 163, 166, 174, 197 Extracellular Matrix, 14, 24, 159, 166, 174 Extracellular Space, 166 Extraction, 149, 166, 194 Extravascular, 33, 166 Extremity, 109, 166 Exudate, 153, 165, 166 F Failure to Thrive, 112, 166 Family Planning, 125, 166 Fat, 112, 145, 152, 154, 160, 161, 166, 177, 197 Fetus, 166, 189 Fibrinogen, 20, 166, 187, 200 Fibroblasts, 166, 174, 180 Fibrosis, 7, 8, 11, 12, 13, 15, 19, 23, 25, 26, 29, 30, 31, 32, 33, 35, 36, 47, 53, 56, 74, 96, 97, 98, 100, 103, 104, 110, 166, 191, 195 Flatus, 166, 167 Fleroxacin, 37, 55, 166 Fluorescence, 36, 166 Foramen, 156, 166, 186 Forearm, 152, 166 Free Radicals, 149, 166, 181 Friction, 146, 167 Fungistatic, 151, 167 G Gallbladder, 97, 145, 151, 167 Gallic Acid, 98, 101, 167 Gamma-interferon, 65, 167, 174 Gangrene, 110, 167 Gas, 12, 16, 18, 35, 102, 130, 142, 147, 154, 162, 166, 167, 171, 181, 183, 190, 193, 194, 199, 203 Gas exchange, 12, 167, 190, 193, 194, 203 Gastric, 147, 164, 167, 170, 171 Gastric Acid, 147, 167 Gastrin, 42, 167, 171 Gastroesophageal Reflux, 4, 5, 167 Gastroesophageal Reflux Disease, 4, 167 Gastrointestinal, 36, 97, 153, 157, 165, 167, 176, 199, 202, 203 Gene Expression, 11, 28, 32, 63, 96, 167
Gene Therapy, 25, 167 Generator, 17, 167 Genetic Code, 168, 183 Genetic Engineering, 152, 157, 168 Genetic Markers, 16, 168 Genetics, 13, 15, 57, 163, 168 Genital, 157, 168, 204 Genotype, 12, 14, 168, 186 Gingivitis, 22, 162, 168 Gland, 11, 24, 168, 178, 185, 190, 195, 198, 199, 200 Glomerular, 168, 193 Glomeruli, 168, 191 Glucans, 22, 168 Glucocorticoid, 10, 168 Glucose, 101, 156, 162, 168, 170, 174 Glucose Intolerance, 162, 168 Glucosyltransferases, 22, 168 Glucuronic Acid, 168, 170 Glycine, 151, 168, 182, 196 Glycoprotein, 57, 88, 146, 149, 158, 166, 168, 169, 175, 181, 200 Glycosidic, 148, 168, 184 Goblet Cells, 23, 30, 80, 169 Gonorrhea, 155, 169 Governing Board, 169, 189 Gp120, 169, 186 Graft, 15, 35, 104, 169, 173, 181 Graft Rejection, 104, 169, 173 Graft-versus-host disease, 169, 181 Gram-negative, 12, 99, 155, 169, 183, 200, 203 Gram-positive, 155, 169, 183, 198 Granulation Tissue, 153, 169 Granule, 30, 169 Granulocyte, 12, 169 Guanylate Cyclase, 169, 183 Gyrase, 166, 169 H Haemophilus influenzae, 19, 39, 42, 58, 60, 70, 98, 169 Half-Life, 29, 155, 169 Haplotypes, 14, 169 Hay Fever, 22, 61, 146, 156, 169 Headache, 169, 174 Health Services, 10, 170 Health Status, 4, 9, 79, 170 Heart attack, 154, 170 Heart failure, 160, 170, 191 Heartburn, 4, 170 Hematopoiesis, 170, 174, 175 Hemoglobin, 148, 165, 170
210
Chronic Bronchitis
Hemoglobinopathies, 167, 170 Hemorrhage, 169, 170, 181, 198 Hemostasis, 170, 174 Heparin, 27, 170, 188, 196 Hepatitis, 112, 170 Hepatocellular, 112, 170 Hepatocellular carcinoma, 112, 170 Hepatocyte, 156, 170 Heredity, 167, 168, 170 Heterodimers, 170, 174 Heterogeneity, 80, 170 Heterozygotes, 163, 170 Histamine, 41, 53, 58, 59, 147, 156, 171, 189 Histamine Release, 41, 58, 147, 171 Histidine, 171 Hoarseness, 4, 171 Homeostasis, 35, 171 Homogeneous, 100, 159, 171 Homologous, 167, 170, 171, 195, 199, 201 Homozygotes, 163, 171 Hormonal, 150, 171 Hormone, 151, 153, 160, 162, 165, 167, 171, 174, 194, 196, 200 Humoral, 169, 171 Hybrid, 171 Hybridization, 18, 171 Hydration, 12, 96, 171 Hydrogen, 145, 147, 151, 154, 171, 177, 180, 182, 183, 184, 186, 190 Hydrogen Peroxide, 171, 177 Hydrogenation, 171, 191 Hydrolysis, 151, 152, 155, 171, 187, 188, 190, 202 Hydrophilic, 100, 162, 171 Hydroxybenzoic Acids, 98, 101, 171 Hygienic, 172, 197 Hyperbilirubinemia, 172, 176 Hyperplasia, 7, 10, 11, 24, 30, 57, 172 Hypersecretion, 22, 23, 24, 30, 32, 97, 172 Hypersensitivity, 44, 146, 162, 164, 172, 194 Hypertension, 154, 169, 172, 188, 200 Hypertrophy, 11, 24, 160, 172, 202 Hypoventilation, 6, 172 Hypoxemia, 60, 67, 172 Hypoxia, 53, 81, 172 Hypoxic, 67, 89, 172 I Idiopathic, 104, 172 Immune response, 13, 21, 60, 61, 104, 148, 169, 172, 173, 178, 199, 202, 203 Immune Sera, 172
Immune system, 10, 21, 103, 172, 173, 178, 202, 204 Immune-response, 21, 172 Immunity, 13, 21, 65, 70, 84, 172, 201 Immunization, 31, 145, 172, 173, 189 Immunocompromised, 45, 172 Immunoglobulins, 172, 187 Immunohistochemistry, 25, 172 Immunologic, 109, 145, 146, 156, 172, 192 Immunology, 13, 15, 39, 52, 54, 62, 68, 172 Immunosuppressant, 173, 179 Immunosuppression, 104, 173, 177, 184 Immunosuppressive, 104, 168, 173, 200 Immunosuppressive Agents, 104, 173 Immunosuppressive therapy, 173 Immunotherapy, 35, 145, 162, 173 Impaction, 57, 173 Impairment, 16, 23, 97, 156, 163, 173, 179 Implant radiation, 173, 175, 192, 204 In vitro, 8, 10, 14, 17, 19, 23, 25, 33, 34, 57, 146, 152, 167, 173, 200 In vivo, 8, 10, 11, 19, 21, 22, 23, 25, 26, 33, 34, 35, 146, 167, 170, 173, 177, 180, 200 Incision, 173, 175, 199 Incompetence, 167, 173 Induction, 13, 20, 34, 35, 84, 173 Infarction, 151, 173, 181, 193 Infiltration, 32, 173, 176 Influenza, 109, 174 Ingestion, 153, 174 Inhalation, 16, 17, 23, 30, 33, 35, 39, 118, 119, 145, 153, 174, 175 Inhalation Exposure, 23, 33, 174 Initiation, 25, 174, 201 Inner ear, 155, 174 Inorganic, 16, 174, 181, 199 Insecticides, 174, 204 Insight, 9, 15, 21, 30, 34, 174 Insulin, 5, 174 Insulin-dependent diabetes mellitus, 174 Integrins, 19, 34, 174 Intercellular Adhesion Molecule-1, 19, 174 Interferon, 167, 174 Interleukin-5, 39, 63, 174 Interleukin-8, 31, 103, 174 Interleukin-9, 67, 175 Interleukins, 173, 175 Intermittent, 99, 163, 175 Internal radiation, 175, 191, 204 Interstitial, 153, 166, 175, 193, 204 Intestine, 175, 192, 197, 198 Intoxication, 175, 204
211
Intracellular, 12, 23, 30, 33, 173, 174, 175, 183, 196 Intramuscular, 175, 185 Intravascular, 175, 176 Intravenous, 104, 175, 185 Invasive, 172, 175 Involuntary, 164, 175, 192 Iodoacetic Acid, 154, 175 Ionizing, 147, 164, 175, 192 Ipratropium, 69, 119, 175 Irradiation, 17, 175, 204 Irritants, 97, 103, 175 Ischemia, 15, 18, 35, 150, 161, 176, 181, 193 Isozymes, 31, 56, 176 J Jaundice, 112, 172, 176 K Kb, 14, 124, 176 Keratinocytes, 174, 176 Keratolytic, 162, 176 Kidney Disease, 36, 108, 109, 124, 176 Kinetic, 175, 176 L Labile, 158, 176 Lacrimal, 176, 182 Lacrimal Apparatus, 176, 182 Larynx, 131, 176, 201 Latent, 64, 176, 189 Lesion, 176, 177 Leukemia, 31, 167, 176 Leukemic Infiltration, 176 Leukostasis, 35, 176 Levofloxacin, 51, 64, 71, 75, 82, 176 Ligament, 176, 186, 190 Ligands, 17, 25, 174, 177 Linkage, 9, 14, 16, 57, 168, 177, 185 Lipid, 33, 65, 174, 177, 184 Lipid Peroxidation, 33, 177, 184 Lipopolysaccharide, 169, 177 Lipoprotein, 169, 177 Liver, 108, 112, 145, 146, 151, 157, 167, 168, 170, 176, 177, 188, 193, 202 Liver cancer, 112, 177 Localization, 16, 172, 177 Localized, 8, 145, 161, 173, 177, 187, 202 Longitudinal study, 10, 177 Lower Esophageal Sphincter, 167, 177 Lung Transplantation, 13, 15, 35, 104, 177 Lung volume, 9, 177, 193 Lymph, 164, 177, 199 Lymphatic, 164, 173, 177, 179, 200 Lymphocyte Depletion, 173, 177
Lymphocytes, 15, 31, 52, 65, 66, 67, 81, 148, 167, 172, 174, 177, 178, 200, 204 Lymphoid, 11, 148, 160, 169, 172, 177, 178 Lysine, 65, 178, 202 M Macrolides, 79, 178 Macrophage, 17, 21, 23, 42, 178 Major Histocompatibility Complex, 169, 178 Malaise, 99, 178 Malignant, 31, 109, 145, 149, 177, 178, 182, 192 Malnutrition, 146, 150, 178 Manifest, 7, 13, 99, 157, 178 Mastitis, 152, 178 Maxillary, 178, 185 Mechanical ventilation, 90, 178 Mechanoreceptors, 178, 193 Mediate, 10, 21, 22, 31, 34, 178 Mediator, 20, 68, 178, 188 Medical Records, 178, 194 MEDLINE, 125, 178 Melanin, 178, 186, 202 Melanocytes, 178, 179 Melanoma, 31, 179 Membrane, 26, 29, 42, 146, 155, 158, 159, 162, 163, 165, 169, 176, 179, 180, 181, 182, 186, 187, 194, 196 Memory, 5, 10, 179 Meninges, 155, 179 Mental, iv, 5, 6, 124, 126, 156, 173, 179, 183, 189, 190, 195, 202 Mental Disorders, 179, 189, 190 Mental Health, iv, 6, 124, 126, 179, 183, 189, 190 Mental Retardation, 5, 179 Mesenchymal, 164, 179 Mesenteric, 179, 189 Metabolic disorder, 112, 179 Metabolite, 152, 179, 189 Metaplasia, 24, 31, 179 Methotrexate, 28, 179 Microbe, 179, 201 Microbiology, 16, 42, 45, 75, 98, 150, 179 Microcirculation, 179, 188 Microorganism, 158, 179, 204 Micro-organism, 161, 179 Microscopy, 18, 25, 30, 151, 157, 179 Migration, 18, 25, 34, 174, 179 Mitosis, 149, 179 Modification, 168, 180, 191 Monitor, 17, 46, 180, 183
212
Chronic Bronchitis
Monoclonal, 34, 175, 180, 192, 204 Monoclonal antibodies, 34, 180 Monocular, 14, 180 Monocyte, 14, 42, 68, 180 Monocyte Chemoattractant Protein-1, 14, 180 Mononuclear, 14, 42, 59, 180 Morphogenesis, 11, 180 Morphological, 24, 163, 178, 180 Morphology, 25, 149, 154, 180 Moxalactam, 64, 180 Mucins, 53, 78, 96, 97, 162, 169, 180 Mucociliary, 12, 29, 50, 68, 84, 96, 97, 180, 197 Mucociliary Clearance, 12, 29, 50, 84, 96, 180 Mucolytic, 69, 73, 145, 153, 154, 180 Mucosa, 19, 25, 56, 67, 181, 182, 198 Mucus, 12, 22, 23, 24, 30, 32, 35, 57, 63, 65, 88, 96, 97, 102, 165, 180, 181 Multicenter study, 28, 65, 71, 181 Muscarinic Agonists, 30, 181 Mustard Gas, 175, 181 Mutagenesis, 30, 181 Mutagens, 181 Myalgia, 174, 181 Mycophenolate mofetil, 104, 181 Mydriatic, 162, 181, 187 Myocardial Ischemia, 160, 181 Myocardial Reperfusion, 181, 193 Myocardial Reperfusion Injury, 181, 193 Myopia, 181, 192, 194 N Narcotic, 145, 182 Nasal Cavity, 182, 185 Nasal Mucosa, 174, 182 Nasolacrimal, 96, 182 Nebramycin, 182, 200 Nebulizer, 80, 182 Necrosis, 149, 173, 181, 182, 193, 196 Neoplasms, 145, 149, 154, 182, 192 Nephropathy, 176, 182 Nervous System, 155, 178, 182, 199, 203 Neural, 171, 178, 182, 193, 194 Neuronal, 182 Neurons, 182, 183, 199 Neuropathy, 109, 182 Neuropeptides, 17, 182 Neuropsychological Tests, 5, 182 Neurotransmitter, 145, 153, 168, 171, 182, 196, 199 Neutrons, 146, 175, 182, 191
Neutrophil, 12, 18, 26, 27, 33, 146, 174, 183 Nicotine, 131, 183, 192 Nitric Oxide, 33, 61, 183 Nuclear, 157, 163, 182, 183 Nuclei, 147, 163, 167, 168, 179, 182, 183, 190 Nucleic acid, 18, 168, 171, 181, 183, 191 Nucleic Acid Hybridization, 171, 183 Nucleus, 149, 156, 161, 177, 180, 182, 183, 190 Nursing Care, 107, 183 Nutritional Status, 3, 183 O Observational study, 73, 183 Occupational Exposure, 5, 9, 20, 183 Occupational Health, 18, 23, 183 Ofloxacin, 49, 71, 183 Ointments, 183, 197, 204 Oligosaccharides, 78, 183 Oncogenic, 174, 184 Opportunistic Infections, 104, 184 Opsin, 184, 194 Oral Health, 3, 109, 184 Organ Culture, 184, 200 Osteoarthritis, 28, 184 Osteoclasts, 153, 184 Otitis, 96, 109, 157, 184 Otitis Media, 96, 184 Outpatient, 51, 184 Ovalbumin, 31, 184, 196 Ovary, 184, 188, 198 Overexpress, 8, 184 Oxidation, 33, 145, 149, 152, 161, 162, 177, 184 Oxidative Stress, 24, 33, 184 Oxides, 184, 199 Oxygen Consumption, 67, 184, 193 Oxygenase, 35, 184 Oxygenation, 69, 172, 184 P Palliative, 185, 200 Pancreas, 145, 151, 157, 174, 185, 198, 202 Pancreatic, 28, 97, 157, 167, 185 Pancreatic Ducts, 97, 185 Pancreatic Juice, 157, 167, 185 Panniculitis, 112, 185 Paranasal Sinuses, 96, 157, 185, 196 Parenteral, 99, 185 Partial remission, 185, 193 Particle, 6, 16, 17, 22, 33, 39, 185, 201 Pathologic, 7, 149, 151, 160, 172, 176, 185 Pathologic Processes, 149, 185
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Pathologies, 35, 185 Pathophysiology, 4, 11, 24, 109, 185 Patient Education, 131, 136, 138, 143, 185 Peak flow, 20, 185 Pedigree, 13, 16, 185 Pelvic, 185, 190 Pelvis, 185, 191 Penicillin, 147, 148, 185 Peptide, 23, 42, 153, 157, 164, 185, 188, 190 Peptide Chain Elongation, 157, 185 Peptide T, 23, 185 Perfusion, 172, 186 Periodontal Attachment Loss, 4, 186 Periodontal disease, 4, 186 Periodontal Ligament, 186 Periodontitis, 168, 186 Peripheral blood, 59, 186 Peritoneal, 31, 34, 150, 186 Peritoneal Cavity, 34, 150, 186 Peritoneum, 186 PH, 36, 186 Pharmacodynamics, 63, 71, 186 Pharmacokinetic, 186 Pharmacologic, 18, 33, 148, 169, 186, 201 Pharynx, 167, 174, 182, 186 Phenotype, 11, 14, 53, 186 Phenylalanine, 186, 202 Phenylephrine, 97, 98, 187 Phospholipases, 187, 196 Phospholipids, 166, 177, 187 Phosphorus, 153, 187 Phosphorylated, 149, 187 Phosphorylation, 26, 31, 34, 187 Physical Therapy, 88, 90, 187 Physiologic, 7, 17, 20, 33, 146, 152, 169, 187, 192 Physiology, 18, 29, 30, 67, 84, 187 Pigment, 178, 179, 187, 194 Plants, 146, 150, 154, 168, 180, 187, 188, 195, 196, 201, 203 Plaque, 22, 187 Plasma, 59, 74, 146, 148, 149, 151, 152, 153, 155, 166, 168, 169, 170, 187, 193, 195 Plasma cells, 148, 169, 187 Plasma protein, 74, 146, 187 Plasma Volume, 152, 187 Plasmin, 149, 187, 188 Plasminogen Activators, 27, 187, 188 Plasminogen Inactivators, 188, 196 Platelet Activation, 188, 196 Platelet Aggregation, 147, 183, 188 Platelet Factor 4, 175, 188
Platelets, 151, 183, 188 Pneumoconiosis, 74, 188 Pneumonia, 28, 46, 51, 64, 71, 96, 97, 98, 100, 109, 153, 160, 188, 202 Pneumonitis, 44, 153, 188, 198 Pollen, 188, 191 Polymers, 98, 101, 188, 190 Polymorphic, 9, 188 Polymorphism, 12, 188 Polypeptide, 147, 164, 166, 171, 187, 188, 204 Polysaccharide, 22, 148, 188 Portal Hypertension, 112, 188 Portal Vein, 112, 188, 189 Postnatal, 29, 189, 198 Postsynaptic, 189, 196, 199 Potentiating, 35, 189 Potentiation, 189, 196 Practice Guidelines, 126, 189 Precancerous, 156, 189 Precipitating Factors, 4, 189 Precursor, 148, 163, 164, 186, 189, 202 Predisposition, 9, 189 Prenatal, 29, 163, 189 Prevalence, 4, 9, 19, 24, 45, 47, 49, 55, 61, 62, 73, 81, 109, 189 Primary Prevention, 67, 189 Probe, 7, 189 Prodrug, 28, 189 Progression, 9, 19, 48, 60, 102, 148, 189 Progressive, 15, 27, 104, 108, 155, 157, 163, 182, 184, 188, 189, 191, 193 Promethazine, 156, 189 Promoter, 8, 11, 12, 20, 190 Prophylaxis, 73, 98, 190, 202 Prospective study, 82, 177, 190 Prostate, 97, 151, 190, 202 Protease, 9, 24, 26, 27, 29, 146, 188, 190 Protein C, 31, 82, 146, 147, 177, 190, 202 Protein S, 18, 152, 157, 165, 168, 190, 200 Proteolytic, 146, 158, 164, 166, 187, 188, 190, 196 Protons, 146, 171, 175, 190, 191 Proximal, 162, 182, 190, 196 Psychiatry, 190, 203 Psychic, 179, 190 Psychoactive, 190, 204 Psychotropic, 5, 190 Public Health, 19, 20, 33, 64, 84, 126, 190 Public Policy, 125, 190 Publishing, 37, 190 Pulmonary Alveoli, 172, 190
214
Chronic Bronchitis
Pulmonary Artery, 152, 191, 203 Pulmonary Circulation, 37, 67, 90, 191 Pulmonary Emphysema, 42, 60, 146, 191 Pulmonary Fibrosis, 13, 17, 104, 191 Pulmonary hypertension, 84, 160, 191 Pulse, 180, 191 Pupil, 162, 181, 191 Purines, 191, 196 Purulent, 44, 99, 100, 191 Putrefaction, 167, 191 Pyelonephritis, 109, 191 Pyrimidines, 191, 196 Q Quality of Life, 10, 26, 40, 80, 103, 112, 191 Quercetin, 22, 191 Quinolones, 80, 191 R Race, 4, 179, 191 Radiation, 16, 164, 165, 166, 173, 175, 191, 192, 204 Radiation therapy, 165, 175, 191, 204 Radioactive, 169, 171, 173, 175, 180, 183, 184, 191, 192, 204 Radiolabeled, 175, 192, 204 Radiopharmaceutical, 167, 192 Radiotherapy, 153, 175, 192, 204 Randomized, 19, 26, 28, 38, 39, 40, 49, 64, 71, 75, 76, 77, 163, 192 Reactivation, 109, 192 Reactive Oxygen Species, 18, 33, 192 Reagent, 162, 167, 192, 196 Receptor, 12, 14, 15, 17, 21, 24, 26, 30, 31, 32, 34, 96, 148, 169, 186, 192, 196 Receptors, Muscarinic, 181, 192 Recombinant, 11, 192 Recombination, 167, 168, 192 Rectum, 149, 158, 166, 167, 190, 192 Recurrence, 156, 192 Red blood cells, 165, 184, 192 Reductase, 179, 192 Refer, 1, 158, 177, 182, 192, 201 Reflex, 192, 193 Reflux, 5, 56, 167, 192 Refraction, 181, 192, 197 Refractory, 104, 192 Regimen, 63, 99, 163, 193 Regurgitation, 167, 170, 193 Reinfection, 109, 193 Relapse, 53, 193 Remission, 88, 192, 193 Renal failure, 36, 193 Renin, 148, 154, 193
Renin-Angiotensin System, 154, 193 Reperfusion, 15, 35, 181, 193 Reperfusion Injury, 15, 193 Respirable, 20, 22, 193 Respiration, 42, 65, 68, 70, 76, 80, 84, 88, 89, 154, 180, 193 Respirator, 178, 193 Respiratory failure, 66, 72, 104, 193 Respiratory Mechanics, 18, 193 Respiratory Paralysis, 145, 193 Respiratory Physiology, 41, 43, 44, 45, 48, 53, 58, 63, 64, 70, 73, 75, 77, 81, 89, 194, 203 Respiratory System, 146, 180, 194 Respite Care, 108, 194 Retina, 159, 181, 194, 195, 202, 204 Retinal, 96, 149, 180, 194 Retinal Detachment, 96, 194 Retinol, 194 Retrospective, 3, 19, 99, 194 Retrospective study, 4, 99, 194 Retroviral vector, 167, 194 Rheology, 65, 194 Rheumatoid, 28, 31, 194 Rheumatoid arthritis, 28, 31, 194 Rhinitis, 78, 156, 175, 194 Rhodopsin, 149, 184, 194 Risk factor, 9, 12, 20, 72, 73, 77, 104, 112, 164, 190, 194 Risk patient, 71, 195 Rod, 150, 195 Rutin, 191, 195 S Saline, 26, 153, 195 Salivary, 162, 195, 199 Schizoid, 195, 204 Schizophrenia, 195, 204 Schizotypal Personality Disorder, 195, 204 Sclerosis, 108, 195 Screening, 5, 27, 112, 157, 195 Sebaceous, 162, 175, 195 Sebaceous gland, 162, 175, 195 Secretion, 23, 24, 30, 32, 57, 164, 171, 172, 174, 175, 180, 181, 195, 203 Secretory, 23, 28, 30, 65, 180, 195, 199 Segmental, 7, 195 Segmentation, 195 Segregation, 16, 150, 192, 195 Semen, 190, 195 Semisynthetic, 147, 155, 157, 195 Senile, 90, 195 Sensor, 35, 195
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Sepsis, 12, 99, 195 Septal, 74, 196 Sequence Homology, 185, 196 Sequester, 27, 196 Serine, 8, 24, 27, 157, 196, 202 Serine Endopeptidases, 196 Serine Proteinase Inhibitors, 196 Serpins, 8, 196 Serum, 12, 20, 26, 42, 47, 99, 145, 146, 147, 158, 172, 177, 196 Shock, 59, 196 Side effect, 12, 108, 117, 145, 196, 201 Signal Transduction, 18, 196 Signs and Symptoms, 26, 109, 193, 196 Silver Staining, 70, 196 Sinusitis, 46, 96, 110, 157, 196 Skin Care, 107, 197 Small intestine, 163, 171, 175, 197, 202 Smoking Cessation, 60, 197 Smooth muscle, 18, 147, 153, 171, 181, 193, 197, 199 Soaps, 197 Social Environment, 191, 197 Social Support, 107, 197 Sodium, 29, 197, 199 Soft tissue, 152, 197 Specialist, 133, 162, 197 Species, 23, 24, 45, 146, 165, 169, 171, 179, 180, 191, 192, 196, 197, 198, 199, 200, 201, 202, 203, 204 Specificity, 27, 196, 197 Spectrum, 112, 166, 180, 197 Sperm, 156, 188, 197 Spermatozoa, 157, 195, 197 Sphenoid, 185, 198 Sphincter, 176, 198 Spinal cord, 155, 156, 179, 182, 192, 193, 198 Spirometry, 9, 27, 130, 198 Splenic Vein, 189, 198 Sputum, 12, 26, 38, 44, 50, 58, 59, 61, 74, 82, 99, 100, 103, 198 Stem Cells, 11, 169, 198 Steroids, 61, 160, 168, 198 Stimulant, 81, 160, 171, 198 Stimulus, 159, 174, 192, 198 Stomach, 145, 165, 167, 171, 176, 177, 186, 192, 197, 198 Stool, 158, 173, 198 Streptococcal, 109, 198 Streptococci, 22, 198 Streptococcus, 22, 41, 42, 99, 198
Stress, 25, 33, 35, 142, 184, 189, 194, 198, 202 Stroke, 5, 108, 124, 154, 198 Stromal, 25, 198 Stromal Cells, 25, 198 Strongyloidiasis, 74, 198 Subacute, 173, 197, 198 Subclinical, 173, 199 Subcutaneous, 112, 185, 199 Sublingual, 73, 199 Submaxillary, 164, 199 Subspecies, 197, 199 Substance P, 165, 179, 195, 199 Sulfur, 6, 17, 68, 199 Sulfur Dioxide, 17, 199 Sulfur Oxides, 68, 199 Superoxide, 35, 199 Supplementation, 89, 199 Support group, 143, 199 Surgical Wound Infection, 109, 199 Sweat, 29, 162, 199 Sweat Glands, 29, 162, 199 Symphysis, 156, 190, 199 Symptomatic, 16, 97, 101, 199 Synaptic, 182, 183, 196, 199 Synaptic Transmission, 183, 199 Systemic, 5, 23, 31, 70, 104, 109, 118, 119, 152, 165, 173, 175, 192, 199, 201, 202, 204 T Tachycardia, 150, 199 Tachypnea, 150, 200 Tacrolimus, 104, 200 Tear Gases, 175, 200 Tetracycline, 25, 200 Therapeutics, 38, 39, 40, 41, 50, 51, 52, 66, 71, 77, 120, 200 Thermoregulation, 91, 200 Threonine, 185, 196, 200 Thrombin, 166, 188, 190, 200 Thrombomodulin, 190, 200 Thrombosis, 35, 151, 174, 181, 190, 198, 200 Thymus, 94, 172, 177, 200 Thyroid, 153, 200, 202 Thyroxine, 146, 186, 196, 200 Tinnitus, 184, 200 Tissue Culture, 23, 36, 200 Tobramycin, 98, 200 Tolerance, 22, 145, 168, 200 Tomography, 37, 201 Tone, 181, 201 Topical, 150, 171, 197, 201, 204
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Chronic Bronchitis
Toxic, iv, 33, 104, 150, 164, 172, 182, 183, 199, 201 Toxicity, 7, 23, 28, 104, 163, 201 Toxicokinetics, 201 Toxicology, 17, 39, 84, 126, 201 Toxin, 164, 200, 201 Toxoplasmosis, 150, 201 Trace element, 156, 157, 201 Trachea, 99, 153, 165, 176, 186, 200, 201 Transcription Factors, 11, 201 Transduction, 196, 201 Transfection, 152, 167, 201 Transfer Factor, 172, 201 Translation, 165, 201 Translocate, 23, 201 Translocation, 157, 165, 201 Transmitter, 145, 178, 201 Transplantation, 13, 15, 25, 36, 104, 172, 177, 178, 201 Triad, 157, 202 Tricuspid Atresia, 160, 202 Trimethoprim-sulfamethoxazole, 49, 71, 202 Trypsin, 24, 146, 157, 164, 202, 204 Tuberculosis, 109, 202 Tumor marker, 146, 151, 202 Tunica, 181, 202 Tyrosine, 26, 30, 202 U Urea, 199, 202 Uremia, 193, 202 Ureters, 202 Urethra, 190, 202 Urinary, 37, 150, 155, 157, 161, 181, 202 Urinary tract, 37, 150, 155, 202 Urinary tract infection, 37, 150, 202 Urine, 148, 150, 152, 164, 202 Urticaria, 156, 202 Uveitis, 149, 202 V Vaccination, 58, 202 Vaccine, 73, 114, 202 Vacuoles, 163, 203 Vagina, 162, 203, 204
Vascular, 34, 35, 53, 81, 162, 164, 169, 173, 179, 183, 188, 202, 203 Vasodilator, 153, 171, 181, 203 Vegetative, 151, 203 Vein, 175, 183, 188, 189, 198, 203 Venous, 102, 151, 190, 202, 203 Venous blood, 102, 203 Ventilation, 17, 194, 203 Ventricle, 150, 160, 191, 202, 203 Ventricular, 160, 181, 202, 203 Venules, 152, 153, 179, 203 Vertigo, 184, 203 Veterinary Medicine, 125, 203 Vibrio, 156, 203 Vibrio cholerae, 156, 203 Viral, 10, 21, 24, 82, 98, 100, 104, 145, 174, 184, 201, 203 Virulence, 201, 203 Virus, 10, 21, 152, 168, 169, 187, 194, 201, 203 Viscosity, 100, 145, 152, 194, 203 Vitreous, 194, 204 Vitreous Humor, 194, 204 Vitro, 8, 20, 23, 170, 204 Vivo, 8, 20, 26, 33, 177, 204 Vulva, 204 Vulvovaginitis, 109, 204 W White blood cell, 148, 151, 169, 177, 178, 180, 181, 183, 187, 204 Windpipe, 153, 186, 200, 204 Withdrawal, 10, 204 Wound Healing, 174, 204 X Xenobiotics, 28, 204 Xenograft, 148, 204 X-ray, 17, 46, 142, 159, 166, 175, 183, 191, 192, 204 X-ray therapy, 175, 204 Y Yeasts, 186, 204 Z Zinc Oxide, 23, 204 Zymogen, 157, 190, 204
