Chronic Obstructive Pulmonary Disease - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

CHRONIC

OBSTRUCTIVE PULMONARY DISEASE 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 Obstructive Pulmonary Disease: 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: 0-497-00252-3 1. Chronic Obstructive Pulmonary Disease-Popular works. I. Title.

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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.

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

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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on chronic obstructive pulmonary disease. 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 OBSTRUCTIVE PULMONARY DISEASE ...................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Chronic Obstructive Pulmonary Disease ..................................... 4 E-Journals: PubMed Central ....................................................................................................... 60 The National Library of Medicine: PubMed ................................................................................ 61 CHAPTER 2. NUTRITION AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE .......................... 107 Overview.................................................................................................................................... 107 Finding Nutrition Studies on Chronic Obstructive Pulmonary Disease .................................. 107 Federal Resources on Nutrition ................................................................................................. 109 Additional Web Resources ......................................................................................................... 109 CHAPTER 3. ALTERNATIVE MEDICINE AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE .... 111 Overview.................................................................................................................................... 111 National Center for Complementary and Alternative Medicine................................................ 111 Additional Web Resources ......................................................................................................... 128 General References ..................................................................................................................... 130 CHAPTER 4. DISSERTATIONS ON CHRONIC OBSTRUCTIVE PULMONARY DISEASE ...................... 131 Overview.................................................................................................................................... 131 Dissertations on Chronic Obstructive Pulmonary Disease ....................................................... 131 Keeping Current ........................................................................................................................ 132 CHAPTER 5. BOOKS ON CHRONIC OBSTRUCTIVE PULMONARY DISEASE .................................... 133 Overview.................................................................................................................................... 133 Book Summaries: Federal Agencies............................................................................................ 133 Book Summaries: Online Booksellers......................................................................................... 134 Chapters on Chronic Obstructive Pulmonary Disease .............................................................. 135 CHAPTER 6. MULTIMEDIA ON CHRONIC OBSTRUCTIVE PULMONARY DISEASE ......................... 139 Overview.................................................................................................................................... 139 Video Recordings ....................................................................................................................... 139 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 143 Overview.................................................................................................................................... 143 NIH Guidelines.......................................................................................................................... 143 NIH Databases........................................................................................................................... 145 Other Commercial Databases..................................................................................................... 147 APPENDIX B. PATIENT RESOURCES ............................................................................................... 149 Overview.................................................................................................................................... 149 Patient Guideline Sources.......................................................................................................... 149 Finding Associations.................................................................................................................. 153 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 157 Overview.................................................................................................................................... 157 Preparation................................................................................................................................. 157 Finding a Local Medical Library................................................................................................ 157 Medical Libraries in the U.S. and Canada ................................................................................. 157 ONLINE GLOSSARIES................................................................................................................ 163 Online Dictionary Directories ................................................................................................... 165 CHRONIC OBSTRUCTIVE PULMONARY DISEASE DICTIONARY .............................. 167 INDEX .............................................................................................................................................. 227

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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 obstructive pulmonary disease 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 obstructive pulmonary disease, 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 obstructive pulmonary disease, 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 obstructive pulmonary disease. 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 obstructive pulmonary disease, 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 obstructive pulmonary disease. The Editors

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

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CHAPTER

1.

STUDIES ON CHRONIC PULMONARY DISEASE

OBSTRUCTIVE

Overview In this chapter, we will show you how to locate peer-reviewed references and studies on chronic obstructive pulmonary disease.

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 obstructive pulmonary disease, 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 obstructive pulmonary disease” (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: •

Effect of Cigar Smoking on the Risk of Cardiovascular Disease, Chronic Obstructive Pulmonary Disease, and Cancer in Men Source: New England Journal of Medicine. 340(23): 1773-1780. June 10, 1999. Summary: Sales of cigars in the United States have been increasing since 1993. Cigar smoking is a known risk factor for certain cancers and for chronic obstructive pulmonary disease (COPD). However, unlike the relation between cigarette smoking and cardiovascular disease, the association between cigar smoking and cardiovascular disease has not been clearly established. This article reports on a cohort study among 17,774 men, 30 to 85 years of age at base line (from 1964 to 1973) who were enrolled in

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Chronic Obstructive Pulmonary Disease

the Kaiser Permanente health plan and who reported that they had never smoked cigarettes and did not currently smoke a pipe. Those who smoked cigars (1546 men) and those who did not (16,228) were followed from 1971 through the end of 1995 for a first hospitalization for or death from a major cardiovascular disease or COPD, and through the end of 1996 for a diagnosis of cancer. In multivariate analyses, cigar smokers, as compared with nonsmokers, were at higher risk for coronary heart disease, COPD, and cancers of the upper aerodigestive tract and lung, with evidence of dose response effects. There appeared to be a synergistic relationship between cigar smoking and alcohol consumption with respect to the risk of oropharyngeal cancers and cancers of the upper aerodigestive tract. The authors conclude that, independent of other risk factors, regular cigar smoking can increase the risk of coronary heart disease, COPD, and cancers of the upper aerodigestive tract and lung. 4 tables. 47 references. (AA-M). •

Chronic Obstructive Pulmonary Disease and Cognitive Impairment in the Elderly Source: International Psychogeriatrics. 8(1): 113-125. 1996. Summary: This cross-sectional epidemiological study in Lieto, Finland, compared 61 men and 21 women with chronic obstructive pulmonary disease (COPD) with agedand sex-matched people from the same community to analyze the associations between COPD, cognitive performance, and occurrence of dementia. The cognitive assessment was based on the Mini-Mental State Examination (MMSE), previous clinical documents, and an assessment made by the research nurse after she had interviewed and tested each patient. These three measures revealed no differences between COPD patients and the age-matched people, and MMSE subtest scores did not differ significantly between these two groups of participants. The findings suggest that the relative contribution of COPD to the occurrence of cognitive impairment and dementia in older people may be none or minimal at the community level. 31 references. (AA-M).

Federally Funded Research on Chronic Obstructive Pulmonary Disease The U.S. Government supports a variety of research studies relating to chronic obstructive pulmonary disease. 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 obstructive pulmonary disease. 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 obstructive pulmonary disease. The following is typical of the type of information found when searching the CRISP database for chronic obstructive pulmonary disease:

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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).

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Project Title: A FUNCTIONAL GENOMICS HEART & LUNG DEVELOP. PROGRAM Principal Investigator & Institution: Hoffman, Eric P.; A James Clark Professor of Pediatrics, b; Children's Research Institute Washington, D.C., Dc 20010 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: Drs. Eric Hoffman and Dietrich Stephan (whose primary interests are focused on muscle disease and leukemia) are PI and Co-PI on the Program's Expression Array Core and have extensive experience with all aspects of array use and data analysis. They have established collaborations with Dr. Michael Bitmer, Dr. Yidony Chen and the entire NHGRI array community. As a post-doctoral fellow in the laboratory of Dr. Jeffery Trent (member of this Program's External Advisory Committee), and a pioneer in DNA microarray technology, Dr. Stephan developed several alternative approaches to label total RNA for efficient signal detection under varying circumstances which have become the standard protocol used at NHGRI and has become a quite robust and reliable system for detecting signals over several orders of magnitude. In addition to building and using 7K expression arrays, Dr. Stephan was the first at NHGRI to develop genomic DNA microarray systems. Dr. Hoffman's laboratory is particularly interested in systematic assessments of the sensitivity and specificity of the Affymetrix vs. cDNA array approaches, and shows preliminary data pointing out the importance of redundant measurements, and correlative studies. Indeed, the proposed systematic comparison of the Affymetrix and cDNA array experimental platforms should be the first of this type of quality control of expression array data, and should prove highly valuable to both Program investigations and the research community at large. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: A PROTEOMICS APPROACH IN THE STUDY OF NOVEL COPD MARKERS Principal Investigator & Institution: Djukanovic, Ratko; University of Southampton Highfield Southampton, Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): COPD is a major health problem worldwide, but our level of understanding of its mechanisms, when compared to the other important airway disease, asthma, is relatively poor. COPD is a disease which progresses at a slow rate, which makes it very difficult to study its natural history and the impact of any therapeutic intervention. For all these reasons, it is vitally important to discover biomarkers that are elective for COPD, i.e., they are not general markers of lung inflammation and remodeling, and are prognostic for the rate of clinical deterioration. A number of non-invasive markers have been studied to date; to our knowledge, none of these have fulfilled the above criteria. As with other inflammatory lung diseases, a host of inflammatory and remodeling processes are involved in the pathogenesis of COPD, which render a singlemarker approach unlikely to succeed. We hypothesize that a number of proteins or protein isoforms are differentially expressed in the airway lining fluid in COPD and that these reflect the chronic pathology of COPD, rather than the chronic and acute effects of smoking. We propose to test this hypothesis using a proteomics approach as our primary, unbiased filter, to identify a set of 15 differentially expressed proteins (DEPs) that are present in a group of meticulously characterized subjects with COPD, but not present in those who have no evidence of lung damage despite an equivalent smoking history. Our programme is staged in a way to optimize the use of the state-of-the-art proteomics technology and precious archival samples

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collected over up to 17 years at the University of Nebraska and more recently in Southampton. Because we believe that patterns (groups) of biomarkers are more strongly related to COPD, we will apply multivariate analyses to identify the DEPs, which will thus become Early Candidate COPD-Selective Biomarkers. We will then develop antibodies against these in order to provide reagents for immunoassays. The latter will be applied to potentially as many as 480 subjects who have COPD, chronic severe asthma, or are healthy smokers or non-smokers. This will allow us to follow a logical sequence of further selection of biomarkers with respect to their selectivity for COPD, presence in early stages of smoke-induced lung damage and their prognostic value in terms of clinical deterioration and decline in lung function. Finally, applying the antibodies to archival lung tissue samples we will be able to localize the COPDselective proteins to the airway and alveoli, adding valuable knowledge to our understanding of COPD mechanisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: A ENHANCEMENT

RANDOMIZED

TRIAL

OF

HOME

SELF-EFFICACY

Principal Investigator & Institution: Jerant, Anthony F.; Family and Community Medicine; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 956165200 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 31-DEC-2007 Summary: (provided by applicant): Background: Key reasons for the "quality chasm" between current and ideal chronic illness care are that our health care system is insensitive to patient preferences, provider-driven, and disease-focused. By contrast, a common goal among proposed patient-centered care models is to foster continuous healing relationships between patients and the health care system. Such relationships allow patients to receive care over time via a variety of communication media, rather than just via episodic office visits. Home health care can foster such relationships and improve outcomes for patients with a variety of conditions. Home interventions may be particularly useful in caring for the growing number of people with chronic illnesses and accompanying functional limitations that might limit their access to communitybased interventions. However, trials comparing the effectiveness and cost-effectiveness of the wide array of home care models are limited, and the mechanisms that underlie their effectiveness remain unclear. Aims/Hypotheses: This study will address these research gaps. The study hypotheses are: a) Each of three home interventions will result in improvements in patient self-efficacy, adherence to care, and health-related quality of life (HRQOL) compared with usual care but will not differ statistically; b) From the payer's perspective, all the interventions will be cost saving compared with usual care, and a standard telephone intervention will be the most cost saving; and c) Self-efficacy will improve temporally before adherence to care and HRQOL. Methods: This will be a randomized controlled study of four groups, comparing the effectiveness and incremental cost-effectiveness of three different home-based care models and usual care in improving chronic illness outcomes. The chronic illnesses targeted will be arthritis, asthma, chronic obstructive pulmonary disease, congestive heart failure, depression, and diabetes mellitus. Trained laypersons will deliver the interventions, a self efficacy enhancement program (vs. usual care). The home care delivery media in the models will be in person visits, videophone calls, and standard telephone calls. The primary outcomes will be HRQOL and costs. Implications: Better understanding of the mechanisms of effectiveness of home care will facilitate the development of optimal

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home interventions. The findings will help policymakers, payers, and providers identify which interventions to implement. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ADMINISTRATIVE/EDUCATION IMMUNITY PGA

CENTER

FOR

INNATE

Principal Investigator & Institution: Weiss, Scott T.; Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: PROPOSED PROGRAM (Adapted from the Applicant's Abstract) Asthma, chronic obstructive pulmonary disease (COPD), myocardial infarction (MI), and deep venous thrombosis (DVT) are among the most common diseases of the lung, heart, and blood (ref). The combined health care costs for these conditions approximate 100 billion dollars per year. The goal of the RFA HL- 99-024 Genomic Applications for Heart, Lung, and Blood Research is to develop and expand genomic knowledge within the heart, lung, and blood community and apply that knowledge to disease pathobiology. There have been considerable advances in the understanding of the disease mechanisms for these conditions, and all four are associated with the development of a local inflammatory process. It has become apparent that cells and cytokines that are part of the innate immune system control the early phases of this process of airway, lung, and blood vessel inflammation. The proposal builds on the strengths of three institutions: the Respiratory Sciences Center at the University of Arizona (UA), the Department of Medicine at Brigham & Women's Hospital (BWH), and the Bioinformatics Program at Children's Hospital in Boston (CH), to develop a human variation discovery program on the theme of non-cognate immunity and its broad relationship to heart, lung, and blood diseases. The Arizona/BWH PGA will provide the scientific community with a complete screen of the genetic variants in a subset of innate immunity genes that are most likely to influence the risk for the four diseases noted above. The investigators will also perform a preliminary assessment of the association of these variants with the four phenotypes under study, to guide researchers in these areas away from variants with low likelihood of being relevant and toward those showing promising functional and epidemiologic evidence of influencing any of the four disease phenotypes. To accomplish this broad goal, the investigators have the following specific aims: (1) To screen for polymorphisms 100 genes known to be directly or indirectly related to the innate immune response; (2) To genotype a sample of individuals of Hispanic, nonHispanic White, and African American ethnicity for all the newly discovered polymorphisms; (3) To perform association studies and phylogenetic analysis to identify SNPs most likely to be involved in the determination of asthma, chronic obstructive pulmonary disease, myocardial infarction, and deep venous thrombosis; (4) To disseminate the information on ethnic-specific and phenotype-specific distribution of the polymorphisms under study on a web site within 60 days of the completion of the genotyping studies; (5) To develop a training program that will allow individuals with different knowledge and experience to become acquainted with modern genetic techniques in the fields of high throughput sequencing and genotyping; study design, data handling and data analysis in genetic epidemiology; and ethical issues in population genetics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: APPLIED GENOMICS IN CARDIOPULMONARY DISEASE Principal Investigator & Institution: Haponik, Edward F.; Professor of Internal Medicine; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: The Clinical Core will serve as the coordinating center for patient recruitment, specimen procurement and data base management. It is the mission of this Core to identify and provide disease-specific candidate genes from patients with such clinical disorders as acute lung injury, COPD, cystic fibrosis, asthma, pulmonary hypertension, pulmonary fibrosis, ischemic heart failure and both lung and cardiac transplant rejection. This core will also be responsible for the establishment of a Cardiopulmonary Tissue Repository that will maintain an archive of cryopreserved tissues and maintain an accurate data base of patient demographic and clinical data for correlation with biological end points produced by cDNA microarray. Following patient consent and registration, tissue samples and peripheral blood are delivered to the Core laboratory. The freezing facility will also serve as a repository for cyropreserved human lung and cardiac specimens. The Core Investigators will meet regularly to review all diagnostic materials on each specimen procured including histochemical stains and biopsies in order to determine a precise diagnosis and relevant demographic and clinical data for entry into the Project's data base which will include critical variables for the analysis of the biological data obtained. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: APPLIED GENOMICS IN CARDIOPULMONARY DISEASE Principal Investigator & Institution: Scott, Alan F.; Director; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: The use of single nucleotide polymorphisms (SNPs) is likely to become a major tool for the discovery of genetic linkage and disease association in the coming decade. New technologies currently entering the laboratory will allow investigators to perform high throughput studies that, until now, were impossible. The Genotyping Core proposes to locate SNPs in genes with demonstrated or presumed relevance to human cardiopulmonary disease. We will select 20 candidate genes for SNP analysis per year in airway diseases (cystic fibrosis, chronic obstructive pulmonary disease, and asthma) and selected from comparisons of our expression profiling analysis in human and animal models of human disease. We anticipate three to five SNPs per gene, which we can then evaluate in well-defined patient populations. We hypothesize SNP may explain phenotypic differences in carefully defined disease severity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: APPLIED GENOMICS IN CARDIOPULMONARY DISEASE-EDUCATION Principal Investigator & Institution: Goldstein, Allan L.; Biochem and Molecular Biology; George Washington University 2121 I St Nw Washington, Dc 20052 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: The Education Core will address an important focus of this Program. Attainment of goals should be ensured by the hierarchical nature of the Program design, emphasis on educational components, timed data release to the public, and history of interactions between many of the individual investigators. The close affiliation of the

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CNMC Research Center for Genetic Medicine with George Washington University, TIGR, and the NIH will also afford the use of pre-existing resources. This Program relies heavily on the web-based educational paradigms developed by Program member Stephen Engraft, who has developed the Frontiers in Genetics web-based lecture and CME course series (see www.frontiersingenetics.com). Development of the proposed web-based educational programs and data repositories will be facilitated by its multidepartmental nature. Our Program will help catalyze other broad- based institutional efforts (e.g. through mini symposia and CME programs based at Johns Hopkins. Finally, through the leadership roles of Hopkins co-investigators within major national specialty societies, delineation of a spectrum of CME activities will be pursued (e.g. at the international meetings of the American Thoracic Society, the American Heart Association and the American College of Chest Physicians, and at the regional meetings of the American Federation for Medical Research. These latter activities generate new collaborators at other medical centers who will be prepared to query the Hopkins database. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BALANCING HOPE & TRUTH-TELLING FOR PATIENTS WITH CA/COPD Principal Investigator & Institution: Curtis, J Randall.; Medicine; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2005 Summary: (provided by investigator): Patients with terminal or life-limiting illness report a strong need to maintain hope that they will overcome their illness while, at the same time, they desire full disclosure about their diagnosis and prognosis. These two goals, to maintain hope and know the truth about one's prognosis for survival and quality of life, are often difficult for clinicians to reconcile. Experts in end-of-life care call for clinicians to redirect patients' hope from hope for cure toward hope for quality of life and quality of dying when prognosis is poor. However, there are no data that help clinicians know how to offer hope and simultaneously provide accurate prognostic information to dying patients. This proposed study would examine the perspectives of patients with terminal cancer and chronic obstructive pulmonary disease (COPD), their families, and their health care providers concerning the often-perceived conflict between the need for hope and the need for truthful information about prognoses. We will conduct a series of open-ended interviews with patients, family members, nurses, and physicians. Interviews will be conducted by trained qualitative researchers serially over a twelve-month period and will be analyzed by the investigators using the principles of grounded theory. In addition, quantitative surveys will be conducted with participants at the same time points to provide descriptive information and permit construct validation of the qualitative data. Participants will be selected to represent culturally and ethnically diverse perspectives and analyses will incorporate this diversity. Finally, the findings will be presented to focus groups to assess the trustworthiness of the analyses and improve generalizability of the findings. The overall objective of this study is to develop strategies for clinicians to use throughout the course of a life-limiting disease to support patients in their dual needs for hope and truthfulness. These strategies will be described and translated into interventions targeting nurses, physicians, and teams who provide care for patients with cancer, COPD, and other lifelimiting diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Chronic Obstructive Pulmonary Disease

Project Title: BDNF IN PLASTICITY OF CHEMOAFFERENT PATHWAY Principal Investigator & Institution: Katz, David M.; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 01-FEB-2002; Project End 31-DEC-2006 Summary: (provided by applicant): The aim of the proposed research is to define the role of Brain-Derived Neurotrophic Factor (BDNF) in activity-dependent plasticity in the developing chemoafferent pathway. Chemoafferent neurons are the link between peripheral chemoreceptors and the brainstem, and thereby play a pivotal role in cardiorespiratory homeostasis. At birth, chemoafferent reflexes are immature, and perturbations in oxygen availability can derange postnatal development of cardiorespiratory responses to acute hypoxia. However, mechanisms that underlie chemoreflex development and plasticity are largely undefined. This proposal is based on our recent discoveries that 1) Chemoafferent neurons in the newborn rat nodosepetrosal ganglion complex (NPG) express high levels of BDNF messenger RNA and protein, 2) BDNF protein is released from NPG neurons in response to patterned electrical stimulation in vitro, and 3) BDNF acutely inhibits glutamatergic AMPA receptors in second-order relay neurons in the nucleus tractus solitarius (nTS), the primary site of chemoafferent projections to the brainstem. Together, these data indicate a new role for BDNF as a modulator of excitatory synaptic transmission between primary chemoafferent neurons and second-order relay neurons in nTS. In view of increasing evidence that BDNF plays a critical role in long-term synaptic plasticity elsewhere in the brain, we hypothesize that BDNF plays a similar role at chemoafferent synapses in nTS. Moreover, based on our preliminary data, we hypothesize that BDNF signaling in nTS is regulated by changes in oxygen availability, and thereby contributes to derangements in chemoreflex function following chronic sustained or intermittent hypoxia. Therefore, the proposed research is designed to further define mechanisms of BDNF expression and release in chemoafferent neurons after birth, including the role of chronic sustained and intermittent hypoxia, in vivo and in vitro. In addition, we will characterize postsynaptic effects of BDNF on developing nTS neurons, including regulation of transmitter receptor expression and dendritic growth. Moreover, we will determine the role of BDNF in functional plasticity in vivo by analyzing development of peripheral chemoreflexes in transgenic mice in which BDNF signaling is disrupted selectively after birth. By defining mechanisms of activity-dependent plasticity in the PG and nTS, the proposed research may shed light on cellular and molecular mechanisms relevant to understanding and improved management of hypoventilation and apnea syndromes in neonates and infants, as well as mechanisms that contribute to altered cardiorespiratory control in adult obstructive sleep apnea and chronic obstructive pulmonary disease. Moreover, it is hoped that elucidating development of this system will, in turn, create a model of neurotrophin function applicable to the nervous system as a whole. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: INSOMNIA

BEHAVIORAL

TREATMENT

FOR

COMORBID

GERIATRIC

Principal Investigator & Institution: Rybarczyk, Bruce D.; Rush University Medical Center Chicago, Il 60612 Timing: Fiscal Year 2002; Project Start 15-AUG-2000; Project End 31-JUL-2004 Summary: Description (adapted from the investigator's abstract): This is a revised application to test the efficacy of an empirically based cognitive-behavioral intervention

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for older adults with insomnia and co-morbid chronic illness recruited from an HMO population. The primary objective of the study will be to compare the efficacy of behavioral treatments for insomnia among patients with 3 common age-related chronic illnesses: osteo-arthritis (OA), chronic obstructive pulmonary disease (COPD) and coronary artery disease (CAD) because exceptionally high rates of co-morbid insomnia have been found in the 3 groups. A second major objective is to determine whether an effective behavioral treatment can diminish the well-established effects of insomnia on quality of life among those with chronic illness. The proposed study will include random assignment of 3 groups of 55 HMO patients 55 years or older with OA, COPD and CAD and co-morbid insomnia to an 8-week cognitive-behavioral treatment class or placebo control class. The behavioral intervention will be empirically based with both cognitive-behavioral and relaxation approaches. The placebo control group will be a wellness/stress management class. Outcomes will be assessed at 4, 8, and 12 months post treatment follow-up intervals. Sleep quantity and quality will be evaluated using polysomnography, actigraphy and self report measures. Quality of life, functional status and mood will also be assessed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BIOINFOMATICS CENTER FOR INNATE IMMUNITY PGA Principal Investigator & Institution: Klimecki, Walter T.; Associate Research Scientist; None; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: PROPOSED PROGRAM (Adapted from the Applicant's Abstract) Asthma, chronic obstructive pulmonary disease (COPD), myocardial infarction (MI), and deep venous thrombosis (DVT) are among the most common diseases of the lung, heart, and blood (ref). The combined health care costs for these conditions approximate 100 billion dollars per year. The goal of the RFA HL- 99-024 Genomic Applications for Heart, Lung, and Blood Research is to develop and expand genomic knowledge within the heart, lung, and blood community and apply that knowledge to disease pathobiology. There have been considerable advances in the understanding of the disease mechanisms for these conditions, and all four are associated with the development of a local inflammatory process. It has become apparent that cells and cytokines that are part of the innate immune system control the early phases of this process of airway, lung, and blood vessel inflammation. The proposal builds on the strengths of three institutions: the Respiratory Sciences Center at the University of Arizona (UA), the Department of Medicine at Brigham & Women's Hospital (BWH), and the Bioinformatics Program at Children's Hospital in Boston (CH), to develop a human variation discovery program on the theme of non-cognate immunity and its broad relationship to heart, lung, and blood diseases. The Arizona/BWH PGA will provide the scientific community with a complete screen of the genetic variants in a subset of innate immunity genes that are most likely to influence the risk for the four diseases noted above. The investigators will also perform a preliminary assessment of the association of these variants with the four phenotypes under study, to guide researchers in these areas away from variants with low likelihood of being relevant and toward those showing promising functional and epidemiologic evidence of influencing any of the four disease phenotypes. To accomplish this broad goal, the investigators have the following specific aims: (1) To screen for polymorphisms 100 genes known to be directly or indirectly related to the innate immune response; (2) To genotype a sample of individuals of Hispanic, nonHispanic White, and African American ethnicity for all the newly discovered polymorphisms; (3) To perform association studies and phylogenetic analysis to identify

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Chronic Obstructive Pulmonary Disease

SNPs most likely to be involved in the determination of asthma, chronic obstructive pulmonary disease, myocardial infarction, and deep venous thrombosis; (4) To disseminate the information on ethnic-specific and phenotype-specific distribution of the polymorphisms under study on a web site within 60 days of the completion of the genotyping studies; (5) To develop a training program that will allow individuals with different knowledge and experience to become acquainted with modern genetic techniques in the fields of high throughput sequencing and genotyping; study design, data handling and data analysis in genetic epidemiology; and ethical issues in population genetics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BIOINFORMATICS CENTER FOR INNATE IMMUNITY PGA Principal Investigator & Institution: Lazarus, Ross; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: PROPOSED PROGRAM (Adapted from the Applicant's Abstract) Asthma, chronic obstructive pulmonary disease (COPD), myocardial infarction (MI), and deep venous thrombosis (DVT) are among the most common diseases of the lung, heart, and blood (ref). The combined health care costs for these conditions approximate 100 billion dollars per year. The goal of the RFA HL- 99-024 Genomic Applications for Heart, Lung, and Blood Research is to develop and expand genomic knowledge within the heart, lung, and blood community and apply that knowledge to disease pathobiology. There have been considerable advances in the understanding of the disease mechanisms for these conditions, and all four are associated with the development of a local inflammatory process. It has become apparent that cells and cytokines that are part of the innate immune system control the early phases of this process of airway, lung, and blood vessel inflammation. The proposal builds on the strengths of three institutions: the Respiratory Sciences Center at the University of Arizona (UA), the Department of Medicine at Brigham & Women's Hospital (BWH), and the Bioinformatics Program at Children's Hospital in Boston (CH), to develop a human variation discovery program on the theme of non-cognate immunity and its broad relationship to heart, lung, and blood diseases. The Arizona/BWH PGA will provide the scientific community with a complete screen of the genetic variants in a subset of innate immunity genes that are most likely to influence the risk for the four diseases noted above. The investigators will also perform a preliminary assessment of the association of these variants with the four phenotypes under study, to guide researchers in these areas away from variants with low likelihood of being relevant and toward those showing promising functional and epidemiologic evidence of influencing any of the four disease phenotypes. To accomplish this broad goal, the investigators have the following specific aims: (1) To screen for polymorphisms 100 genes known to be directly or indirectly related to the innate immune response; (2) To genotype a sample of individuals of Hispanic, nonHispanic White, and African American ethnicity for all the newly discovered polymorphisms; (3) To perform association studies and phylogenetic analysis to identify SNPs most likely to be involved in the determination of asthma, chronic obstructive pulmonary disease, myocardial infarction, and deep venous thrombosis; (4) To disseminate the information on ethnic-specific and phenotype-specific distribution of the polymorphisms under study on a web site within 60 days of the completion of the genotyping studies; (5) To develop a training program that will allow individuals with different knowledge and experience to become acquainted with modern genetic techniques in the fields of high throughput sequencing and genotyping; study design,

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data handling and data analysis in genetic epidemiology; and ethical issues in population genetics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BIOMARKERS OF OXIDATIVE STRESS AND INFLAMMATION IN COPD Principal Investigator & Institution: Macnee, William; University of Edinburgh Edinburgh Eh8 9Yl, Scotland Edinburgh, Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Chronic Obstructive Pulmonary Disease (COPD) is a disease with a major unmet medical need, for which at present there is no effective treatment that will halt the decline in lung function. Development of new therapies is hampered by the lack of well defined clinical biomarkers to both characterize patients and assess drug efficacy. Oxidative stress and the associated inflammatory responses in the lungs are key elements in the pathogenesis of COPD. However, there have been no longitudinal studies to assess the utility of representative markers of oxidative stress and inflammation as biomarkers of disease severity and hence their potential as surrogate endpoints for assessment of the effectiveness of new therapeutic agents. The purpose of this project is to identify and characterize candidate markers of oxidative stress and inflammation in both cross sectional and longitudinal studies. The proposed biomarkers for these studies are the lipid peroxidation products 4-hydroxy-2-nonenal, F2alpha-isoprostanes, and cytokines such as interleukin (IL) IL-8, IL-6, IL-1, tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor in a well characterized cohort of COPD patients in both cross sectional and longitudinal studies. A further aim is to relate the levels of these markers of oxidative stress to inflammatory mediators and differential cell counts in induced sputum. In addition, a population of COPD patients will be characterized according to the levels of surrogate markers of airway inflammation and oxidative stress, which will be related to disease severity and to the clinical phenotype of COPD. Sophisticated techniques such gas chromatography/mass spectrometry (GC/MS) will be used to measure specific and stable lipid peroxidation products in peripheral blood, induced sputum and exhaled breath condensate. Moreover, mindful of the possibility that no single molecule will be a biomarker which is applicable to all patients with COPD, metabonomic and genomic technologies will be exploited to assess a spectrum of potential biomarkers, thus generating a 'finger print' characteristic of the disease. Such information will allow the identification of novel biomarkers and the fingerprints themselves may represent a mechanism to stratify COPD patients and allow the assessment of novel therapies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CHALLENGING LIFE EVENTS IN OLDER PERSONS Principal Investigator & Institution: Daaleman, Timothy P.; Family Medicine; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-AUG-2006 Summary: (provided by applicant): Timothy P. Daaleman, DO, is a family physician researcher with expertise in examining the influence of religious and spiritual variables in healthcare settings. This application will provide a period of mentored training comprised of: a research practicum within the Center on Aging at the University of Kansas Medical Center (KUMC); coursework in the Masters in Public Health (MPH) program and at the University of Kansas in Lawrence; and a research project to test a

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Chronic Obstructive Pulmonary Disease

theoretical model of the relationship between spirituality and patient conceptualization of death and dying in a population of community-dwelling elders with serious illness. The plan outlines the training and research experience he will require, in order to develop and launch a fully independent research career that will focus on understanding and improving the dying process and end-of-life care among elders in the United States. Career Development Plan: Course work from MPH program forms the core portion of the didactic training period and will be complimented by practical training in study design, subject recruitment, data collection and analysis, and project management within the KUMC Center on Aging. Research Program: The SUPPORT trial not only awakened American medicine to reexamine the way it cares for seriously ill and dying patients, but also has indirectly promoted a rapprochement among the realms of spirituality, religion, and the practice of medicine. An understanding of the psychological, social, cultural, and now spiritual elements and processes that are involved in the composition of death and dying attitudes holds promise in comprehending and potentially improving the difficult transition that older patients make from serious illness to dying. The overall objective of this research project is to describe and understand the determinants of elders attitudes toward serious illness, death, the dying process, and discussions of advance care planning. Both rural and urban primary care physicians (N=10) who have been members of the Kansas Hartford Geriatric Project, and older community-dwelling patients with serious illness from their practices (N=270), will participate in three phases of the study: a cross-sectional survey, a prospective, longitudinal cohort study, and qualitative semi-structured interviews. The primary aim is to determine the social, psychological, spiritual, and cultural influences that comprise attitudes towards death and the dying process in older persons. Our hypothesis is that patient spirituality is a significant explanatory factor in death attitudes after accounting for multiple covariates, i.e. social support, mental health status. Secondary aims include learning how a baseline measure of patient spirituality predicts future death attitudes and discussions of advance care planning. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CHEMOKINE BLOCKADE TO PRESERVE LUNG DEVELOPMENT Principal Investigator & Institution: Auten, Richard L.; Pediatrics; Duke University Durham, Nc 27710 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: Chronic lung disease in prematurity (CLD) may affect as many as 50% of very low birthweight newborns. CLD confers added risk for abnormal neurodevelopmental outcome. Inflammation in response to adequate antioxidant defenses in premature newborns is central to the pathophysiology of lung injury leading to CLD. Present therapy includes glucocorticoids which may adversely affect lung, somatic and central nervous system development.,. Targeted immunotherapy blocking early inflammatory-induced lung injury may prevent the development of CLD and avoid adverse steroid effects. Our hypothesis is that blocking leukocyte influx and/of function will prevent chronic lung disease in the hyperoxia-exposed rodent model. The proposed studies will use hyperoxia-exposed newborn rodents to study the mechanisms of inflammatory effects on lung development in response to serve oxidant stress, as a model of CLD. Neutrophil and macrophage influx/function will be modified by using specific anti- chemokine antibodies and chemokine receptor antagonists. The contribution of key neutrophil functions will e studied in gene knockout mice lacking these functions. Aim 1 will determine which aspect of neutrophil and/or macrophage influx/function contributes most to biochemical oxidant stress in newborn lung during

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initiation of hyperoxia-induced lung injury. Aim 1 will determine which aspect of neutrophil and/or macrophage influx/function contributes most to biochemical oxidant stress in newborn lung during initiation of hyperoxia-induced lung injury. Aim 2 will determine the specific contributions of leukocyte influx/function to DNA damage, growth arrest, and pathologic apoptosis, which contribute to abnormal alveolar development. Aim 3 will determine whether blockade of leukocyte function can safely preserve normal alveolar development during recovery from severe oxidant stress. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CHEMOPREVENTION OF LUNG CARCINOGENESIS USING GREEN TEA Principal Investigator & Institution: Hakim, Iman A.; None; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2003; Project Start 07-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant) Many laboratory studies have shown an inhibitory action of green tea or the polyphenolic fraction of green tea in animal models of lung carcinogenesis. Thus, the role of tea drinking as a potential inhibitor of carcinogenesis merits careful evaluation. In our attempt at translating the abundant pre-clinical information and epidemiological data to the human population, we are proposing a Phase IIb 3-arm randomized, placebo controlled, double blinded green tea intervention trial among former smokers with chronic obstructive pulmonary disease (COPD) and >= 40 pack-years of smoking history. This population is targeted because they have been identified as having a high prevalence of premalignant dysplasia. Subjects will be randomly assigned to consume daily for six months either a standardized green tea (GT) beverage, or a defined green tea polyphenol (GTP) extract in capsule form, or placebo preparations. The hypotheses to be tested in the proposed research are 1) high consumption of GT or GTP can protect against cellular oxidative damage and 2) high consumption of GT or GTP can modulate the expression of genes involved in proliferation and apoptosis in a population at elevated risk of lung cancer. The primary endpoints will be improvement in markers of oxidative damage in DNA, lipids, and proteins (levels of 8-OHdG, 8-epi-PGF2, MDA, di-tyrosine, and catalase and glutathione peroxidase activities). The secondary endpoints will be exploratory to assess changes in the gene expression of biomarkers of proliferation (EGFR, PCNA, JUN, FOS, Ki-67) and apoptosis (bcl-2, caspase-3) in induced sputum, in addition, we will seek to determine if there are differences in adherence between the green tea preparation groups. We believe that a program of nutritional intervention by realistic dietary modifications that are effective, safe, and acceptable should be the cornerstone of lung cancer prevention strategy. 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; Institute of 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 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

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Chronic Obstructive Pulmonary Disease

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: CLARA CELLS, THEIR SECRETIONS IN LUNG IMMUNOREGULATION Principal Investigator & Institution: Stripp, Barry R.; Associate Professor; Environ & Occupational Health; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-JUL-2005 Summary: (provided by applicant): Even though cytokine production by cells of the immune system can significantly impact epithelial cell function, little is known of reciprocal roles for epithelial cells in regulation of the immune system. This is a significant issue when trying to understand the complex series of events that lead to deteriorating lung function among individuals with chronic inflammatory and/or immunological lung diseases such as COPD and asthma. There is a growing recognition that the conducting airway epithelium is dynamic in its function and that chronic lung disease results in predictable changes to epithelial cells. Among these changes are alterations in nonciliated airway epithelial cell function, for which reduced abundance of Clara cell secretory protein (CCSP) serves as a biomarker. Whether changes to Clara cells are a cause or a nonciliated airway epithelial cells contribute to exacerbation of lung disease and a continuing decline in lung function. Our recent studies in CCSP null mice (CCSP-/-) demonstrate that Clara cells fulfill important roles in defense against environmental agents in addition to serving critical immunoregulatory functions. Central to this proposal is the observation that CCSP-/- mice have elevated local production of IgA. Moreover, expression of IgA is dramatically up regulated following in vivo endotoxin exposure of CCSP-/- but not wild type mice, demonstrating fundamental differences in B-cell responsiveness with CCSP deficiency. We hypothesize that CCSP functions to suppress the immune system through either directly or indirectly regulating local B-cell function, and that these changes in B-cell function impact innate mucosal defense. If correct, changes in Clara cell function may lead to hyperstimulation

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of the local immune response which, although beneficial with respect to the acute clearance of colonizing microorganisms, could exacerbate airway disease and dysfunction. Aims will address four specific aspects of altered lung function that accompanies CCSP deficiency: 1) does CCSP deficiency result in altered innate and/or adaptive immunity, 2) are changes in lung immunoregulation and innate defense directly related to loss of CCSP, 3) are differences in innate defense with CCSP deficiency directly related to altered B-and/or T-cell function, and 4) which cell types are most sensitive to CCSP-dependent alterations in endotoxin signaling. By addressing these aims we will define mechanisms by which CCSP deficiency leads to altered immunoregulation within the lung. This knowledge may help in the development of strategies to block inappropriate immunological responses that lead to deteriorating lung function among individuals with chronic lung disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CLINICAL CENTER IN COPD Principal Investigator & Institution: Bailey, William C.; Professor and Director; Medicine; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Chronic Obstructive Pulmonary Disease (COPD) is a serious public health problem responsible for more than 500, 000 hospitalizations, 100,000 deaths, and $15 billion in direct costs of medical care in the United States each year. We propose to form a collaborative COPD CRN Clinical Center at the University of Alabama at Birmingham (UAB) and the Birmingham Veterans Affairs Medical Center (BVAMC). The UAB/BVAMC Clinical Center will be headed by, Drs. William C. Bailey and J. Allen D. Cooper. The proposed investigators and their research staff have extensive experience in recruitment and retention for clinical trials, as well as study design and implementation. The collaborative effort between UAB and the BVAMC will allow us to quickly and efficiently recruit large numbers of COPD patients for clinical research studies. In addition, the UAB/BVAMC COPD Clinical Center will have access to a large network of experts at the University of Alabama at Birmingham who can assist in the design and implementation of clinical trials. The UAB/BVAMC Clinical Center proposes two studies aimed at enhancing treatment for moderate-to severe COPD. The first study will examine measures of inflammation and responsiveness to bronchodilator challenge, responsiveness to systemic steroid treatment, and responsiveness to inhaled steroid treatment. This study may provide a new method for identifying subgroups of COPD patients who are most likely to respond to inhaled corticosteroids. The second project will examine the causes of poor responsiveness to the pneumococcal vaccine with the long term goal of using this information to reduce pneumococcal infections and related exacerbations in COPD patients. The UAB/BVAMC Clinical Center also proposes a Clinical Research Skills Training Core. Dr. J. Allen D. Cooper, the Director for fellowship training in Pulmonary and Critical Care Medicine at UAB, will head this core. Trainees will be funded for a total of two years and will be required to enroll in one of the UAB K30 Clinical Research Curriculum Development Award components (either the Clinical Research Training Program or the Master's of Science in Public Health in Clinical Research). Trainees will also receive funding for a pilot project, which will be developed and conducted under the supervision of the Training Core Investigators. These Investigators have expertise in COPD, Clinical Research and Study Design, Behavioral Science, Epidemiology, and Statistics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Chronic Obstructive Pulmonary Disease

Project Title: CLINICAL CENTER-COPD CLINICAL RESEARCH NETWORK Principal Investigator & Institution: Scharf, Steven M.; Professor; Medicine; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Chronic obstructive pulmonary disease is a major problem worldwide with increasing prevalence and morbidity/mortality. Current therapy is based on smoking cessation, maximizing lung function, treating infection and rehabilitation. The increase in knowledge about basic disease mechanisms affords the opportunity to explore new methods for treating this disorder. We propose the development of a clinical center at the University of Maryland to participate in the NIH COPD Clinical Research Network. In addition to describing the patient population and recruitment strategies, we present 2 model proposals for consideration by the network. The first proposal relies on recent findings that there is a strong inflammatory component in patients with end-stage COPD which may lead to weight loss, muscle wasting and increased mortality. A key inflammatory cytokine is tumor necrosis factor alpha (TNFalpha). We propose evaluating the effects of anti-TNFalpha therapy (inflixamab) in moderate to severe COPD patients in a 3-arm randomized blinded trial. Patients will receive 26 weeks of infliximab, 24 weeks inflixamab/12 weeks' placebo or 36 weeks of placebo treatment. Our primary outcome will be 6 minute walking distance, a measure of exercise tolerance. A number of secondary variables including proinflammatory cytokines in sputum and blood, pulmonary physiological and metabolic outcomes, body composition and quality of life (QOL) indices will be measured as well. The second proposal is on the use of inhaled steroids in COPD. Results from previous trials have in general been disappointing. However, there are likely to be subsets of patients who respond. We predict that patients with a prominent airway inflammatory component to their disease will be likely to respond to inhaled steroids and would be candidates for long-term treatment. We will determine if the sputum level of proinflamamtory cytokines is predictive of the response to steroid inhalers in COPD. We will determine if the presence of a single nucleotide substitution in the glucocorticoid receptor has a negative impact on the response. Outcomes from this randomized clinical trial will be gauged in terms of health related QOL. In addition to presenting these formal proposals, we have developed several concept proposals. We have also offered the development of a health cost utilization core for the COPD CRN. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: COGNITIVE EFFECTS OF LUNG VOLUME REDUCTION SURGERY Principal Investigator & Institution: Kozora, Elizabeth; National Jewish Medical & Res Ctr and Research Center Denver, Co 80206 Timing: Fiscal Year 2002; Project Start 01-FEB-2000; Project End 31-JAN-2005 Summary: The primary goal of this study is to examine the neuropsychological functioning of emphysema patients undergoing lung volume reduction surgery (MT+LVRS) compared to medical therapy alone (MT). The study will include patients at two clinical sites for the National Emphysema Treatment Trial (NETT). Enhancements of ventilation and functional capacity are expected to contribute to greater long-term improvements in utilization of oxygen in the brain, thereby leading to improvements in cognitive performance greater than those observed among patients who exercise but do not receive LVRS (Specific Aim 1). A health control group will be retested on similar neuropsychological tests in order to control for practice effects (Specific Aim 2). Although we do not expect significant differences in emotional (depression and anxiety)

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functioning across groups, this study will enable us to evaluate the relationship between emotional status and neuropsychological scores in the MT+ LVRS and MT groups following randomization. In addition, since major neurological events are more likely following surgery, and major neurological events affect cognitive function, we will evaluate the incidence of neurological events in our sample and will determine the degree to which neurological events are associated with cognitive function (Specific Aim 3). No studies have examined the relationship between change in cognition and improve quality of life in COPD patients following LVRS surgery, therefore, we aim to explore these associations in Specific Aim 4. We propose to compare changes following LVRS and MT by examining 84 NETT patients (42 in MT, 42 in LVRS) at three times points (baseline, post 6-10 week medical treatment MT, and 6 months post MT or LVRS randomization) using select neuropsychological, psychological, neurological and QoL tests. Forty normal controls will be tested at baseline and 6-10 weeks follow- up. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CONTINUOUS MEASUREMENT OF BREATHLESSNESS Principal Investigator & Institution: Baird, John C.; Psychological Applications, Llc 74 N Pinnacle Ridge Rd Waterbury, Vt 05676 Timing: Fiscal Year 2003; Project Start 10-SEP-2001; Project End 31-JAN-2005 Summary: (provided by applicant): The objective of this research is to evaluate a computer-assisted, continuous method for measuring breathlessness during exercise. The method represents a new approach to obtain subjective ratings from patients exercising on a cycle ergometer or treadmill. Whereas the "gold standard" Borg scale for measuring breathlessness is employed in over one million patients per year, it is limited by the fact that each estimate occurs at a discrete point in time cued or signaled by the health professional, rather than when the patient senses a change in symptom intensity. Moreover, if the patient cannot verbalize a response (e.g., while breathing through a mouthpiece), the rating must be indicated on the scale by finger pointing. During exercise this can lead to uncertainty on the part of the clinician as to exactly where the patient is pointing. The continuous method for obtaining patient-initiated ratings is unencumbered by these limitations, while also providing a direct measure of the absolute threshold and peak of breathlessness. The software to obtain such ratings has been shown to be reliable, valid, and easy to use. Thus far, the method has been successfully applied in patients with chronic obstructive pulmonary disease. The goal of Phase II is to evaluate the new methodology with a wider sample of adult patients afflicted with asthma, interstitial lung disease, respiratory muscle weakness, and pulmonary vascular disease, as well as with a group of children with asthma. Tests will also be conducted to investigate the responsiveness of the continuous method to track the effects of bronchodilator therapy and respiratory load. PROPOSED COMMERCIAL APPLICATION. The commercial goal is to replace the discrete scale with a computeradministered continuous method for measuring breathlessness during exercise. The product marketed in Phase III will be a computer software package that will be purchased by physicians, clinics and hospitals throughout the world. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: COPD CLINICAL RESEARCH NETWORK Principal Investigator & Institution: Lazarus, Stephen C.; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2008

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Chronic Obstructive Pulmonary Disease

Summary: (provided by applicant): Investigators in the Division of Pulmonary and Critical Care Medicine at the University of California, San Francisco hereby apply to participate in a cooperative COPD Clinical Research Network, to examine existing and novel therapies and management strategies for COPD, and to rapidly disseminate the findings of this Network to the medical community. COPD is the 4th leading cause of death in the United States, and the associated financial and social burden is enormous. As new information on the pathobiology of COPD and new approaches for management appear, large, carefully conducted, collaborative multicenter studies are required to define the position of these new strategies in our therapeutic algorithm. Two specific protocols are included in this application; both test novel therapeutic approaches to important clinical problems associated with COPD. The first proposal, "The Effects of TNF-alpha Inhibition in COPD", examines the ability of a monoclonal antibody against the potent proinflammatory cytokine TNF-alpha to reduce the rate of exacerbations in patients with moderate-to-severe COPD. Exacerbations account for most of the emergency department visits, hospitalizations, and deaths associated with COPD. This proposal will examine the effect of anti-TNF-alpha therapy on exacerbations, and the relationship between exacerbations, symptoms, lung function, quality of life, markers of inflammation in airway secretions, and expression of epithelial cell genes related to mucus production. The second project, "Inhibition of Endothelin-1 in COPD-related Pulmonary Arterial Hypertension" will examine whether treatment with the Endothelin A and B receptor antagonist bosentan improves capacity in patients with pulmonary arterial hypertension, and the prognosis for these patients is poor. Evidence suggests that the pulmonary artery lesion is not due solely to hypoxemia, and that vasodilator therapy may be beneficial. This study will test an orally-administered therapy with bosentan, and clinically-important endpoints including exercise capacity, functional class, dyspnea, quality of life, and overall clinical status. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: COPD CLINICAL RESEARCH NETWORK - DATA COORDINATING CENT* Principal Investigator & Institution: Connett, John E.; Professor; Biostatistics; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The Division of Biostatistics in the School of Public Health at the University of Minnesota (John Connett, PI), in collaboration with the Divisions of Epidemiology and Pulmonary Medicine, proposes to establish and operate the Data Coordinating Center (DCC) for the Chronic Obstructive Pulmonary Disease Clinical Research Network. The goals of the Network are to identify preventive and therapeutic interventions to reduce mortality, exacerbations, and disability in patients with moderate-to-severe COPD. Clinical trials undertaken by the Network must have relevance to clinical practice for the treatment of this common and serious chronic disease, and must provide efficient answers to questions regarding treatment alternatives. As described in RFA HL-03-002, four-to-six clinical centers and the DCC will launch and complete 4-5 clinical trials in a 5-year period, with 2-3 protocols in operation simultaneously. As the DCC for the Network we will perform the following key functions: 1) establish the Network's organizational structure and facilitate internal communications; 2) provide statistical input on study design; 3) develop and maintain Manuals of Procedures; 4) establish a distributed data entry/data management system; 5) train and certify clinical center personnel; 6) create subcontracts with central laboratories and reading centers, as needed; 7) generate randomization schedules and

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reports to monitor data quality, recruitment progress, retention, outcomes, and adverse events; 8) carry out data analyses for the investigators and contribute to manuscripts and scientific presentations. Our group brings to this project over 16 years of experience in the design, conduct, and analysis of multicenter clinical trials of COPD and emphysema, including the Lung Health Studies I, II, and the Feasibility of Retinoid Therapy for Emphysema (FORTE) study. We have assembled a solid and productive team of investigators and professional staff with relevant expertise in biostatistics, clinical trials, epidemiology, and pulmonary medicine, and ample experience in data management, data quality control, and statistical analysis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DRUG THERAPY FOR PREVENTING COPD EXACERBATIONS Principal Investigator & Institution: Niewoehner, Dennis E.; Minnesota Veterans Reserach Inst 1 Veterans Dr Minneapolis, Mn 55417 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Chronic obstructive pulmonary disease (COPD) is a rapidly growing global health problem and in the United States is now the fourth commonest cause of death. Symptomatic treatment for this disease is only modestly effective. Oxygen for hypoxemic patients and cigarette smoking cessation are the only known interventions that alter the natural history of the disease. Patients with established COPD frequently develop exacerbations, clinical episodes that are characterized by cough, sputum, and worsening dypsnea and caused mostly by infections. Exacerbations are very morbid and extraordinarily costly events that also accelerate deterioration in lung function. Hospitalization for COPD accounts for about two thirds of all health care expenditures for this disease. Antibiotics and systemic corticoteroids, common treatments for severe COPD exacerbations, are only marginally effective and their widespread use may be harmful to the patient and to society at large. Reducing the frequency of severe COPD exacerbations is very important, because even small reductions would confer large human and economic benefits. Described in this application is a proposal for two separate randomized clinical trials to determine whether low-dose theophylline or inhaled corticosteroids will reduce the frequency of severe COPD exacerbations. Once widely prescribed, theophylline has fallen into disfavor as a COPD treatment, partly due to safety issues. However, recent studies indicate that theophylline may prevent severe COPD exacerbations and that antiinflammatory activity is retained at lower and safer doses. Recent trials suggest that inhaled corticosteroids may also prevent severe COPD exacerbations, but these findings have yet to be fully confirmed. Each of the two proposed trials will randomize about 700 patients with moderate-to-severe COPD (FEV1 < 60% predicted) in equal numbers to active drug (low-dose theophylline or inhaled corticosteroids) or placebo for a one-year period. The primary outcome variable is the first occurrence of a severe COPD exacerbation (defined as an unscheduled clinic or urgent care visit requiring systemic corticosteroid therapy or hospitalization) or death from any cause. Secondary outcomes include spirometry, several measures of health care utilization, respiratory medication use, and safety. Both trials are designed with 80% power to show a 30% reduction in severe exacerbations at a significance level of 0.05. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: EFFICACY OF YOGA FOR SELF-MANAGEMENT OF DYSPNEA IN COPD Principal Investigator & Institution: Carrieri-Kohlman, Virginia L.; Professor; Physiological Nursing; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 31-MAY-2004 Summary: (provided by applicant): Management of dyspnea (shortness of breath) is a major problem for patients with chronic obstructive lung diseases (COPD). The effectiveness of traditional supervised and home-based exercise programs for decreasing dyspnea is well established. The remaining knowledge gap is the efficacy of complementary exercises that patients report they are using to manage dyspnea, that may be more congruent with pulmonary patients' lifestyles and values, and that can be adapted to changes in illness severity and disability. Yoga practice is a complementary therapy that people use to manage their dyspnea. Previous studies lack controlled designs, large samples, protocol descriptions, or valid instruments for measuring dyspnea. The aims of this exploratory study are: 1) to develop a safe and feasible yoga program for patients with COPD; 2) to test the efficacy of this program, while establishing the decrease in dyspnea that may be expected with such a program; 3) to determine whether secondary outcomes of physical performance, psychological well being, and health related quality of life (HRQL) are positively affected by yoga practice; 4) to identify and contact community resources including physicians, nurses, yoga practitioners and facilities to support the testing of yoga training for patients with COPD in targeted communities. In a prospective randomized controlled trial three cohorts of subjects with moderate to severe COPD (N=36) will be randomly assigned to either an experimental yoga training or a usual care control for12 weeks. Outcomes will be measured at baseline, after each session, and immediately after the training program. If yoga is shown to affect dyspnea in patients with COPD, the findings of this exploratory study will serve as a foundation for the writing of a multi-center controlled trial to compare the effect of yoga training on dyspnea and multivariate outcomes to an attention control group and a usual care group with a larger sample of patients with moderate to severe COPD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ELECTROCHEMICAL OXYGEN CONCENTRATOR FOR HOME THERAPY Principal Investigator & Institution: Andrews, Craig C.; Lynntech, Inc. College Station, Tx 77840 Timing: Fiscal Year 2003; Project Start 01-MAY-2000; Project End 31-MAR-2005 Summary: (provided by applicant): The beneficial effects of Long-term Oxygen Therapy (LTOT) in the home for patients with Chronic Obstructive Pulmonary Disease (COPD), and other lung diseases causing hypoxemia, are well known. The number of patients with COPD is increasing in most countries, and in the U.S., it is now one of the leading causes of death. LTOT increases a patient's survival rate and also has the potential to improve considerably a patient's quality of life. Since LTOT must be given for as long as possible during the day, it is important to extend daily hours of oxygen therapy into the mobile period of the day. This can be achieved through the use of compact, lightweight, portable sources of oxygen gas. Thus, there exists a clear need for a new technologybased oxygen generator that satisfies all the requirements for LTOT both within and outside the home. Currently, providing ambulatory oxygen with LOX systems is

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problematic because of the cost of LOX and hence lower profit margins for suppliers. The aims of portable oxygen are to increase exercise tolerance, reduce exercise dyspnea, improve quality of life, and extend the daily hours of LTOT. In response to the identified need, this project is specifically aimed at improving the delivery of oxygen to ambulatory patients in the home and office setting using an innovative electrochemical life support system. The technology will have a dramatic improvement in clinical benefits, patient convenience and delivery costs. The portable electrochemical system will produce on demand a supply of humidified, but otherwise pure, oxygen gas, while having a system weight less than 10 Ib and system power requirements less than 600 Watts. The system will provide instantaneous start-up and it is estimated that the oxygen generator will cost less than $1,000. A dual-use development approach will be adopted because the portable electrochemical oxygen generator technology has both government and other commercial applications such as battlefield life support, forward medical treatment areas, casualty transport vehicles, "oxygen trickle charger" for commercial and military aircraft, and hyperbaric oxygen therapy for decompression sickness, air embolism, and carbon monoxide poisoning. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ENVIRONMENTAL AGENTS AS MODULATORS OF DISEASE PROCESSES Principal Investigator & Institution: Cory-Slechta, Deborah A.; Professor; Environmental Medicine; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2002; Project Start 01-AUG-1980; Project End 31-MAR-2005 Summary: OVERALL (Taken from the Applicant's Description) Despite a marked increase in the human life span, questions about the role of environmental and occupational agents as modulators of disease and dysfunction continue to arise. These questions are provoked by such observations as the increased incidence of asthma in children, reports that Parkinson's disease (PD) has an environmental rather than a genetic basis, of correlations between ultra fine particles and cardiovascular respiratory morbidity and even mortality, and of endocrine-like chemical and reproductive dysfunction, among others. The goal of the University of Rochester NIEHS Environmental Health Sciences Center (EHSC) is to define the scope of the contribution of toxic agents to disease processes and dysfunctions and to understand the mechanisms by which they occur. The Center strives to provide a sound scientific basis for evaluating the health risks posed by chemical exposures to human populations and ultimately to prevent their occurrence. This is achieved through the efforts of four Research Cores. Studies within the Neurotoxicology Research Core seek to identify mechanisms by which toxicants affect nervous system function and thereby contribute to behavioral, neurological and psychiatric disturbances of the nervous system, such as Parkinson's disease, autism, and cognitive impairments. The Osteotoxicology Research Core focuses primarily on the extent to which lead exposure serves as a risk factor for disturbances of skeletal function, particularly its involvement in dental caries in osteoporosis. The Pulmonary Toxicology Research Core examines inflammatory and oxidative stress-induced mechanisms of lung injury and how disease states such as asthma, chronic obstructive pulmonary disease and others modulate these mechanisms. The Protein Modulators of Toxicity Research Core seeks to identify the ways in which toxicants modulate biologically active proteins critical to normal homeostatic function, thereby inducing changes contributing to disease processes. The scientific efforts of the Research Cores are promoted and assisted through five Facility/Service Cores: Transgenic Services, Pathology/Morphology/Imaging,

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Biostatistics, University Facilities and Shared Instrumentation. In addition, collaborations and new directions are significantly enhanced through the Enrichment Program of the EHSC, which includes a Pilot Project Program, a Visiting Scientist Program, the EHSC Seminar Series and the Rochester Conference Series. The Community Outreach and Education Program with its new Director, has instituted a Community Advisory Board that provides communication between the EHSC and the Community and has established educational programs for various segments of the community, including students and teachers, medical professionals and even senior scientists Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DEFICIENCY

ENVIRONMENTAL

FACTORS

IN

ALPHA

1-ANTITRYPSIN

Principal Investigator & Institution: Newman, Lee S.; Professor; National Jewish Medical & Res Ctr and Research Center Denver, Co 80206 Timing: Fiscal Year 2002; Project Start 01-JUN-2001; Project End 31-MAY-2004 Summary: Occupational dust, fume, and gas exposures have been associated with the development of chronic obstructive pulmonary disease (COPD). Genetic and familial factors also contribute to the risk of COPD. Individuals with alpha1-antitrypsin deficiency (alpha11ATD) comprise one of these genetically susceptible populations. The major environmental risk factor for COPD and for alpha1AT deficient individuals who are homozygous (PI*Z) is personal tobacco use. However, preliminary studies suggest that occupational respiratory exposures may also contribute to the severity of this disease. We hypothesize that exposure to occupational and environmental respiratory irritants (dust, fumes, smoke, and gas) increases the risk of both chronic respiratory symptoms and airflow obstruction in genetically susceptible individuals with PI* Z alpha1AT deficiency. This hypothesis will be tested through the following specific aims: 1) To evaluate the association between specific types of occupational and environmental respiratory exposures and the presence and severity of specific pulmonary symptoms and airflow obstruction. 2) To assess the potential interaction or confounding effects between different types of respiratory irritant exposures and/or personal and environmental tobacco smoke in predicting risk of respiratory symptoms. 3) To assess the potential interaction between personal or environmental tobacco smoke and respiratory infections in predicting risk of respiratory symptoms and airflow limitation. 4) To validate the model developed as a predictive model by repeated re-sampling of the original data set, i.e. bootstrapping, that could help health professionals counsel and educate PI*Z patients concerning their risks from environmental and occupational exposures. A cross-sectional design will be used in an expanded cohort of >300 patients with alpha1At deficiency PI*Z. The goal of this proposal is to better understand the burden of obstructive lung disease due to occupational exposures in PI*Z individuals. Such research offers an opportunity to investigate environmental and genetic interactions in which the gene trait that confers susceptibility is known but in which the environmental triggers are not. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EXERCISE AND DISABILITY IN COPD PATIENTS Principal Investigator & Institution: Berry, Michael J.; Health and Exercise Science; Wake Forest University 1834 Wake Forest Road Winston-Salem, Nc 27106 Timing: Fiscal Year 2002; Project Start 01-AUG-1995; Project End 31-AUG-2006

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Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EXHALED AIR BIOMARKERS IN COPD Principal Investigator & Institution: Voelkel, Norbert E.; Professor; Medicine; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, Co 800450508 Timing: Fiscal Year 2002; Project Start 26-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): COPD is a world-wide health problem of increasing prevalence. Non-invasive markers of disease phenotype, severity and rate of progression of the disease, markers characterizing exacerbations of COPD are badly needed. We propose to analyze ultrafiltered exhaled air samples, to establish optimal protocols for sample collection following a FEV1 maneuver, to survey lipids including phospholipids, eicosanoids, steroids, nucleosides, proteins and peptides as markers of potential disease (activity). We propose to establish quantitative mass spectroscopic techniques (using stable isotope dilution protocols) for target marker assays. We propose to investigate stable COPD patients before and during supplemental continuous flow oxygen treatment, before and during alpha-l-antitrypsin infusion therapy, before and after smoking cessation and before and after lung transplantation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: FISH OIL INTAKE, BIOMARKERS AND CHANGE IN LUNG FUNCTION Principal Investigator & Institution: Barr, R Graham.; Medicine; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 31-MAR-2008 Summary: (provided by applicant): We have recently observed a potentially protective effect of fish oil intake on the development of chronic obstructive pulmonary disease (COPD) using validated, questionnaire-based definitions of fish oil intake and COPD in the Nurses' Health Study. The primary aims of the current application are to replicate this promising finding with more precise measures of exposures and outcomes and to investigate potential molecular and genetic intermediaries in a population of 557 older, current and former smokers. The main hypotheses are: 1) dietary fish intake and n-3 PUFA levels are inversely associated with longitudinal lung function decline and CT lung density; 2) n-3 PUFA levels are inversely associated with biological intermediaries, such as leukotriene (LT)-B4, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and soluble adhesion molecules, and these intermediaries are on the causal pathway between n-3 PUFA levels and lung function decline; 3) related genes variants, such as those in genes coding for TNF-alpha, ICAM-1 and nitric oxide synthase (NOS) isoforms, identify individuals at higher risk of lung function decline. Baseline questionnaire, spirometry, and chest CT data and blood specimens have been collected for 557 participants, and one-year follow-up visits for questionnaire, spirometry and chest CT measures are currently ongoing. We propose to study the above hypotheses in this cohort of older, former and current smokers by extending follow-up for an additional four years; the total of six measures would yield adequate power to examine the important relationships between fish intake, n-3 polyunsaturated fatty acids (PUFA), inflammatory mediators, related gene variants and longitudinal lung function. Use of this existing cohort with previously collected blood samples will provide relatively costeffective results about this potentially promising and safe therapy for COPD.

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

Project Title: FUNCTIONAL GENOMIC BIOMARKERS IN COPD Principal Investigator & Institution: Reilly, John J.; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 23-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Chronic Obstructive Pulmonary Disease (COPD) affects over 18 million Americans. It is clear that the major environmental risk factor for this debilitating syndrome is cigarette smoking. It is not clear, however, what factors are responsible for the fact that some smokers develop the disease while most do not. Studies of potential therapies have been hampered by the lack of easily measurable characteristics that predict the course of the disease. Most studies have used measures of lung function as a marker of disease activity. Such studies typically require large numbers of patients and an observation period of months to years. This application proposes studies to develop alternative biomarkers associated with COPD. The research proposed will develop a set of candidate biomarkers by utilizing expression array profiling to characterize gene expression patterns in lung tissue and peripheral blood associated with the presence of COPD. These candidates will then be assessed in studies performed in populations previously characterized for COPD-related phenotypes: the Boston Early Onset COPD Study and the Normative Aging Study. The initial studies will involve expressionprofiling in both lung tissue and peripheral blood in samples obtained from patients undergoing pulmonary resections at Brigham and Women's Hospital. Samples from 20 patients with airflow obstruction on spirometry and emphysema demonstrated on chest CT scans will be compared to samples from 20 matched control patients. State of the art bioinformatic analytic techniques will be used to analyze these data and develop a list of candidate biomarkers based on expression differences. Polymorphisms in the candidate genes will then be studied for genetic association in two characterized populations with different disease distributions. The Boston Early Onset COPD Study consists of patients who have been diagnosed at an early age with severe COPD and their family members. In contrast, the Normative Aging Study includes participants with a broad spectrum of COPD. Studies in these populations will be directed at establishing whether differences in gene expression or gene polymorphisms are associated with COPD. It is hoped that these markers will provide insight into disease pathogenesis and serve as outcome assessment parameters. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: FUNCTIONAL GENOMICS CENTER FOR INNATE IMMUNITY PGA Principal Investigator & Institution: Vercelli, Donata; Professor; None; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: PROPOSED PROGRAM (Adapted from the Applicant's Abstract) Asthma, chronic obstructive pulmonary disease (COPD), myocardial infarction (MI), and deep venous thrombosis (DVT) are among the most common diseases of the lung, heart, and blood (ref). The combined health care costs for these conditions approximate 100 billion dollars per year. The goal of the RFA HL- 99-024 Genomic Applications for Heart, Lung, and Blood Research is to develop and expand genomic knowledge within the heart, lung, and blood community and apply that knowledge to disease pathobiology. There have been considerable advances in the understanding of the disease mechanisms for these conditions, and all four are associated with the development of a local

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inflammatory process. It has become apparent that cells and cytokines that are part of the innate immune system control the early phases of this process of airway, lung, and blood vessel inflammation. The proposal builds on the strengths of three institutions: the Respiratory Sciences Center at the University of Arizona (UA), the Department of Medicine at Brigham & Women's Hospital (BWH), and the Bioinformatics Program at Children's Hospital in Boston (CH), to develop a human variation discovery program on the theme of non-cognate immunity and its broad relationship to heart, lung, and blood diseases. The Arizona/BWH PGA will provide the scientific community with a complete screen of the genetic variants in a subset of innate immunity genes that are most likely to influence the risk for the four diseases noted above. The investigators will also perform a preliminary assessment of the association of these variants with the four phenotypes under study, to guide researchers in these areas away from variants with low likelihood of being relevant and toward those showing promising functional and epidemiologic evidence of influencing any of the four disease phenotypes. To accomplish this broad goal, the investigators have the following specific aims: (1) To screen for polymorphisms 100 genes known to be directly or indirectly related to the innate immune response; (2) To genotype a sample of individuals of Hispanic, nonHispanic White, and African American ethnicity for all the newly discovered polymorphisms; (3) To perform association studies and phylogenetic analysis to identify SNPs most likely to be involved in the determination of asthma, chronic obstructive pulmonary disease, myocardial infarction, and deep venous thrombosis; (4) To disseminate the information on ethnic-specific and phenotype-specific distribution of the polymorphisms under study on a web site within 60 days of the completion of the genotyping studies; (5) To develop a training program that will allow individuals with different knowledge and experience to become acquainted with modern genetic techniques in the fields of high throughput sequencing and genotyping; study design, data handling and data analysis in genetic epidemiology; and ethical issues in population genetics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FUNCTONAL GENOMICS CENTER FOR INNATE IMMUNITY PGA Principal Investigator & Institution: Stampfer, Meir J.; Professor and Chair; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: PROPOSED PROGRAM (Adapted from the Applicant's Abstract) Asthma, chronic obstructive pulmonary disease (COPD), myocardial infarction (MI), and deep venous thrombosis (DVT) are among the most common diseases of the lung, heart, and blood (ref). The combined health care costs for these conditions approximate 100 billion dollars per year. The goal of the RFA HL- 99-024 Genomic Applications for Heart, Lung, and Blood Research is to develop and expand genomic knowledge within the heart, lung, and blood community and apply that knowledge to disease pathobiology. There have been considerable advances in the understanding of the disease mechanisms for these conditions, and all four are associated with the development of a local inflammatory process. It has become apparent that cells and cytokines that are part of the innate immune system control the early phases of this process of airway, lung, and blood vessel inflammation. The proposal builds on the strengths of three institutions: the Respiratory Sciences Center at the University of Arizona (UA), the Department of Medicine at Brigham & Women's Hospital (BWH), and the Bioinformatics Program at Children's Hospital in Boston (CH), to develop a human variation discovery program on the theme of non-cognate immunity and its broad relationship to heart, lung, and blood

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diseases. The Arizona/BWH PGA will provide the scientific community with a complete screen of the genetic variants in a subset of innate immunity genes that are most likely to influence the risk for the four diseases noted above. The investigators will also perform a preliminary assessment of the association of these variants with the four phenotypes under study, to guide researchers in these areas away from variants with low likelihood of being relevant and toward those showing promising functional and epidemiologic evidence of influencing any of the four disease phenotypes. To accomplish this broad goal, the investigators have the following specific aims: (1) To screen for polymorphisms 100 genes known to be directly or indirectly related to the innate immune response; (2) To genotype a sample of individuals of Hispanic, nonHispanic White, and African American ethnicity for all the newly discovered polymorphisms; (3) To perform association studies and phylogenetic analysis to identify SNPs most likely to be involved in the determination of asthma, chronic obstructive pulmonary disease, myocardial infarction, and deep venous thrombosis; (4) To disseminate the information on ethnic-specific and phenotype-specific distribution of the polymorphisms under study on a web site within 60 days of the completion of the genotyping studies; (5) To develop a training program that will allow individuals with different knowledge and experience to become acquainted with modern genetic techniques in the fields of high throughput sequencing and genotyping; study design, data handling and data analysis in genetic epidemiology; and ethical issues in population genetics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETICS AND CONSEQUENCES OF NICOTINE ADDICTION Principal Investigator & Institution: Hoidal, John R.; Professor; Internal Medicine; University of Utah Salt Lake City, Ut 84102 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): This is a revised application from faculty members at the University of Utah for support of a Program Project Grant (PPG) on the genetics and consequences of nicotine addiction. The broad objective of this PPG is to systematically dissect the genetic and molecular mechanisms of addiction and to determine the role of nicotine in the devastating clinical conditions caused by cigarette smoking, identifying specific facets that can ultimately be manipulated to prevent and/or effectively treat this devastating affliction. The thematic hypothesis being tested is that the susceptibility to both nicotine addiction and its consequences has underlying genetic components. In this hypothesis, nicotinic acetylcholine receptors (nAChRs) are critically involved in initiating the determining susceptibility to addiction and the consequences of cigarette smoking, including the dysregulated inflammation and abnormal repair that lead to chronic obstructive pulmonary disease (COPD). The hypothesis will be addressed by combining studies of candidate gene and linkage analysis using the powerful Utah family database and a well-established COPD database with studies using mouse genetics and biology. The studies are designed to generate new knowledge that will improve our understanding of the genetics of addiction and its consequences. In the PPG, productive established investigators with excellent track records of interaction have combined to direct three projects and four cores. Each project addresses novel mechanisms and is oriented around the central theme. Each project is supported by new preliminary data that document the importance and feasibility of the proposed studies. We believe that the proposal offers the special advantages of established research programs, proven multidisciplinary collaborative interactions and a rich environment for productive basic and clinical

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research. By orienting the proposal around the genetics of addiction and its consequences, all three projects interact and intrinsically reinforce each other in almost every phase of their studies. The "intellectual structure" of the PPG is as follows: Project 1, combines the use of unique patient populations with "state of the art" techniques for genotyping and large scale nucleotide sequencing to investigate the genetics of nicotine addiction in humans. Project 2 complements the studies of Project I by delineating the genetic mechanisms that contribute to the formation and maintenance of tolerance to nicotine through nAChRs using well-characterized inbred mice and gene-targeting approaches. Project 3 uses the genetic approaches employed in Project I and animal models developed in the inbred mouse strains used in Project 2 to explore the role of nicotine in the pathogenesis of COPD and the genetic basis for COPD. An Administrative Core, an Animal Core, a Microarray Core and a Resequencing and Genomic Analysis Core support the three projects. The revised proposal has been restructured in response to the initial review and is much stronger. It offers established research programs coming together in multi-disciplinary collaborative interactions for productive basic and clinical research on an important societal problem. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENOTYPING CENTER FOR INNATE IMMUNITY PGA Principal Investigator & Institution: Kwiatkowski, David J.; Associate Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: PROPOSED PROGRAM (Adapted from the Applicant's Abstract) Asthma, chronic obstructive pulmonary disease (COPD), myocardial infarction (MI), and deep venous thrombosis (DVT) are among the most common diseases of the lung, heart, and blood (ref). The combined health care costs for these conditions approximate 100 billion dollars per year. The goal of the RFA HL- 99-024 Genomic Applications for Heart, Lung, and Blood Research is to develop and expand genomic knowledge within the heart, lung, and blood community and apply that knowledge to disease pathobiology. There have been considerable advances in the understanding of the disease mechanisms for these conditions, and all four are associated with the development of a local inflammatory process. It has become apparent that cells and cytokines that are part of the innate immune system control the early phases of this process of airway, lung, and blood vessel inflammation. The proposal builds on the strengths of three institutions: the Respiratory Sciences Center at the University of Arizona (UA), the Department of Medicine at Brigham & Women's Hospital (BWH), and the Bioinformatics Program at Children's Hospital in Boston (CH), to develop a human variation discovery program on the theme of non-cognate immunity and its broad relationship to heart, lung, and blood diseases. The Arizona/BWH PGA will provide the scientific community with a complete screen of the genetic variants in a subset of innate immunity genes that are most likely to influence the risk for the four diseases noted above. The investigators will also perform a preliminary assessment of the association of these variants with the four phenotypes under study, to guide researchers in these areas away from variants with low likelihood of being relevant and toward those showing promising functional and epidemiologic evidence of influencing any of the four disease phenotypes. To accomplish this broad goal, the investigators have the following specific aims: (1) To screen for polymorphisms 100 genes known to be directly or indirectly related to the innate immune response; (2) To genotype a sample of individuals of Hispanic, nonHispanic White, and African American ethnicity for all the newly discovered polymorphisms; (3) To perform association studies and phylogenetic analysis to identify

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SNPs most likely to be involved in the determination of asthma, chronic obstructive pulmonary disease, myocardial infarction, and deep venous thrombosis; (4) To disseminate the information on ethnic-specific and phenotype-specific distribution of the polymorphisms under study on a web site within 60 days of the completion of the genotyping studies; (5) To develop a training program that will allow individuals with different knowledge and experience to become acquainted with modern genetic techniques in the fields of high throughput sequencing and genotyping; study design, data handling and data analysis in genetic epidemiology; and ethical issues in population genetics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: H. INFLUENZAE MODULINS IN COPD AIRWAY INFLAMMATION Principal Investigator & Institution: Clemans, Daniel L.; Biology; Eastern Michigan University Ypsilanti, Mi 48197 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 31-DEC-2005 Summary: (provided by applicant): Non-typeable Haemophilus influenzae (NTHi) is the most common bacterial cause of exacerbations of chronic obstructive pulmonary disease (COPD). These exacerbations are characterized by a brisk inflammatory response with the accumulation of polymorphonuclear leukocytes (PMN) in the lungs of patients with COPD. Essential to this inflammatory response is the expression and secretion of proinflammatory cytokines by host respiratory cells in response to NTHi. The mechanisms, by which NTHi stimulate a proinflammatory response by host respiratory cells and the progressive airway destruction in COPD, is unclear. Therefore, the overlying hypothesis of the proposed research is that secreted, nonlipooligosaccharide (LOS), NTHi proteins (i.e., modulins) stimulate the production of proinflammatory cytokines from human respiratory cells contributing to the endobronchial inflammation in COPD. The long-term goal of this project is to define the mechanisms by which specific secreted NTHi modulin(s) affect the recruitment and activation of effector cells in NTHi endobronchial infection. This goal will be met through identifying, purifying, and characterizing one such secreted modulin and its corresponding gene from model H. influenzae strain Rd and analyzing the modulin's role in respiratory inflammation in vitro. We will study the following Specific Aims to address the hypothesis. Specific Aim I will identify the secreted modulin from H. influenzae that stimulates a proinflammatory response in respiratory epithelial cells by 1) isolating the secreted modulin from H. influenzae strain Rd; 2) analyzing the secreted modulin gene from H. influenzae strain Rd; and 3) reconstituting the H. influenzae strain Rd modulin activity using the purified modulin. Specific Aim II will assess the distribution and expression of the secreted modulin gene from clinical isolates of NTHi. These studies will provide important insights into the mechanisms of the host inflammatory response in NTHi endobronchial infection of COPD and potentially identify novel therapeutic strategies to be employed in the treatment of this debilitating disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: HE3 MR DIFFUSION & LOW DOSE CT QUANTITATION OF EMPHYSEMA Principal Investigator & Institution: Gierada, David S.; Radiology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 23-SEP-2002; Project End 31-JUL-2006

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Summary: (provided by applicant): The goal of this proposal is to develop and evaluate hyperpolarized helium-3 diffusion magnetic resonance imaging (He-3 dMRI) and low dose quantitative computed tomography (LD-QCT) indexes of emphysema as noninvasive biomarkers for the presence, severity, and progression of emphysema. Emphysema is a pathologic abnormality of the lungs defined by enlargement of terminal airspaces and destruction of airspace walls, and is commonly present in the millions of patients with chronic obstructive pulmonary disease. Increased knowledge regarding the role of inflammatory mechanisms and proteinases in the pathogenesis of COPD is leading to searches for newer anti-inflammatory strategies and enzyme inhibitors. Though in the early stages of development, some of these new approaches may eventually provide therapy that alters the course of the disease. Accurate biomarkers of emphysema would allow for early diagnosis, intervention, and evaluation of new therapies. Though spirometry is used to diagnose COPD, it is a relatively inaccurate means of assessing for emphysema. Conventional CT is a highly accurate way to assess the severity of emphysema, which can be quantified by the decrease in xray attenuation of the lungs that results from airspace enlargement and alveolar destruction. However, CT is performed using relatively high doses of ionizing radiation, which limits its acceptability as a screening and follow-up test, particularly in early or mild disease. In recent years, other noninvasive imaging tests for emphysema have been designed that require no or greatly reduced ionizing radiation. One new test, He-3 dMRI, uses a specially constructed MRI pulse sequence to measure the degree to which diffusivity of inhaled hyperpolarized He-3 gas is restricted by alveolar walls. This measurement, the apparent diffusion coefficient (ADC), is increased (gas diffusion is less restricted) when alveolar spaces are enlarged in emphysema. Another test, low dose CT scanning, allows depiction of substantial lung detail at less than 20 percent of the radiation dose of conventional CT, but has not been developed for quantitation of emphysema. Though promising, the optimal technique and validity of both He-3 dMRI and LD-QCT have yet to be established. We hypothesize that 1) Optimizing He-3 dMRI and LD-QCT techniques will allow sensitive and accurate assessment of emphysema, compared to lung morphometry, 2) The optimized He-3 dMRI and LD-QCT techniques will provide valid biomarkers of emphysema that can be applied to other populations, and 3) He-3 dMRI and LD-QCT will allow identification of emphysema progression over time. We will study three separate groups of subjects. In the first group, we will determine which scanning and analysis parameters provide ADC and LD-QCT biomarkers that most accurately quantify the amount of emphysema present pathologically in lobectomy specimens (Aim I). We will then use the optimized scanning and analysis techniques to validate these measurements in a different group, compared to the amount of emphysema present in lobectomy specimens (Aim II). In a third group of subjects, we will determine ADC and LD-QCT lung attenuation measurements at serial time points to assess for emphysema progression (Aim III). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HEALTH EFFECTS OF AIR POLLUTION IN AN ELDERLY POPULATION Principal Investigator & Institution: Sullivan, Jeffrey H.; Environmental and Occupational Health Studies; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 05-AUG-2002; Project End 31-MAY-2007 Summary: (provided by applicant) The long term goal of the candidate is to develop a patient oriented research program in Pulmonary Medicine and Environmental Health at

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the University of Washington that determines mechanisms of pulmonary and cardiovascular effect from environmental pollutants. The candidate will perform two studies to determine the effects of PM2.5 on cardiac function. The first study is a casecrossover study which will determine the association of sudden cardiac arrest to PM2.5 and co-pollutant levels. The second is a panel study in elderly individuals that will expand on the understanding of mechanism of cardiac effect by determining whether inflammatory cytokine and thrombotic responses to particulate matter (PM), CO or N02 occur in susceptible sub-populations. It hypothesizes that these air pollutants induce an inflammatory cascade within the lung that results in measurable elevations in local and systemic inflammatory mediators that induce a decompensation of cardiac function, especially in susceptible groups. These proposed studies of inflammatory markers will be coupled to measures of intra-individual changes in thrombotic proteins (D-dimer and fibrinogen) with varying levels of air pollution exposure in this cohort of elderly participants with and without lung and heart disease. The proposed study builds on an established project within the UW EPA PM Research Center repeatedly measuring personal PM exposures and health effects, in 108 elderly individuals with and without cardiac or respiratory diseases during a high and low pollution season. By assessing intra-individual differences, this project will: 1) Determine whether PM exposure-effect relationships can be detected for exhaled nitric oxide and for serum TNF-alpha and TNF-alpha receptors, IL-6 and IL-6 receptor, endothelin-1 and C-reactive protein (CRP) and whether these effects are associated with sub-clinical morbidity including a reduction in heart rate variability. 2) Determine whether elevated PM 2.5 is associated with increased susceptibility to thrombosis by measuring intra-individual variation of D-dimer and fibrinogen levels. Elucidating molecular mechanisms of susceptibility to air pollution induced morbidity will aid in designing public health policy to prevent morbidity and mortality from air pollution. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HEART ATTACKS AND TRAFFIC POLLUTION Principal Investigator & Institution: Schwartz, Joel D.; Director of Research & Development; Environmental Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 26-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant ): Since the late 1980's, numerous studies have found particulate air pollutant concentrations to be responsible for excess mortality. More recent studies have clarified that most of these deaths are sudden deaths. We have recently shown that particles from traffic are more specifically associated with acute cardiovascular effects. We have also shown the pre-existing diabetes was an important modifier of the particle effect. All of these studies have looked at immediate effects. Two prospective cohort studies have indicated that long-term exposure to particles is also associated with noticeable reductions in life expectancies. To replicate the association between chronic exposure and deaths, and examine the specific role of traffic particles we will conduct a case-control study of myocardial infarctions, using data from the Worcester Heart Attack Study. We will use a GIS system to code the latitude and longitude of home and work locations of cases and controls, and fit models relating concentrations of elemental carbon (a tracer for traffic particles) to population density, distance from roadways, and traffic counts in the Worcester MSA. From this, we will assign exposures to each subject. Controls will be sampled from town census books, which are conducted annually in Massachusetts. Controls will be matched by age, sex, and 10 year age group. Socio-economic data will be merged from the block group of the

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subjects, and questionnaire data will assess smoking history, alcohol consumption, aspirin and other medication use, educational level, height, weight, age, race, exercise, and air conditioner use. We will also ask about the presence of medical conditions, such as diabetes, that may be modifiers of the effect of pollution. Nonlinearities in covariates will be assessed and controlled for using penalized splines, in conditional logistic regressions. A preliminary analysis will use retrospective data, and not obtain questionnaire data. Effect modification by diabetes, prior MI, COPD, smoking, and angina will be tested using interaction terms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HOW ACCESS AFFECTS OUTCOMES OF REHABILITATION SERVICES Principal Investigator & Institution: Iezzoni, Lisa L.; Associate Professor; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2004; Project Start 01-JAN-2004; Project End 31-DEC-2005 Summary: (provided by applicant): With the aging population, the number of Americans with functional limitations will rise by over 300% by 2049 if the age-specific prevalence of major chronic conditions remains unchanged. While medical interventions can sometimes dramatically improve physical functioning, restoring functional abilities is unrealistic for many people. The focus shifts to preserving function, slowing its decline; and preventing secondary complications. Rehabilitation services, including physical therapy (PT) and occupational therapy (OT), are central to these efforts. Few studies have examined the outcomes of PT and OT as they are routinely practiced throughout communities in the United States. This project will use a longitudinal, nationwide survey of Medicare beneficiaries over and under age 65 (the 1994-2001 Medicare Current Beneficiary Surveys), linked with respondents' Medicare claims, to examine outcomes of PT and OT. A major change in Medicare payment policy -- the 1997 Balanced Budget Act, which tightened payments for rehabilitation services -- will serve as a "natural experiment" of conditions under which access to routine rehabilitation care is constrained. The proposed study aims to examine the association between the intensity of PT and OT services and likelihood of good outcomes, including lower rates of: self-reported functional decline; worsening overall health; activities of daily living (ADL) and instrumental ADL dependence; institutionalization; acute care hospitalization; injury prompting medical attention; decubitus ulcer development; purchase of assistive technology; social isolation; and death. The study will examine persons within five conditions: arthritis; stroke; acute myocardial infarction; chronic obstructive pulmonary disease; and lower extremity mobility problems, regardless of cause. Two inter-related hypotheses will guide this work: (1) increased intensity of PT and OT is associated with better outcomes; and (2) decreased access to PT and OT is associated with worse outcomes. These hypotheses will be tested using cross-sectional and longitudinal analyses; analytic techniques will include time series, propensity score, instrumental variable, and proportional hazards regression modeling. The primary outcome of the proposed study will be an assessment of the association of PT and OT, as routinely practiced nationwide and important outcomes of care. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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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

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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 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: INNATE IMMUNITY IN HEART, LUNG, AND BLOOD DISEASE Principal Investigator & Institution: Martinez, Fernando D.; Professor of Pediatrics; Pediatrics; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004 Summary: PROPOSED PROGRAM (Adapted from the Applicant's Abstract) Asthma, chronic obstructive pulmonary disease (COPD), myocardial infarction (MI), and deep venous thrombosis (DVT) are among the most common diseases of the lung, heart, and blood (ref). The combined health care costs for these conditions approximate 100 billion dollars per year. The goal of the RFA HL- 99-024 Genomic Applications for Heart, Lung, and Blood Research is to develop and expand genomic knowledge within the heart, lung, and blood community and apply that knowledge to disease pathobiology. There have been considerable advances in the understanding of the disease mechanisms for these conditions, and all four are associated with the development of a local inflammatory process. It has become apparent that cells and cytokines that are part of

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the innate immune system control the early phases of this process of airway, lung, and blood vessel inflammation. The proposal builds on the strengths of three institutions: the Respiratory Sciences Center at the University of Arizona (UA), the Department of Medicine at Brigham & Women's Hospital (BWH), and the Bioinformatics Program at Children's Hospital in Boston (CH), to develop a human variation discovery program on the theme of non-cognate immunity and its broad relationship to heart, lung, and blood diseases. The Arizona/BWH PGA will provide the scientific community with a complete screen of the genetic variants in a subset of innate immunity genes that are most likely to influence the risk for the four diseases noted above. The investigators will also perform a preliminary assessment of the association of these variants with the four phenotypes under study, to guide researchers in these areas away from variants with low likelihood of being relevant and toward those showing promising functional and epidemiologic evidence of influencing any of the four disease phenotypes. To accomplish this broad goal, the investigators have the following specific aims: (1) To screen for polymorphisms 100 genes known to be directly or indirectly related to the innate immune response; (2) To genotype a sample of individuals of Hispanic, nonHispanic White, and African American ethnicity for all the newly discovered polymorphisms; (3) To perform association studies and phylogenetic analysis to identify SNPs most likely to be involved in the determination of asthma, chronic obstructive pulmonary disease, myocardial infarction, and deep venous thrombosis; (4) To disseminate the information on ethnic-specific and phenotype-specific distribution of the polymorphisms under study on a web site within 60 days of the completion of the genotyping studies; (5) To develop a training program that will allow individuals with different knowledge and experience to become acquainted with modern genetic techniques in the fields of high throughput sequencing and genotyping; study design, data handling and data analysis in genetic epidemiology; and ethical issues in population genetics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INOS GENE TRANSFECTION IN PULMONARY HYPERTENSION Principal Investigator & Institution: Chicoine, Louis G.; Pediatrics; University of New Mexico Albuquerque Controller's Office Albuquerque, Nm 87131 Timing: Fiscal Year 2002; Project Start 01-APR-1999; Project End 31-MAR-2004 Summary: Pulmonary hypertension (PH) is a significant cause of morbidity and mortality affecting a broad range of patients. Neonatal pulmonary hypertension is the second leading cause for admission to neonatal intensive care units for respiratory support. In adults, PH causes significant morbidity and mortality in patients with chronic obstructive pulmonary disease. In all patients, PH is characterized by cellular proliferation and altered vasoreactivity in the pulmonary vascular bed. The objectives of this proposal are to evaluate the vasodilator efficacy and toxicity of NO produced by virally mediated inducible nitric oxide synthase (iNOS) gene transfection in the lung and to determine the effect of virally transfected iNOS on the pathogenesis of PH. The general hypothesis is that virally transfected iNOS will result in sufficient NO formation to modulate pulmonary vasoconstriction and attenuate pulmonary vascular changes associated with pulmonary hypertension, but insufficient NO formation to result in toxicity. Utilizing human iNOS gene and, as a control, the E. coli lac Z reporter gene coding for beta-galactosidase (beta-gal) adenovirus constructs our goals set forth in this proposal are: 1) to optimize iNOS gene delivery and expression in the rat lung, 2) to determine the role of transfected iNOS on the development of pulmonary hypertension, and 3) to compare intravascular and intratracheal delivery of the iNOS gene in terms of

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gene expression, vascular reactivity and toxicity. These goals are addressed in the following specific aims: Specific Aim number 1: Assess the effectiveness of adenovirusmediated iNOS gene transfection in attenuating acute pulmonary vasoconstrictor responses. Specific Aim number 2: Assess iNOS gene transfection-mediated effects on the development of chronic hypoxia-induced pulmonary hypertension. Specific Aim number 3: Assess the efficacy and toxicity of intravascularly and intratracheally administered adenoviral iNOS constructs. The methods will involve using adenovirus constructs containing the gene for iNOS or beta-gal that will be administered intravascularly; the lungs will then be studied to determine vascular reactivity, NO production, and localization of transfected iNOS. Some rats will be transfected and exposed to chronic hypoxia. Finally, intravascular and intratracheal delivery will be compared in terms of gene localization and toxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEURONS

INTEGRATION

BY

AIRWAY

PARASYMPATHIC

GANGLIA

Principal Investigator & Institution: Myers, Allen C.; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 01-APR-1992; Project End 31-MAY-2005 Summary: In the airway, the autonomic nervous system controls smooth muscle tone, secretion by glands, and blood flow. Although there is abundant physiological and pharmacological evidence indicating that dysfunction of this autonomic control of the airways contributes to the causes and symptoms of pulmonary diseases such as bronchial asthma, chronic obstructive pulmonary disease and emphysema, little is actually known about the regulation of these nerves. Our long term goal is to provide knowledge of how autonomic tone is regulated in the airway, especially that provided by the parasympathetic nervous system. Control of smooth muscle in the trachea and bronchi is predominantly by nerve fibers that emanate from neuronal cell bodies in parasympathetic ganglia, small clusters of cell bodies located near the airway wall. The parasympathetic tone of the airway smooth muscle is thought to be under the control of the central nervous system where signals are transmitted rhythmically during respiration to the parasympathetic neurons in the airway wall. This signal activates airway parasympathetic ganglia neurons by release of a neurotransmitter which mediates cholinergic synaptic transmission in the ganglia. Separate, but potentially important, forms of neural regulation of parasympathetic neurons in the airways are by the so-called local peripheral reflex pathway and the intraganglionic pathways. In the peripherals reflex pathway, a sensory nerve is activated by changes in the airway and communicates directly with the parasympathetic neuron in the nearby ganglia by releasing neuropeptides from branches of the sensory axon, evoking non-cholinergic synaptic transmission. In other words, this is an sensory- parasympathetic reflex, independent of the central nervous system. A peripheral reflex would thus allow local increases in parasympathetic tone in an airway segment, independent of changes in another segment. In the intraganglionic pathway, postganglionic axons leaving a bronchial ganglion serve to innervate, and modulate the function of neighboring ganglia within the airway tree. This proposal describes experiments that will address our central hypothesis, namely that the parasympathetic nerve activity in the airways is shaped by the integration of three separate inputs: 1.) input from the central nervous system {classical cholinergic nicotinic input), 2.) input from the peripheral reflex sensory fibers, and 3.) input from surrounding postganglionic parasympathetic ganglia. We feel that an understanding of the mechanism of this integration is a prerequisite to obtaining

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knowledge on the mechanisms by which airway neurophysiology is regulated in health and disregulated in disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INTRACELLULAR PATHWAYS MEDIATING AIRWAY MUCIN SECRETION Principal Investigator & Institution: Davis, C William.; Cystic Fib/Pulmonary Trtmt Ctr; University of North Carolina Chapel Hill Aob 104 Airport Drive Cb#1350 Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 15-FEB-2000; Project End 31-JAN-2004 Summary: Mucin hyperproduction is a common component of obstructive airways disease and comprises a principle problem faced by patients and their attending physicians. A major long-term goal of this laboratory is the identification of molecular targets for pharmacologic therapies against mucin hypersecretion. Using SPOC1 cells as a model for airway mucin secretion, we have shown that phospholipase C-coupled P2Y2 receptors localized in the apical membrane form the dominate regulatory pathway in these cells. Because all airway epithelial cells likely possess P2Y2 receptors for extracellular ATP and UTP, targets for the selective inhibition of mucin secretion need to be located at points distal to activation of PLC, and IP3 and DAG generation. The two downstream elements of the PLC pathway, Ca2+-protein kinase C (PKC), appear to be independent in their activation of mucin release, and preliminary data suggest strongly that nPKCdelta, a Ca2+-insensitive isoform, is uniquely activated by agonist. This proposal will test whether the Ca2+ and PKC pathways leading to mucin secretion are fully additive and independent, or whether they converge at a rate limiting step proximal to mucin granule/plasma membrane fusion and exocytosis. A likely candidate for this proximal barrier to secretion is the cortical cytoskeleton, comprised of actin microfilaments. Specific Aim 1 will use wild-type and mutant nPKCdelta retroviral expression vectors to test whether nPKCdelta, in fact, mediates the effects of agonist of mucin secretion, and it will examine the means by which nPKCdelta is activated. Specific Aim II tests the independence between Ca2+- and PKC-activated mucin secretory pathways by probing the transit of mucin granules across the cortical microfilament barrier and the plasma membrane. We focus on the roles of scinderin, a gelsolin-related, F-acting severing enzyme, and Rab3 isoforms, respectively. In each case, we will test whether these elements participate in the regulation of agoniststimulated exocytosis and whether they lie in the pathways modulated by nPKCdelta and/or Ca2+. Lastly, we will exploit the different binding kinetics of BAPTA and EGTRA to test the degree of independence between PKC and Ca2+ in the final steps of exocytosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: LOCAL BIOLOGICAL RESPONSE PROFILES IN THE LOWER RESPIRATORY TRACT Principal Investigator & Institution: Plopper, Charles G.; Professor and Chairperson; University of Alabama Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: Exposure to ozone, the principal component of photochemical smog, produces a heterogeneous pattern of response within the respiratory system of adults. Epidemiologic studies suggest that exposure to ozone during early childhood can have long lasting effects including decrements in small airways function. Recent experimental

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work by our group supports these findings. Extensive exposure (5 months) of infant rhesus monkeys (30 days old) to ozone profoundly remodeled the tracheobronchial airways to produce the features of chronic airways disease in adults: mucous cell hyperplasia, basement membrane thickening, altered epithelial innervation, smooth muscle hypertrophy, inflammatory cell infiltration, elevated baseline airway resistance, as well as loss of conducting airways. Taken together, this suggests that immature airways of infants are more susceptible to oxidant injury than are adults and that the postnatal developmental process itself is subject to perturbation by oxidant stress. Project 2 will define cellular basis of local antioxidant protective mechanisms in immature tracheobronchial airways of infants and how they are modulated by growth, development and allergic sensitization. The overall hypothesis that we will test is that the following four characteristics of immature airways contribute to the heightened susceptibility of infants to oxidant exposure: 1)immature airway geometry and cellular organization; 2) alterations in O3 deposition patterns during postnatal growth; 3) local differences in levels of cellular and extracellular antioxidants and 4) airway specific differences in ability to generate in inflammatory response. Project 2 will coordinate closely with Project 1 on defining the cellular basis of local antioxidant protective mechanisms in the tracheobronchial airways, with Project 3 on the relationship of evens in tracheobronchial airways to those in the nasal cavity, and with Project 4 on the development of a dynamic model of airway growth and development as it impacts on susceptibility of infants and young children to growth altering exposures to air pollutants allergens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LONG ACTING AGONISTS OF ADENOSINE A2A RECEPTORS Principal Investigator & Institution: Thompson, Robert D.; Interim Director of Chemistry; Adenosine Therapeutics, Llc Charlottesville, Va 22902 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 31-OCT-2004 Summary: (provided by applicant): Adenosine is an endogenous nucleoside that exerts its physiological effects through four G-protein coupled receptors A1, A2A, A2B, and A3. Adenosine Therapeutics, LLC is interested in the anti-inflammatory actions mediated by the A2A receptor subtype. A lead compound, ATL-146e, is being developed for coronary artery imaging and has also been shown to be efficacious in several animal models of inflammation. Due to its short half-life, it is not an ideal candidate for chronic inflammatory disorders such as chronic obstructive pulmonary disease (COPD), which would be better treated with a longer-acting compound. Recently, we discovered a novel class of compounds that shows greater potency and duration of action than ATL-146e, but exhibit decreased selectivity. Thus, the goal of this proposal is to synthesize long acting A2A agonists that are potent and selective. We will evaluate these compounds in a functional bioassay that has already been demonstrated to be a useful and efficient tool in predicting a compound's duration of action. As oral dosing may be a preferable route of administration, a secondary goal will be to identify compounds that have oral bioavailability. Finally, we will evaluate standard PK parameters for our best candidates using standard LC/MS protocols that we have developed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: LUNG HEALTH STUDY--LONG TERM FOLLOW UP Principal Investigator & Institution: Altose, Murray D.; Chief of Staff (W); Medicine; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106

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Timing: Fiscal Year 2002; Project Start 01-FEB-1998; Project End 31-JAN-2003 Summary: The Lung Health Study (LHS), conducted from 1986-1994, demonstrated that a smoking intervention program in middle-aged long-term cigarette smokers can result in a highly significant beneficial effect on the rate of FEV1 decline over five years. However, FEV1 is only a surrogate marker for clinical outcomes of respiratory morbidity and mortality. The present study proposes long-term post-trial follow-up of former LHS participants to assess the incidence of morbidity and mortality from respiratory and cardiovascular diseases and other causes, as documented by hospital, clinic, and death records. A pulmonary function test 11 to 12 years after entry into the LHS is also proposed to determine long- term effects of the LHS smoking intervention program on lung function. The main objectives of the study are as follows: 1) to determine, using an intent-to-treat analysis, whether the LHS smoking intervention significantly reduces the incidence of clinically important respiratory and cardiovascular disease over a 12- to 15-year period following study enrollment; 2) to determine whether the beneficial effect of the smoking intervention program on measures of lung function persists through 11 to 12 years of follow-up; 3) to estimate the magnitude of the effects of FEV1 and FVC on the risks of cardiovascular and respiratory morbidity and mortality, after controlling for smoking history; 4) to study the role of other factors (gender, airways reactivity, weight gain, and co- morbidities) in determining the rate of decline in pulmonary function and the risks of cardiovascular and respiratory morbidity and mortality. All ten of the original LHS clinical centers plan to participate. To minimize bias, all surviving participants of the LHS will be invited to participate, giving a potential sample size of 5600. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LUNG HEALTH STUDY--LONG TERM FOLLOW-UP Principal Investigator & Institution: Buist, Aline S.; Associate Professor of Medicine; Medicine; Oregon Health & Science University Portland, or 972393098 Timing: Fiscal Year 2002; Project Start 01-FEB-1998; Project End 31-JAN-2004 Summary: The Lung Health Study (LHS), conducted from 1986-1994, demonstrated that a smoking intervention program in middle-aged long-term cigarette smokers can result in a highly significant beneficial effect on the rate of FEV1 decline over five years. However, FEV1 is only a surrogate marker for clinical outcomes of respiratory morbidity and mortality. The present study proposes long-term post-trial follow-up of former LHS participants to assess the incidence of morbidity and mortality from respiratory and cardiovascular diseases and other causes, as documented by hospital, clinic, and death records. A pulmonary function test 11 to 12 years after entry into the LHS is also proposed to determine long- term effects of the LHS smoking intervention program on lung function. The main objectives of the study are as follows: 1) to determine, using an intent-to-treat analysis, whether the LHS smoking intervention significantly reduces the incidence of clinically important respiratory and cardiovascular disease over a 12- to 15-year period following study enrollment; 2) to determine whether the beneficial effect of the smoking intervention program on measures of lung function persists through 10 to 12 years of follow-up; 3) to estimate the magnitude of the effects of FEV1 and FVC on the risks of cardiovascular and respiratory morbidity and mortality, after controlling for smoking history; 4) to study the role of other factors [gender, airways reactivity, weight gain, and co- morbidities] in determining the rate of decline in pulmonary function and the risks of cardiovascular and respiratory morbidity and mortality. All ten of the original LHS clinical centers plan to participate. To

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minimize bias, all surviving participants of the LHS will be invited to participate, giving a potential sample size of 5600. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LUNG INFLATION AND AIRWAY HYPERRESPONSIVENESS Principal Investigator & Institution: Adkinson, N Franklin.; Professor of Medicine; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 15-DEC-1998; Project End 31-AUG-2007 Summary: (provided by applicant): Airways hyperresponsiveness (AHR) is a central feature of asthma, strongly related to the severity of the disease. However, its mechanisms are not understood. In the first period of this grant, we examined how lung inflation (deep inspiration) influences airways responsiveness. We identified that lung inflation has two distinct beneficial effects in healthy humans: it acts as a bronchoprotector and as a bronchodilator against bronchoconstrictive stimuli. We also found that the bronchoprotective effect of lung inflation is lost in individuals with AHR and is also absent against the bronchoconstriction induced by an allergic reaction. Preliminary findings indicate that the bronchodilatory effect is lost in subjects with COPD and in those with severe asthma. We now propose 3 specific aims: Specific aim 1 will test the hypothesis that nitric oxide (NO), which affects the airways smooth muscle by increasing the levels of cGMP, mediates the bronchoprotective effects of lung inflation and that the NO effect is impaired in AHR. This will be tested with the use of inhaled NO in healthy subjects and subjects with asthma with the intent to demonstrate that NO can mimic deep inspiration-induced bronchoprotection only in the former group. An analogous approach will be used by pre-treatment with sildenafil citrate, an approved inhibitor of PDE V, the enzyme responsible for cGMP degradation. Specific aim 2 will be devoted to the understanding of the mechanisms behind the absence of bronchoprotection against a respiratory allergic reaction. We will first examine whether an allergic reaction leads to the loss of bronchoprotection against other stimuli, such as methacholine. By using inhaled NO, we will examine whether the bronchoprotective action of this molecule is absent against an allergic reaction. With antagonists to products of the allergic reaction (primarily antileukotrienes and antihistamines), we will test whether we can restore the bronchoprotective effects of lung inflation against allergen. In specific aim 3 we will examine the reasons behind the loss of the bronchodilatory effect of lung inflation. Our hypothesis is that, in COPD, bronchodilation is lost as a result of impairment in lung elastic recoil, whereas in severe asthma, as a result of airway wall stiffness. To test this hypothesis, we will investigate these subject groups in comparison to healthy controls by simultaneously testing airways distensibility through high resolution computerized tomography imaging, recoil pressure at various lung volumes and bronchodilation by lung inflation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MECHANISMS AND LOCALIZATION OF CO2 SENSITIVE CNS NEURONS Principal Investigator & Institution: Richerson, George B.; Associate Professor; Neurology; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 01-AUG-1995; Project End 31-JUL-2006 Summary: (provided by applicant): The major source of feedback for control of breathing comes from central respiratory chemoreceptor that monitor blood CO2 levels. Dysfunction of these neurons occurs in many common diseases, including chronic

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obstructive pulmonary disease (COPD), sleep apnea, and possibly sudden infant death syndrome (SIDS). The first step in finding specific treatments for these diseases is to identify the neurons responsible for chemoreception, and define their mechanisms. Although the central chemoreceptors were localized to the ventrolateral medulla (VLM) 40 years ago, the specific neurons responsible have still not been clearly identified. We recently obtained evidence that serotonin-containing neurons within the VLM are central respiratory chemoreceptors, but the majority of neurons with identical properties are located in the medullary raphe. This is exciting, because chemosensitivity of serotonergic neurons could provide a biological basis for the interaction between sleep and breathing. The proposed work is aimed at further defining the cellular mechanisms of these neurons, and the role that they play in central chemoreception. We propose to use a combination of patch clamp recordings from neurons in tissue culture and brain slices, imaging of intracellular pH, immunohistochemistry, confocal microscopy, and computer modeling to address basic unanswered questions about chemosensitive raphe neurons. 1) Do medullary raphe neurons have properties that would make them uniquely specialized to sense changes in blood CO2? We will look at their anatomical relationship with blood vessels, the co-transmitters they contain, and their projections. 2) Are there differences between chemosensitive neurons in the medullary raphe and the VLM? 3) Does chemosensitivity of midbrain raphe neurons explain the arousal that occurs in response to hypercapnia during sleep? 4) What ion channels are responsible for chemosensitivity? 5) Does CO2 act through a change in intracellular pH alone? 6) Can the depression of breathing during sleep be explained in part by the effects of reticular activating system neurotransmitters on raphe neurons? Disturbances of breathing are common in human diseases, particularly during sleep. Understanding the basic mechanisms involved in modulation of neuronal activity by CO2, and the mechanisms by which breathing is affected by sleep, may help provide successful treatment for these diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MENTORED DEVELOPMENT AWARD

PATIENT-ORIENTED

RESEARCH

CAREER

Principal Investigator & Institution: Zeidler, Michelle R.; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Asthma is an enormous medical and economic burden worldwide and affects over 14 million Americans. Despite treatment with inhaled corticosteroid therapy, many asthmatic patients exhibit persistent symptoms of asthma, as well as accelerated decline in lung function. While asthma has classically been described as a disease of the proximal airways, physiologic, histologic, and immunologic data indicate that the distal lung is significantly involved in asthma and may be a cause of uncontrolled disease. Understanding the role of the distal lung in asthma has been hampered by difficulties in studying and treating this area. Chlorofluorcarbon (CFC) inhaled corticosteroids (ICS), the mainstay of asthma treatment, cannot effectively reach the distal lung due to their relatively large particle size. The recent transition to non-CFC inhalers has created a new class of extra-fine ICS aerosols which, theoretically, have a sufficiently small particle size to reach this region. To date, the effect of extra-fine ICS on distal lung inflammation remains unknown. The proposed study will evaluate the change in distal lung inflammation in mild to moderate steroid naive asthmatics at baseline and after treatment with a conventional ICS which mainly targets the proximal lung versus an extra-fine ICS which targets both

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the proximal and distal lung. The study will be conducted using a double-blinded, randomized crossover trial design. Before and after treatment, distal lung inflammation will be evaluated using: 1) messenger ribonucleic acid (mRNA) measures of inducible nitric oxide synthase, eotaxin, rantes, and interleukin-4 (IL-4) receptor alpha in distal airways obtained via distal lung brushings; and 2) lipopolysaccharide (LPS)-stimulated production of tumor necrosis factor (TNF)-alpha and MIP-1 alpha by alveolar macrophage obtained from distal bronchoalveolar lavage (BAL) aliquots. Non-invasive measures of small airways disease will also be obtained before and after treatment and correlated with the molecular and cellular markers of distal lung inflammation in an attempt to identify a valid non-invasive marker of small airways inflammation. Noninvasive markers of distal disease include: 1) quantitative analysis of thoracic computed tomography at residual volume (RV) before and after methacholine challenge; 2) physiologic measures of small airways disease including RV, FRC, isovolume FEF 25-75, and closing volume; and 3) the alveolar portion of exhaled nitric oxide (NO). This study will determine the potential to modify distal airways inflammation which may ultimately improve asthma control. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: METALS IN EXHALED BREATH CONDENSATE AS COPD BIOMARKERS Principal Investigator & Institution: Mutti, Antonio; University of Parma Via Cavestro 7 Parma, Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Chronic obstructive pulmonary disease (COPD) is a major health problem worldwide and is increasing with a high prevalence, high morbidity and high cost. COPD is an important medical area for which biomarkers are needed for the study of the pathogenesis, the diagnosis and the clinical management. Exhaled breath condensate (EBC) can be collected with non-invasive methods and is a promising medium to develop biomarkers of COPD. The present research project is aimed at applying the most sensitive, selective and specific reference analytical techniques to the study of the composition of EBC in COPD patients. EBC levels of toxic metals and essential trace elements will be measured in COPD patients by electrothermal atomic absorption spectroscopy (ETAAS) and inductively coupled plasma mass spectrometry (ICP-MS). Such a novel approach (never done before) will be applied to identify and validate biomarkers of exposure and susceptibility to toxic metals, known to be contained in tobacco smoke, and probably playing a fundamental etiologic role in the pathogenetic path leading to COPD. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) will be used as a complementary approach to develop biomarkers of effect (aldehydes from lipid peroxidation) suitable for the long-term monitoring of COPD patients. This novel approach represents a significant advance over the analysis of alternative media (BALF, blood, serum, urine, hair), which are not as reliable (owing to interfering substances in the complex matrix) and reflect systemic rather than lung (target tissue) levels of both toxic metals and essential trace elements. Tobacco smoke and polluted environments substantially increase the lung burden of pneumotoxic chemicals, particularly heavy metals. Biomarkers of exposure (EBC levels of AI, Cd, Cr, Ni, Pb) should provide a quantitative estimate of the target tissue dose, thus distinguishing exposed from non-exposed controls. The lung response to inhaled pneumotoxic substances shows a high inter-individual variability as a function of different detoxifying capacity. Biomarkers of susceptibility will be developed relying on the consideration that some trace elements (Mn, Cu, Zn, Se, and Mo) are components of

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metalloproteins (superoxide dismutase, glutathione peroxidase, xanthine oxidase) known to modulate the response to toxic substances, possibly accounting for the limited proportion (15-20%) of smokers developing COPD. Biomarkers of susceptibility could be useful to identify and counsel people who are at increased risk of disease when exposed to tobacco smoke or environmental pollutants. Biomarkers of effect will be developed starting from aldehydes released into the EBC after lipid peroxidation in cell membranes. The pattern of aldehydes could distinguish membrane damage due to either oxidative stress or other mechanisms, such as a direct attack by free radicals. In summary, we propose a novel approach to the development of COPD biomarkers, relying on (i) noninvasive collection procedures to obtain (ii) a simple, interference-free matrix (EBC is practically water) to be analyzed by (iii) reference analytical methods, which are highly selective and specific (mainly, if not entirely, based on mass spectrometry), to determine (iv) stable analytes (heavy metals and trace elements). Through EBC biomarkers we sought to address two specific aims: a) to determine the validity of metals and aldehydes levels in EBC as biomarkers of exposure, of susceptibility and of effect in patients with COPD; b) to determine the clinical utility of EBC biomarkers as prognostic tools to predict the natural history of COPD. Establishing heavy and toxic metal levels in EBC as novel biomarkers of exposure, effect and susceptibility in patients with COPD could assist health care providers in devising new primary and secondary interventions, including drugs, to improve the quality of life and outcome of patients with COPD worldwide. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MOLECULAR EPIDEMIOLOGY AND GENE-ENVIRONMENT INTERACTION Principal Investigator & Institution: Zhang, Zuo-Feng; Director/Professor; Epidemiology; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-MAR-2005 Summary: (provided by applicant): This planning grant of molecular epidemiology presents a multidisciplinary approach to an important aspect of molecular epidemiology: gene-environment interaction. Crosstalk among the multidisciplinary team and collaborations to integrate novel technologies and/or methodologies into epidemiologic research are planned. The investigators will explore air pollution-related genetic susceptibility and instability for future population studies of gene-environment interactions on the risk of airborne pollutant-related diseases such as asthma, chronic obstructive pulmonary disease (COPD), and airway cancers. They will develop microarray gene chips to measure the genetic susceptibility (genotypes) and instability as measured by gene expression, and explore new statistical methodology to deal with exposure, genetic susceptibility, gene expression and related illnesses. The specific aims of the project are: Aim 1. To establish a multidisciplinary team and to increase crosstalk in order to foster collaborations to integrate novel technologies and methodologies into molecular epidemiology; and Aim 2. To conduct 3 pilot studies to identify allelic variants (polymorphisms) of environmental disease susceptibility genes; to examine air pollution-related global gene expressions; and to explore the related statistical methodology to analyze data with exposures, genotypes and gene expression matrix in order to foster future population-based molecular epidemiological studies of geneenvironment interaction in determining the risk of environmentallyinduced diseases. The planned University of California at Los Angeles (UCLA) Molecular Epidemiology Project in Environmental Genome Projects builds upon existing resources and

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researches of the Southern California Particle Center and Supersite (SCPCS) and the UCLA Center for Occupational and Environmental Health (COEH). It takes advantage of the wide range of expertise and skill in epidemiology, molecular biology, environmental health sciences, toxicology, occupational medicine, and biostatistics/bioinformatics. The planning grant will address critical research questions in a broad-based effort to understand the mechanism of air pollution and its related susceptibility genotypes and gene expressions, to explore gene-environmental interactions, and to develop more effective methods for the identification of high risk individuals for prevention of air pollution-related diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEW METHODS FOR EVAL OF ORGANIC DUST AEROSOLS Principal Investigator & Institution: Reynolds, Stephen J.; Professor; Environmental & Radiological Hlth Scis; Colorado State University-Fort Collins Fort Collins, Co 80523 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2007 Summary: More than 700,000 men, women, and children working in livestock production are at risk for occupational lung disease related to organic dust exposures. The primary goals of this project are to evaluate new methods for measuring inhalable particulates, endotoxins, and glucans/ergosterols that can be used to help establish occupational exposure guidelines for complex organic dusts in swine, poultry, and dairy environments, and to evaluate and develop correction factors for direct-reading aerosol instruments that can be readily used by practitioners for interventions. The performance of inhalable samplers including the IOM, IOM with Multifoam discs, and Button Sampler will be compared to traditional gravimetric methods for total and respirable dusts under controlled laboratory conditions and in the field. The utility and performance of these devices for measuring endotoxins and glucans/ergosterols will also be determined. Analysis using both assay (LAL and monoclonal antibody) and chemical (mass spectrometry) methods will help elucidate relationships between specific chemical components and potency of these bacterial and fungal products in the various organic dust matrices. In the same laboratory and field experiments two directreading devices, the DataRAM and HAM, will be compared to the gravimetric methods, and their performance characterized in response to particle size distributions determined using a Grimm. Their suitability for practical applications in these environments will also be determined. This project addresses the need for more research related to organic dusts in agriculture identified by the NIOSH Board of Scientific Counselors, as well as developing practical cost-effective tools for application in engineering and other interventions, also identified as a priority. This study will address several priority areas of the National Occupational Research Agenda (NORA): Asthma and Chronic Obstructive Pulmonary Disease, Mixed Exposures, and Exposure Assessment Methods. This project also addresses the NIOSH Agricultural Centers priority area to develop and conduct research related to the prevention of occupational disease of agricultural workers and their families, with an emphasis on multidisciplinary research and the development and evaluation of control technologies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: NOVEL STRATEGIES TARGETING ACUTE EXACERBATION OF COPD Principal Investigator & Institution: Albert, Richard K.; Denver Health and Hospital Authority 777 Bannock St Denver, Co 802044507

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Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The overall objective of this proposal is to test three novel treatments aimed at reducing the frequency and/or the severity of acute exacerbations of COPD. We describe two randomized placebo-controlled trials. The first will determine whether long-term administration of N-acetyl cysteine (a thiol compound that decreases mucus viscosity and also has anti-oxidant, anti-inflammatory and cytoprotective effects), or clarithromycin (a macrolide antibiotic having both antiinflammatory and antibiotic effects) will reduce the frequency and severity of COPD exacerbations. The second will determine whether administering bronchodilators via nebulizers that are powered with heliox (a mixture of helium and oxygen), as opposed to air, will more rapidly reverse the physiologic abnormalities, and reduce the length of hospital stay, associated with severe acute exacerbations of COPD as a result of the lower density of heliox reducing turbulent flow, thereby increasing bronchodilator deposition in more distal airways. As a sub goal we also propose to use a number of biomarkers (i.e., levels of adenosine in exhaled air, levels of interleukins 6 and 8 in sputum, levels of interleukins 6 and 8, surfactant protein D, vascular endothelial growth factor, fibrinogen, C-reactive peptide, Factor VIII activity, and von Willebrand's factor antigen in blood), to identify and characterize those patients who are more likely to have acute exacerbations. This information will, at the same time, also provide information regarding the pathobiology of COPD exacerbations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: O2-CHEMOSENSING BY REATIVE OXYGEN SPECIES/NADPH OXIDASE Principal Investigator & Institution: Fidone, Salvatore J.; Professor of Physiology; Physiology; University of Utah Salt Lake City, Ut 84102 Timing: Fiscal Year 2004; Project Start 01-JUL-1978; Project End 31-AUG-2008 Summary: (provided by applicant): O2-sensing in the carotid body occurs in neuroectoderm-derived type I glomus cells where hypoxia elicits a complex chemotransduction cascade involving membrane depolarization, Ca 2+ entry and the release of excitatory neurotransmitters. Efforts to understand the exquisite O2sensitivity of these cells focus primarily on the relationship between PO2 and the activity of K+-channels. A current hypothesis proposes that coupling between local PO2 and the open-closed state of K+-channels is mediated by a phagocytic-like multisubunit enzyme, NADPH oxidase, which produces reactive oxygen species (ROS) in proportion to the prevailing PO2. In O2-sensitive cells contained in lung neuroepithelial bodies (NEB), experiments have confirmed that ROS levels decrease in hypoxia, and that E M and K+-channel activity are indeed controlled by ROS produced by NADPH oxidase. However, recent studies in our laboratory suggest that ROS generated by a nonphagocytic form of NADPH oxidase, are important contributors to chemotransduction, but that their role in type I cells differs fundamentally from the mechanism utilized by NEB. We propose to test the hypothesis that in response to hypoxia, NADPH oxidase activity is increased in type I cells, and further, that increased ROS levels generated in response to low-O2 facilitate membrane re-polarization via the activation of a subset of K+-channels. In addition, we will examine the hypothesis that a non-phagocytic NADPH oxidase mediates adaptive morphological and physiological adjustments induced by exposure of the carotid body to chronic hypoxia (CH), a condition that occurs clinically in sleep apnea and chronic obstructive pulmonary disease (COPD). Studies will include: I. An examination of the sources and mechanisms of ROS production in type I cells, II. Evaluation of the involvement of NADPH oxidase and ROS

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in the carotid body response to acute hypoxia; III. The expression of NADPH oxidase subunits in the carotid body; and the effects of CH; and IV. The role of NADPH oxidase and ROS in carotid body adaptation to CH. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PORTABLE CONTINUOUS OXYGEN SYSTEM Principal Investigator & Institution: Appel, W Scot.; Sequal Technologies, Inc. 11436 Sorrento Valley Rd San Diego, Ca 92121 Timing: Fiscal Year 2003; Project Start 04-AUG-2003; Project End 31-JAN-2004 Summary: (provided by applicant): Chronic obstructive pulmonary disease (COPD) is a serious public health problem that is responsible for more than 500,000 hospitalizations, 100,000 deaths, and $15 billion in direct costs of medical care in the U.S. each year. In addition, millions of Americans are disabled by lung disease. It is estimated that more than 16 million people have undiagnosed COPD. Patients, whom have developed emphysema or obstructive bronchitis or who are afflicted with longstanding, low, blood-oxygen levels (chronic hypoxemia), typically require supplemental oxygen. Oxygen concentrators--electrically powered mechanical devices that extract oxygen from air by a process known as Pressure Swing Adsorption (PSA)--are the most prevalent devices used to provide supplemental oxygen (0.5 - 3.0 liters per minute). When low-flow supplemental oxygen is prescribed for the treatment of COPD or chronic hypoxemia, a patient is provided with a stationary oxygen concentrator for use in their home, plus several small tanks of gaseous oxygen and accessories (an oxygen conserving device & pressure regulator) for ambulation or excursions outside their home, including airline travel. SeQual Technologies has developed an advanced PSA gas separation system for the generation of oxygen for medical applications. This proprietary system incorporates a rapid vacuum-pressure-swing adsorption process that enables SeQual to provide a PSA unit with both the highest recovery (the ratio of output oxygen molecules to input oxygen molecules) and the greatest productivity (the oxygen output flow rate per unit volume of the system) of any medical oxygen concentrator. The Company's proprietary PSA devices--in combination with state-ofthe-art, high efficiency, lightweight motors and compressors--have enabled SeQual to produce a unique, portable, battery-operated, oxygen concentrator system. SeQual's continued efforts remain in the improvement of the efficiency, productivity and recovery of oxygen molecules during the PSA process to effectively miniaturize the oxygen generation device that will lead to a very small scale portable oxygen concentrator that can deliver continuous oxygen to a patient at all times. The focus of this research is on novel monolithic structured adsorbents. The study proposes to characterize the surface area of the structures, study the effectiveness of the unique pressure swing adsorption cycles and parameters and design a very small system for the concentration of oxygen. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PREDICTING DEPRESSION OUTCOMES IN MEDICALLY ILL ELDERS Principal Investigator & Institution: Koenig, Harold G.; Associate Professor; Psychiatry; Duke University Durham, Nc 27710 Timing: Fiscal Year 2002; Project Start 15-AUG-1999; Project End 31-JUL-2004 Summary: Older adults with congestive heart failure (CHF) and chronic pulmonary disease (CPD) are increasing in number. Their lives and ability to function are greatly

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affected by these illnesses, which frequently lead to recurrent hospital admissions to manage exacerbations. We have found that 26 percent of older persons with CHF or CPD fulfill criteria for major depressive disorder when hospitalized. Depression is often prolonged, affects recovery, and increases use of health services. About one-third of these depressed patients, however, will go into full remission within three months of hospital discharge, often without specific treatment for depression. Many of these patients improve because their physical illness improves. The other two-thirds of depressed patients will have persistent depression, whether or not their health improves. Minor depression is even more common than major depression, being present in 32 percent of such patients, and while it may have a better prognosis than major depression, it is nevertheless associated with considerable disability and poorer quality of life. Research Questions: We are interested in studying four conjoint trajectories of depression-physical health outcome in the first six months after hospital discharge: depression and health both improve, depression improves but health does not, health improves but depression does not, and neither depression nor health improves. What proportion of patients follow each trajectory? What psychosocial and health characteristics predict which trajectory they will follow? What are the barriers to effective treatment, how is depression currently treated in these patients, and what are predictors of treatment intensity? Methods: 1000 older patients with CHF or CPD and major (n=500) or minor depression (n=500) will be recruited from the inpatient services of Duke Hospital and two community hospitals and followed for six months after discharge. Detailed assessments of depression and severity of medical illness will be conducted by a research nurse during telephone and in-person evaluations. Significance: Such information is necessary to determine which of the many patients with major or minor depression need specific treatment, and which patients will improve on their own after discharge as their medical illness improves or fails to improve. It will also provide important information to both guide future clinical trials and identify barriers to effective treatment of depression in these patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF MUCIN GENE EXPRESSION BY ELASTASE Principal Investigator & Institution: Voynow, Judith A.; Associate Professor; Pediatrics; Duke University Durham, Nc 27710 Timing: Fiscal Year 2002; Project Start 05-AUG-2000; Project End 31-JUL-2004 Summary: (adapted from the application): Neutrophil-predominant airway inflammation is a major pathologic feature of chronic airway diseases. Neutrophils release neutrophil elastase that stimulates increased production of mucins. This action is likely to be a key link between neutrophilic inflammation and mucus obstruction of the airways. Presently, the molecular mechanisms by which elastase increases the production of mucins are unknown. Three preliminary findings are cited upon which a hypothetical model will be tested: 1) neutrophil elastase increases the stability of mRNAs coding for two major respiratory tracts mucins, MUC5AC and MUC4; 2) neutrophil elastase treatment of airway epithelial cells triggers generation of reactive oxygen species; and 3) hydroxyl radical and hydrogen peroxide scavengers inhibit neutrophil elastase-induced increases in MUC5AC and MUC4 mRNA levels. This leads to the following hypotheses. In respiratory epithelial cells neutrophil elastase treatment enhances mRNA stability of MUC genes via the following mechanisms. Neutrophil elastase alters the cellular oxidant/antioxidant balance resulting in the generation of reactive oxygen species. These reactive oxygen species, specifically hydrogen peroxide and hydroxyl radical, mediate the interaction between RNA-binding proteins and mucin

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mRNA stability sequences, resulting in increased mucin mRNA stability. Emphasizing the importance of post-translational regulation of mucin gene expression, experiments will test critical steps in the hypothetical pathway of elastase-reguated mucin mRNA expression. Aim 1 studies the effect of elastase treatment on the interaction between RNA-binding proteins and mucin mRNA stability sequences. Aim 2a studies the effect of hydrogen peroxide and hydroxyl radical on mediating the elastase-induced increase in mucin mRNA stability and mucin mRNA levels, while Aim 2b studies the effect of reactive oxygen species on the interaction between RNA-binding proteins and mucin mRNA stability sequences, leading to increased mRNA stability and mRNA levels. The ultimate goal is to use information from this project to identify new biologic targets for therapeutic interventions to prevent mucus obstruction in chronic inflammatory airway diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF TOLL-LIKE RECEPTOR IN AIRWAY INFECTION Principal Investigator & Institution: Li, Jian-Dong; Scientist Ii Section Chief; House Ear Institute 2100 W 3Rd St Los Angeles, Ca 900571922 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Non-typeable Haemophilus influenzae (NTHi) causes infections in chronic obstructive pulmonary disease (COPD) and otitis media (OM). Both are characterized by inflammation. The molecular mechanisms underlying NTHi-induced inflammation remain poorly defined. Our long-term objective is to understand the molecular mechanisms by which the inflammatory response is induced and regulated in NTHi infections. Our recent studies showed that NTHi strongly activates nuclear factor-kappaB (NF-kappaB) via Toll-like Receptor 2 (TLR2). Because TLR2 expression in airway epithelial cells is low and overexpression of TLR2 greatly enhances NTHi-induced NF-kappaB activation, we hypothesize that NTHi up-regulates TLR2 via a specific signaling network. Our preliminary results indeed indicate that NTHi strongly up-regulates TLR2 via positive NF-kappaB and TGF-beta pathways and a negative EGFR-p38 MAPK pathway. Moreover, glucocorticoids synergistically enhance NTHi-induced TLR2 up-regulation. These encouraging results have thus laid a solid foundation for further investigation of the molecular mechanisms underlying NTHi-induced TLR2 upregulation (short-term objective). Aim 1. Determine the contribution of NF-kappaB and TGF-beta pathways to NTHi-induced TLR2 upregulation by perturbing their signaling. Aim 2. Determine the contribution of EGFRp38 MAPK pathway to NTHi-induced TLR2 up-regulation by perturbing their signaling. Aim 3. Determine the signaling mechanisms by which glucocorticoids synergistically enhance NTHi-induced TLR2 up-regulation by studying the effect of increased MKP-1 expression on NTHi-induced activation of p38 and TLR2 upregulation. Significance: Understanding the signaling mechanisms underlying NTHiinduced TLR2 up-regulation will not only bring new insights into the regulation of inflammation, but will also open up novel therapeutic targets for modulating inflammatory responses in COPD and OM. Moreover, elucidating the molecular mechanisms by which glucocorticoids enhance NTHi-induced TLR2 up-regulation will provide instructive information regarding how to use glucocorticoids more appropriately in the clinic. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: RESEARCH CORE 2 - ENVIRONMENTAL LUNG DISEASE Principal Investigator & Institution: Tesfaigzi, Yohannes; Staff Scientist; University of New Mexico Albuquerque Controller's Office Albuquerque, Nm 87131 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: SUBPROJECT ABSTRACT NOT PROVIDED Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ROLE OF ELASTOLYTIC CATHEPSINS IN EMPHYSEMA Principal Investigator & Institution: Chapman, Harold A.; Professor; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 01-JUN-2001; Project End 31-MAY-2006 Summary: (Applicant's Abstract): Although excessive proteolysis is a key element in the pathogenesis of emphysema, pathways of protease dysregulation in this disorder remain uncertain. New studies implicate lymphocyte-derived cytokines in emphysema. Interferon-y acts on macrophages as well as non-inflammatory cells such as smooth muscle cells to promote expression and secretion of the active cysteine protease cathepsin S, a potent elastase stable at neutral pH. Transgenic mice expressing either IL13 or interferon-y on airway surfaces develop cysteine protease-dependent emphysematous changes. Further, a significant correlation was recently found between serum levels of cystatin C, the major cysteine protease inhibitor, and severe reductions in FEV1 (<20 percent predicted) in a cohort of 30 patients with early-onset emphysema compared to controls with normal FEV1 and comparable smoking history. These studies invite the hypothesis that pro-inflammatory cytokines and possibly cigarette smoke stimulate mesenchymal lung cells and macrophages to secrete elastolytic cysteine proteases and downregulate their cystatin C release. This imbalance creates an accelerated process of collagen and elastin degradation important to the development of emphysema and COPD. The research plan is centered on the question of whether dysregulation of elastolytic cathepsins is important to the pathogenesis of emphysema. Parallel tracks of animal and human experiments are proposed: Mouse cathepsin S/L and cystatin C "knockouts" are used in Aims 1 and 2 to answer the question of whether excess elastolytic cathepsin activity exacerbates the development of interferon-yinduced emphysema and whether mesenchymal cells in the lung are a source of these enzymes. Aim 3 is designed to determine if low levels of cystatin C and/or polymorphic markers in or near the major genes regulating cystatin C (and elastolytic cathepsins) are associated with increased risk of COPD. Together, these studies should determine if some patients with early-onset COPD can be grouped, based on either phenotypic (cystatin C) or genetic markers, into a functional subset defined by a common pathogenic pathway involving dysregulation of elastolytic cathepsins. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SMALL GTPASES AND LUNG BETA RECEPTOR REGULATION Principal Investigator & Institution: Knoll, Brian J.; Pharmacological and Pharmaceutical Sciences; University of Houston 316 E Cullen Houston, Tx 772042015 Timing: Fiscal Year 2002; Project Start 10-JUL-1994; Project End 31-MAY-2004 Summary: A characteristic of G protein-coupled receptors is their desensitization after activation, as exemplified by human beta2- adrenergic receptors (beta2ARs). These receptors stimulate adenylyl cyclase after binding catecholamine agonists, and mediate such physiologic actions such as the relaxation of airway smooth muscle. Beta2ARs thus

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are important targets for drugs used to treat asthma and chronic obstructive pulmonary disease. Desensitization of beta2ARs occurs first by receptor phosphorylation, causing uncoupling from G-protein, then by internalization of receptors away from the cell surface and into sorting endosomes. Most internalized receptors are dephosphorylated and recycle to the cell surface, but receptors are also sorted to lysosomes for degradation (downregulation) or to perinuclear 'recycling' endosomes. Endocytosis and intracellular sorting events are thus critical mechanisms for the regulation of ligand-activated signal transducing receptors. Our long-term goals are to determine how receptor movements from one cell compartment to another are regulated, and the relationship of these movements to receptor activity. Trafficking between cellular compartments is regulated by ras-related GTPases called rabs, and by proteins interact with rabs. Rab5 and its interacting proteins control the fusion of endocytic vesicles with the sorting endosome, and re implicated in the traffic between sorting and recycling endosomes. Rab4 and rab11 also participate in sorting among endosomal compartments. Using the yeast twohybrid method we identified a novel, membrane associated rab5 interacting (rab5ip) that appears to be localized to endosomal membranes. The specific goals of the present study are to determine how rab proteins regulate beta2AR activity and number by movements between intracellular compartments, and to determine how rab5ip regulates endosome fusion. Transfected cells will be examined by confocal microscopy and radioligand binding to determine how rabs and rab5ip regulate traffic among the sorting endosome, the recycling endosome, the plasma membrane and lysosomes. These movements also will be correlated with beta2AR dephosphorylation. The function of rab5ip will be studied with rab5ip mutants and an endosome fusion assay in vitro. Rab5ip domains required for interaction with rab5 will be determined, and potential interactions with other regulators of endosome fusion will be assessed. Finally, a screen will be performed for other novel proteins that interact with rab5ip. These studies will provide insight into the mechanisms of endocytic trafficking events, and how they regulate the activity and number of an important signal-transducing receptor. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EVALUATION

SPANISH

CHRONIC

DISEASE

EDUCATION

PROGRAM

Principal Investigator & Institution: Lorig, Kate R.; Associate Professor; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 01-APR-1998; Project End 31-DEC-2003 Summary: (Adapted from the Investigator's Abstract): For health services to be efficient, and relevant for patients with chronic disease, patients must play an active role in management. Past studies have demonstrated that English-speaking patients can benefit from chronic disease self-management education. Initial results suggest that these same benefits occur for Spanish-speaking arthritis patients. This is especially important because Hispanics are the fastest growing population in the United States and, at the same time, carry a disproportionate burden of chronic disease. In addition, they often encounter limited access to health care and health education due to certain economic, language and cultural barriers. The proposed project will address these issues by: 1. Developing and implementing an experimental community-based Spanish language health education program for self-management for patients with three chronic diseases (coronary artery disease, chronic obstructive pulmonary disease and type II diabetes). Patients with different conditions will attend the same program together as has been successful with English-speaking patients. 2. Conduct a 4-month randomized trial to determine the impact of the program on: a.) the subsequent use of self-management

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practices; b.) self-efficacy to manage disease-related problems and symptoms; c.) the physical and emotional health status of the participants; and, d.) the health service utilization of the participants. 3. Conduct a 1-year longitudinal study to determine the long-term effectiveness of the program. 4. Conduct exploratory studies to 1) determine if the program is more beneficial for some subgroups, and 2) to explore the mechanisms by which health status improves. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SUPPLEMENTAL SE AND VITAMIN E AND PULMONARY FUNCTION Principal Investigator & Institution: Cassano, Patricia A.; Div/Nutritional Sciences; Cornell University Ithaca Office of Sponsored Programs Ithaca, Ny 14853 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): This proposed project is a randomized clinical trial testing whether supplementation with selenium and/or vitamin E affects pulmonary function. There is compelling evidence from observational epidemiologic studies that high antioxidant intakes are associated with reduced risks of chronic obstructive disease (COPD) and increased lung function. This proposal is an ancillary study to the multisite selenium and Vitamin E Cancer Prevention Trial (SELECT), a 4-arm placebo-controlled, double-blinded randomized trial in 32,400 men testing whether daily supplementation with vitamin E (400mg alpha-tocopherol), selenium (200 micrograms selenomethionine) or both vitamin E and selenium can prevent prostate cancer. We will enroll 3,000 SELECT participants for this respiratory ancillary study, and extend data collection to include pulmonary function, respiratory disease, and respiratory symptoms. We also will collect biological measures of nutrient exposure (serum vitamin E and selenium) and plasma lipids (total and high-density lipoprotein cholesterol) on all participants and oxidant burden (urinary F2-isoprostane) on a sub sample of heavy smokers and men with COPD. The primary outcome will be change between baseline and year 3 in forced expiratory volume in the first second (FEV1). FEV1 is a valid and reliable measure of respiratory function that strongly predicts COPD and mortality. Extensive data on diet and dietary supplement use are being collected by the SELECT parent study. All specific aims examine pre-specified contrasts between the 4 arms of the SELECT randomized trial. The underlying hypothesis is that antioxidants will reduce the age related decline in FEV1, and thus at the 3-year follow-up FEV1 will be higher in the groups receiving antioxidant supplements compared to controls. A secondary aim considers whether the effect of supplementation is greater among smokers (high burden of exogenous oxidants) who, by purposive selection of the study sites, will comprise 25% of the sample. The proposed study addresses important and timely questions about diet and lung disease, and makes cost efficient use of the research infrastructure of SELECT. This study could have enormous public health significance, because supplementation with antioxidant nutrients would be an inexpensive and practicable means to reduce morbidity and mortality from pulmonary disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SURFACE PROTEINS OF MORAXELLA CATARRHALIS Principal Investigator & Institution: Hansen, Eric; Professor; Microbiology; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002; Project Start 01-JUL-1996; Project End 31-MAR-2007

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Summary: (provided by applicant): Moraxella (Branhamella) catarrhalis is now acknowledged to be an important cause of otitis media in infants and young children and can also cause lower respiratory tract infections in adults with chronic obstructive pulmonary disease. Little is known about the gene products that allow M. catarrhalis to colonize the nasopharynx and then cause disease in the respiratory tract. However, the ability to attach to human cells and to resist killing by normal human serum (i.e., serum resistance) are well-recognized bacterial virulence factors. We have identified two different proteins (UspA1 and UspA2) that are exposed on the surface of this pathogen and that perform distinct functions relevant to the ability of M. catarrhalis to colonize and survive in vivo. We already have established that UspA1 is an adhesin that binds human epithelial cells in vitro. We also have proven that UspA2 is directly involved in the expression of serum resistance by this organism. This research project involves investigation of the structure-function relationships inherent in these two proteins and also addresses two other topics that are relevant to the infectious process involving M. catarrhalis. In the first Specific Aim, we will identify the amino acid sequence(s) in the UspA1 protein that allows it to bind human epithelial cells. In the second Specific Aim, we will identify both the mechanism by which UspA2 confers serum resistance on M. catarrhalis and the amino acid sequence(s) in UspA2 responsible for this activity. Experiments designed to determine the level of UspA2 required for serum resistance and how UspA2 expression is regulated constitute the third Specific Aim. Finally, we will investigate biofilm formation by M. catarrhalis and identify gene products involved in this biologically relevant process in the fourth Specific Aim. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: T CELL INFLAMMATION AND MUCIN HYPERSECRETION IN COPD Principal Investigator & Institution: Fahy, John V.; Associate Professor of Medicine; Cardiovascular Research Inst; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 01-AUG-2001; Project End 31-JUL-2005 Summary: The mechanisms of mucus hypersecretion in COPD are poorly understood, even though sputum production is associated with an accelerated rate of decline in FEV1 and with increased mortality from COPD. In addition, the reasons why only a minority of cigarette smokers develop COPD is unknown. To date, clinical research in COPD has been significantly hampered by problems in measuring outcome indicators related to mucus hypersecretion. We hypothesize that smokers with COPD have a T cell phenotype characterized by predominance of CD4+ T cells of the subtype which contributes to overexpression of mucin genes, increased numbers of goblet cells, and increased levels of both stored and secreted mucin. In addition, we hypothesize that the airway phenotype in smokers without COPD will not be normal but will be intermediate to that observed in healthy subjects and smokers with COPD. Finally, we hypothesize that treatment of smokers with COPD with inhaled corticosteroids will decrease lymphocytic inflammation, mucin gene expression, and the levels of stored and secreted mucin. We propose to test our hypotheses in three groups of human subjects smokers with COPD, smokers without COPD and healthy non smoking controls. We will apply methods recently developed in our laboratory for measuring mucin gene expression, goblet cell hyperplasia and secreted mucin levels as well as methods we have adopted from others for purifying and phenotyping airway T cells. Aim 1 will determine the phenotype of the airway mucosa in smokers with COPD compared to smokers without COPD and non smoking controls with emphasis on the numbers and

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subtypes of T lymphocytes, the numbers of goblet cells, and the relationship between stored and secreted mucin glycoproteins. Aim 2 will determine which of the nine currently identified mucin genes are overexpressed in smokers with and without COPD. Aim 3 will determine in inhaled corticosteroid treatment in smokers with COPD is associated with a reduction in lymphocyte number, mucin gene expression, goblet cell number, or in the levels of stored and secreted mucin. The proposed studies address an unmet need, because no clinical studies have been published focusing on T cell subtypes, mucin genes, and goblet cells in human COPD. The application of the methods described here provide the opportunity to begin to understand the relationship between lymphocytic inflammation and mucin gene expression in COPD, and may suggest strategies for improving treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: THE CARDIOPULMONARY EFFECTS OF PARTICULATE EXPOSURE Principal Investigator & Institution: Christiani, David C.; Professor; Environmental Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 31-MAR-2007 Summary: (provided by applicant): 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. Similar associations have been observed for rates of hospital admissions for respiratory and cardiovascular diseases for subjects over age 65. Results from the first phase of this study (ES R01 09860) showed significant cardiac and airway changes after both environmental and occupational particulate exposures. The objective of this application is to investigate the role of both occupational and non-occupational exposure to particulates in the development of respiratory and cardiac responses in boilermakers. We will employ a detailed, continuous exposure assessment to PM2.5 with and PM1.0 with repeated measures of biologic and physiologic markers of response. In addition, we will employ novel techniques for the assessment of particulate-induced physiologic responses, including gene expression using mRNA microarrays. Hypotheses to be addressed in this established cohort of boilermakers include: (1) Short-term exposure to particulates from occupational, ambient, and indoor exposures results in airway inflammation and obstruction measured by serial expired NO and FEV1; (2) Chronic exposures to particulates result in long-term decreases in expired NO and FEV1; (3) Exposure to particulates results in acute changes in cardiovascular function measured as heart-rate variability, heart-rate, and blood pressure; (4) Exposure to particulates results in increased acute phase reactant (c-reactive protein, fibrinogen) concentration in the serum; (5) Exposure to particulates induces systemic responses resulting in alterations in white blood cell gene expression assessed by mRNA microarray analysis pre- and postexposure; (6) Common chronic medical conditions such as hypertension, COPD, and asthma predispose particulate-exposed individuals to changes in cardiac function (heart rate, heart rate variability, and blood pressure). The results of this work will have important implications for preventive efforts aimed at reducing particle-associated morbidity and mortality. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: THE REGULATION AND ROLE OF NITRIC OXIDE IN ASTHMA Principal Investigator & Institution: Erzurum, Serpil C.; Professor; Molecular Medicine; Cleveland Clinic Lerner Col/Med-Cwru Cleveland, Oh 44195 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): High output nitric oxide (NO) synthesis has been linked to airway inflammation in asthma. NO is produced by human airway epithelial cells (HAEC) which have increased NO synthase 2 (NOS2) expression in asthma due to transcriptional activation of the gene. Our preliminary results show that interferon gamma (IFNgamma) induces, and interleukin-4 augments, NOS2 expression in HAEC in vitro through mechanisms that require physical interaction between activator protein (AP)-I and IFNgamma-activated signal transducer and activator of transcription (STAT)I prior to DNA binding. In the context that asthma results from inflammatory processes that injure or modify airway function, excessive NO may participate in the pathogenesis of asthma through reactive nitrogen species formation and subsequent nitration of proteins which modifies their biologic functions. In support of this, nitrated proteins are increased in the asthmatic airway. Using an innovative proteomic approach, we have identified tyrosine nitration of specific proteins in lung epithelial cells after NOS2 induction, and in the human airway, e.g. Mn superoxide dismutase and catalase. Nitration of antioxidants leads to inactivation, and biologic consequence of apoptosis. Taken together, we hypothesize that NO synthesis is increased in asthma due to NOS2 gene induction by AP-1 and STAT-1 signaling mechanisms in the airway epithelial cell, and that the generation of excess NO leads to protein tyrosine nitration which modifies protein functions and contributes to airway injury/inflammation. To test this hypothesis, we will (1) define the regulation of NOS2 gene expression using HAEC in culture, and airway cells freshly obtained from asthmatic and healthy control lungs, and (2) determine the role of NO in asthma by a proteomic approach to identify nitrated proteins before and after NOS2 induction in HAEC in culture, and in clinical samples from asthmatics in comparison to patients with chronic obstructive pulmonary disease (COPD) and controls. Identification of nitrated proteins and consequences of biological tyrosine nitration will provide clear and detailed information on the role of NO in asthma. Since all the studies are performed in the physiologically relevant context of the human lung or in primary airway epithelial cells, these studies will provide a valuable comprehensive picture of the mechanisms that control NO synthesis in the human airway, and alterations in those mechanisms that lead to asthma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: T-LYMPHOCYTES, PATHOGENESIS

LATENT

VIRUS

AND

EMPHYSEMA

Principal Investigator & Institution: Diaz, Philip T.; Associate Professor of Medicine; Internal Medicine; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 31-DEC-2003 Summary: (provided by applicant): Recent data has suggested that latent adenoviral infections may up-regulate inflammatory processes in the lung and be an important cofactor in emphysema development. In addition recent lung biopsy studies have demonstrated that lung lymphocytes, particularly CD8+ cells are found more commonly in the airway as well as the lung parenchyma in individuals with chronic obstructive pulmonary disease. It has thus been hypothesized that lymphocytes associated with chronic obstructive pulmonary disease represent a cytotoxic T-lymphocyte (CTL) response to latent virus. In support of this hypothesis is data demonstrating a marked

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increased susceptibility of HIV infected smokers to emphysema. Furthermore, the presence of emphysema in this precocious process is associated with increased numbers of cytotoxic lymphocytes on broncho- alveolar lavage. With this as a background, the central hypothesis of the present study is that CTL's represent a response to latent viral infection in the lung and contribute directly to emphysema pathogenesis by accelerating apoptotic cell death of lung parenchyma. To address this hypothesis, we examine use lung tissue obtained from subjects enrolled in the National Emphysema Treatment Trial undergoing lung volume reduction surgery (LVRS). The specific aims of the current proposal are: Specific Aim 1: To determine the relationship between latent virus infection of lung epithelium, CTL infiltration and programmed cell death in patients with advanced emphysema. Specific Aim 2: To determine whether latent viral infection of alveolar epithelium predicts progression of emphysema following LVRS. In conclusion, we believe that successful completion of this project will provide us with very important information regarding the role of latent viral infection, upregulation of the inflammatory response and the pathogenesis of emphysema. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: TOXIC INFLAMMATION

ALDEHYDES

AS

MODULATORS

OF

LUNG

Principal Investigator & Institution: Van Der Vliet, Albert; Associate Professor; Pathology; University of Vermont & St Agric College 340 Waterman Building Burlington, Vt 05405 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Reactive aldehydes such as acrolein (2,3-propenal) are major components of air pollution and are proposed to contribute to the adverse effects of smoking in lung diseases such as chronic obstructive pulmonary disease (COPD). In addition, acrolein and similarly reactive aldehydes (such as 4hydroxynonenal) are also generated endogenously, as presumed bioactive products of oxidative stress such as during inflammation. Acute and chronic lung diseases, including COPD, are often dominated by recruitment and activation of neutrophils, and tobacco smoke-derived aldehydes have been shown to alter several neutrophil properties, including stimulation of cytokine release, inhibition of the respiratory burst, and interference with constitutive neutrophil apoptosis. Overall, these various observations may help explain why smoking contributes to persistent airway inflammation, by increasing neutrophil recruitment and by interfering with neutrophil apoptosis, the latter a critical event in the termination of inflammatory processes. Preliminary studies in mice have shown that exposure to environmental tobacco smoke augments neutrophil inflammation by lipopolysaccharide, perhaps due to interference of tobacco smoke aldehydes with neutrophil apoptosis and clearance. Based on their chemical reactivity, these aldehydes react primarily with cellular GSH or with redoxsensitive cysteine residues in proteins, thereby altering cellular redox status and/or interfering with various cell signaling pathways. A better understanding of biochemical mechanisms by which these aldehydes modulate inflammatory processes may provide additional links between environmental/oxidative stress and inflammatory lung diseases such as COPD. Our hypothesis is that reactive aldehydes can contribute to chronic lung inflammation by interfering with granulocyte apoptosis, thereby increasing survival and/or necrosis, resulting in continued and increased inflammation. We aim to explore the effects of aldehydes on pathways that regulate neutrophil survival and death pathways, and their consequences for neutrophil phagocytic clearance and/or release of toxic granule components. We plan to study this in freshly isolated human

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neutrophils (alone or in co-culture experiments with cultured macrophages or airway epithelial cells) and in a mouse model of acute transient airway inflammation. Finally, we aim to determine the major cellular targets for these aldehydes, using various derivatization strategies and proteomics approaches (2-D electrophoresis, MALDI mass spectrometry), in an attempt to relate specific protein modifications by these aldehydes to their cellular effects. We propose that thus identified cellular targets and its modifications could be used as mechanism-based biomarkers to explore a role of these aldehydes in the etiology of such diseases as COPD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: TRAINING IN TRANSLATIONAL LUNG RESEARCH Principal Investigator & Institution: Schluger, Neil W.; Associate Professor of Medicine & Public; Medicine; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2004; Project Start 15-APR-2004; Project End 31-MAR-2009 Summary: (provided by applicant): Progress in pulmonary medicine in several areas has been limited by an incomplete understanding of basic mechanisms of the pathogenesis of disorders such as chronic obstructive pulmonary disease (COPD), asthma, acute lung injury and the adult respiratory distress syndrome, tuberculosis, interstitial lung disease (including idiopathic pulmonary fibrosis), and lung cancer. In the past few years however, advances in basic science have brought a greater understanding of some of the processes likely to be involved in these diseases, and advances in basic investigative techniques such as genomics and proteomics, hold promise for broad application in clinical medicine. Crucial to the application of advances in basic science to important problems in clinical pulmonary medicine will be the development of a cadre of physician-scientists with an both an understanding of relevant basic science and lung biology as well as the tools to apply that knowledge in the clinical setting in order to carry our rigorous translational studies in lung disease that can test and confirm hypotheses developed at the bench, with the ultimate goal of developing potent new therapeutic approaches for a variety of disorders. Our goal in this application is consistent with that set forth by NIH itself in its introduction of career development awards for young investigators with an interest in clinical or patient oriented research: "to encourage research-oriented clinicians to develop independent research skills and gain experience in advanced methods and experimental approaches needed to conduct patient-oriented research." The training program described in this application will enable trainees to successfully apply for these NIH-sponsored career development awards, or their equivalent. The rationale behind the establishment of this training program is a follows: 1. There is a manifest need to prepare physician-scientists to conduct translational research in pulmonary medicine. 2. As basic science research reaches this translational stage, it will be important to Wain individuals to develop an integrated understanding of a variety of processes in cell biology, immunology, genetics, molecular biology, clinical research, epidemiology, and clinical medicine. 3. The College of Physicians and Surgeons of Columbia University and the Columbia Presbyterian Medical Center provide an outstanding environment for a comprehensive and integrated training program in pulmonary translational research, owing to the depth and breadth of basic and clinical academic programs at the institutions. 4. By providing formal didactic instruction, mentoring, and well-structured research opportunities, the program will attract basic and clinical scientist trainees who wish to receive rigorous training in the area of pulmonary translational research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TREATMENT EFFECTIVENESS IN DEPRESSED PATIENTS WITH COPD Principal Investigator & Institution: Alexopoulos, George S.; Professor and Vice Chair; Psychiatry; Weill Medical College of Cornell Univ New York, Ny 10021 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): COPD affects 15 percent of older adults and is the fourth leading cause of death in the US. Approximately 20 percent of COPD patients have major depression, a condition that contributes to suffering but also to poor treatment adherence leading to increased disability and morbidity. The study will investigate the effectiveness of an intervention aimed at facilitating the implementation and adherence to a treatment algorithm based on AHCPR guidelines in depressed COPD patients. The cornerstone of the intervention is the use of Health Specialists (HS), who will collaborate with the patients? own physicians and help them to offer timely and appropriately targeted treatment recommendations for pharmacotherapy. The HS will also visit patients at their homes and offer education, directions and support aimed at improving their adherence to medical, psychiatric, and rehabilitative recommendations. In addition, the HS will provide to families, and physicians education on depression. We hypothesize that this intervention will increase the prescription of adequate antidepressant treatment by physicians, enhance treatment adherence by patients, and reduce depressive symptomatology, suicidal ideation, and disability over a 26-week post-discharge follow-up period. The subjects will be 180 elderly patients consecutively admitted to two pulmonary rehabilitation centers (2-week length of stay), suffering from major depression and COPD. The impact of the intervention (offered to half of the sample, N=90) will be contrasted with that of usual care (N=90). We targeted in this study one of the most disabled and suffering segments of the population. We used, in our design, our research experience with depressed COPD patients, the PROSPECT multicenter study of primary care elderly patients, our home care study, and the geriatric depression studies of our Intervention Research Center. If found effective, this "intervention" can be broadly implemented, as it can be used by visiting nurse staff after retraining. Finally, we believe that our approach to the care of depressed, medically ill patients can generate a practice model that has the ability to rapidly incorporate advances made in clinical science. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TREATMENT GOALS AT THE END OF LIFE Principal Investigator & Institution: Fried, Terri R.; Associate Professor; Internal Medicine; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 15-FEB-2002; Project End 31-JAN-2007 Summary: (provided by applicant): A geriatrician with both quantitative and qualitative research skills, Dr. Fried is poised to consolidate her career as an independent investigator. The K02, described as a time-off clinical duties award, would permit her to avoid the additional clinical responsibilities she would otherwise be expected to assume as her early career development awards end. Her research program is focused on the elicitation of older persons preferences for different intensities and sites of in care and on the outcomes of these alternative care strategies. It began with projects examining attitudes toward life-sustaining treatment and advance directives, and outcomes of pneumonia in nursing home residents treated with and without hospital transfer. Additional studies have examined the use of and older persons attitudes toward home as a treatment site in acute and terminal illness. Recent work has focused on older

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Chronic Obstructive Pulmonary Disease

persons treatment preferences in serious and terminal illness. Results of this work include reliable and valid new patient-centered measures of treatment preference and the development of a unique cohort of seriously ill older outpatients. Building upon this earlier work, the overall objective of the proposed study is to examine changes in the preferences of both patients and their families across a spectrum of diseases. The primary aim is to determine the effect of primary diagnosis, health status, and healthcare utilization on the preferences of patients and their families. The study will involve 226 terminally ill older persons and a family member. They will be interviewed in their homes every four months if medically stable, and as frequently as every month if the illness is progressing. The relationship of disease diagnosis, health status (functional status, symptoms, self-rated health), healthcare utilization, and understanding of the illness prognosis to preferences will be examined using longitudinal repeated measures analysis. Dr. Fried s research program also consists of additional cohort studies examining communication, symptoms, and function in this study group and intervention studies to enhance physician-patient communication. With colleagues skilled in patient-centered research, extensive data management and analysis support, and senior faculty and administration committed to Dr. Fried s continued success, Yale offers the resources necessary to ensure Dr. Fried s continued development as an independent investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: UNDERSTANDING AND LIVING WITH COPD: A SELF-CARE CDROM Principal Investigator & Institution: Mcfarren, Ann E.; Principal; Healthmark Multimedia, Llc 1828 L St Nw, Ste 250 Washington, Dc 20036 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-MAR-2003 Summary: (provided by applicant): Chronic obstructive pulmonary disease (COPD) currently affects the lives of 16 million Americans and is the only major cause of death that is increasing in the U.S. The societal costs of COPD are great, with an estimated $26 billion total direct costs each year. An additional $12.4 billion per year has been estimated as indirect societal costs due to lost earnings. COPD is irreversible and progressive; however, rehabilitation and skill training can positively affect a patient?s quality of life. This Phase I SBIR will result in a multimedia CD-ROM that will provide education and skill training for persons with COPD. In Phase I, HealthMark will (1) Develop a content outline for the full program; (2) Work with individuals with COPD to identify interactive methods and tools to help them cope with COPD; and (3) Develop one area of information (e.g., What is COPD?) and 2 self-care skill lessons as a prototype; (4) test prototype with 40 individuals with COPD and (5) review prototype with subject matter experts. During Phase I we will also determine the effectiveness of the interactive education and self-care guide in helping persons with COPD learn about and manage their disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: UW-FHCRC VARIATION DISCOVERY RESOURCE Principal Investigator & Institution: Kruglyak, Leonid; Associate Investigator, Howard Hughes m; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-JUL-2004

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Summary: Inflammation is one of the most basic responses linked to a wide variety of common human disorders including asthma, chronic obstructive pulmonary disease, coronary artery disease and stroke. In this application, the investigators propose a joint program between the University of Washington and the Fred Hutchinson Cancer Research Center (UW-FHCRC) to establish a Variation Discovery Resource (VDR) focused on finding single nucleotide polymorphisms (SNPs) in the genes and pathways underlying inflammatory responses in humans. The goals are: (1) to establish a high throughput variation discovery group that will scan more than 200 of the genes involved in inflammation; (2) to identify the common variable sites, their relative frequencies, and haplotypes in these genes for two populations having different evolutionary historics; (3) to rapidly disseminate this information to the biomedical community via national databases such as dbSNP and Genbank, and by a resource generated website; and (4) to establish a training and education program on human variation analysis that provides on-site training as well as a formalized workshop. Overall, the studies will provide a wealth of new information for testing the important relationships that exist between variations in human DNA sequence, and variations in risk for common human diseases. (End of Abstract) Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: WORKPLACE AEROSOL SAMPLING AT REALISTIC LOW WINDSPEEDS Principal Investigator & Institution: Vincent, James H.; Professor of Industrial Hygiene; Environmental Health Sciences; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2004; Project Start 01-SEP-2004; Project End 31-AUG-2007 Summary: Aerosol samplers remain important through their role in the assessment (and hence control) of workers' exposures to airborne particles. Respiratory ill-health, including asthma and chronic obstructive pulmonary disease, remain major NORA priority areas. The proposed research is a continuation of a body of work carried out under RO1-OH 02984-02 (1994-1998), and then 5 RO1-OH 03687-03 (1998-2002) and 5 RO1 OH 02984-06 (1999-2003), complementing field studies supported from other resources. This new project will contain further laboratory research to develop meaningful aerosol sampling methodology under realistically low windspeed conditions not covered by previous research (0.05 to 0.5 m/s). The specific aims are to: a) develop a novel laboratory-based experimental system by which to evaluate aerosol samplers at the low windspeeds found in most workplaces; (b) use it to evaluate cascade impactor- based aerosol sampling systems that will provide information about the particle size distributions in workers' aerosol exposures; (c) define the efficiency of human inhalation (using a mannequin) at very low windspeed, allowing for the effects of the breathing patterns of the subject and body heat; (d) characterize the performances of a range of candidate personal inhalable aerosol samplers when used under such conditions; and (e) use such performance information to explain the mass biases between different samplers when they are used in realistic laboratory environments (and to relate the conclusions to what is observed in field studies). Earlier work has been influential in the setting of occupational exposure standards and in establishing relevant exposure assessment methods. Yet there remain considerable knowledge gaps. We are still unable to explain the extent to which specific personal samplers reflect actual worker exposure, or to explain differences between workplace exposure assessments using various recommended samplers. The new research will fill these gaps and place occupational aerosol exposure assessment on a still firmer footing.

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

E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “chronic obstructive pulmonary disease” (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 obstructive pulmonary disease in the PubMed Central database: •

Bacterial Infection in Chronic Obstructive Pulmonary Disease in 2000: a State-of-theArt Review. by Sethi S, Murphy TF.; 2001 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=88978

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Detecting chronic obstructive pulmonary disease using peak flow rate: cross sectional survey. by Jackson H, Hubbard R.; 2003 Sep 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=196392

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Detecting patients at a high risk of developing chronic obstructive pulmonary disease in general practice: cross sectional case finding study. by van Schayck CP, Loozen JM, Wagena E, Akkermans RP, Wesseling GJ.; 2002 Jun 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=115215

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Identifying asthma and chronic obstructive pulmonary disease in patients with persistent cough presenting to general practitioners: descriptive study. by Thiadens HA, de Bock GH, Dekker FW, Huysman JA, van Houwelingen JC, Springer MP, Postma DS.; 1998 Apr 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28529

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Measuring health-related quality of life in patients with chronic obstructive pulmonary disease in a routine hospital setting: Feasibility and perceived value. by Bendtsen P, Leijon M, Sofie Sommer A, Kristenson M.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=155632

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Steady-state pharmacokinetics and sputum penetration of lomefloxacin in patients with chronic obstructive pulmonary disease and acute respiratory tract infections. by Kovarik JM, Hoepelman AI, Smit JM, Sips PA, Rozenberg-Arska M, Glerum JH, Verhoef J.; 1992 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=284353

3 4

Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.

With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.

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

A 62-year-old woman with chronic obstructive pulmonary disease. Author(s): Celli BR. Source: Jama : the Journal of the American Medical Association. 2003 November 26; 290(20): 2721-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14645315

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A computer simulation model of the natural history and economic impact of chronic obstructive pulmonary disease. Author(s): Borg S, Ericsson A, Wedzicha J, Gulsvik A, Lundback B, Donaldson GC, Sullivan SD. Source: Value in Health : the Journal of the International Society for Pharmacoeconomics and Outcomes Research. 2004 March-April; 7(2): 153-67. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15164805

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A new unsupported upper limb exercise test for patients with chronic obstructive pulmonary disease. Author(s): Takahashi T, Jenkins SC, Strauss GR, Watson CP, Lake FR. Source: Journal of Cardiopulmonary Rehabilitation. 2003 November-December; 23(6): 430-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14646791

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A randomized controlled trial of the effect of psychotherapy on anxiety and depression in chronic obstructive pulmonary disease. Author(s): de Godoy DV, de Godoy RF. Source: Archives of Physical Medicine and Rehabilitation. 2003 August; 84(8): 1154-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12917854

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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Acute exacerbations in chronic obstructive pulmonary disease: current strategies with pharmacological therapy. Author(s): Hall CS, Kyprianou A, Fein AM. Source: Drugs. 2003; 63(14): 1481-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12834365

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Acute exacerbations of chronic obstructive pulmonary disease. Author(s): Palm KH, Decker WW. Source: Emergency Medicine Clinics of North America. 2003 May; 21(2): 331-52, Viii. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12793617

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Adaptation to disability in chronic obstructive pulmonary disease: neglected relationships to older adults' perceptions of independence. Author(s): Falter LB, Gignac MA, Cott C. Source: Disability and Rehabilitation. 2003 July 22; 25(14): 795-806. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12959360

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Advances in the management of chronic obstructive pulmonary disease. Author(s): Ziedalski TM, Sankaranarayanan V, Chitkara RK. Source: Expert Opinion on Pharmacotherapy. 2003 July; 4(7): 1063-82. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12831334

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Air pollution and hospital admissions for chronic obstructive pulmonary disease in three metropolitan areas in the United States. Author(s): Moolgavkar SH. Source: Inhalation Toxicology. 2000; 12 Suppl 4: 75-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12881887

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Airway inflammation in chronic obstructive pulmonary disease: comparisons with asthma. Author(s): Sutherland ER, Martin RJ. Source: The Journal of Allergy and Clinical Immunology. 2003 November; 112(5): 81927; Quiz 828. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14610463

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Alveolar macrophages from subjects with chronic obstructive pulmonary disease are deficient in their ability to phagocytose apoptotic airway epithelial cells. Author(s): Hodge S, Hodge G, Scicchitano R, Reynolds PN, Holmes M. Source: Immunology and Cell Biology. 2003 August; 81(4): 289-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12848850

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An international survey of chronic obstructive pulmonary disease in young adults according to GOLD stages. Author(s): de Marco R, Accordini S, Cerveri I, Corsico A, Sunyer J, Neukirch F, Kunzli N, Leynaert B, Janson C, Gislason T, Vermeire P, Svanes C, Anto JM, Burney P; European Community Respiratory Health Survey Study Group. Source: Thorax. 2004 February; 59(2): 120-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14760151

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An outreach programme for patients with an exacerbation of chronic obstructive pulmonary disease. Author(s): Murphy NM, Byrne CC, O'Neill SJ, McElvaney NG, Costello RW. Source: Ir Med J. 2003 May; 96(5): 137-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12846274

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Antiinflammatory effects of the phosphodiesterase-4 inhibitor cilomilast (Ariflo) in chronic obstructive pulmonary disease. Author(s): Gamble E, Grootendorst DC, Brightling CE, Troy S, Qiu Y, Zhu J, Parker D, Matin D, Majumdar S, Vignola AM, Kroegel C, Morell F, Hansel TT, Rennard SI, Compton C, Amit O, Tat T, Edelson J, Pavord ID, Rabe KF, Barnes NC, Jeffery PK. Source: American Journal of Respiratory and Critical Care Medicine. 2003 October 15; 168(8): 976-82. Epub 2003 June 19. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12816740

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Anxiety and chronic obstructive pulmonary disease: prevalence, impact, and treatment. Author(s): Brenes GA. Source: Psychosomatic Medicine. 2003 November-December; 65(6): 963-70. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14645773

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Anxiety and depression in patients with chronic obstructive pulmonary disease (COPD). A review. Author(s): Mikkelsen RL, Middelboe T, Pisinger C, Stage KB. Source: Nordic Journal of Psychiatry. 2004; 58(1): 65-70. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14985157

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Arm exercise capacity and dyspnea ratings in subjects with chronic obstructive pulmonary disease. Author(s): McKeough ZJ, Alison JA, Bye PT. Source: Journal of Cardiopulmonary Rehabilitation. 2003 May-June; 23(3): 218-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12782907

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Aspiration of dead space in the management of chronic obstructive pulmonary disease patients with respiratory failure. Author(s): Liu YN, Zhao WG, Xie LX, Cao DS, Chen LA, Zhang JP, Zhang B, Ma YM, Li YZ, Zhang XG, Jia YH. Source: Respiratory Care. 2004 March; 49(3): 257-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14982645

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Associations between periodontal disease and risk for nosocomial bacterial pneumonia and chronic obstructive pulmonary disease. A systematic review. Author(s): Scannapieco FA, Bush RB, Paju S. Source: Ann Periodontol. 2003 December; 8(1): 54-69. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14971248

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Asthma mistaken for chronic obstructive pulmonary disease. Author(s): Bhattarai MD. Source: Lancet. 2003 May 31; 361(9372): 1914-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12788613

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Bacteria and exacerbations of chronic obstructive pulmonary disease. Author(s): Anthonisen NR. Source: The New England Journal of Medicine. 2002 August 15; 347(7): 526-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12181408

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Bacterial infection in chronic obstructive pulmonary disease in 2000: a state-of-the-art review. Author(s): Sethi S, Murphy TF. Source: Clinical Microbiology Reviews. 2001 April; 14(2): 336-63. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11292642

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Baseline oxygen saturation predicts exercise desaturation below prescription threshold in patients with chronic obstructive pulmonary disease. Author(s): Knower MT, Dunagan DP, Adair NE, Chin R Jr. Source: Archives of Internal Medicine. 2001 March 12; 161(5): 732-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11231707

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Benefits and risks of inhaled corticosteroids in chronic obstructive pulmonary disease. Author(s): Bonay M, Bancal C, Crestani B. Source: Drug Safety : an International Journal of Medical Toxicology and Drug Experience. 2002; 25(1): 57-71. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11820912

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Benefits of supplemental oxygen in exercise training in nonhypoxemic chronic obstructive pulmonary disease patients. Author(s): Emtner M, Porszasz J, Burns M, Somfay A, Casaburi R. Source: American Journal of Respiratory and Critical Care Medicine. 2003 November 1; 168(9): 1034-42. Epub 2003 July 17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12869359

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Benzimidazolone activators of chloride secretion: potential therapeutics for cystic fibrosis and chronic obstructive pulmonary disease. Author(s): Singh S, Syme CA, Singh AK, Devor DC, Bridges RJ. Source: The Journal of Pharmacology and Experimental Therapeutics. 2001 February; 296(2): 600-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11160649

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beta-Adrenoceptor-mediated thermogenesis and lipolysis in patients with chronic obstructive pulmonary disease. Author(s): Schiffelers SL, Blaak EE, Baarends EM, Van Baak MA, Saris WH, Wouters EF, Schols AM. Source: American Journal of Physiology. Endocrinology and Metabolism. 2001 February; 280(2): E357-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11158941

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Beta-blocker therapy combined with low-dose pimobendan in patients with idiopathic dilated cardiomyopathy and chronic obstructive pulmonary disease: report on two cases. Author(s): Shiga T, Wakaumi M, Yajima T, Kajimoto K, Matsuda N, Kawana M, Kasanuki H. Source: Cardiovascular Drugs and Therapy / Sponsored by the International Society of Cardiovascular Pharmacotherapy. 2002 May; 16(3): 259-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12374905

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Bilateral lung transplantation and pulmonary artery reconstruction in a patient with chronic obstructive pulmonary disease and a giant pulmonary artery aneurysm. Author(s): Force SD, Lau CL, Moazami N, Trulock EP, Patterson GA. Source: The Journal of Thoracic and Cardiovascular Surgery. 2003 September; 126(3): 864-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14502171

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Bilateral versus single lung transplantation for chronic obstructive pulmonary disease: intermediate-term results. Author(s): Pochettino A, Kotloff RM, Rosengard BR, Arcasoy SM, Blumenthal NP, Kaiser LR, Bavaria JE. Source: The Annals of Thoracic Surgery. 2000 December; 70(6): 1813-8; Discussion 18189. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11156077

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Biopsy neutrophilia, neutrophil chemokine and receptor gene expression in severe exacerbations of chronic obstructive pulmonary disease. Author(s): Qiu Y, Zhu J, Bandi V, Atmar RL, Hattotuwa K, Guntupalli KK, Jeffery PK. Source: American Journal of Respiratory and Critical Care Medicine. 2003 October 15; 168(8): 968-75. Epub 2003 July 11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12857718

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Bone loss in patients with untreated chronic obstructive pulmonary disease is mediated by an increase in bone resorption associated with hypercapnia. Author(s): Dimai HP, Domej W, Leb G, Lau KH. Source: Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research. 2001 November; 16(11): 2132-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11697811

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Bone mineral density in patients with chronic obstructive pulmonary disease treated with budesonide Turbuhaler. Author(s): Johnell O, Pauwels R, Lofdahl CG, Laitinen LA, Postma DS, Pride NB, Ohlsson SV. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 June; 19(6): 1058-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12108857

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Bronchodilator effect of zafirlukast in subjects with chronic obstructive pulmonary disease. Author(s): Nannini LJ Jr, Flores DM. Source: Pulmonary Pharmacology & Therapeutics. 2003; 16(5): 307-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12877822

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Bronchodilator reversibility in Australian adults with chronic obstructive pulmonary disease. Author(s): Reid DW, Soltani A, Johns DP, Bish R, Williams TJ, Burns GP, Walters EH. Source: Internal Medicine Journal. 2003 December; 33(12): 572-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14656230

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Bronchodilator reversibility testing in chronic obstructive pulmonary disease. Author(s): Calverley PM, Burge PS, Spencer S, Anderson JA, Jones PW. Source: Thorax. 2003 August; 58(8): 659-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12885978

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Budesonide/formoterol: in chronic obstructive pulmonary disease. Author(s): Reynolds NA, Perry CM, Keating GM. Source: Drugs. 2004; 64(4): 431-41; Discussion 433-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14969576

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Burden of chronic obstructive pulmonary disease. Author(s): Rossi A, Confalonieri M. Source: Lancet. 2000 December; 356 Suppl: S56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11191515

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Can high resolution computed tomography predict lung function in patients with chronic obstructive pulmonary disease? Author(s): Spiropoulos K, Trakada G, Kalamboka D, Kalogeropoulou C, Petsas T, Efremidis G, Tsiamita M, Trakada A, Dimopoulos I. Source: Lung. 2003; 181(4): 169-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14692557

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Chronic obstructive pulmonary disease and community-based pharmacological care. Author(s): Scullion JE. Source: British Journal of Community Nursing. 2004 March; 9(3): 97-101. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15028994

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Chronic obstructive pulmonary disease and sleep. Author(s): Gay PC. Source: Respiratory Care. 2004 January; 49(1): 39-51; Discussion 51-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14733621

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Chronic obstructive pulmonary disease, pollution, pulmonary vascular disease, transplantation, pleural disease, and lung cancer in AJRCCM 2003. Author(s): Tobin MJ. Source: American Journal of Respiratory and Critical Care Medicine. 2004 January 15; 169(2): 301-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14718243

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Chronic obstructive pulmonary disease. Family physicians' role in management. Author(s): Kaplan A. Source: Can Fam Physician. 2004 May; 50: 750, 752, 754-5. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15171678

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Chronic obstructive pulmonary disease. National clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and secondary care. Author(s): National Collaborating Centre for Chronic Conditions. Source: Thorax. 2004 February; 59 Suppl 1: 1-232. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15041752

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Chronic obstructive pulmonary disease: emerging medical therapies. Author(s): MacIntyre NR. Source: Respiratory Care. 2004 January; 49(1): 64-9; Discussion 69-71. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14733623

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Chronic obstructive pulmonary disease: resource list for healthcare professionals & consumers. Author(s): Frey AL. Source: Natl Netw. 2004 January; 28(3): 16-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15015390

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Chronic obstructive pulmonary disease: the last year of life. Author(s): Hansen-Flaschen J. Source: Respiratory Care. 2004 January; 49(1): 90-7; Discussion 97-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14733625

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Cigarette smoking, periodontal disease: and chronic obstructive pulmonary disease. Author(s): Hyman JJ, Reid BC. Source: J Periodontol. 2004 January; 75(1): 9-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025211

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CLCA1 gene polymorphisms in chronic obstructive pulmonary disease. Author(s): Hegab AE, Sakamoto T, Uchida Y, Nomura A, Ishii Y, Morishima Y, Mochizuki M, Kimura T, Saitoh W, Massoud HH, Massoud HM, Hassanein KM, Sekizawa K. Source: Journal of Medical Genetics. 2004 March; 41(3): E27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14985398

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Clinical relevance of inter-method differences in fat-free mass estimation in chronic obstructive pulmonary disease. Author(s): Kilduff LP, Fuld JP, Neder JA, Pitsiladis YP, Carter R, Stevenson R, Ward SA. Source: Respiration; International Review of Thoracic Diseases. 2003 NovemberDecember; 70(6): 585-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14732788

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Clinical significance of hilar thoracic index and width of right descending branch of pulmonary artery in chronic obstructive pulmonary disease. Author(s): Chhabra SK, De S. Source: Indian J Chest Dis Allied Sci. 2004 April-June; 46(2): 91-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15072323

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Combination therapy for chronic obstructive pulmonary disease: one size fits all? Author(s): Rabe KF. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 December; 22(6): 874-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14680071

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Controlled breathing and dyspnea in patients with chronic obstructive pulmonary disease (COPD). Author(s): Gosselink R. Source: Journal of Rehabilitation Research and Development. 2003 September-October; 40(5 Suppl 2): 25-33. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15074451

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Corticosteroid resistance in chronic obstructive pulmonary disease: inactivation of histone deacetylase. Author(s): Barnes PJ, Ito K, Adcock IM. Source: Lancet. 2004 February 28; 363(9410): 731-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15001333

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Corticosteroids and chronic obstructive pulmonary disease in the nursing home. Author(s): Rich A. Source: Journal of the American Medical Directors Association. 2004 January-February; 5(1): 31-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14706126

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Cost-effectiveness of inhaled corticosteroids for chronic obstructive pulmonary disease according to disease severity. Author(s): Sin DD, Golmohammadi K, Jacobs P. Source: The American Journal of Medicine. 2004 March 1; 116(5): 325-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14984818

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Cytokines and dietary energy restriction in stable chronic obstructive pulmonary disease patients. Author(s): Godoy I, Campana AO, Geraldo RR, Padovani CR, Paiva SA. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 December; 22(6): 920-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14680079

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Delivery of ipratropium and albuterol combination therapy for chronic obstructive pulmonary disease: effectiveness of a two-in-one inhaler versus separate inhalers. Author(s): Chrischilles E, Gilden D, Kubisiak J, Rubenstein L, Shah H. Source: Am J Manag Care. 2002 October; 8(10): 902-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12395958

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Detecting chronic obstructive pulmonary disease using peak flow rate: cross sectional survey. Author(s): Jackson H, Hubbard R. Source: Bmj (Clinical Research Ed.). 2003 September 20; 327(7416): 653-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14500437

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Detection of asthma and chronic obstructive pulmonary disease in primary care. Author(s): van Schayck CP, Chavannes NH. Source: Eur Respir J Suppl. 2003 January; 39: 16S-22S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12572697

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Development of the chronic obstructive pulmonary disease activity rating scale: reliability, validity and factorial structure. Author(s): Morimoto M, Takai K, Nakajima K, Kagawa K. Source: Nursing & Health Sciences. 2003 March; 5(1): 23-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12603718

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Diaphragm length during tidal breathing in patients with chronic obstructive pulmonary disease. Author(s): Gorman RB, McKenzie DK, Pride NB, Tolman JF, Gandevia SC. Source: American Journal of Respiratory and Critical Care Medicine. 2002 December 1; 166(11): 1461-9. Epub 2002 September 11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12406839

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Dietary change, nutrition education and chronic obstructive pulmonary disease. Author(s): Brug J, Schols A, Mesters I. Source: Patient Education and Counseling. 2004 March; 52(3): 249-57. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14998594

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Dietary factors in the pathogenesis of asthma and chronic obstructive pulmonary disease. Author(s): Denny SI, Thompson RL, Margetts BM. Source: Curr Allergy Asthma Rep. 2003 March; 3(2): 130-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12562552

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Differences in airway inflammation in patients with fixed airflow obstruction due to asthma or chronic obstructive pulmonary disease. Author(s): Fabbri LM, Romagnoli M, Corbetta L, Casoni G, Busljetic K, Turato G, Ligabue G, Ciaccia A, Saetta M, Papi A. Source: American Journal of Respiratory and Critical Care Medicine. 2003 February 1; 167(3): 418-24. Epub 2002 November 08. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12426229

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Difficult to wean chronic obstructive pulmonary disease patients: avoid heat and moisture exchangers? Author(s): Hilbert G. Source: Critical Care Medicine. 2003 May; 31(5): 1580-1. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12771638

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Disease of the airways in chronic obstructive pulmonary disease. Author(s): Cosio Piqueras MG, Cosio MG. Source: Eur Respir J Suppl. 2001 December; 34: 41S-49S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12392034

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Disease severity and the effect of fluticasone propionate on chronic obstructive pulmonary disease exacerbations. Author(s): Jones PW, Willits LR, Burge PS, Calverley PM; Inhaled Steroids in Obstructive Lung Disease in Europe study investigators. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 January; 21(1): 68-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12570111

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Disorders of sex hormone status in patients with chronic obstructive pulmonary disease. Author(s): Makarevich AE. Source: Wiad Lek. 2003; 56(3-4): 140-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12923960

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Disturbances in leptin metabolism are related to energy imbalance during acute exacerbations of chronic obstructive pulmonary disease. Author(s): Creutzberg EC, Wouters EF, Vanderhoven-Augustin IM, Dentener MA, Schols AM. Source: American Journal of Respiratory and Critical Care Medicine. 2000 October; 162(4 Pt 1): 1239-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11029324

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Does long-term oxygen therapy reduce hospitalisation in hypoxaemic chronic obstructive pulmonary disease? Author(s): Ringbaek TJ, Viskum K, Lange P. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 July; 20(1): 38-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12166578

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Does oxidative stress alter quadriceps endurance in chronic obstructive pulmonary disease? Author(s): Koechlin C, Couillard A, Simar D, Cristol JP, Bellet H, Hayot M, Prefaut C. Source: American Journal of Respiratory and Critical Care Medicine. 2004 May 1; 169(9): 1022-7. Epub 2004 March 04. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15001462

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Does the inhalation device affect the bronchodilatory dose response curve of salbutamol in asthma and chronic obstructive pulmonary disease patients? Author(s): Broeders ME, Molema J, Hop WC, Vermue NA, Folgering HT. Source: European Journal of Clinical Pharmacology. 2003 September; 59(5-6): 449-55. Epub 2003 August 12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12920494

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Doxapram for ventilatory failure due to exacerbations of chronic obstructive pulmonary disease. Author(s): Greenstone M, Lasserson TJ. Source: Cochrane Database Syst Rev. 2003; (1): Cd000223. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12535393

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Drug treatment for chronic obstructive pulmonary disease. Author(s): Wark P. Source: Idrugs. 2003 September; 6(9): 874-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12964067

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Dual dopamine D2 receptor and beta2-adrenoceptor agonists for the treatment of chronic obstructive pulmonary disease: the pre-clinical rationale. Author(s): Dougall IG, Young A, Ince F, Jackson DM. Source: Respiratory Medicine. 2003 January; 97 Suppl A: S3-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12564606

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Early discharge of people with chronic obstructive pulmonary disease. Author(s): Burton S. Source: Nurs Times. 2004 February 10-16; 100(6): 65-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15000033

Studies

73

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Early mobilization with walking aids following hospital admission with acute exacerbation of chronic obstructive pulmonary disease. Author(s): Yohannes AM, Connolly MJ. Source: Clinical Rehabilitation. 2003 August; 17(5): 465-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12952150

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Economic evaluation of influenza vaccination in Thai chronic obstructive pulmonary disease patients. Author(s): Wongsurakiat P, Lertakyamanee J, Maranetra KN, Jongriratanakul S, Sangkaew S. Source: J Med Assoc Thai. 2003 June; 86(6): 497-508. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12924797

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Effect of exacerbations on quality of life in patients with chronic obstructive pulmonary disease: a 2 year follow up study. Author(s): Miravitlles M, Ferrer M, Pont A, Zalacain R, Alvarez-Sala JL, Masa F, Verea H, Murio C, Ros F, Vidal R; IMPAC Study Group. Source: Thorax. 2004 May; 59(5): 387-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15115864

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Effect of the combination of two bronchodilators on breathlessness in patients with chronic obstructive pulmonary disease. A crossover clinical trial. Author(s): Sansores R, Ramirez-Vanegas A, Reddy C, Mejia-Alfaro R. Source: Archives of Medical Research. 2003 July-August; 34(4): 292-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12957526

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Effects of a comprehensive self-management programme in patients with chronic obstructive pulmonary disease. Author(s): Monninkhof E, van der Valk P, van der Palen J, van Herwaarden C, Zielhuis G. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 November; 22(5): 815-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621090

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Effects of inhaled furosemide on exertional dyspnea in chronic obstructive pulmonary disease. Author(s): Ong KC, Kor AC, Chong WF, Earnest A, Wang YT. Source: American Journal of Respiratory and Critical Care Medicine. 2004 May 1; 169(9): 1028-33. Epub 2004 February 20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14977622

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Efficacy of the novel phosphodiesterase-4 inhibitor BAY 19-8004 on lung function and airway inflammation in asthma and chronic obstructive pulmonary disease (COPD). Author(s): Grootendorst DC, Gauw SA, Benschop N, Sterk PJ, Hiemstra PS, Rabe KF. Source: Pulmonary Pharmacology & Therapeutics. 2003; 16(6): 341-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14580925

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Elevated urinary 8-hydroxydeoxyguanosine, a biomarker of oxidative stress, and lack of association with antioxidant vitamins in chronic obstructive pulmonary disease. Author(s): Igishi T, Hitsuda Y, Kato K, Sako T, Burioka N, Yasuda K, Sano H, Shigeoka Y, Nakanishi H, Shimizu E. Source: Respirology (Carlton, Vic.). 2003 December; 8(4): 455-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14629648

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Endocrinological disturbances in chronic obstructive pulmonary disease. Author(s): Creutzberg EC, Casaburi R. Source: Eur Respir J Suppl. 2003 November; 46: 76S-80S. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621109

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Endothelin-1 levels in the pathophysiology of chronic obstructive pulmonary disease and bronchial asthma. Author(s): Spiropoulos K, Trakada G, Nikolaou E, Prodromakis E, Efremidis G, Pouli A, Koniavitou A. Source: Respiratory Medicine. 2003 August; 97(8): 983-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12924528

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Epidemiology of respiratory viruses in patients hospitalized with near-fatal asthma, acute exacerbations of asthma, or chronic obstructive pulmonary disease. Author(s): Tan WC, Xiang X, Qiu D, Ng TP, Lam SF, Hegele RG. Source: The American Journal of Medicine. 2003 September; 115(4): 272-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12967691

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Erythropoietin response after correction of severe hypoxaemia due to acute respiratory failure in chronic obstructive pulmonary disease patients. Author(s): Pavlisa G, Vrbanic V, Kusec V, Jaksic B. Source: Clinical Science (London, England : 1979). 2004 January; 106(1): 43-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12917010

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Evaluation of arterial endothelin-1 levels, before and during a sleep study, in patients with bronchial asthma and chronic obstructive pulmonary disease. Author(s): Nikolaou E, Trakada G, Prodromakis E, Efremidis G, Pouli A, Koniavitou A, Spiropoulos K. Source: Respiration; International Review of Thoracic Diseases. 2003 NovemberDecember; 70(6): 606-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14732791

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Evaluation of oxygen uptake kinetics and oxygen kinetics of peripheral skeletal muscle during recovery from exercise in patients with chronic obstructive pulmonary disease. Author(s): Okamoto T, Kanazawa H, Hirata K, Yoshikawa J. Source: Clinical Physiology and Functional Imaging. 2003 September; 23(5): 257-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12950322

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Exacerbations of chronic obstructive pulmonary disease. Author(s): Wedzicha JA, Donaldson GC. Source: Respiratory Care. 2003 December; 48(12): 1204-13; Discussion 1213-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14651761

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Exercise training in chronic obstructive pulmonary disease. Author(s): Rochester CL. Source: Journal of Rehabilitation Research and Development. 2003 September-October; 40(5 Suppl 2): 59-80. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15074454

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Factor analysis of laboratory and clinical measurements of dyspnea in patients with chronic obstructive pulmonary disease. Author(s): Nguyen HQ, Altinger J, Carrieri-Kohlman V, Gormley JM, Stulbarg MS. Source: Journal of Pain and Symptom Management. 2003 February; 25(2): 118-27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12590027

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Factor analysis of quality of life, dyspnea, and physiologic variables in patients with chronic obstructive pulmonary disease before and after rehabilitation. Author(s): Fuchs-Climent D, Le Gallais D, Varray A, Desplan J, Cadopi M, Prefaut CG. Source: American Journal of Physical Medicine & Rehabilitation / Association of Academic Physiatrists. 2001 February; 80(2): 113-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11212011

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Factors associated with improvement in breathing capacity during exercise in patients with chronic obstructive pulmonary disease. Author(s): Ong KC, Wang YT. Source: Respirology (Carlton, Vic.). 2003 September; 8(3): 332-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12911827

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Factors contributing to alterations in skeletal muscle and plasma amino acid profiles in patients with chronic obstructive pulmonary disease. Author(s): Engelen MP, Wouters EF, Deutz NE, Menheere PP, Schols AM. Source: The American Journal of Clinical Nutrition. 2000 December; 72(6): 1480-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11101475

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Factors influencing airway inflammation in chronic obstructive pulmonary disease. Author(s): Hill A, Gompertz S, Stockley R. Source: Thorax. 2000 November; 55(11): 970-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11050270

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Factors predicting a hospital stay of over 3 days in patients with acute exacerbation of chronic obstructive pulmonary disease. Author(s): de la Iglesia F, Valino P, Pita S, Ramos V, Pellicer C, Nicolas R, Diz-Lois F. Source: Journal of Internal Medicine. 2002 June; 251(6): 500-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12028505

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Family support and self-care behavior of Chinese chronic obstructive pulmonary disease patients. Author(s): Xiaolian J, Chaiwan S, Panuthai S, Yijuan C, Lei Y, Jiping L. Source: Nursing & Health Sciences. 2002 March-June; 4(1-2): 41-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12084020

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Fatal Aspergillus myocarditis following short-term corticosteroid therapy for chronic obstructive pulmonary disease. Author(s): Carrascosa Porras M, Herreras Martinez R, Corral Mones J, Ares Ares M, Zabaleta Murguiondo M, Ruchel R. Source: Scandinavian Journal of Infectious Diseases. 2002; 34(3): 224-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12035764

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Fatigue in patients with chronic obstructive pulmonary disease. Author(s): Theander K, Unosson M. Source: Journal of Advanced Nursing. 2004 January; 45(2): 172-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14706002

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Following protocol: weaning difficult-to-wean patients with chronic obstructive pulmonary disease. Author(s): Hill NS. Source: American Journal of Respiratory and Critical Care Medicine. 2001 July 15; 164(2): 186-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11463583

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Formoterol as dry powder oral inhalation compared with salbutamol metered-dose inhaler in acute exacerbations of chronic obstructive pulmonary disease. Author(s): Cazzola M, D'Amato M, Califano C, Di Perna F, Calderaro E, Matera MG, D'Amato G. Source: Clinical Therapeutics. 2002 April; 24(4): 595-604. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12017404

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Formoterol in patients with chronic obstructive pulmonary disease: a randomized, controlled, 3-month trial. Author(s): Aalbers R, Ayres J, Backer V, Decramer M, Lier PA, Magyar P, Malolepszy J, Ruffin R, Sybrecht GW. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 May; 19(5): 936-43. Erratum In: Eur Respir J 2002 July; 20(1): 245. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12030736

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Formoterol therapy for chronic obstructive pulmonary disease: a review of the literature. Author(s): Friedman M, Della Cioppa G, Kottakis J. Source: Pharmacotherapy. 2002 September; 22(9): 1129-39. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12222549

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Formoterol: a review of its use in chronic obstructive pulmonary disease. Author(s): Cheer SM, Scott LJ. Source: American Journal of Respiratory Medicine : Drugs, Devices, and Other Interventions. 2002; 1(4): 285-300. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14720051

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Fracture risk associated with inhaled corticosteroid use in chronic obstructive pulmonary disease. Author(s): Lee TA, Weiss KB. Source: American Journal of Respiratory and Critical Care Medicine. 2004 April 1; 169(7): 855-9. Epub 2004 January 07. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14711795

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Function of pulmonary neuronal M(2) muscarinic receptors in stable chronic obstructive pulmonary disease. Author(s): On LS, Boonyongsunchai P, Webb S, Davies L, Calverley PM, Costello RW. Source: American Journal of Respiratory and Critical Care Medicine. 2001 May; 163(6): 1320-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11371395

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Functional evaluation in patients with chronic obstructive pulmonary disease: pulmonary function test versus cardiopulmonary exercise test. Author(s): Fink G, Moshe S, Goshen J, Klainman E, Lebzelter J, Spitzer S, Kramer MR. Source: Journal of Occupational and Environmental Medicine / American College of Occupational and Environmental Medicine. 2002 January; 44(1): 54-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11802466

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Functional involvement of central nervous system in acute exacerbation of chronic obstructive pulmonary disease A preliminary transcranial magnetic stimulation study. Author(s): Clin Evid. 2002 Dec;(8):1530-45 Source: Journal of Neurology. 2002 September; 249(9): 1232-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12603952

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Future research directions in chronic obstructive pulmonary disease. Author(s): Croxton TL, Weinmann GG, Senior RM, Hoidal JR. Source: American Journal of Respiratory and Critical Care Medicine. 2002 March 15; 165(6): 838-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11897653

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Future treatment of chronic obstructive pulmonary disease. Author(s): Di Maria G, Spicuzza L, Mazzarella G. Source: Monaldi Arch Chest Dis. 2002 June-August; 57(3-4): 200-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12619385

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Gaps in the care of patients admitted to hospital with an exacerbation of chronic obstructive pulmonary disease. Author(s): Choi PP, Day A, Etchells E. Source: Cmaj : Canadian Medical Association Journal = Journal De L'association Medicale Canadienne. 2004 April 27; 170(9): 1409-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15111474

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Gender-related differences in severe, early-onset chronic obstructive pulmonary disease. Author(s): Silverman EK, Weiss ST, Drazen JM, Chapman HA, Carey V, Campbell EJ, Denish P, Silverman RA, Celedon JC, Reilly JJ, Ginns LC, Speizer FE. Source: American Journal of Respiratory and Critical Care Medicine. 2000 December; 162(6): 2152-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11112130

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Genetic polymorphisms of matrix metalloproteinases: functional importance in the development of chronic obstructive pulmonary disease? Author(s): Wallace AM, Sandford AJ. Source: American Journal of Pharmacogenomics : Genomics-Related Research in Drug Development and Clinical Practice. 2002; 2(3): 167-75. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12383023

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Genetic risk factors for chronic obstructive pulmonary disease. Author(s): Sandford AJ, Joos L, Pare PD. Source: Current Opinion in Pulmonary Medicine. 2002 March; 8(2): 87-94. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11845002

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Genetic risk factors for chronic obstructive pulmonary disease. Author(s): Sandford AJ, Pare PD. Source: Clinics in Chest Medicine. 2000 December; 21(4): 633-43. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11194775

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Genetic risk factors of chronic obstructive pulmonary disease. Author(s): Joos L, Pare PD, Sandford AJ. Source: Swiss Medical Weekly : Official Journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology. 2002 January 26; 132(3-4): 27-37. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11953903

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Genetic variants of human beta-defensin-1 and chronic obstructive pulmonary disease. Author(s): Matsushita I, Hasegawa K, Nakata K, Yasuda K, Tokunaga K, Keicho N. Source: Biochemical and Biophysical Research Communications. 2002 February 15; 291(1): 17-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11829455

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Genetics of chronic obstructive pulmonary disease. Author(s): Silverman EK. Source: Novartis Found Symp. 2001; 234: 45-58; Discussion 58-64. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11199103

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Genome-wide linkage analysis of bronchodilator responsiveness and postbronchodilator spirometric phenotypes in chronic obstructive pulmonary disease. Author(s): Palmer LJ, Celedon JC, Chapman HA, Speizer FE, Weiss ST, Silverman EK. Source: Human Molecular Genetics. 2003 May 15; 12(10): 1199-210. Erratum In: Hum Mol Genet. 2003 August 15; 12(16): 2085. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12719384

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Genomewide linkage analysis of quantitative spirometric phenotypes in severe earlyonset chronic obstructive pulmonary disease. Author(s): Silverman EK, Palmer LJ, Mosley JD, Barth M, Senter JM, Brown A, Drazen JM, Kwiatkowski DJ, Chapman HA, Campbell EJ, Province MA, Rao DC, Reilly JJ, Ginns LC, Speizer FE, Weiss ST. Source: American Journal of Human Genetics. 2002 May; 70(5): 1229-39. Epub 2002 March 25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11914989

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Genome-wide linkage analysis of severe, early-onset chronic obstructive pulmonary disease: airflow obstruction and chronic bronchitis phenotypes. Author(s): Silverman EK, Mosley JD, Palmer LJ, Barth M, Senter JM, Brown A, Drazen JM, Kwiatkowski DJ, Chapman HA, Campbell EJ, Province MA, Rao DC, Reilly JJ, Ginns LC, Speizer FE, Weiss ST. Source: Human Molecular Genetics. 2002 March 15; 11(6): 623-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11912177

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Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines for chronic obstructive pulmonary disease. Author(s): Gomez FP, Rodriguez-Roisin R. Source: Current Opinion in Pulmonary Medicine. 2002 March; 8(2): 81-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11845001

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Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Author(s): Pauwels RA, Buist AS, Calverley PM, Jenkins CR, Hurd SS; GOLD Scientific Committee. Source: American Journal of Respiratory and Critical Care Medicine. 2001 April; 163(5): 1256-76. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11316667

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Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: National Heart, Lung, and Blood Institute and World Health Organization Global Initiative for Chronic Obstructive Lung Disease (GOLD): executive summary. Author(s): Pauwels RA, Buist AS, Ma P, Jenkins CR, Hurd SS; GOLD Scientific Committee. Source: Respiratory Care. 2001 August; 46(8): 798-825. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11463370

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Granulocyte inflammatory markers and airway infection during acute exacerbation of chronic obstructive pulmonary disease. Author(s): Aaron SD, Angel JB, Lunau M, Wright K, Fex C, Le Saux N, Dales RE. Source: American Journal of Respiratory and Critical Care Medicine. 2001 February; 163(2): 349-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11179105

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Guidelines for management of chronic obstructive pulmonary disease (COPD) in India: a guide for physicians (2003). Author(s): Jindal SK, Gupta D, Aggarwal AN; WHO-Government of India Biennium (2002-2003) Programme. Source: Indian J Chest Dis Allied Sci. 2004 April-June; 46(2): 137-53. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15072332

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Guidelines for the management of chronic obstructive pulmonary disease. Author(s): Buist AS. Source: Respiratory Medicine. 2002 August; 96 Suppl C: S11-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12199486

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Guidelines versus clinical practice in the treatment of chronic obstructive pulmonary disease. Author(s): Miravitlles M. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 July; 20(1): 243-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12166576

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Guidelines versus clinical practice in the treatment of chronic obstructive pulmonary disease. Author(s): Roche N, Lepage T, Bourcereau J, Terrioux P. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2001 December; 18(6): 903-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11829094

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Haemophilus influenzae in acute exacerbations of chronic obstructive pulmonary disease. Author(s): Leanord A, Williams C. Source: International Journal of Antimicrobial Agents. 2002 May; 19(5): 371-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12007844

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Health care utilization in chronic obstructive pulmonary disease. A case-control study in a health maintenance organization. Author(s): Mapel DW, Hurley JS, Frost FJ, Petersen HV, Picchi MA, Coultas DB. Source: Archives of Internal Medicine. 2000 September 25; 160(17): 2653-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10999980

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Health status measurement in chronic obstructive pulmonary disease. Author(s): Jones PW. Source: Thorax. 2001 November; 56(11): 880-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11641515

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Health surveillance for occupational chronic obstructive pulmonary disease. Author(s): Meijer E, Grobbee DE, Heederik DJ. Source: Journal of Occupational and Environmental Medicine / American College of Occupational and Environmental Medicine. 2001 May; 43(5): 444-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11382179

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Health-related quality of life and mortality in male patients with chronic obstructive pulmonary disease. Author(s): Domingo-Salvany A, Lamarca R, Ferrer M, Garcia-Aymerich J, Alonso J, Felez M, Khalaf A, Marrades RM, Monso E, Serra-Batlles J, Anto JM. Source: American Journal of Respiratory and Critical Care Medicine. 2002 September 1; 166(5): 680-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12204865

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Heliox for treatment of exacerbations of chronic obstructive pulmonary disease. Author(s): Rodrigo G, Pollack C, Rodrigo C, Rowe B. Source: Cochrane Database Syst Rev. 2002; (2): Cd003571. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12076487

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Helium/oxygen mixture reduces the work of breathing at the end of the weaning process in patients with severe chronic obstructive pulmonary disease. Author(s): Diehl JL, Mercat A, Guerot E, Aissa F, Teboul JL, Richard C, Labrousse J. Source: Critical Care Medicine. 2003 May; 31(5): 1415-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12771612

Studies

83

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Helium-oxygen reduces work of breathing in mechanically ventilated patients with chronic obstructive pulmonary disease. Author(s): Gainnier M, Arnal JM, Gerbeaux P, Donati S, Papazian L, Sainty JM. Source: Intensive Care Medicine. 2003 October; 29(10): 1666-70. Epub 2003 July 25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12897990

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History of chronic obstructive pulmonary disease (COPD), wheezes, and forced expiratory time (FET)--in evaluating test measures for COPD and for assessing time intervals for performing bedside maneuvers. Author(s): Nardone DA. Source: Journal of General Internal Medicine : Official Journal of the Society for Research and Education in Primary Care Internal Medicine. 2003 January; 18(1): 74; Author Reply 74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12534770

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Home based neuromuscular electrical stimulation as a new rehabilitative strategy for severely disabled patients with chronic obstructive pulmonary disease (COPD). Author(s): Neder JA, Sword D, Ward SA, Mackay E, Cochrane LM, Clark CJ. Source: Thorax. 2002 April; 57(4): 333-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11923552

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Home care by outreach nursing for chronic obstructive pulmonary disease. Author(s): Smith B, Appleton S, Adams R, Southcott A, Ruffin R. Source: Cochrane Database Syst Rev. 2001; (3): Cd000994. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11686972

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Home hospitalisation of exacerbated chronic obstructive pulmonary disease patients. Author(s): Hernandez C, Casas A, Escarrabill J, Alonso J, Puig-Junoy J, Farrero E, Vilagut G, Collvinent B, Rodriguez-Roisin R, Roca J; CHRONIC project. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 January; 21(1): 58-67. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12570110

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Horizontal transfer of the gene encoding outer membrane protein P2 of nontypeable Haemophilus influenzae, in a patient with chronic obstructive pulmonary disease. Author(s): Hiltke TJ, Schiffmacher AT, Dagonese AJ, Sethi S, Murphy TF. Source: The Journal of Infectious Diseases. 2003 July 1; 188(1): 114-7. Epub 2003 June 23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12825179

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Hospital at home for acute exacerbations of chronic obstructive pulmonary disease. Author(s): Ram FS, Wedzicha JA, Wright J, Greenstone M. Source: Cochrane Database Syst Rev. 2003; (4): Cd003573. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14583984

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Hospital at home services for acute exacerbation of chronic obstructive pulmonary disease: a survey of British practice. Author(s): Johnson MK, Flanigan U, Fuld J, Irwin A, Stewart C, Stevenson RD. Source: Health Bull (Edinb). 2001 May; 59(3): 163-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12664756

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Hospital re-admission in patients with acute exacerbation of chronic obstructive pulmonary disease. Author(s): Lau AC, Yam LY, Poon E. Source: Respiratory Medicine. 2001 November; 95(11): 876-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11716201

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Host-pathogen interaction during pneumococcal infection in patients with chronic obstructive pulmonary disease. Author(s): Bogaert D, van der Valk P, Ramdin R, Sluijter M, Monninkhof E, Hendrix R, de Groot R, Hermans PW. Source: Infection and Immunity. 2004 February; 72(2): 818-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14742525

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Human diaphragm remodeling associated with chronic obstructive pulmonary disease: clinical implications. Author(s): Levine S, Nguyen T, Kaiser LR, Rubinstein NA, Maislin G, Gregory C, Rome LC, Dudley GA, Sieck GC, Shrager JB. Source: American Journal of Respiratory and Critical Care Medicine. 2003 September 15; 168(6): 706-13. Epub 2003 July 11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12857719

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Human immune response to outer membrane protein CD of Moraxella catarrhalis in adults with chronic obstructive pulmonary disease. Author(s): Murphy TF, Kirkham C, Liu DF, Sethi S. Source: Infection and Immunity. 2003 March; 71(3): 1288-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12595444

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Hyperhomocysteinemia and changed plasma thiol redox status in chronic obstructive pulmonary disease. Author(s): Andersson A, Ankerst J, Lindgren A, Larsson K, Hultberg B. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2001 March; 39(3): 229-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11350020

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Identification and assessment of chronic obstructive pulmonary disease in the elderly. Author(s): Doherty DE. Source: Journal of the American Medical Directors Association. 2003 SeptemberOctober; 4(5 Suppl): S116-20. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14501807

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Impact of chronic obstructive pulmonary disease on family functioning. Author(s): Kanervisto M, Paavilainen E, Astedt-Kurki P. Source: Heart & Lung : the Journal of Critical Care. 2003 November-December; 32(6): 360-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14652527

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Implementation of British Thoracic Society guidelines for acute exacerbation of chronic obstructive pulmonary disease: impact on quality of life. Author(s): Dheda K, Crawford A, Hagan G, Roberts CM. Source: Postgraduate Medical Journal. 2004 March; 80(941): 169-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15016940

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Importance of chronic obstructive pulmonary disease for prognosis and diagnosis of congestive heart failure in patients with acute myocardial infarction. Author(s): Kjoller E, Kober L, Iversen K, Torp-Pedersen C; Trace Study Group. Source: European Journal of Heart Failure : Journal of the Working Group on Heart Failure of the European Society of Cardiology. 2004 January; 6(1): 71-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15012921

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In vivo evidence of endothelial injury in chronic obstructive pulmonary disease by lung scintigraphic assessment of (123)I-metaiodobenzylguanidine. Author(s): Arao T, Takabatake N, Sata M, Abe S, Shibata Y, Honma T, Takahashi K, Okada A, Takeishi Y, Kubota I. Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 2003 November; 44(11): 1747-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14602855

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Induced sputum CD8+ T-lymphocyte subpopulations in chronic obstructive pulmonary disease. Author(s): Tzanakis N, Chrysofakis G, Tsoumakidou M, Kyriakou D, Tsiligianni J, Bouros D, Siafakas NM. Source: Respiratory Medicine. 2004 January; 98(1): 57-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14959815

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Inflammation 2003-Sixth World Congress. Focus on chronic obstructive pulmonary disease. 2-6 August 2003, Vancouver, Canada. Author(s): Rossi AG. Source: Idrugs. 2003 September; 6(9): 838-40. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14565167

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Inflammatory cell profiles and T-lymphocyte subsets in chronic obstructive pulmonary disease and severe persistent asthma. Author(s): Tsoumakidou M, Tzanakis N, Kyriakou D, Chrysofakis G, Siafakas NM. Source: Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology. 2004 February; 34(2): 234-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14987303

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Influence of lung volume reduction surgery (LVRS) on health related quality of life in patients with chronic obstructive pulmonary disease. Author(s): Goldstein RS, Todd TR, Guyatt G, Keshavjee S, Dolmage TE, van Rooy S, Krip B, Maltais F, LeBlanc P, Pakhale S, Waddell TK. Source: Thorax. 2003 May; 58(5): 405-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12728160

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Inhaled corticosteroids and chronic obstructive pulmonary disease: are we barking up the wrong tracheobronchial tree? Author(s): Epstein PE. Source: Annals of Internal Medicine. 2003 June 17; 138(12): 1001-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12809460

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Inhaled corticosteroids in chronic obstructive pulmonary disease. Author(s): Sutherland ER. Source: Annals of Internal Medicine. 2003 November 18; 139(10): 864; Author Reply 8645. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14623628

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Inhaled corticosteroids in the long-term management of patients with chronic obstructive pulmonary disease. Author(s): Sin DD, Man SF. Source: Drugs & Aging. 2003; 20(12): 867-80. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14565780

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Inhaled corticosteroids reduce the progression of airflow limitation in chronic obstructive pulmonary disease: a meta-analysis. Author(s): Sutherland ER, Allmers H, Ayas NT, Venn AJ, Martin RJ. Source: Thorax. 2003 November; 58(11): 937-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14586043

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Inhaled corticosteroids should not be prescribed to all chronic obstructive pulmonary disease patients. Author(s): Bourbeau J, McIvor A. Source: Can Respir J. 2003 April; 10(3): 148-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12712224

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Inhaled salmeterol/fluticasone propionate combination in chronic obstructive pulmonary disease. Author(s): Lyseng-Williamson KA, Keating GM. Source: American Journal of Respiratory Medicine : Drugs, Devices, and Other Interventions. 2002; 1(4): 273-82; Discussion 283-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14720047

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Introduction: systemic effects in chronic obstructive pulmonary disease. Author(s): Wouters EF. Source: Eur Respir J Suppl. 2003 November; 46: 1S. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621100

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Invasive pulmonary aspergillosis complicating chronic obstructive pulmonary disease in an immunocompetent patient. Author(s): Ali ZA, Ali AA, Tempest ME, Wiselka MJ. Source: Journal of Postgraduate Medicine. 2003 January-March; 49(1): 78-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12865577

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Investigation into the nutritional status, dietary intake and smoking habits of patients with chronic obstructive pulmonary disease. Author(s): Cochrane WJ, Afolabi OA. Source: Journal of Human Nutrition and Dietetics : the Official Journal of the British Dietetic Association. 2004 February; 17(1): 3-11; Quiz 13-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14718026

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Is there a role for systemic corticosteroids in the management of stable chronic obstructive pulmonary disease? Author(s): Wood-Baker R. Source: American Journal of Respiratory Medicine : Drugs, Devices, and Other Interventions. 2003; 2(6): 451-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14719984

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Isolated fatal renal mucormycosis in a patient with chronic obstructive pulmonary disease and tuberculosis. Author(s): Lin CY, Lee SC, Lin CC, Chan SC, Lee CT. Source: Int J Clin Pract. 2003 December; 57(10): 916-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14712898

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JAMA patient page. Chronic obstructive pulmonary disease. Author(s): Parmet S, Lynm C, Glass RM. Source: Jama : the Journal of the American Medical Association. 2003 November 5; 290(17): 2362. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14600198

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Knowledge and practice of medical doctors on chronic obstructive pulmonary disease: a preliminary survey from a state hospital. Author(s): Fauzi AR. Source: Med J Malaysia. 2003 June; 58(2): 205-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14569740

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Legionella spp. in acute exacerbations of chronic obstructive pulmonary disease: what is the evidence? Author(s): Ewig S. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 March; 19(3): 387-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11936511

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Length of ICU stay for chronic obstructive pulmonary disease varies among large community hospitals. Author(s): Keenan SP, Dodek P, Chan K, Hogg RS, Craib KJ, Anis AH, Spinelli JJ. Source: Intensive Care Medicine. 2003 April; 29(4): 590-5. Epub 2003 March 15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12640521

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Length of stay in a hospital emergency room due to asthma and chronic obstructive pulmonary disease: implications for air pollution studies. Author(s): Perez-Hoyos S, Ballester F, Tenias JM, Merelles A, Rivera ML. Source: European Journal of Epidemiology. 2000 May; 16(5): 455-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10997833

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Leptin and TNF-alpha levels in patients with chronic obstructive pulmonary disease and their relationship to nutritional parameters. Author(s): Calikoglu M, Sahin G, Unlu A, Ozturk C, Tamer L, Ercan B, Kanik A, Atik U. Source: Respiration; International Review of Thoracic Diseases. 2004 January-February; 71(1): 45-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14872110

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Limitation to exercise tolerance in chronic obstructive pulmonary disease: look to the muscles of ambulation. Author(s): Casaburi R. Source: American Journal of Respiratory and Critical Care Medicine. 2003 August 15; 168(4): 409-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12912729

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Local and systemic inflammation in patients with chronic obstructive pulmonary disease: soluble tumor necrosis factor receptors are increased in sputum. Author(s): Vernooy JH, Kucukaycan M, Jacobs JA, Chavannes NH, Buurman WA, Dentener MA, Wouters EF. Source: American Journal of Respiratory and Critical Care Medicine. 2002 November 1; 166(9): 1218-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12403691

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Long-acting beta2-agonists for chronic obstructive pulmonary disease patients with poorly reversible airflow limitation. Author(s): Appleton S, Poole P, Smith B, Veale A, Bara A. Source: Cochrane Database Syst Rev. 2002; (3): Cd001104. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12137617

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Long-term effects of inhaled corticosteroids on FEV1 in patients with chronic obstructive pulmonary disease. A meta-analysis. Author(s): Highland KB, Strange C, Heffner JE. Source: Annals of Internal Medicine. 2003 June 17; 138(12): 969-73. Erratum In: Ann Intern Med. 2003 November 18; 139(10): 873. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12809453

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Long-term use of Viozan (sibenadet HCl) in patients with chronic obstructive pulmonary disease: results of a 1-year study. Author(s): Hiller FC, Alderfer V, Goldman M. Source: Respiratory Medicine. 2003 January; 97 Suppl A: S45-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12564610

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Lower respiratory tract infections in chronic obstructive pulmonary disease outpatients with tracheostomy and persistent colonization by P. aeruginosa. Author(s): Lusuardi M, Capelli A, Di Stefano A, Zaccaria S, Balbi B, Donner CF. Source: Respiratory Medicine. 2003 November; 97(11): 1205-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14635975

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Lymphocyte proliferative response to P6 of Haemophilus influenzae is associated with relative protection from exacerbations of chronic obstructive pulmonary disease. Author(s): Abe Y, Murphy TF, Sethi S, Faden HS, Dmochowski J, Harabuchi Y, Thanavala YM. Source: American Journal of Respiratory and Critical Care Medicine. 2002 April 1; 165(7): 967-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11934723

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Maintenance therapy with budesonide and formoterol in chronic obstructive pulmonary disease. Author(s): Calverley PM, Boonsawat W, Cseke Z, Zhong N, Peterson S, Olsson H. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 December; 22(6): 912-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14680078

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Management of chronic obstructive pulmonary disease in the elderly. Author(s): Antonelli Incalzi R. Source: Aging Clin Exp Res. 2004 February; 16(1): 13-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15132286

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Management of chronic obstructive pulmonary disease. Author(s): Ewart RM. Source: Jama : the Journal of the American Medical Association. 2004 March 3; 291(9): 1066; Author Reply 1067. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14996771

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Management of chronic obstructive pulmonary disease. Author(s): Barr RG. Source: Jama : the Journal of the American Medical Association. 2004 March 3; 291(9): 1066-7; Author Reply 1067. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14996770

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Medical management of chronic obstructive pulmonary disease. Author(s): Sciurba FC. Source: Chest Surg Clin N Am. 2003 November; 13(4): 615-29. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14682598

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Methylxanthines for exacerbations of chronic obstructive pulmonary disease: metaanalysis of randomised trials. Author(s): Barr RG, Rowe BH, Camargo CA Jr. Source: Bmj (Clinical Research Ed.). 2003 September 20; 327(7416): 643. Erratum In: Bmj. 2003 October 18; 327(7420): 919. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14500434

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Microalbuminuria in chronic obstructive pulmonary disease. Author(s): Komurcuoglu A, Kalenci S, Kalenci D, Komurcuoglu B, Tibet G. Source: Monaldi Arch Chest Dis. 2003 October-December; 59(4): 269-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15148835

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Mortality after first hospitalization for chronic obstructive pulmonary disease: changes in 1980-1998. Author(s): Saynajakangas O, Lampela P, Koiranen M, Keistinen T. Source: Cent Eur J Public Health. 2004 March; 12(1): 19-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15068201

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Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease. Author(s): Jagoe RT, Engelen MP. Source: Eur Respir J Suppl. 2003 November; 46: 52S-63S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621107

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Myopathological features in skeletal muscle of patients with chronic obstructive pulmonary disease. Author(s): Gosker HR, Kubat B, Schaart G, van der Vusse GJ, Wouters EF, Schols AM. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 August; 22(2): 280-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12952261

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N-acetylcysteine is unlikely to reduce hospitalisation for chronic obstructive pulmonary disease. Author(s): Ernst P, Suissa S. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 November; 22(5): 865; Author Reply 865-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621098

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New developments in the pathogenesis of acute exacerbations of chronic obstructive pulmonary disease. Author(s): Sethi S. Source: Current Opinion in Infectious Diseases. 2004 April; 17(2): 113-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15021050

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New therapies for chronic obstructive pulmonary disease. Author(s): Krishna G, Sankaranarayanan V, Chitkara RK. Source: Expert Opinion on Investigational Drugs. 2004 March; 13(3): 255-67. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15013944

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Noninvasive positive pressure ventilation for respiratory failure caused by exacerbations of chronic obstructive pulmonary disease: a standard of care? Author(s): Hill NS. Source: Critical Care (London, England). 2003 December; 7(6): 400-1. Epub 2003 May 30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14624671

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Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Author(s): Ram FS, Picot J, Lightowler J, Wedzicha JA. Source: Cochrane Database Syst Rev. 2004; (1): Cd004104. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14974057

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Noninvasive positive pressure ventilation using a helmet in patients with acute exacerbation of chronic obstructive pulmonary disease: a feasibility study. Author(s): Antonelli M, Pennisi MA, Pelosi P, Gregoretti C, Squadrone V, Rocco M, Cecchini L, Chiumello D, Severgnini P, Proietti R, Navalesi P, Conti G. Source: Anesthesiology. 2004 January; 100(1): 16-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14695719

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Noninvasive ventilation for chronic obstructive pulmonary disease. Author(s): Hill NS. Source: Respiratory Care. 2004 January; 49(1): 72-87; Discussion 87-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14733624

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Noninvasive ventilation in patients with acute hypercapnic exacerbation of chronic obstructive pulmonary disease who refused endotracheal intubation. Author(s): Chu CM, Chan VL, Wong IW, Leung WS, Lin AW, Cheung KF. Source: Critical Care Medicine. 2004 February; 32(2): 372-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14758150

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Non-pharmacological treatment for chronic obstructive pulmonary disease. Author(s): Clini E, Costi S, Lodi S, Rossi G. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2003 December; 9(12): Ra300-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14646985

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Obtaining evidence for use by healthcare payers on the success of chronic obstructive pulmonary disease management. Author(s): Mapel D, Pearson M. Source: Respiratory Medicine. 2002 August; 96 Suppl C: S23-30. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12199488

Studies

93

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Operating a sustainable disease management program for chronic obstructive pulmonary disease. Author(s): Endicott L, Corsello P, Prinzi M, Tinkelman DG, Schwartz A. Source: Lippincott's Case Management : Managing the Process of Patient Care. 2003 November-December; 8(6): 252-62; Quiz 263-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14646783

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Oral theophylline for chronic obstructive pulmonary disease. Author(s): Ram FS, Jones PW, Castro AA, De Brito JA, Atallah AN, Lacasse Y, Mazzini R, Goldstein R, Cendon S. Source: Cochrane Database Syst Rev. 2002; (4): Cd003902. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12519617

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Osteoporosis in chronic obstructive pulmonary disease. Author(s): Ionescu AA, Schoon E. Source: Eur Respir J Suppl. 2003 November; 46: 64S-75S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621108

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Outcome measures in chronic obstructive pulmonary disease (COPD). Author(s): Dirksen A. Source: Thorax. 2003 December; 58(12): 1007-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14645957

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Outpatient oral prednisone after emergency treatment of chronic obstructive pulmonary disease. Author(s): Aaron SD, Vandemheen KL, Hebert P, Dales R, Stiell IG, Ahuja J, Dickinson G, Brison R, Rowe BH, Dreyer J, Yetisir E, Cass D, Wells G. Source: The New England Journal of Medicine. 2003 June 26; 348(26): 2618-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12826636

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Oxidant metabolism in chronic obstructive pulmonary disease. Author(s): Boots AW, Haenen GR, Bast A. Source: Eur Respir J Suppl. 2003 November; 46: 14S-27S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621103

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Oxidative stress and gene transcription in asthma and chronic obstructive pulmonary disease: antioxidant therapeutic targets. Author(s): Rahman I. Source: Current Drug Targets. Inflammation and Allergy. 2002 September; 1(3): 291-315. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14561194

94

Chronic Obstructive Pulmonary Disease

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Oxygen in the rehabilitation of patients with chronic obstructive pulmonary disease: an old tool revisited. Author(s): Brusasco V, Pellegrino R. Source: American Journal of Respiratory and Critical Care Medicine. 2003 November 1; 168(9): 1021-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14581283

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Oxygen supplementation before or after submaximal exercise in patients with chronic obstructive pulmonary disease. Author(s): Nandi K, Smith AA, Crawford A, MacRae KD, Garrod R, Seed WA, Roberts CM. Source: Thorax. 2003 August; 58(8): 670-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12885981

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Personal exposures to particles and their relationships with personal activities for chronic obstructive pulmonary disease patients living in Boston. Author(s): Rojas-Bracho L, Suh HH, Catalano PJ, Koutrakis P. Source: J Air Waste Manag Assoc. 2004 February; 54(2): 207-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14977322

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Predicting factors contributing to length of stay in hospitalized chronic obstructive pulmonary disease (COPD) patients: the role of the emergency room. Author(s): Diaz-Peromingo JA, Grandes-Ibanez J, Fandino-Orgeira JM, BarcalaVillamarin P, Garrido-Sanjuan JA. Source: Acta Medica (Hradec Kralove). 2004; 47(1): 29-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15168878

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Predicting outcomes in chronic obstructive pulmonary disease. Author(s): Ussetti P, Laporta R. Source: The New England Journal of Medicine. 2004 May 27; 350(22): 2308-10; Author Reply 2308-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15168424

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Predicting outcomes in chronic obstructive pulmonary disease. Author(s): Garcia-Pachon E, Padilla-Nava I. Source: The New England Journal of Medicine. 2004 May 27; 350(22): 2308-10; Author Reply 2308-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15163786

Studies

95

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Predicting outcomes in chronic obstructive pulmonary disease. Author(s): Kostianev SS, Iluchev DH. Source: The New England Journal of Medicine. 2004 May 27; 350(22): 2308-10; Author Reply 2308-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15168426

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Predicting outcomes in chronic obstructive pulmonary disease. Author(s): Sankaranarayanan V, Ziedalski T, Gould MK. Source: The New England Journal of Medicine. 2004 May 27; 350(22): 2308-10; Author Reply 2308-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15168425

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Prospective study of postmenopausal hormone use and newly diagnosed asthma and chronic obstructive pulmonary disease. Author(s): Barr RG, Wentowski CC, Grodstein F, Somers SC, Stampfer MJ, Schwartz J, Speizer FE, Camargo CA Jr. Source: Archives of Internal Medicine. 2004 February 23; 164(4): 379-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14980988

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Pulmonary disease: pneumonia, chronic obstructive pulmonary disease, asthma, and thromboembolic disease. Author(s): de Palo VA. Source: Journal of the American Podiatric Medical Association. 2004 March-April; 94(2): 157-67. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15028793

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Pulmonary mucormycosis in a patient with chronic obstructive pulmonary disease: diagnosis by fine needle aspiration cytology. Author(s): Benekli M, Crane JK, Conti RR, Kremzier JE, Bidani R. Source: The Journal of Thoracic and Cardiovascular Surgery. 2004 February; 127(2): 5889. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14762378

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Pulmonary scintigraphy in chronic obstructive pulmonary disease. Author(s): Cantinho G. Source: Pediatr Pulmonol Suppl. 2004; 26: 238-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15029661

96

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Quadriceps fatigability after single muscle exercise in patients with chronic obstructive pulmonary disease. Author(s): Mador MJ, Deniz O, Aggarwal A, Kufel TJ. Source: American Journal of Respiratory and Critical Care Medicine. 2003 July 1; 168(1): 102-8. Epub 2003 April 10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12689846

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Quadriceps fatigue after cycle exercise in patients with chronic obstructive pulmonary disease. Author(s): Jeffery Mador M, Kufel TJ, Pineda L. Source: American Journal of Respiratory and Critical Care Medicine. 2000 February; 161(2 Pt 1): 447-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10673184

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Quadriceps muscle endurance in patients with chronic obstructive pulmonary disease. Author(s): Van't Hul A, Harlaar J, Gosselink R, Hollander P, Postmus P, Kwakkel G. Source: Muscle & Nerve. 2004 February; 29(2): 267-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14755493

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Quality of life and exercise tolerance in chronic obstructive pulmonary disease: effects of a short and intensive inpatient rehabilitation program. Author(s): Fuchs-Climent D, Le Gallais D, Varray A, Desplan J, Cadopi M, Prefaut C. Source: American Journal of Physical Medicine & Rehabilitation / Association of Academic Physiatrists. 1999 July-August; 78(4): 330-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10418838

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Quality of life and functional parameters in patients with chronic obstructive pulmonary disease (COPD): an update. Author(s): Gigliotti F, Grazzini M, Stendardi L, Romagnoli I, Scano G. Source: Respiratory Medicine. 2002 June; 96(6): 373-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12117034

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Quality of life assessment after patient education in a randomized controlled study on asthma and chronic obstructive pulmonary disease. Author(s): Gallefoss F, Bakke PS, Rsgaard PK. Source: American Journal of Respiratory and Critical Care Medicine. 1999 March; 159(3): 812-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10051255

Studies

97

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Quantitative 15 steps exercise oximetry as a marker of disease severity in patients with chronic obstructive pulmonary disease. Author(s): Kramer MR, Krivoruk V, Lebzelter J, Liani M, Fink G. Source: Isr Med Assoc J. 1999 November; 1(3): 165-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10731326

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Questioning the use of heart rate and dyspnea in the prescription of exercise in subjects with chronic obstructive pulmonary disease. Author(s): Brolin SE, Cecins NM, Jenkins SC. Source: Journal of Cardiopulmonary Rehabilitation. 2003 May-June; 23(3): 228-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12782909

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Reduced mechanical efficiency in chronic obstructive pulmonary disease but normal peak VO2 with small muscle mass exercise. Author(s): Richardson RS, Leek BT, Gavin TP, Haseler LJ, Mudaliar SR, Henry R, Mathieu-Costello O, Wagner PD. Source: American Journal of Respiratory and Critical Care Medicine. 2004 January 1; 169(1): 89-96. Epub 2003 September 18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14500263

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Regional chest wall volumes during exercise in chronic obstructive pulmonary disease. Author(s): Aliverti A, Stevenson N, Dellaca RL, Lo Mauro A, Pedotti A, Calverley PM. Source: Thorax. 2004 March; 59(3): 210-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14985554

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Regular inhaled short acting beta2 agonists for the management of stable chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis. Author(s): Ram FS, Sestini P. Source: Thorax. 2003 July; 58(7): 580-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12832670

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Regulation of TNF-alpha- and IFN-gamma-induced CXCL10 expression: participation of the airway smooth muscle in the pulmonary inflammatory response in chronic obstructive pulmonary disease. Author(s): Hardaker EL, Bacon AM, Carlson K, Roshak AK, Foley JJ, Schmidt DB, Buckley PT, Comegys M, Panettieri RA Jr, Sarau HM, Belmonte KE. Source: The Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology. 2004 January; 18(1): 191-3. Epub 2003 November 03. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14597565

98

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Rehabilitation for patients with chronic obstructive pulmonary disease: meta-analysis of randomized controlled trials. Author(s): Salman GF, Mosier MC, Beasley BW, Calkins DR. Source: Journal of General Internal Medicine : Official Journal of the Society for Research and Education in Primary Care Internal Medicine. 2003 March; 18(3): 213-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12648254

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Relationship between exercise performance and water distribution measured by new bioelectrical impedance analysis in patients with chronic obstructive pulmonary disease. Author(s): Mamoto T, Fujiwara H, Toyama Y, Hirata K, Yoshikawa J, Fujimoto S. Source: Clinical Physiology and Functional Imaging. 2003 July; 23(4): 230-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12914563

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Respiratory failure in chronic obstructive pulmonary disease. Author(s): Calverley PM. Source: Eur Respir J Suppl. 2003 November; 47: 26S-30S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621114

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Respiratory mechanics in morbid obese patients with chronic obstructive pulmonary disease and hypertension during pneumoperitoneum. Author(s): Salihoglu Z, Demiroluk S, Dikmen Y. Source: European Journal of Anaesthesiology. 2003 August; 20(8): 658-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12932069

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Respiratory response to carbon dioxide stimulation during low flow supplemental oxygen therapy in chronic obstructive pulmonary disease. Author(s): Chiang LL, Hung TC, Ho SC, Lin HC, Yu CT, Wang CH, Kuo HP. Source: J Formos Med Assoc. 2002 September; 101(9): 607-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12645187

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Response of whole-body protein and urea turnover to exercise differs between patients with chronic obstructive pulmonary disease with and without emphysema. Author(s): Engelen MP, Deutz NE, Mostert R, Wouters EF, Schols AM. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4): 868-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12663285

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Sharpening the clinical diagnostic borders of chronic obstructive pulmonary disease. Author(s): Jenkins C. Source: Internal Medicine Journal. 2003 December; 33(12): 551-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14656225

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99

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Short- and long-term efficacy of fluticasone propionate in subjects with early signs and symptoms of chronic obstructive pulmonary disease. Results of the DIMCA study. Author(s): van Grunsven P, Schermer T, Akkermans R, Albers M, van den Boom G, van Schayck O, van Herwaarden C, van Weel C. Source: Respiratory Medicine. 2003 December; 97(12): 1303-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14682412

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Shuttle walking test and 6-minute walking test induce a similar cardiorespiratory performance in patients recovering from an acute exacerbation of chronic obstructive pulmonary disease. Author(s): Vagaggini B, Taccola M, Severino S, Marcello M, Antonelli S, Brogi S, De Simone C, Giardina A, Paggiaro PL. Source: Respiration; International Review of Thoracic Diseases. 2003 NovemberDecember; 70(6): 579-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14732787

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Six-minute walking and pulmonary function test outcomes during the early period after lung cancer surgery with special reference to patients with chronic obstructive pulmonary disease. Author(s): Nomori H, Watanabe K, Ohtsuka T, Naruke T, Suemasu K. Source: Jpn J Thorac Cardiovasc Surg. 2004 March; 52(3): 113-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15077844

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Smoking cessation care received by veterans with chronic obstructive pulmonary disease. Author(s): Sherman SE, Lanto AB, Nield M, Yano EM. Source: Journal of Rehabilitation Research and Development. 2003 September-October; 40(5 Suppl 2): 1-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15074449

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Strategies for screening for chronic obstructive pulmonary disease. Author(s): Enright PL, Kaminsky DA. Source: Respiratory Care. 2003 December; 48(12): 1194-201; Discussion 1201-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14651760

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Supplemental oxygen increases arterial stiffness in chronic obstructive pulmonary disease. Author(s): Bartels MN, Jelic S, Basner RC, Ngai P, Gonzalez JM, De Meersman RE. Source: Respiratory Medicine. 2004 January; 98(1): 84-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14959818

100

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Supraventricular tachyarrythmia prophylaxis after coronary artery surgery in chronic obstructive pulmonary disease patients (early amiodarone prophylaxis trial). Author(s): Kuralay E, Cingoz F, Kilic S, Bolcal C, Gunay C, Demirkilic U, Tatar H. Source: European Journal of Cardio-Thoracic Surgery : Official Journal of the European Association for Cardio-Thoracic Surgery. 2004 February; 25(2): 224-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14747117

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Surgical therapies for chronic obstructive pulmonary disease. Author(s): Benditt JO. Source: Respiratory Care. 2004 January; 49(1): 53-61; Discussion 61-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14733622

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Systemic inflammation in chronic obstructive pulmonary disease. Author(s): Oudijk EJ, Lammers JW, Koenderman L. Source: Eur Respir J Suppl. 2003 November; 46: 5S-13S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621102

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Targeting adenosine receptors: novel therapeutic targets in asthma and chronic obstructive pulmonary disease. Author(s): Rorke S, Holgate ST. Source: American Journal of Respiratory Medicine : Drugs, Devices, and Other Interventions. 2002; 1(2): 99-105. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14720064

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The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. Author(s): Celli BR, Cote CG, Marin JM, Casanova C, Montes de Oca M, Mendez RA, Pinto Plata V, Cabral HJ. Source: The New England Journal of Medicine. 2004 March 4; 350(10): 1005-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14999112

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The cost of chronic obstructive pulmonary disease and its effects on managed care. Author(s): Mapel D, Chen JC, George D, Halbert RJ. Source: Manag Care Interface. 2004 April; 17(4): 61-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15108761

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The cost-effectiveness of mini peak expiratory flow as a screening test for chronic obstructive pulmonary disease among the Bangkok elderly. Author(s): Maranetra N, Chuaychoo B, Naruman C, Lertakyamanee J, Dejsomritrutai W, Chierakul N, Nana A, Thamlikitkul W, Suthamsmai T, Saengkaew S, Sreelum W, Aksornin M, Dechapol A, Reungcham C. Source: J Med Assoc Thai. 2003 December; 86(12): 1133-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14971521

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The effect of a minimal contact smoking cessation programme in out-patients with chronic obstructive pulmonary disease: a pre-post-test study. Author(s): Monninkhof E, van der Valk P, van der Palen J, Mulder H, Pieterse M, van Herwaarden C, Zielhuis G. Source: Patient Education and Counseling. 2004 March; 52(3): 231-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14998591

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The most cost-effective screening method for chronic obstructive pulmonary disease among the Bangkok elderly. Author(s): Chuaychoo B, Maranetra N, Naruman C, Dejsomritrutai W, Lertakyamanee J, Chierkul N, Nana A, Thamlikitkul W, Suthamsmai T, Saengkaew S, Sreelum W, Aksornin M, Dechapol A, Sathet W. Source: J Med Assoc Thai. 2003 December; 86(12): 1140-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14971522

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The SCOPE study: health-care consumption related to patients with chronic obstructive pulmonary disease in France. Author(s): Detournay B, Pribil C, Fournier M, Housset B, Huchon G, Huas D, Godard P, Voinet C, Chanal I, Jourdanne C, Durand-Zaleski I; SCOPE Group. Source: Value in Health : the Journal of the International Society for Pharmacoeconomics and Outcomes Research. 2004 March-April; 7(2): 168-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15164806

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Theophylline: mechanism of action and use in asthma and chronic obstructive pulmonary disease. Author(s): Hansel TT, Tennant RC, Tan AJ, Higgins LA, Neighbour H, Erin EM, Barnes PJ. Source: Drugs Today (Barc). 2004 January; 40(1): 55-69. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14988770

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Transforming growth factor-beta1 genotype and susceptibility to chronic obstructive pulmonary disease. Author(s): Wu L, Chau J, Young RP, Pokorny V, Mills GD, Hopkins R, McLean L, Black PN. Source: Thorax. 2004 February; 59(2): 126-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14760152

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Translating new understanding into better care for the patient with chronic obstructive pulmonary disease. Author(s): Pierson DJ. Source: Respiratory Care. 2004 January; 49(1): 99-109. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14733626

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Underdiagnosis of chronic obstructive pulmonary disease in Northern Sweden. Author(s): Lindstrom M, Jonsson E, Larsson K, Lundback B. Source: The International Journal of Tuberculosis and Lung Disease : the Official Journal of the International Union against Tuberculosis and Lung Disease. 2002 January; 6(1): 76-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11931405

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Underdiagnosis of chronic obstructive pulmonary disease: a rationale for spirometry as a screening tool. Author(s): McIvor RA, Tashkin DP. Source: Can Respir J. 2001 May-June; 8(3): 153-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11420591

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University of Cincinnati Dyspnea Questionnaire for Evaluation of Dyspnoea during physical and speech activities in patients with chronic obstructive pulmonary disease: a validation analysis. Author(s): Hodgev V, Kostianev S, Marinov B. Source: Clinical Physiology and Functional Imaging. 2003 September; 23(5): 269-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12950324

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Update on chronic obstructive pulmonary disease. Author(s): Boyle AH, Locke DL. Source: Medsurg Nursing : Official Journal of the Academy of Medical-Surgical Nurses. 2004 February; 13(1): 42-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15029932

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Urban air pollution and chronic obstructive pulmonary disease: a review. Author(s): Sunyer J. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2001 May; 17(5): 1024-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11488305

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Urinary desmosine excretion is inversely correlated with the extent of emphysema in patients with chronic obstructive pulmonary disease. Author(s): Cocci F, Miniati M, Monti S, Cavarra E, Gambelli F, Battolla L, Lucattelli M, Lungarella G. Source: The International Journal of Biochemistry & Cell Biology. 2002 June; 34(6): 594604. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11943590

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Use of heliox in patients with severe exacerbation of chronic obstructive pulmonary disease. Author(s): Gerbeaux P, Gainnier M, Boussuges A, Rakotonirina J, Nelh P, Torro D, Arnal JM, Jean P. Source: Critical Care Medicine. 2001 December; 29(12): 2322-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11801835

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Usefulness of a linear analog scale questionnaire to measure health-related quality of life in elderly patients with chronic obstructive pulmonary disease. Author(s): Katsura H, Yamada K, Kida K. Source: Journal of the American Geriatrics Society. 2003 August; 51(8): 1131-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12890078

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Using economic evaluations to reduce the burden of asthma and chronic obstructive pulmonary disease. Author(s): Sculpher M. Source: Pharmacoeconomics. 2001; 19 Suppl 2: 21-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11700785

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Utilization of health care services by patients with chronic obstructive pulmonary disease. Author(s): O'Brien JA, Ward AJ, Jones MK, McMillan C, Lordan N. Source: Respiratory Medicine. 2003 January; 97 Suppl A: S53-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12564611

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Validation of a chronic obstructive pulmonary disease screening questionnaire for population surveys. Author(s): Mullerova H, Wedzicha J, Soriano JB, Vestbo J. Source: Respiratory Medicine. 2004 January; 98(1): 78-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14959817

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Validation of self-reported chronic obstructive pulmonary disease in a cohort study of nurses. Author(s): Barr RG, Herbstman J, Speizer FE, Camargo CA Jr. Source: American Journal of Epidemiology. 2002 May 15; 155(10): 965-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11994237

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Validity of spirometric testing in a general practice population of patients with chronic obstructive pulmonary disease (COPD). Author(s): Schermer TR, Jacobs JE, Chavannes NH, Hartman J, Folgering HT, Bottema BJ, van Weel C. Source: Thorax. 2003 October; 58(10): 861-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14514938

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Variation in intubation decisions for patients with chronic obstructive pulmonary disease in one critical care network. Author(s): Wildman MJ, O'Dea J, Kostopoulou O, Tindall M, Walia S, Khan Z. Source: Qjm : Monthly Journal of the Association of Physicians. 2003 August; 96(8): 58391. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12897344

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Ventilation of patients with asthma and chronic obstructive pulmonary disease. Author(s): Peigang Y, Marini JJ. Source: Current Opinion in Critical Care. 2002 February; 8(1): 70-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12205409

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Ventilation-perfusion inequality and carbon dioxide sensitivity in hypoxaemic chronic obstructive pulmonary disease (COPD) and effects of 6 months of long-term oxygen treatment (LTOT). Author(s): Sandek K, Bratel T, Hellstrom G, Lagerstrand L. Source: Clinical Physiology (Oxford, England). 2001 September; 21(5): 584-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11576160

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Ventilatory limitations in chronic obstructive pulmonary disease. Author(s): O'Donnell DE. Source: Medicine and Science in Sports and Exercise. 2001 July; 33(7 Suppl): S647-55. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11462073

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Video-assisted lobectomy for a lung cancer patient with chronic obstructive pulmonary disease. Author(s): Koizumi K, Haraguchi S, Hirata T, Hirai K, Mikami I, Fukushima M, Okada D, Yamagishi S, Nakajima Y, Tanaka S. Source: Jpn J Thorac Cardiovasc Surg. 2003 November; 51(11): 569-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14650585

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Viral infection and exacerbations of chronic obstructive pulmonary disease. Author(s): Hogg JC. Source: American Journal of Respiratory and Critical Care Medicine. 2001 November 1; 164(9): 1555-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11719291

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Viral respiratory infections in elderly patients and patients with chronic obstructive pulmonary disease. Author(s): Greenberg SB. Source: The American Journal of Medicine. 2002 April 22; 112 Suppl 6A: 28S-32S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11955457

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Weight loss in chronic obstructive pulmonary disease. Mechanisms and implications. Author(s): Agust AG, Gari PG, Sauleda J, Busquets X. Source: Pulmonary Pharmacology & Therapeutics. 2002; 15(5): 425-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12406664

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What do chronic obstructive pulmonary disease patients die from? A multiple cause coding analysis. Author(s): Hansell AL, Walk JA, Soriano JB. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2003 November; 22(5): 809-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14621089

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What is the "best PEEP" in chronic obstructive pulmonary disease? Author(s): Wrigge H, Putensen C. Source: Intensive Care Medicine. 2000 September; 26(9): 1167-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11089736

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What is the optimal treatment strategy for chronic obstructive pulmonary disease exacerbations? Author(s): Willaert W, Daenen M, Bomans P, Verleden G, Decramer M. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 May; 19(5): 928-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12030735

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Which patients with acute exacerbation of chronic obstructive pulmonary disease benefit from noninvasive positive-pressure ventilation? A systematic review of the literature. Author(s): Keenan SP, Sinuff T, Cook DJ, Hill NS. Source: Annals of Internal Medicine. 2003 June 3; 138(11): 861-70. Review. Summary for Patients In: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12779296

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Which spirometric indices best predict subsequent death from chronic obstructive pulmonary disease? Author(s): Thomason MJ, Strachan DP. Source: Thorax. 2000 September; 55(9): 785-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10950899

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Why are patients with chronic obstructive pulmonary disease at increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic obstructive pulmonary disease. Author(s): Sin DD, Man SF. Source: Circulation. 2003 March 25; 107(11): 1514-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12654609

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Worldwide epidemiology of chronic obstructive pulmonary disease. Author(s): Chen JC, Mannino DM. Source: Current Opinion in Pulmonary Medicine. 1999 March; 5(2): 93-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10813258

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Worldwide guidelines for chronic obstructive pulmonary disease: a comparison of diagnosis and treatment recommendations. Author(s): Iqbal A, Schloss S, George D, Isonaka S. Source: Respirology (Carlton, Vic.). 2002 September; 7(3): 233-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12153689

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Xanthine oxidase is involved in exercise-induced oxidative stress in chronic obstructive pulmonary disease. Author(s): Heunks LM, Vina J, van Herwaarden CL, Folgering HT, Gimeno A, Dekhuijzen PN. Source: The American Journal of Physiology. 1999 December; 277(6 Pt 2): R1697-704. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10600916

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Z and S mutations of the alpha1-antitrypsin gene and the risk of chronic obstructive pulmonary disease. Author(s): Sandford AJ, Weir TD, Spinelli JJ, Pare PD. Source: American Journal of Respiratory Cell and Molecular Biology. 1999 February; 20(2): 287-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9922220

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CHAPTER 2. NUTRITION AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and chronic obstructive pulmonary disease.

Finding Nutrition Studies on Chronic Obstructive Pulmonary Disease 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 obstructive pulmonary disease” (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 obstructive pulmonary disease” (or a synonym): •

Dry powder ipratropium bromide is as safe and effective as metered-dose inhaler formulation: a cumulative dose-response study in chronic obstructive pulmonary disease patients. Author(s): Service de Pneumologie, Hopital de Bois-Guillaume, CHU de Rouen 76031 Rouen Cedex, France. [email protected] Source: Cuvelier, Antoine Muir, Jean Francois Benhamou, Daniel Weitzenblum, Emmanuel Zuck, Pierre Delacenserie, Robert Taytard, Andre Iacono, Philippe RespirCare. 2002 February; 47(2): 159-66 0020-1324

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Enteral feeding in stable chronic obstructive pulmonary disease patients. Author(s): Nutritional Science and Technology Division, Food and Nutrition Research Institute, Department of Science and Technology, University of the Philippines, Manila, Philippines. [email protected] Source: Tanchoco, C C Castro, C A Villadolid, M F Casino, G Rodriguez, M P Roa, C de la Cruz, C M Tangcongco, F Jr Respirology. 2001 March; 6(1): 43-50 1323-7799

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Evidence of muscarinic receptor subtypes in airway smooth muscle of normal volunteers and of chronic obstructive pulmonary disease patients. Author(s): Department of Pharmacology and Toxicology, 1st Faculty of Medicine and Surgery, University of Naples, Italy. Source: Cazzola, M Matera, M G D'Amato, G De Santis, D Maione, S Lisa, M Cenicola, M L Marmo, E Int-J-Clin-Pharmacol-Res. 1989; 9(1): 65-70 0251-1649

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Gas exchange response to naloxone in chronic obstructive pulmonary disease with hypercapnic respiratory failure. Author(s): Department of Medicine, Hospital Clinic, Universitat de Barcelona, Spain. Source: Roca, J Montserrat, J M Rodriguez Roisin, R Guitart, R Torres, A Agusti, A G Wagner, P D Bull-Eur-Physiopathol-Respir. 1987 May-June; 23(3): 249-54 0395-3890

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Induced sputum of patients with chronic obstructive pulmonary disease (COPD) contains adhesion-promoting, therapy-sensitive factors. Author(s): Department of Respiratory Medicine, University of Antwerp, AntwerpenWilrijk, Belgium. [email protected] Source: van Overveld, F J Vermeire, P A De Backer, W A Inflamm-Res. 2000 January; 49(1): 8-13 1023-3830

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Intravenous therapy of chronic obstructive pulmonary disease with sodium glycinate theophylline monitored by a new bed side theophylline assay. Author(s): Universitatsklinik fur Innere Medizin I, Abteilung fur Hamatologie und Hamostaseologie, Vienna, Austria. Source: Knobl, P N Burghuber, O C Acta-Med-Austriaca. 1992; 19(4): 114-7 0303-8173

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Multifocal atrial tachycardia as a prognostic indicator in patients with severe chronic obstructive pulmonary disease requiring mechanical ventilation. Author(s): Department of Chest Medicine, Chang Gung Memorial Hospital, Taipei, Taiwan, R.O.C. Source: Tsai, Y H Lee, C J Lan, R S Lee, C H Changgeng-Yi-Xue-Za-Zhi. 1991 September; 14(3): 163-7

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Nocturnal oxygen saturation and sleep quality in patients with advanced chronic obstructive pulmonary disease during treatment with moderate dose CRtheophylline. Author(s): Department of Pulmonary Medicine, Helsinki University, Finland. Source: Brander, P E Salmi, T Eur-J-Clin-Pharmacol. 1992; 43(2): 125-9 0031-6970

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Role of increased environmental Aspergillus exposure for patients with chronic obstructive pulmonary disease (COPD) treated with corticosteroids in an intensive care unit. Author(s): Institute of Hygiene and Public Health, University of Bonn, Sigmund-FreudStr. 25, D-53105 Bonn, Germany. Source: Kistemann, Thomas Huneburg, HilMarch Exner, Martin Vacata, Vladimir Engelhart, Steffen Int-J-Hyg-Environ-Health. 2002 February; 204(5-6): 347-51 1438-4639

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Treatment of chronic obstructive pulmonary disease and its exacerbations in general practice. EOLO Group. Estudio Observacional de la Limitacion Obstructiva al Flujo aEreo. Author(s): Servei de Pneumologia, Hospital General Universitari Vall d'Hebron, Barcelona, Spain. [email protected] Source: Miravitlles, M Mayordomo, C Artes, M Sanchez Agudo, L Nicolau, F Segu, J L Respir-Med. 1999 March; 93(3): 173-9 0954-6111

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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WebMDHealth: 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 obstructive pulmonary disease; 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 C Source: Healthnotes, Inc.; www.healthnotes.com

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Minerals Carnitine Source: Prima Communications, Inc.www.personalhealthzone.com L-Carnitine Source: Healthnotes, Inc.; www.healthnotes.com Magnesium Source: Healthnotes, Inc.; www.healthnotes.com

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CHAPTER 3. ALTERNATIVE MEDICINE AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to chronic obstructive pulmonary disease. 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 obstructive pulmonary disease 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 obstructive pulmonary disease” (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 obstructive pulmonary disease: •

133Xenon washout patterns during diaphragmatic breathing. Studies in normal subjects and patients with chronic obstructive pulmonary disease. Author(s): Brach BB, Chao RP, Sgroi VL, Minh VD, Ashburn WL, Moser KM. Source: Chest. 1977 June; 71(6): 735-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=862443

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A comparison of autogenic drainage and the active cycle of breathing techniques in patients with chronic obstructive pulmonary diseases. Author(s): Savci S, Ince DI, Arikan H. Source: Journal of Cardiopulmonary Rehabilitation. 2000 January-February; 20(1): 37-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10680096

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A study of the long-term effect of therapy in chronic obstructive pulmonary disease. Author(s): Emirgil C, Sobol BJ, Norman J, Moskowitz E, Goyal P, Wadhwani B. Source: The American Journal of Medicine. 1969 September; 47(3): 367-77. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4897276

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Acute dyspnea as perceived by patients with chronic obstructive pulmonary disease. Author(s): Heinzer MM, Bish C, Detwiler R. Source: Clinical Nursing Research. 2003 February; 12(1): 85-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12583501

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Acute effects of different nutritional supplements on symptoms and functional capacity in patients with chronic obstructive pulmonary disease. Author(s): Vermeeren MA, Wouters EF, Nelissen LH, van Lier A, Hofman Z, Schols AM. Source: The American Journal of Clinical Nutrition. 2001 February; 73(2): 295-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11157327

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Adjunct therapy in chronic obstructive pulmonary disease. Author(s): Lefcoe NM, Paterson NA. Source: The American Journal of Medicine. 1973 March; 54(3): 343-50. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4569964

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An occupational therapy program for the chronic obstructive pulmonary disease patient. Author(s): Berzins GF. Source: Am J Occup Ther. 1970 April; 24(3): 181-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5418047

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Arm training reduces the VO2 and VE cost of unsupported arm exercise and elevation in chronic obstructive pulmonary disease. Author(s): Epstein SK, Celli BR, Martinez FJ, Couser JI, Roa J, Pollock M, Benditt JO. Source: Journal of Cardiopulmonary Rehabilitation. 1997 May-June; 17(3): 171-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9187983

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Arrhythmias in patients with chronic obstructive pulmonary disease. Author(s): Brashear RE. Source: The Medical Clinics of North America. 1984 July; 68(4): 969-81. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6381932

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Athletic training in chronic obstructive pulmonary disease. Author(s): Shayevitz MB, Shayevitz BR.

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Source: Clinics in Sports Medicine. 1986 July; 5(3): 471-91. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3521897 •

Biofeedback training for reduced respiratory rate in chronic obstructive pulmonary disease: a preliminary study. Author(s): Sitzman J, Kamiya J, Johnston J. Source: Nursing Research. 1983 July-August; 32(4): 218-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6553245

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Breathing pattern retraining and exercise in persons with chronic obstructive pulmonary disease. Author(s): Collins EG, Langbein WE, Fehr L, Maloney C. Source: Aacn Clinical Issues. 2001 May; 12(2): 202-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11759548

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Breathing retraining and exercise conditioning in patients with chronic obstructive pulmonary disease (COPD): a physiological approach. Author(s): Gigliotti F, Romagnoli I, Scano G. Source: Respiratory Medicine. 2003 March; 97(3): 197-204. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12645825

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Breathing retraining in chronic obstructive pulmonary disease. Author(s): Breslin EH. Source: Journal of Cardiopulmonary Rehabilitation. 1995 January-February; 15(1): 25-33. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8529084

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Bronchopulmonary hygiene physical therapy in bronchiectasis and chronic obstructive pulmonary disease: a systematic review. Author(s): Jones A, Rowe BH. Source: Heart & Lung : the Journal of Critical Care. 2000 March-April; 29(2): 125-35. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10739489

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Causes and effects of chronic obstructive pulmonary disease. Author(s): Jones A. Source: British Journal of Nursing (Mark Allen Publishing). 2001 July 12-25; 10(13): 84550. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11927884

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Chest physiotherapy for chronic obstructive pulmonary disease. Author(s): Kass I, Rubin H.

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Source: Postgraduate Medicine. 1970 October; 48(4): 145-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5505754 •

Chiropractic management of chronic obstructive pulmonary disease. Author(s): Meyer JJ. Source: Journal of Manipulative and Physiological Therapeutics. 1989 August; 12(4): 314-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2769095

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Chiropractic management of chronic obstructive pulmonary disease. Author(s): Masarsky CS, Weber M. Source: Journal of Manipulative and Physiological Therapeutics. 1988 December; 11(6): 505-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3253396

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Chronic obstructive pulmonary disease (COPD). Author(s): Pope BB. Source: Nursing. 2004 March; 34(3): 56-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15180007

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Chronic obstructive pulmonary disease 8: non-pharmacological management of COPD. Author(s): Morgan MD, Britton JR. Source: Thorax. 2003 May; 58(5): 453-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12728173

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Chronic obstructive pulmonary disease and intake of catechins, flavonols, and flavones: the MORGEN Study. Author(s): Tabak C, Arts IC, Smit HA, Heederik D, Kromhout D. Source: American Journal of Respiratory and Critical Care Medicine. 2001 July 1; 164(1): 61-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11435239

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Chronic obstructive pulmonary disease symptom effects of long-term cumulative exposure to ambient levels of total suspended particulates and sulfur dioxide in California Seventh-Day Adventist residents. Author(s): Euler GL, Abbey DE, Magie AR, Hodgkin JE. Source: Archives of Environmental Health. 1987 July-August; 42(4): 213-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3662608

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Elevation of serum theophylline levels by ipriflavone in a patient with chronic obstructive pulmonary disease. Author(s): Takahashi J, Kawakatsu K, Wakayama T, Sawaoka H. Source: European Journal of Clinical Pharmacology. 1992; 43(2): 207-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1425881

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Randomised controlled trial of transcutaneous electrical muscle stimulation of the lower extremities in patients with chronic obstructive pulmonary disease. Author(s): Bourjeily-Habr G, Rochester CL, Palermo F, Snyder P, Mohsenin V. Source: Thorax. 2002 December; 57(12): 1045-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12454299

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Reliability of a commercially available threshold loading device in healthy subjects and in patients with chronic obstructive pulmonary disease. Author(s): Gosselink R, Wagenaar RC, Decramer M. Source: Thorax. 1996 June; 51(6): 601-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8693441

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Resistive breathing training in patients with chronic obstructive pulmonary disease. Author(s): Belman MJ, Thomas SG, Lewis MI. Source: Chest. 1986 November; 90(5): 662-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3769566

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Resistive breathing training in severe chronic obstructive pulmonary disease. A pilot study. Author(s): Andersen JB, Dragsted L, Kann T, Johansen SH, Nielsen KB, Karbo E, Bentzen L. Source: Scand J Respir Dis. 1979 June; 60(3): 151-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=493905

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Respiratory muscle endurance training in chronic obstructive pulmonary disease: impact on exercise capacity, dyspnea, and quality of life. Author(s): Scherer TA, Spengler CM, Owassapian D, Imhof E, Boutellier U. Source: American Journal of Respiratory and Critical Care Medicine. 2000 November; 162(5): 1709-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11069801

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Respiratory muscle function in patients with chronic obstructive pulmonary disease: its relationship to disability and to respiratory therapy. Author(s): Sharp JT, Danon J, Druz WS, Goldberg NB, Fishman H, Machnach W. Source: Am Rev Respir Dis. 1974 December; 110(6 Pt 2): 154-68. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4613221

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Respiratory muscle training for patients with chronic obstructive pulmonary disease. Author(s): Reid WD, Samrai B. Source: Physical Therapy. 1995 November; 75(11): 996-1005. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7480129

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Reversal of electrocardiogram to normal in chronic obstructive pulmonary disease with emphysema. Author(s): Dines DE, Parkin TW. Source: Archives of Internal Medicine. 1967 December; 120(6): 721-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4228639

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Rib cage dimensions in hyperinflated patients with severe chronic obstructive pulmonary disease. Author(s): Cassart M, Gevenois PA, Estenne M. Source: American Journal of Respiratory and Critical Care Medicine. 1996 September; 154(3 Pt 1): 800-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8810622

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Right ventricular function at rest and during exercise in chronic obstructive pulmonary disease. Author(s): Matthay RA, Arroliga AC, Wiedemann HP, Schulman DS, Mahler DA. Source: Chest. 1992 May; 101(5 Suppl): 255S-262S. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1576846

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Strategies to forestall morbidity and mortality in chronic obstructive pulmonary disease. Author(s): Petty TL. Source: Med Sect Proc. 1983; : 67-78. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6379640

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Targeted inspiratory muscle training improves respiratory muscle function and reduces dyspnea in patients with chronic obstructive pulmonary disease. Author(s): Harver A, Mahler DA, Daubenspeck JA. Source: Annals of Internal Medicine. 1989 July 15; 111(2): 117-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2742247

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Targeted resistive ventilatory muscle training in chronic obstructive pulmonary disease. Author(s): Belman MJ, Shadmehr R. Source: Journal of Applied Physiology (Bethesda, Md. : 1985). 1988 December; 65(6): 2726-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3215873

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The chronic obstructive pulmonary disease exacerbation. Author(s): Sherk PA, Grossman RF. Source: Clinics in Chest Medicine. 2000 December; 21(4): 705-21. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11194781

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The effect of postrehabilitation programmes among individuals with chronic obstructive pulmonary disease. Author(s): Brooks D, Krip B, Mangovski-Alzamora S, Goldstein RS. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2002 July; 20(1): 20-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12166571

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The effect of the pulsatile electromagnetic field in patients suffering from chronic obstructive pulmonary disease and bronchial asthma. Author(s): Sadlonova J, Korpas J, Vrabec M, Salat D, Buchancova J, Kudlicka J. Source: Bratisl Lek Listy. 2002; 103(7-8): 260-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12518999

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The respiratory muscles in chronic obstructive pulmonary disease (COPD). Author(s): Rochester DF, Arora NS, Braun NM, Goldberg SK. Source: Bull Eur Physiopathol Respir. 1979 September-October; 15(5): 951-75. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=389331

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Therapeutic exercise in patients with chronic obstructive pulmonary disease. Author(s): Weg JG. Source: Cardiovasc Clin. 1985; 15(2): 261-75. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3912052

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Thymostimulin administration modulates polymorph metabolic pathway in patients with chronic obstructive pulmonary disease. Author(s): Tortorella C, Ottolenghi A, Moretti AM, Jirillo E, Antonaci S. Source: Immunopharmacology and Immunotoxicology. 1992; 14(3): 421-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1325490

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Training in the rehabilitation of pulmonary patients with chronic obstructive pulmonary disease. Author(s): Celli BR. Source: Monaldi Arch Chest Dis. 1998 August; 53(4): 438-49. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9828601

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Treating dyspnea in a patient with advanced chronic obstructive pulmonary disease. Author(s): Runo JR, Ely EW. Source: The Western Journal of Medicine. 2001 September; 175(3): 197-201. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11527853

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Voluntary regularization method of the respiratory act applied to chronic obstructive pulmonary disease. Author(s): Brigo B, Campacci R, Avesani R, Zambito A, Schinina V. Source: International Journal of Rehabilitation Research. Internationale Zeitschrift Fur Rehabilitationsforschung. Revue Internationale De Recherches De Readaptation. 1983 September; 6(3): 283-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6642817

Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •

Alternative Medicine Foundation, Inc.: http://www.herbmed.org/

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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats

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Chinese Medicine: http://www.newcenturynutrition.com/

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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html

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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm

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Google: http://directory.google.com/Top/Health/Alternative/

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Healthnotes: http://www.healthnotes.com/

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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine

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Open Directory Project: http://dmoz.org/Health/Alternative/

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HealthGate: http://www.tnp.com/

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WebMDHealth: http://my.webmd.com/drugs_and_herbs

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/

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The following is a specific Web list relating to chronic obstructive pulmonary disease; 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 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 Osteoporosis Source: Prima Communications, Inc.www.personalhealthzone.com Pulmonary Hypertension Source: Integrative Medicine Communications; www.drkoop.com

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Alternative Therapy Ionized Air (negative Ions) Source: Healthnotes, Inc.; www.healthnotes.com

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Herbs and Supplements Amino Acids Overview Source: Healthnotes, Inc.; www.healthnotes.com Coenzyme Q10 Source: Healthnotes, Inc.; www.healthnotes.com Docosahexaenoic Acid Source: Healthnotes, Inc.; www.healthnotes.com Elecampane Alternative names: Inula helenium Source: Healthnotes, Inc.; www.healthnotes.com Eucalyptus Alternative names: Eucalyptus globulus Source: Healthnotes, Inc.; www.healthnotes.com Ipratropium Bromide Source: Healthnotes, Inc.; www.healthnotes.com Ipriflavone Source: Prima Communications, Inc.www.personalhealthzone.com

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Ivy Leaf Alternative names: Hedera helix Source: Healthnotes, Inc.; www.healthnotes.com Lobelia Alternative names: Lobelia inflata Source: Healthnotes, Inc.; www.healthnotes.com Mullein Alternative names: Verbascum thapsus Source: Healthnotes, Inc.; www.healthnotes.com N-Acetyl Cysteine Source: Healthnotes, Inc.; www.healthnotes.com Theophylline/Aminophylline Source: Healthnotes, Inc.; www.healthnotes.com

General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.

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CHAPTER 4. DISSERTATIONS ON CHRONIC OBSTRUCTIVE PULMONARY DISEASE Overview In this chapter, we will give you a bibliography on recent dissertations relating to chronic obstructive pulmonary disease. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “chronic obstructive pulmonary disease” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on chronic obstructive pulmonary disease, we have not necessarily excluded non-medical dissertations in this bibliography.

Dissertations on Chronic Obstructive Pulmonary Disease ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to chronic obstructive pulmonary disease. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •

A COMPARISON OF SMOKING PATTERNS BETWEEN COUNSELINGASSISTED AND UNASSISTED HEAVY SMOKERS WITH EARLY CHRONIC OBSTRUCTIVE PULMONARY DISEASE (SMOKING CESSATION, PULMONARY DISEASE) by GONZALES, DAVID H., PHD from OREGON STATE UNIVERSITY, 1991, 157 pages http://wwwlib.umi.com/dissertations/fullcit/9220494

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AN APPLICATION OF LOCUS-OF-CONTROL THEORY TO CHRONIC OBSTRUCTIVE PULMONARY DISEASE EDUCATION by NEISH, CHRISTINE MARGARET GERKEN, PHD from THE CLAREMONT GRADUATE UNIVERSITY, 1988, 527 pages http://wwwlib.umi.com/dissertations/fullcit/8820112

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Effect of strength training on functional fitness in older chronic obstructive pulmonary disease patients by Alexander, Jeffrey Lester, PhD from ARIZONA STATE UNIVERSITY, 2003, 46 pages http://wwwlib.umi.com/dissertations/fullcit/3084699

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Epidemiology of asthma and chronic obstructive pulmonary disease in the Nurses' Health Study by Barr, R. Graham, DPH from HARVARD UNIVERSITY, 2003 http://wwwlib.umi.com/dissertations/fullcit/f579793

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Health-related quality of life, functional status, and exercise tolerance of adults with chronic obstructive pulmonary disease following three treatment situations: Exercise alone, exercise with a lecture series, and exercise with activity training by Migliore, Anna, PhD from NEW YORK UNIVERSITY, 2003, 255 pages http://wwwlib.umi.com/dissertations/fullcit/3071163

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Outcomes in chronic obstructive pulmonary disease (COPD) patients cared for in physician pulmonary practices with and without advanced practice nurses (APNS) by Neisser-Frankson, Cheryl Lynn, PhD from UNIVERSITY OF PENNSYLVANIA, 2003, 309 pages http://wwwlib.umi.com/dissertations/fullcit/3095925

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THE EFFECTS OF AEROBIC AND VENTILATORY MUSCLE TRAINING ON PULMONARY FUNCTION AND SUBMAXIMAL WORK PERFORMANCE IN SUBJECTS WITH PRE-CLINICAL CHRONIC OBSTRUCTIVE PULMONARY DISEASE (LUNG DISEASE) by KRAMER, PETER GEORGE, EDD from THE UNIVERSITY OF TENNESSEE, 1984, 101 pages http://wwwlib.umi.com/dissertations/fullcit/8421393

Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.

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CHAPTER

5.

BOOKS ON CHRONIC PULMONARY DISEASE

OBSTRUCTIVE

Overview This chapter provides bibliographic book references relating to chronic obstructive pulmonary disease. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on chronic obstructive pulmonary disease 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 obstructive pulmonary disease” (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 obstructive pulmonary disease: •

Cigars: Health Effects and Trends Source: Bethesda, MD: National Cancer Institute (NCI), National Institutes of Health (NIH). February 1998. 348 p. Contact: Available from National Cancer Institute (NCI). Publications Ordering Service, P.O. Box 24128, Baltimore, MD 21227. Voice (800) 422-6237. TTY (800) 332-8615. Fax (301) 330-7968. Website: rex.nci.nih.gov. PRICE: Single copy free. NIH Publication Number 98-4302. Summary: The recent increase in cigar consumption began in 1993 and was dismissed by many in public health as a passing fad that would quickly dissipate. Recently released data from the U.S. Department of Agriculture (USDA) suggests that the upward trend in cigar use might not be as temporary as some had predicted. This

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monograph from the National Cancer Institute addresses the questions that arise from this dramatic surge in tobacco use. Eight chapters cover an overview of cigar smoking, trends in cigar consumption and smoking prevalence, chemistry and toxicology, the disease consequences of cigar smoking, indoor air pollution from cigar smoke, pharmacology and abuse potential of cigars, marketing and promotion of cigars, and policies regulating cigars. There is sufficient evidence to conclude that a causal relationship exists between regular cigar use and cancers of the lung, larynx, oral cavity, and esophagus. Heavy cigar smoking, particularly for those who inhale, causes an increased risk of coronary heart disease and chronic obstructive pulmonary disease. There is also suggestive evidence for a relationship between cigar smoking and cancer of the pancreas, but the evidence is insufficient at this time to draw a causal inference. Each chapter concludes with references. •

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), 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 obstructive pulmonary disease” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “chronic obstructive pulmonary disease” (or a synonym) in their titles. The following is indicative of

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the results you might find when searching for “chronic obstructive pulmonary disease” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •

21st Century Complete Medical Guide to Chronic Obstructive Pulmonary Disease (COPD) and Emphysema, Authoritative Government Documents, Clinical References, and Practical Information for Patients and Physicians (CD-ROM) by PM Medical Health News; ISBN: 1592487297; http://www.amazon.com/exec/obidos/ASIN/1592487297/icongroupinterna

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Acute Exacerbations of Chronic Obstructive Pulmonary Disease (Lung Biology in Health and Disease) by N. M. Siafakas, et al; ISBN: 0824741285; http://www.amazon.com/exec/obidos/ASIN/0824741285/icongroupinterna

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Asthma and Chronic Obstructive Pulmonary Disease (COPD) by Tim Peters; ISBN: 1879874490; http://www.amazon.com/exec/obidos/ASIN/1879874490/icongroupinterna

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Diseases Explained: Chronic Obstructive Pulmonary Disease Wall Chart by LexiComp; ISBN: 1930598335; http://www.amazon.com/exec/obidos/ASIN/1930598335/icongroupinterna

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Lung-volume reduction surgery for end-stage chronic obstructive pulmonary disease (SuDoc HE 20.6512/7:996/10) by Thomas V. Holohan; ISBN: B00010VY5Y; http://www.amazon.com/exec/obidos/ASIN/B00010VY5Y/icongroupinterna

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Management of Acute Exacerbations of Chronic Obstructive Pulmonary Disease (Evidence report/technology assessment) by Douglas C. McCrory (Other Contributor); ISBN: 1587630508; http://www.amazon.com/exec/obidos/ASIN/1587630508/icongroupinterna

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Out-Patient Rehabilitation in Chronic Obstructive Pulmonary Disease (Acta Biomedica Lovaniensia 203) by Thierry Troosters; ISBN: 906186982X; http://www.amazon.com/exec/obidos/ASIN/906186982X/icongroupinterna

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Respiratory Muscles in Chronic Obstructive Pulmonary Disease (Current Topics in Rehabilitation) by A. Grassino, et al; ISBN: 0387195092; http://www.amazon.com/exec/obidos/ASIN/0387195092/icongroupinterna

Chapters on Chronic Obstructive Pulmonary Disease In order to find chapters that specifically relate to chronic obstructive pulmonary disease, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and chronic obstructive pulmonary disease 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 obstructive pulmonary disease” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on chronic obstructive pulmonary disease: •

Pulmonary Disease Source: in Little, J.W., et al. Dental Management of the Medically Compromised Patient. 6th ed. St. Louis, MO: Elsevier Science. 2002. p. 125-146.

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Contact: Available from Elsevier Science. Customer Service Department, 11830 Westline Industrial Drive, St. Louis, MO 63146 (800) 545-2522. Fax (800) 535-9935. Email: [email protected]. Website: www.elsevierhealth.com. PRICE: $56.95. ISBN: 323011713. Summary: Many types of pulmonary (lung) disorders may influence routine dental care and require special management of the patient. The more commonly encountered pulmonary diseases include chronic obstructive pulmonary disease (COPD), asthma, and tuberculosis. This chapter on pulmonary disease is from a resource text that helps dental professionals work with medically compromised patients. For each condition, the chapter provides a brief overview of the basic disease process, epidemiology, pathophysiology, signs and symptoms, laboratory findings, currently-accepted medical therapy, prevention of medical complications, and recommendations for specific dental treatment planning. 14 figures. 2 tables. 79 references. •

Aging Voice: Normal Changes or Disease? Source: in Linville, S.E. Vocal Aging. San Diego, CA: Singular Publishing Group. 2001. p. 203-216. Contact: Available from Thomson Learning Group. P.O. Box 6904, Florence, KY 41022. (800) 842-3636. Fax (606) 647-5963. Website: www.singpub.com. PRICE: $43.95 plus shipping and handling. ISBN: 1565939026. Summary: Normal elderly speakers vary considerably across a wide range of measures involving breathing function, phonatory characteristics, and articulatory precision. This variability results from differences among people in the rate and extent of physiological aging, as well as differences in variables such as lifestyle, genetics, and environmental factors. This chapter on the aging voice is from a text devoted to the properties of the aging voice, with emphasis on diagnosis and treatment of voice disorders in elderly patients. In this chapter, the author explores issues involved in differentiating normal laryngeal aging from pathological states. Topics include glottal gap, vocal fold atrophy, variable mucosal wave patterns, chronic obstructive pulmonary disease, and diagnostic tests. Pathological conditions producing laryngeal dysfunction are examined relative to normal changes in laryngeal function with aging. Respiratory disorders that occur frequently in elderly patients are also contrasted with normal aging. The author describes environmental factors that can influence the aged voice, including physical fitness and cigarette smoking. 43 references.

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Management of the Medically Compromised Patient Source: in Kwon, P.H. and Laskin, D.M. Clinician's Manual of Oral and Maxillofacial Surgery. Chicago, IL: Quintessence Publishing Co, Inc. 2001. p. 227-262. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail: [email protected]. Website: www.quintpub.com. PRICE: $58.00 plus shipping and handling. ISBN: 0867153962. Summary: This chapter on management of the medically compromised patient is from a spiral-bound handbook that offers quick reference information to the oral and maxillofacial surgeon. The outline and chart-based format is designed to offer quick access to information that may be needed in situations that do not allow time for a leisurely perusal of textbooks and journals. The chapter covers cardiac disease, including coronary artery disease, congestive heart failure, dysrhythmias and

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conduction disturbances, valvular heart disease, prosthetic valves, and congenital heart disease; respiratory disease, including obstructive lung disease (chronic obstructive pulmonary disease and asthma) and infiltrative diseases of the lung; renal (kidney) disease, including the four different stages of chronic renal failure and acute renal failure; hypertension (high blood pressure); blood disorders, including anemia, erythrocytosis, leukocyte disorders, platelet disorders, coagulation disorders, and causes of bleeding disorders; endocrine diseases, notably diabetes mellitus; adrenal disease; thyroid disease; pituitary disease; neurological diseases, including cerebrovascular disease (including stroke), seizure disorders, and neuromuscular diseases; liver disease; autoimmune diseases; and the immunocompromised patient. For each condition, the chapter discusses preoperative evaluation, history, physical examination, laboratory examinations, preoperative therapy, and perioperative monitoring. 3 tables. •

Patients with Common Systemic Diseases Source: in Newman, M.G. and van Winkelhoff, A.J., eds. Antibiotic and Antimicrobial Use in Dental Practice. 2nd ed. Chicago, IL: Quintessence Publishing Co, Inc. 2001. p. 243-255. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail: [email protected]. Website: www.quintpub.com. PRICE: $32.00 plus shipping and handling. ISBN: 0867153970. Summary: This chapter on the use of antibiotics in patients with common systemic diseases is from a textbook that integrates basic facts and principles of antibiotic therapy with recently emerged concepts of care in dentistry. The authors note that patients being treated for chronic systemic disorders are often on multiple drug regimens; it is therefore essential that clinicians obtain a complete medical history and consider possible drug interactions before prescribing any medications. Because dental procedures may produce considerable bacteremia, it is particularly important that dentists have an understanding of a patient's underlying pathophysiology before making appropriate treatment planning decisions. Clinicians also should consult with the physicians of patients at increased risk of infection before prescribing an antibiotic regimen. Topics covered include diabetes mellitus, bleeding and coagulation disorders, anemias, white blood cell disorders (leukemia, lymphoma, multiple myeloma), rheumatoid arthritis, systemic lupus erythematosus, Sjogren syndrome, renal (kidney) disease, liver diseases, cardiovascular diseases, chronic obstructive pulmonary disease, asthma, and tuberculosis. Important principles, key facts, and clinical insights are highlighted and the chapter concludes with a list of references. 1 figure. 2 tables. 33 references.

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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

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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. •

Patients' Experiences with Their Disease: Learning from the Differences and Sharing the Common Problems Source: in Assal, J., Golay, A., and Visser, A.P., eds. New Trends in Patient Education: A Trans-Cultural and Inter-Disease Approach. Amsterdam, The Netherlands: Elsevier Science B.V. 1995. p. 301-312. Contact: Available from Elsevier Science. Regional Sales Office, Customer Support Department, 655 Avenue of the Americas, New York, NY 10010. (212) 633-3730. Fax (212) 633-3680. E-mail: [email protected]. PRICE: $209.50. ISBN: 0444822348. Summary: This chapter, from the proceedings of an international patient education conference, presents patients' experiences and views about the psychological, professional, family, cognitive, and financial costs of several chronic diseases. Diseases covered include arterial hypertension, autonomous dialysis, back pain, bronchial asthma, chronic obstructive pulmonary disease, colostomy, diabetes mellitus, epilepsy, laryngectomy, and Parkinson's disease. (AA-M).

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CHAPTER 6. MULTIMEDIA ON CHRONIC OBSTRUCTIVE PULMONARY DISEASE Overview In this chapter, we show you how to keep current on multimedia sources of information on chronic obstructive pulmonary disease. 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 obstructive pulmonary disease is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “chronic obstructive pulmonary disease” 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 obstructive pulmonary disease” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on chronic obstructive pulmonary disease: •

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

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genetic disorder that affects infants, children, and adults. It is the most common 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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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 Institute8: •

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

•

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

•

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

•

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

•

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

•

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

•

National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375

•

National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/

8

These publications are typically written by one or more of the various NIH Institutes.

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•

National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm

•

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

•

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

•

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

•

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

•

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

•

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

•

Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm

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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.9 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:10 •

Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html

•

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

•

NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html

•

Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/

•

Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html

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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

9

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). 10 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 Gateway11 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.12 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “chronic obstructive pulmonary disease” (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 20323 135 839 81 200 21578

HSTAT13 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.14 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.15 Simply search by “chronic obstructive pulmonary disease” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

11

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

12

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). 13 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 14 15

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 Biologists16 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.17 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.18 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/.

16 Adapted 17

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. 18 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 obstructive pulmonary disease can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.

Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to chronic obstructive pulmonary disease. 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 obstructive pulmonary disease. 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 obstructive pulmonary disease”:

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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 Heart Diseases http://www.nlm.nih.gov/medlineplus/heartdiseases.html Laboratory Tests http://www.nlm.nih.gov/medlineplus/laboratorytests.html Pulmonary Fibrosis http://www.nlm.nih.gov/medlineplus/pulmonaryfibrosis.html Respiratory Diseases http://www.nlm.nih.gov/medlineplus/respiratorydiseases.html

Within the health topic page dedicated to chronic obstructive pulmonary disease, 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 Bronchoscopy: Pulmonary Branch Protocols Source: National Institutes of Health, Clinical Center http://www.cc.nih.gov/ccc/patient_education/pepubs/bronchoscopy.pdf Lung - Diagnosis of COPD and Asthma Source: National Lung Health Education Program http://www.nlhep.org/lung_diagnosis.html Recognizing Signs and Symptoms of Chronic Obstructive Pulmonary Disease Source: National Jewish Medical and Research Center http://www.nationaljewish.org/medfacts/recognizing_copd.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

•

Treatment Current Treatment for Emphysema/COPD Source: National Jewish Medical and Research Center http://www.nationaljewish.org/medfacts/treatment_copd.html

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Lung - Treatment of COPD and Asthma Source: National Lung Health Education Program http://www.nlhep.org/lung_trtmnt.html •

Nutrition Nutritional Guidelines for People with COPD Source: Cleveland Clinic Foundation http://www.clevelandclinic.org/health/healthinfo/docs/2400/2411.asp?index=9451

•

Coping Around the Clock with COPD Source: American Lung Association http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35015

•

From the National Institutes of Health Chronic Obstructive Pulmonary Disease Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/lung/other/copd_fact.pdf What Is Chronic Obstructive Pulmonary Disease (COPD)? Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/dci/Diseases/Copd/Copd_WhatIs.html

•

Latest News Early Care Helps When Lung Disease Flares Up Source: 06/22/2004, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_18503 .html Flu Vaccination Helpful for Lung-disease Patients Source: 06/15/2004, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_18385 .html Simple Test Can Detect Lung Diseases Source: 06/25/2004, United Press International http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_18589 .html

•

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 Inhaled Steroids for Chronic Obstructive Lung Disease Source: American College of Physicians http://www.annals.org/cgi/content/full/138/12/I-46 Noninvasive Positive-Pressure Ventilation for Severe Worsening of Chronic Obstructive Pulmonary Disease Source: American College of Physicians http://www.annals.org/cgi/content/full/138/11/I-27

•

Statistics FASTATS: Chronic Obstructive Pulmonary Disease (COPD) Source: National Center for Health Statistics http://www.cdc.gov/nchs/fastats/copd.htm

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 obstructive pulmonary disease. 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: •

Year 200 dietary guidelines: the case for fruits and vegetables first Source: Produce for Better Health Foundation. Contact: Produce for Better Health Foundation, 5301 Limestone Road, Suite 101, Wilmington, DE 19808-1249. (302) 235-ADAY. Summary: This booklet reviews the ever-growing evidence of the unique health benefits derived from eating fruits and vegetables. Researchers continue to find a strong link between increased fruit and vegetable consumption and the decreased risk of chronic diseases such as cancer, heart disease, and stroke. Evidence is also emerging about the positive role of fruit and vegetable consumption and a reduced incidence of cataracts, diverticulosis, hypertension, and chronic obstructive pulmonary disease. This booklet also discusses the important role of fruits and vegetables in weight management and the control of diabetes.

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Healthfinder™ Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •

Recognizing Signs and Symptoms of Chronic Obstructive Pulmonary Disease (COPD) Summary: Because early treatment is most effective for COPD, it is important to be able to identify symptoms and changes in symptoms. This online patient education guide is designed to assist you. Source: National Jewish Medical and Research Center http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2457 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 obstructive pulmonary disease. 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. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats

•

Family Village: http://www.familyvillage.wisc.edu/specific.htm

•

Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/

•

Med Help International: http://www.medhelp.org/HealthTopics/A.html

•

Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/

•

Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/

•

WebMDHealth: http://my.webmd.com/health_topics

Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to chronic obstructive pulmonary disease. By

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consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with chronic obstructive pulmonary disease. 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 obstructive pulmonary disease. 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 obstructive pulmonary disease” (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 obstructive pulmonary disease”. 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 obstructive pulmonary disease” (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

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obstructive pulmonary disease” (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.19

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

19

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)20: •

Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/

•

Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)

•

Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm

•

California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html

•

California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html

•

California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html

•

California: Gateway Health Library (Sutter Gould Medical Foundation)

•

California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/

•

California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp

•

California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html

•

California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/

•

California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/

•

California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/

•

California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html

•

California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/

•

Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/

•

Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/

•

Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/

20

Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.

Finding Medical Libraries

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•

Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml

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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

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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html

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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

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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

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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html

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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/

•

Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm

•

Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/

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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/

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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

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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

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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

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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/

Finding Medical Libraries

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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm

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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/

•

New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm

•

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

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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

163

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 obstructive pulmonary disease: •

Basic Guidelines for Chronic Obstructive Pulmonary Disease Chronic obstructive pulmonary disease Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000091.htm COPD Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000091.htm

•

Signs & Symptoms for Chronic Obstructive Pulmonary Disease Breath sounds Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003323.htm Cough Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003072.htm Cyanosis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003215.htm

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Dyspnea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003075.htm Lung disease Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000066.htm Nasal flaring Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003055.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 Tachycardia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003077.htm Tachypnea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003071.htm Wheezing Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003070.htm •

Diagnostics and Tests for Chronic Obstructive Pulmonary Disease Arterial blood gas Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003855.htm Blood gases Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003855.htm CAT scan Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003330.htm CBC Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003642.htm Chest X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003804.htm Contraction Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003405.htm Diffusing capacity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003854.htm Pulmonary function Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003443.htm Pulmonary function tests Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003853.htm

Online Glossaries 165

X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm •

Surgery and Procedures for Chronic Obstructive Pulmonary Disease Lung transplant Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003010.htm

•

Background Topics for Chronic Obstructive Pulmonary Disease Acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002215.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Inspection Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002388.htm Lung disease - support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002158.htm Noninvasive Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002269.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

•

MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html

•

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 OBSTRUCTIVE PULMONARY DISEASE 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] Acatalasia: A rare autosomal recessive disorder resulting from the absence of catalase activity. Though usually asymptomatic, a syndrome of oral ulcerations and gangrene may be present. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] 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] Actin: Essential component of the cell skeleton. [NIH] Activities of Daily Living: The performance of the basic activities of self care, such as dressing, ambulation, eating, etc., in rehabilitation. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH]

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Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]

Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] 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 Embolism: Occurs when the lungs over expand to the point that air bubbles are forced through the air sacs of the lungs into the circulatory system. [NIH] 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

Dictionary 169

general anesthesia. [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] Albuterol: A racemic mixture with a 1:1 ratio of the r-isomer, levalbuterol, and s-albuterol. It is a short-acting beta 2-adrenergic agonist with its main clinical use in asthma. [NIH] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] 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] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alprenolol: 1-((1-Methylethyl)amino)-3-(2-(2-propenyl)phenoxy)-2-propanol. Adrenergic beta-blocker used as an antihypertensive, anti-anginal, and anti-arrhythmic agent. [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] Alternative Splicing: A process whereby multiple protein isoforms are generated from a single gene. Alternative splicing involves the splicing together of nonconsecutive exons during the processing of some, but not all, transcripts of the gene. Thus a particular exon may be connected to any one of several alternative exons to form messenger RNA. The alternative forms produce proteins in which one part is common while the other part is different. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH]

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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] Amiodarone: An antianginal and antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting Na,K-activated myocardial adenosine triphosphatase. There is a resulting decrease in heart rate and in vascular resistance. [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] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] 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] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] 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]

Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] 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] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angina Pectoris: The symptom of paroxysmal pain consequent to myocardial ischemia usually of distinctive character, location and radiation, and provoked by a transient stressful situation during which the oxygen requirements of the myocardium exceed the capacity of the coronary circulation to supply it. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Anomalies: Birth defects; abnormalities. [NIH]

Dictionary 171

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] Antiallergic: Counteracting allergy or allergic conditions. [EU] Antianginal: Counteracting angina or anginal conditions. [EU] 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] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] 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] 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] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Apnea: A transient absence of spontaneous respiration. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid

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transport and metabolism. [NIH] Aponeurosis: Tendinous expansion consisting of a fibrous or membranous sheath which serves as a fascia to enclose or bind a group of muscles. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Approximate: Approximal [EU] Aqueous: Having to do with water. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriosus: Circle composed of anastomosing arteries derived from two long posterior ciliary and seven anterior ciliary arteries, located in the ciliary body about the root of the iris. [NIH]

Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Aspergillosis: Infections with fungi of the genus Aspergillus. [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] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astringent: Causing contraction, usually locally after topical application. [EU] Atmospheric Pressure: The pressure at any point in an atmosphere due solely to the weight of the atmospheric gases above the point concerned. [NIH] Atrial: Pertaining to an atrium. [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,

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mainly Solanaceae. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Autogenic: A type of succession when the developing vegetation itself is the cause for the succession. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Back Pain: Acute or chronic pain located in the posterior regions of the trunk, including the thoracic, lumbar, sacral, or adjacent regions. [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] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]

Beta-Galactosidase: A group of enzymes that catalyzes the hydrolysis of terminal, nonreducing beta-D-galactose residues in beta-galactosides. Deficiency of beta-Galactosidase A1 may cause gangliodisosis GM1. EC 3.2.1.23. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its

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composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [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] Bioassay: 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] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bladder: The organ that stores urine. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [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] Body Composition: The relative amounts of various components in the body, such as percent body fat. [NIH] Body Fluids: Liquid components of living organisms. [NIH]

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Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Resorption: Bone loss due to osteoclastic activity. [NIH] Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Breathing Exercises: Therapeutic exercises aimed to deepen inspiration or expiration or even to alter the rate and rhythm of respiration. [NIH] 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] 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] 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] Bronchopulmonary: Pertaining to the lungs and their air passages; both bronchial and pulmonary. [EU] Bronchoscopy: Endoscopic examination, therapy or surgery of the bronchi. [NIH] Bronchus: A large air passage that leads from the trachea (windpipe) to the lung. [NIH] Budesonide: A glucocorticoid used in the management of asthma, the treatment of various skin disorders, and allergic rhinitis. [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] 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

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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] 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] Carbon Monoxide Poisoning: Toxic asphyxiation due to the displacement of oxygen from oxyhemoglobin by carbon monoxide. [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] Cardiac arrest: A sudden stop of heart function. [NIH] Cardiomyopathy: A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] 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] Carotid Body: A small cluster of chemoreceptive and supporting cells located near the bifurcation of the internal carotid artery. The carotid body, which is richly supplied with fenestrated capillaries, senses the pH, carbon dioxide, and oxygen concentrations in the blood and plays a crucial role in their homeostatic control. [NIH] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Catalase: An oxidoreductase that catalyzes the conversion of hydrogen peroxide to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in acatalasia. EC 1.11.1.6. [NIH] Cataracts: In medicine, an opacity of the crystalline lens of the eye obstructing partially or totally its transmission of light. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and

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secreted during physiological stress. [NIH] 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] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Count: A count of the number of cells of a specific kind, usually measured per unit volume of sample. [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 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 Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [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] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] 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] 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]

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Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] 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] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [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] Clathrin: The main structural coat protein of coated vesicles which play a key role in the intracellular transport between membranous organelles. Clathrin also interacts with cytoskeletal proteins. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [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] Closing Volume: The lung volume at which the dependent lung zones cease to ventilate presumably as a result of airway closure. [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] Coated Vesicles: Vesicles formed when cell-membrane coated pits invaginate and pinch off.

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The outer surface of these vesicles are covered with a lattice-like network of coat proteins, such as clathrin, coat protein complex proteins, or caveolins. [NIH] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH] Cognitive restructuring: A method of identifying and replacing fear-promoting, irrational beliefs with more realistic and functional ones. [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] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colostomy: An opening into the colon from the outside of the body. A colostomy provides a new path for waste material to leave the body after part of the colon has been removed. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [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

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activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [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] Computer Simulation: Computer-based representation of physical systems and phenomena such as chemical processes. [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] Conduction: The transfer of sound waves, heat, nervous impulses, or electricity. [EU] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constriction: The act of constricting. [NIH]

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Constriction, Pathologic: The condition of an anatomical structure's being constricted beyond normal dimensions. [NIH] 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] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]

Conus: A large, circular, white patch around the optic disk due to the exposing of the sclera as a result of degenerative change or congenital abnormality in the choroid and retina. [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 Artery Bypass: Surgical therapy of ischemic coronary artery disease achieved by grafting a section of saphenous vein, internal mammary artery, or other substitute between the aorta and the obstructed coronary artery distal to the obstructive lesion. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] C-Reactive Protein: A plasma protein that circulates in increased amounts during inflammation and after tissue damage. [NIH] Critical Care: Health care provided to a critically ill patient during a medical emergency or crisis. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other

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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] 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] 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]

Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytochrome b: Cytochromes (electron-transporting proteins) with protoheme or a related heme as the prosthetic group. The prosthetic group is not covalently bound to the protein moiety. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decompensation: Failure of compensation; cardiac decompensation is marked by dyspnea, venous engorgement, and edema. [EU] Decompression: Decompression external to the body, most often the slow lessening of external pressure on the whole body (especially in caisson workers, deep sea divers, and persons who ascend to great heights) to prevent decompression sickness. It includes also sudden accidental decompression, but not surgical (local) decompression or decompression applied through body openings. [NIH] Decompression Sickness: A condition occurring as a result of exposure to a rapid fall in ambient pressure. Gases, nitrogen in particular, come out of solution and form bubbles in body fluid and blood. These gas bubbles accumulate in joint spaces and the peripheral

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circulation impairing tissue oxygenation causing disorientation, severe pain, and potentially death. [NIH] 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] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] 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 protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]

Dentists: Individuals licensed to practice dentistry. [NIH] Deoxyribonucleic: A polymer of subunits called deoxyribonucleotides which is the primary genetic material of a cell, the material equivalent to genetic information. [NIH] Deoxyribonucleic acid: A polymer of subunits called deoxyribonucleotides which is the primary genetic material of a cell, the material equivalent to genetic information. [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] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Dermis: A layer of vascular connective tissue underneath the epidermis. The surface of the dermis contains sensitive papillae. Embedded in or beneath the dermis are sweat glands, hair follicles, and sebaceous glands. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and

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immunotherapy. [EU] Desmosine: 4-(4-Amino-4-carboxybutyl)-1-(5-amino-5-carboxypentyl)-3,5-bis(3-amino-3carboxypropyl)pyridinium. A rare amino acid found in elastin, formed by condensation of four molecules of lysine into a pyridinium ring. [NIH] Detergents: Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action that depends on possessing both hydrophilic and hydrophobic properties. [NIH] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] 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] Diastolic: Of or pertaining to the diastole. [EU] 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] Diffusivity: Of a reverberant sound field. The degree to which the directions of propagation of waves are random from point to point. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digitalis: A genus of toxic herbaceous Eurasian plants of the Scrophulaceae which yield cardiotonic glycosides. The most useful are Digitalis lanata and D. purpurea. [NIH] Dilated cardiomyopathy: Heart muscle disease that leads to enlargement of the heart's chambers, robbing the heart of its pumping ability. [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] Dilution: A diluted or attenuated medicine; in homeopathy, the diffusion of a given quantity of a medicinal agent in ten or one hundred times the same quantity of water. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases. [NIH] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Diuretic: A drug that increases the production of urine. [NIH] Diverticula: Plural form of diverticulum. [NIH]

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Diverticulitis: Inflammation of a diverticulum or diverticula. [NIH] Diverticulosis: A condition marked by small sacs or pouches (diverticula) in the walls of an organ such as the stomach or colon. These sacs can become inflamed and cause a condition called diverticulitis, which may be a risk factor for certain types of cancer. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dorsum: A plate of bone which forms the posterior boundary of the sella turcica. [NIH] 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] Double-blinded: A clinical trial in which neither the medical staff nor the person knows which of several possible therapies the person is receiving. [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] Dysphoric: A feeling of unpleasantness and discomfort. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Dyspnoea: Difficult or laboured breathing. [EU] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Eicosanoids: A class of oxygenated, endogenous, unsaturated fatty acids derived from arachidonic acid. They include prostaglandins, leukotrienes, thromboxanes, and hydroxyeicosatetraenoic acid compounds (HETE). They are hormone-like substances that act near the site of synthesis without altering functions throughout the body. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU]

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Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]

Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emergency Treatment: First aid or other immediate intervention for accidents or medical conditions requiring immediate care and treatment before definitive medical and surgical management can be procured. [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] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endorphins: One of the three major groups of endogenous opioid peptides. They are large peptides derived from the pro-opiomelanocortin precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; opioid peptides is used for the broader group. [NIH] Endosomes: Cytoplasmic vesicles formed when coated vesicles shed their clathrin coat. Endosomes internalize macromolecules bound by receptors on the cell surface. [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] Endotracheal intubation: Insertion of an airtube into the windpipe. [NIH] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Enkephalins: One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health.

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[NIH]

Environmental Pollutants: Substances which pollute the environment. Use environmental pollutants in general or for which there is no specific heading. [NIH]

for

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] 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] Epidemiology, Molecular: The application of molecular biology to the answering of epidemiological questions. The examination of patterns of changes in DNA to implicate particular carcinogens and the use of molecular markers to predict which individuals are at highest risk for a disease are common examples. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Ergometer: An instrument for measuring the force of muscular contraction. [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] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]

Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH]

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Exercise Test: Controlled physical activity, more strenuous than at rest, which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used. The intensity of exercise is often graded, using criteria such as rate of work done, oxygen consumption, and heart rate. Physiological data obtained from an exercise test may be used for diagnosis, prognosis, and evaluation of disease severity, and to evaluate therapy. Data may also be used in prescribing exercise by determining a person's exercise capacity. [NIH] Exercise Therapy: Motion of the body or its parts to relieve symptoms or to improve function, leading to physical fitness, but not physical education and training. [NIH] Exercise Tolerance: The exercise capacity of an individual as measured by endurance (maximal exercise duration and/or maximal attained work load) during an exercise test. [NIH]

Exocrine: Secreting outwardly, via a duct. [EU] 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] 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] 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 Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] 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] Fasciculation: A small local contraction of muscles, visible through the skin, representing a spontaneous discharge of a number of fibres innervated by a single motor nerve filament. [EU]

Fat: Total lipids including phospholipids. [NIH]

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Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]

Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] 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] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [EU] Flatus: Gas passed through the rectum. [NIH] Focus Groups: A method of data collection and a qualitative research tool in which a small group of individuals are brought together and allowed to interact in a discussion of their opinions about topics, issues, or questions. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Forced Expiratory Volume: Measure of the maximum amount of air during a forced vital capacity determination that can be expelled in a given number of seconds. It is usually given as FEV followed by a subscript indicating the number of seconds over which the measurement is made, although it is sometimes given as a percentage of forced vital capacity. [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 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] Furosemide: A sulfamyl saluretic and diuretic. It has a fast onset and short duration of action and is used in edema and chronic renal insufficiency. [NIH] Galactosides: Glycosides formed by the reaction of the hydroxyl group on the anomeric

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carbon atom of galactose with an alcohol to form an acetal. They include both alpha- and beta-galactosides. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [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] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gelsolin: A 90-kD protein produced by macrophages that severs actin filaments and forms a cap on the newly exposed filament end. Gelsolin is activated by calcium ions and participates in the assembly and disassembly of actin, thereby increasing the motility of some cells. [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] General practitioner: A medical practitioner who does not specialize in a particular branch of medicine or limit his practice to a specific class of diseases. [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] Genetic Markers: A phenotypically recognizable genetic trait which can be used to identify a genetic locus, a linkage group, or a recombination event. [NIH]

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Genetic Techniques: Chromosomal, biochemical, intracellular, and other methods used in the study of genetics. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genomics: The systematic study of the complete DNA sequences (genome) of organisms. [NIH]

Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Geriatric: Pertaining to the treatment of the aged. [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] 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] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]

Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]

Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]

Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] 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] Glycols: A generic grouping for dihydric alcohols with the hydroxy groups (-OH) located on different carbon atoms. They are viscous liquids with high boiling points for their molecular weights. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Goblet Cells: Cells of the epithelial lining that produce and secrete mucins. [NIH] Gonadal: Pertaining to a gonad. [EU] Governing Board: The group in which legal authority is vested for the control of health-

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related institutions and organizations. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] 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] Grafting: The operation of transfer of tissue from one site to another. [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] Granulomatous Disease, Chronic: A recessive X-linked defect of leukocyte function in which phagocytic cells ingest but fail to digest bacteria, resulting in recurring bacterial infections with granuloma formation. [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] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Care Costs: The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from health expenditures, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost. [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Health Expenditures: The amounts spent by individuals, groups, nations, or private or public organizations for total health care and/or its various components. These amounts may or may not be equivalent to the actual costs (health care costs) and may or may not be shared among the patient, insurers, and/or employers. [NIH] 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] Heartbeat: One complete contraction of the heart. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated

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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] 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]

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] Histone Deacetylase: Hydrolyzes N-acetyl groups on histones. [NIH] Histones: Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] 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] 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] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH]

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Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxides: Inorganic compounds that contain the OH- group. [NIH] Hydroxyl Radical: The univalent radical OH that is present in hydroxides, alcohols, phenols, glycols. [NIH] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hygienic: Pertaining to hygiene, or conducive to health. [EU] Hyperbaric: Characterized by greater than normal pressure or weight; applied to gases under greater than atmospheric pressure, as hyperbaric oxygen, or to a solution of greater specific gravity than another taken as a standard of reference. [EU] Hyperbaric oxygen: Oxygen that is at an atmospheric pressure higher than the pressure at sea level. Breathing hyperbaric oxygen to enhance the effectiveness of radiation therapy is being studied. [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypercapnia: A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood. [NIH] Hyperoxia: An abnormal increase in the amount of oxygen in the tissues and organs. [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] Hyperstimulation: Excessive stimulation. [EU] 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] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypoventilation: A reduction in the amount of air entering the pulmonary alveoli. [NIH] Hypoxanthine: A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway. [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] Idiopathic: Describes a disease of unknown cause. [NIH] Imaging procedures: Methods of producing pictures of areas inside the body. [NIH] Immersion: The placing of a body or a part thereof into a liquid. [NIH]

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Immune response: The activity of the immune system against foreign substances (antigens). [NIH]

Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]

effects

of

foreign

Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [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] Immunosuppressive: Describes the ability to lower immune system responses. [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] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] 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.

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[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 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] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [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] Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] Inorganic: Pertaining to substances not of organic origin. [EU] Inotropic: Affecting the force or energy of muscular contractions. [EU] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insomnia: Difficulty in going to sleep or getting enough sleep. [NIH] Institutionalization: The caring for individuals in institutions and their adaptation to routines characteristic of the institutional environment, and/or their loss of adaptation to life outside the institution. [NIH] Intensive Care: Advanced and highly specialized care provided to medical or surgical patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [NIH]

Intensive Care Units: Hospital units providing continuous surveillance and care to acutely ill patients. [NIH] Intercostal: Situated between the ribs. [EU] 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] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [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

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stimuli. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intervention Studies: Epidemiologic investigations designed to test a hypothesized causeeffect relation by modifying the supposed causal factor(s) in the study population. [NIH] Intracellular: Inside a cell. [NIH] Intracellular Membranes: Membranes of subcellular structures. [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is usually performed for the introducing or withdrawing of fluids from the body. [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]

Investigative Techniques: Investigative techniques used in pre-clinical and clinical research, epidemiology, chemistry, immunology, genetics, etc. They do not include techniques specifically applied to diagnosis; therapeutics; anesthesia and analgesia, surgery, operative, and dentistry. [NIH] Involuntary: Reaction occurring without intention or volition. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] 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] 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] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] 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]

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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] 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] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Laryngeal: Having to do with the larynx. [NIH] Laryngectomy: Total or partial excision of the larynx. [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] Length of Stay: The period of confinement of a patient to a hospital or other health facility. [NIH]

Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Lesion: An area of abnormal tissue change. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocyte Disorders: Disordered formation of various types of leukocytes or an abnormal accumulation or deficiency of these cells. [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] 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] Lipolysis: The hydrolysis of lipids. [NIH] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH]

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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]

Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Lobectomy: The removal of a lobe. [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 Studies: Studies in which variables relating to an individual or group of individuals are assessed over a period of time. [NIH] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] 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] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [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 Subsets: A classification of lymphocytes based on structurally or functionally different populations of cells. [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 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]

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Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] 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] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

Mammary: Pertaining to the mamma, or breast. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Mechanical ventilation: Use of a machine called a ventilator or respirator to improve the exchange of air between the lungs and the atmosphere. [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 Staff: Professional medical personnel who provide care to patients in an organized facility, institution or agency. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH]

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Melanin: The substance that gives the skin its color. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Fusion: The adherence of cell membranes, intracellular membranes, or artifical membrane models of either to each other or to viruses, parasites, or interstitial particles through a variety of chemical and physical processes. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [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] Menopause: Permanent cessation of menstruation. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Health: The state wherein the person is well adjusted. [NIH] 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] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metoprolol: Adrenergic beta-1-blocking agent with no stimulatory action. It is less bound to plasma albumin than alprenolol and may be useful in angina pectoris, hypertension, or cardiac arrhythmias. [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] Microfilaments: The smallest of the cytoskeletal filaments. They are composed chiefly of actin. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living 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

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cannot be properly seen by the unaided eye. [NIH] Mineralocorticoids: A group of corticosteroids primarily associated with the regulation of water and electrolyte balance. This is accomplished through the effect on ion transport in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by plasma volume, serum potassium, and angiotensin II. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]

Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] 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] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Motility: The ability to move spontaneously. [EU] Mucinous: Containing or resembling mucin, the main compound in mucus. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucolytic: Destroying or dissolving mucin; an agent that so acts : a mucopolysaccharide or 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,

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water, inorganic salts, and exfoliated cells. [NIH] Multicenter Studies: Controlled studies which are planned and carried out by several cooperating institutions to assess certain variables and outcomes in specific patient populations, for example, a multicenter study of congenital anomalies in children. [NIH] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]

Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Muscle Hypertonia: Abnormal increase in skeletal or smooth muscle tone. Skeletal muscle hypertonicity may be associated with pyramidal tract lesions or basal ganglia diseases. [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] Myalgia: Pain in a muscle or muscles. [EU] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocarditis: Inflammation of the myocardium; inflammation of the muscular walls of the heart. [EU] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors. [NIH] 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] Nasal Septum: The partition separating the two nasal cavities in the midplane, composed of cartilaginous, membranous and bony parts. [NIH] Nasopharynx: The nasal part of the pharynx, lying above the level of the soft palate. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Nephropathy: Disease of the kidneys. [EU] Nerve Fibers: Slender processes of neurons, especially the prolonged axons that conduct nerve impulses. [NIH]

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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] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Diseases: A general term encompassing lower motor neuron disease; peripheral nervous system diseases; and certain muscular diseases. Manifestations include muscle weakness; fasciculation; muscle atrophy; spasm; myokymia; muscle hypertonia, myalgias, and musclehypotonia. [NIH] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropeptides: Peptides released by neurons as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells. [NIH] Neurophysiology: The scientific discipline concerned with the physiology of the nervous system. [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] 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]

Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by

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volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nodose: Having nodes or projections. [EU] Nonverbal Communication: Transmission of emotions, ideas, and attitudes between individuals in ways other than the spoken language. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nosocomial: Pertaining to or originating in the hospital, said of an infection not present or incubating prior to admittance to the hospital, but generally occurring 72 hours after admittance; the term is usually used to refer to patient disease, but hospital personnel may also acquire nosocomial infection. [EU] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] 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] 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] Occupational Medicine: Medical specialty concerned with the promotion and maintenance of the physical and mental health of employees in occupational settings. [NIH] Occupational Therapy: The field concerned with utilizing craft or work activities in the rehabilitation of patients. Occupational therapy can also refer to the activities themselves. [NIH]

Office Visits: Visits made by patients to health service providers' offices for diagnosis, treatment, and follow-up. [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] Opacity: Degree of density (area most dense taken for reading). [NIH] Opiate: A remedy containing or derived from opium; also any drug that induces sleep. [EU] 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]

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Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] 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] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [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]

Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oximetry: The determination of oxygen-hemoglobin saturation of blood either by withdrawing a sample and passing it through a classical photoelectric oximeter or by electrodes attached to some translucent part of the body like finger, earlobe, or skin fold. It includes non-invasive oxygen monitoring by pulse oximetry. [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate and the posterior soft palate. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Panniculitis: General term for inflammation of adipose tissue, usually of the skin, characterized by reddened subcutaneous nodules. [NIH]

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Parasympathetic Nervous System: The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system. [NIH] Parenchyma: The essential elements of an organ; used in anatomical nomenclature as a general term to designate the functional elements of an organ, as distinguished from its framework, or stroma. [EU] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [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] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [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] 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] 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] 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] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [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] Perioperative: Around the time of surgery; usually lasts from the time of going into the hospital or doctor's office for surgery until the time the patient goes home. [NIH]

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Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Nervous System Diseases: Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves. [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] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [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] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] 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] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [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]

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Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Fitness: A state of well-being in which performance is optimal, often as a result of physical conditioning which may be prescribed for disease therapy. [NIH] 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] Pilot study: The initial study examining a new method or treatment. [NIH] Pitch: The subjective awareness of the frequency or spectral distribution of a sound. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [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] 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] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pleura: The thin serous membrane enveloping the lungs and lining the thoracic cavity. [NIH] Pleural: A circumscribed area of hyaline whorled fibrous tissue which appears on the surface of the parietal pleura, on the fibrous part of the diaphragm or on the pleura in the interlobar fissures. [NIH]

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Pneumococcal Infections: Infections with bacteria of the species Streptococcus pneumoniae. [NIH]

Pneumonia: Inflammation of the lungs. [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] 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] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Population Density: Number of individuals in a population relative to space. [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 cirrhosis. [NIH] Portal Vein: A short thick vein formed by union of the superior mesenteric vein and the splenic vein. [NIH] Positive pressure ventilation: Provision of oxygen under pressure by a mechanical respirator. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [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] 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] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Premalignant: A term used to describe a condition that may (or is likely to) become cancer. Also called precancerous. [NIH]

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Preoperative: Preceding an operation. [EU] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary endpoint: The main result that is measured at the end of a study to see if a given treatment worked (e.g., the number of deaths or the difference in survival between the treatment group and the control group). What the primary endpoint will be is decided before the study begins. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] 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] Prostaglandins: A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes. [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 Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein Isoforms: Different forms of a protein that may be produced from different genes, or from the same gene by alternative splicing. [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

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recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycans: Glycoproteins which have a very high polysaccharide content. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] 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] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychotherapy: A generic term for the treatment of mental illness or emotional disturbances primarily by verbal or nonverbal communication. [NIH] 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 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 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] Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [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.

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[NIH]

Pupil: The aperture in the iris through which light passes. [NIH] Purifying: Respiratory equipment whose function is to remove contaminants from otherwise wholesome air. [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] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Racemic: Optically inactive but resolvable in the way of all racemic compounds. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [NIH] Radiopharmaceutical: Any medicinal product which, when ready for use, contains one or more radionuclides (radioactive isotopes) included for a medicinal purpose. [NIH] Random Allocation: A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects. [NIH] Randomization: Also called random allocation. Is allocation of individuals to groups, e.g., for experimental and control regimens, by chance. Within the limits of chance variation, random allocation should make the control and experimental groups similar at the start of an investigation and ensure that personal judgment and prejudices of the investigator do not influence allocation. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Randomized Controlled Trials: Clinical trials that involve at least one test treatment and

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one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table. Treatment allocations using coin flips, odd-even numbers, patient social security numbers, days of the week, medical record numbers, or other such pseudo- or quasi-random processes, are not truly randomized and trials employing any of these techniques for patient assignment are designated simply controlled clinical trials. [NIH] RANTES: A chemokine that is a chemoattractant for eosinophils, monocytes, and lymphocytes. It is a potent and selective eosinophil chemotaxin that is stored in and released from platelets and activated T-cells. [NIH] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] 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] 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] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Rehabilitation Centers: Facilities which provide programs for rehabilitating the mentally or physically disabled individuals. [NIH] Rehabilitative: Instruction of incapacitated individuals or of those affected with some mental disorder, so that some or all of their lost ability may be regained. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [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] Residual Volume: The volume of air remaining in the lungs at the end of a maximal expiration. Common abbreviation is RV. [NIH] Respirable: Dust particles smaller than 0. 005 mm, which are deposited in the respiratory region of the lungs. [NIH]

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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 Burst: A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (granulomatous disease, chronic) often die as a result of recurrent bacterial infections. [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [NIH] Respiratory Muscles: These include the muscles of the diaphragm and the intercostal muscles. [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] Respiratory Therapy: Care of patients with deficiencies and abnormalities associated with the cardiopulmonary system. It includes the therapeutic use of medical gases and their administrative apparatus, environmental control systems, humidification, aerosols, ventilatory support, bronchopulmonary drainage and exercise, respiratory rehabilitation, assistance with cardiopulmonary resuscitation, and maintenance of natural, artificial, and mechanical airways. [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] Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Reticular: Coarse-fibered, netlike dermis layer. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Reverberant: The sound field prevailing in a large enclosure with moderately reflecting surfaces. [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] Ribonucleic acid: RNA. One of the two nucleic acids found in all cells. The other is deoxyribonucleic acid (DNA). Ribonucleic acid transfers genetic information from DNA to proteins produced by the cell. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [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] Rod: A reception for vision, located in the retina. [NIH] Saline: A solution of salt and water. [NIH] Saphenous: Applied to certain structures in the leg, e. g. nerve vein. [NIH] Saphenous Vein: The vein which drains the foot and leg. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed pictures of organs inside the body. MRI scans use a large magnet connected to a computer to create pictures of areas inside the body. [NIH] 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] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Selenomethionine: Diagnostic aid in pancreas function determination. [NIH] Self Care: Performance of activities or tasks traditionally performed by professional health care providers. The concept includes care of oneself or one's family and friends. [NIH] 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] Sensitization: 1. Administration of antigen to induce a primary immune response; priming; immunization. 2. Exposure to allergen that results in the development of hypersensitivity. 3.

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The coating of erythrocytes with antibody so that they are subject to lysis by complement in the presence of homologous antigen, the first stage of a complement fixation test. [EU] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Shivering: Involuntary contraction or twitching of the muscles. It is a physiologic method of heat production in man and other mammals. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skin Care: Maintenance of the hygienic state of the skin under optimal conditions of cleanliness and comfort. Effective in skin care are proper washing, bathing, cleansing, and the use of soaps, detergents, oils, etc. In various disease states, therapeutic and protective solutions and ointments are useful. The care of the skin is particularly important in various occupations, in exposure to sunlight, in neonates, and in decubitus ulcer. [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] 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 Isolation: The separation of individuals or groups resulting in the lack of or minimizing of social contact and/or communication. This separation may be accomplished by physical separation, by social barriers and by psychological mechanisms. In the latter, there may be interaction but no real communication. [NIH]

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Social Security: Government sponsored social insurance programs. [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] Solitary Nucleus: Gray matter located in the dorsomedial part of the medulla oblongata associated with the solitary tract. The solitary nucleus receives inputs from most organ systems including the terminations of the facial, glossopharyngeal, and vagus nerves. It is a major coordinator of autonomic nervous system regulation of cardiovascular, respiratory, gustatory, gastrointestinal, and chemoreceptive aspects of homeostasis. The solitary nucleus is also notable for the large number of neurotransmitters which are found therein. [NIH] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectroscopic: The recognition of elements through their emission spectra. [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] 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]

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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] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]

Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [NIH] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] 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] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stress management: A set of techniques used to help an individual cope more effectively with difficult situations in order to feel better emotionally, improve behavioral skills, and often to enhance feelings of control. Stress management may include relaxation exercises, assertiveness training, cognitive restructuring, time management, and social support. It can be delivered either on a one-to-one basis or in a group format. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stroma: The middle, thickest layer of tissue in the cornea. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Substrate: A substance upon which an enzyme acts. [EU] Sudden death: Cardiac arrest caused by an irregular heartbeat. The term "death" is somewhat misleading, because some patients survive. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S,

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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] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [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] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]

Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatology: 1. That branch of medicine with treats of symptoms; the systematic discussion of symptoms. 2. The combined symptoms of a disease. [EU] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [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 second-

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messenger 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] Synaptic Vesicles: Membrane-bound compartments which contain transmitter molecules. Synaptic vesicles are concentrated at presynaptic terminals. They actively sequester transmitter molecules from the cytoplasm. In at least some synapses, transmitter release occurs by fusion of these vesicles with the presynaptic membrane, followed by exocytosis of their contents. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tachypnea: Rapid breathing. [NIH] Tear Gases: Gases that irritate the eyes, throat, or skin. Severe lacrimation develops upon irritation of the eyes. [NIH] Tendon: A discrete band of connective tissue mainly composed of parallel bundles of collagenous fibers by which muscles are attached, or two muscles bellies joined. [NIH] Theophylline: Alkaloid obtained from Thea sinensis (tea) and others. It stimulates the heart and central nervous system, dilates bronchi and blood vessels, and causes diuresis. The drug is used mainly in bronchial asthma and for myocardial stimulation. Among its more prominent cellular effects are inhibition of cyclic nucleotide phosphodiesterases and antagonism of adenosine receptors. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thermogenesis: The generation of heat in order to maintain body temperature. The uncoupled oxidation of fatty acids contained within brown adipose tissue and shivering are examples of thermogenesis in mammals. [NIH] Thoracic: Having to do with the chest. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]

Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They

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are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and 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] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonus: A state of slight tension usually present in muscles even when they are not undergoing active contraction. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [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] Trace element: Substance or element essential to plant or animal life, but present in

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extremely small amounts. [NIH] Tracer: A substance (such as a radioisotope) used in imaging procedures. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Tracheostomy: Surgical formation of an opening into the trachea through the neck, or the opening so created. [NIH] Traction: The act of pulling. [NIH] Tractus: A part of some structure, usually that part along which something passes. [NIH] Transcutaneous: Transdermal. [EU] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Translating: Conversion from one language to another language. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [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] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] 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] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH]

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Ulceration: 1. The formation or development of an ulcer. 2. An ulcer. [EU] Univalent: Pertaining to an unpaired chromosome during the zygotene stage of prophase to first metaphase in meiosis. [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] 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] 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] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Valves: Flap-like structures that control the direction of blood flow through the heart. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vascular Resistance: An expression of the resistance offered by the systemic arterioles, and to a lesser extent by the capillaries, to the flow of blood. [NIH] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Venous Thrombosis: The formation or presence of a thrombus within a vein. [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] Ventricular Function: The hemodynamic and electrophysiological action of the ventricles. [NIH]

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

Dictionary 225

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] 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] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral Afferents: The sensory fibers innervating the viscera. [NIH] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Vital Capacity: The volume of air that is exhaled by a maximal expiration following a maximal inspiration. [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] Voice Disorders: Disorders of voice pitch, loudness, or quality. Dysphonia refers to impaired utterance of sounds by the vocal folds. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]

Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xanthine: An urinary calculus. [NIH] Xanthine Oxidase: An iron-molybdenum flavoprotein containing FAD that oxidizes hypoxanthine, some other purines and pterins, and aldehydes. Deficiency of the enzyme, an autosomal recessive trait, causes xanthinuria. EC 1.1.3.22. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] 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]

227

INDEX A Abdominal, 167, 168, 184, 206, 208 Acatalasia, 167, 176 Acceptor, 167, 198, 206 Acetylcholine, 28, 167, 178, 204 Acetylcysteine, 91, 167 Actin, 37, 167, 190, 201 Activities of Daily Living, 33, 167 Acute renal, 137, 167 Adaptability, 167, 177 Adaptation, 46, 62, 122, 167, 196, 209 Adenine, 167, 213 Adenocarcinoma, 167, 193 Adenosine, 38, 45, 100, 167, 170, 194, 208, 221 Adenovirus, 35, 167 Adipocytes, 168, 198 Adipose Tissue, 168, 206, 221 Adjustment, 167, 168 Adrenal Cortex, 168, 181, 211 Adrenal Medulla, 168, 176, 186, 187, 205 Adrenergic, 49, 168, 169, 185, 187, 201, 220 Adsorption, 46, 168 Adsorptive, 168 Adverse Effect, 55, 168, 217 Aerobic, 168, 188 Aerosol, 44, 59, 168 Afferent, 168, 198 Affinity, 168, 218 Agonist, 37, 168, 169, 185, 203, 204 Air Embolism, 23, 168 Air Pollutants, 32, 38, 168 Air Sacs, 168, 169 Airway Resistance, 38, 169 Albumin, 169, 201, 209 Albuterol, 70, 169 Aldehydes, 42, 55, 169, 225 Algorithms, 169, 174 Alkaloid, 169, 172, 204, 221 Allergen, 40, 169, 183, 216 Allergic Rhinitis, 169, 175 Alpha Particles, 169, 213 Alprenolol, 169, 201 Alternative medicine, 169 Alternative Splicing, 169, 211 Alveoli, 6, 169, 224 Amino Acid Sequence, 52, 169, 171

Amino Acids, 129, 169, 170, 187, 207, 210, 212, 220, 224 Amiodarone, 100, 170 Ammonia, 170, 224 Ampulla, 170, 177 Amyloid, 170 Anaesthesia, 170, 195 Anal, 26, 33, 170, 187, 189, 199 Analog, 103, 170 Analogous, 40, 170, 223 Analytes, 43, 150, 170 Anatomical, 41, 170, 172, 177, 181, 186, 195, 207, 216 Androgens, 168, 170, 181 Anemia, 137, 170, 175, 203 Anesthesia, 169, 170, 197 Aneurysm, 65, 170 Angina, 33, 170, 171, 201 Angina Pectoris, 170, 201 Animal model, 8, 15, 29, 34, 38, 170 Anions, 169, 170, 197, 220 Anomalies, 170, 203 Antagonism, 171, 221 Antiallergic, 171, 181 Antianginal, 170, 171 Antiarrhythmic, 170, 171, 197 Antibacterial, 171, 218 Antibiotic, 45, 137, 171, 178, 187, 218 Antibodies, 6, 14, 171, 195, 209 Antibody, 20, 44, 168, 171, 179, 193, 195, 200, 202, 213, 217, 218 Anticoagulant, 171, 211 Antidepressant, 57, 171 Antigen, 45, 168, 171, 179, 193, 194, 195, 200, 216 Anti-infective, 171, 193, 217 Anti-inflammatory, 21, 31, 38, 45, 171, 172, 181, 191, 210 Anti-Inflammatory Agents, 171, 172, 181 Antineoplastic, 171, 181 Antioxidant, 14, 38, 47, 51, 74, 93, 171, 206, 220 Antiseptic, 171, 225 Antiviral, 167, 171, 196 Anus, 170, 171, 179 Anxiety, 18, 61, 63, 117, 171 Aorta, 171, 181, 224 Apnea, 10, 171

228

Chronic Obstructive Pulmonary Disease

Apolipoproteins, 171, 199 Aponeurosis, 172, 190 Apoptosis, 15, 54, 55, 172, 176 Approximate, 7, 11, 12, 26, 27, 29, 34, 172 Aqueous, 172, 173, 177, 182, 193, 198 Arachidonic Acid, 172, 185, 198, 211 Arginine, 172, 193, 204 Arterial, 20, 75, 99, 120, 138, 164, 172, 178, 194, 212, 221 Arteries, 171, 172, 174, 181, 199, 203, 212, 222 Arterioles, 172, 174, 224 Arteriosus, 172, 212 Artery, 11, 38, 50, 59, 65, 100, 136, 170, 172, 176, 181, 186, 212 Ascites, 140, 172 Aspergillosis, 87, 172 Aspiration, 64, 95, 172 Aspirin, 33, 172 Assay, 44, 50, 108, 172 Astringent, 172, 225 Atmospheric Pressure, 172, 194 Atrial, 108, 119, 122, 170, 172 Atrium, 172, 224 Atrophy, 136, 172, 204 Atropine, 172, 197 Attenuated, 173, 184 Attenuation, 31, 173 Autogenic, 111, 173 Autoimmune disease, 137, 173 Autonomic Nervous System, 36, 173, 207, 208, 218, 220 Axons, 36, 173, 203 B Back Pain, 138, 173 Bacteremia, 137, 173 Bacteria, 64, 168, 171, 173, 178, 183, 186, 188, 192, 201, 210, 214, 218, 222, 224 Bacterial Infections, 173, 192, 215 Bacterial Physiology, 167, 173 Basal Ganglia, 173, 190, 203 Base, 3, 8, 167, 173, 198 Basement Membrane, 38, 173, 188, 198 Basophils, 173, 192 Benign, 173, 190, 192 Beta-Galactosidase, 35, 173 Bile, 173, 174, 197, 199, 219 Bile Pigments, 174, 197 Biliary, 174, 177 Bioassay, 38, 174 Bioavailability, 38, 174 Biochemical, 14, 55, 79, 174, 191, 217

Biological response modifier, 174, 196 Biological Transport, 174, 184 Biomarkers, 5, 13, 15, 26, 31, 42, 45, 56, 174 Biopsy, 54, 66, 174 Biotechnology, 60, 61, 145, 174 Biotransformation, 174 Bladder, 174, 211, 224 Blood Platelets, 174, 217 Blood pressure, 53, 137, 140, 174, 176, 177, 194, 202, 210, 212, 218 Blood vessel, 7, 11, 12, 27, 29, 35, 41, 174, 175, 176, 177, 178, 186, 197, 199, 201, 207, 209, 217, 219, 221, 224 Body Composition, 18, 174 Body Fluids, 174, 218, 223 Bone Marrow, 175, 190, 195, 199, 202, 203 Bone Resorption, 66, 175 Bone scan, 175, 216 Bowel, 170, 175 Bradykinin, 175, 204, 209 Brain Stem, 175, 207 Breathing Exercises, 116, 117, 175 Bronchi, 36, 175, 187, 221, 223 Bronchial, 36, 74, 75, 127, 138, 140, 175, 197, 221 Bronchiectasis, 113, 138, 140, 175 Bronchioles, 169, 175, 212 Bronchitis, 15, 34, 46, 80, 115, 134, 138, 140, 150, 175 Bronchoalveolar Lavage, 42, 175 Bronchoconstriction, 40, 175 Bronchodilator, 17, 19, 40, 45, 66, 80, 175 Bronchopulmonary, 113, 175, 215 Bronchoscopy, 150, 175 Bronchus, 175 Budesonide, 66, 67, 90, 175 C Cadmium, 34, 175 Cadmium Poisoning, 175 Calcium, 175, 179, 190, 200 Carbohydrate, 118, 176, 181, 191, 210 Carbon Dioxide, 98, 104, 176, 189, 190, 194, 215 Carbon Monoxide Poisoning, 23, 176 Carcinogenesis, 15, 176 Carcinogenic, 176, 196, 219 Carcinogens, 176, 187, 203, 206 Carcinoma, 176 Cardiac, 8, 32, 34, 53, 136, 171, 176, 182, 187, 201, 203, 215, 219 Cardiac arrest, 32, 176, 219 Cardiomyopathy, 176

229

Cardiopulmonary, 8, 61, 63, 78, 97, 111, 112, 113, 119, 120, 121, 176, 215 Cardiorespiratory, 10, 99, 176 Cardiotonic, 176, 184 Cardiovascular, 3, 23, 32, 39, 52, 53, 65, 95, 106, 134, 137, 176, 188, 198, 217, 218 Cardiovascular disease, 3, 39, 53, 106, 134, 137, 176 Carotid Body, 45, 176, 177 Caspase, 15, 176 Catalase, 15, 54, 167, 176 Cataracts, 152, 176 Catecholamine, 49, 176, 185, 208 Cathepsins, 49, 177 Catheter, 177, 197 Catheterization, 177, 197 Causal, 25, 134, 177, 187, 197 Cause of Death, 20, 21, 57, 58, 177 Cell Count, 13, 177 Cell Death, 55, 172, 177, 203 Cell Division, 173, 177, 200, 202, 209, 211, 216 Cell membrane, 43, 174, 177, 183, 188, 190, 201, 208 Cell Respiration, 177, 215 Central Nervous System, 14, 36, 78, 167, 173, 177, 190, 191, 192, 198, 204, 217, 221 Cerebrovascular, 134, 137, 176, 177 Cerebrum, 177 Chemoreceptor, 40, 177 Chest wall, 97, 177 Chin, 64, 177, 201 Cholestasis, 140, 177 Cholesterol, 51, 174, 177, 178, 181, 199, 201, 219 Cholesterol Esters, 178, 199 Cholinergic, 36, 178, 204 Chromatin, 172, 178, 199 Chromosome, 178, 198, 216, 223, 224 Chronic Disease, 20, 50, 138, 152, 178 Chronic renal, 178 Chylomicrons, 178, 199 Circulatory system, 168, 178 Cirrhosis, 140, 178, 210 Clamp, 41, 178 Clarithromycin, 45, 178 Clathrin, 178, 179, 186 Clinical Medicine, 56, 178, 210 Clinical trial, 4, 17, 20, 47, 73, 145, 178, 181, 185, 203, 212, 213 Cloning, 174, 178 Closing Volume, 42, 178

Coagulation, 137, 174, 176, 178, 193, 209, 221 Coated Vesicles, 178, 186 Cognition, 19, 179 Cognitive restructuring, 179, 219 Cohort Studies, 32, 58, 179, 187 Collagen, 49, 173, 179, 188, 200, 209, 211 Collapse, 179, 217 Colloidal, 169, 179, 186 Colon, 179, 185 Colostomy, 138, 179 Combination Therapy, 70, 179 Complement, 179, 180, 200, 209, 217 Complementary and alternative medicine, 111, 130, 180 Complementary medicine, 111, 180 Complete remission, 180, 214 Computational Biology, 145, 180 Computed tomography, 31, 42, 67, 180, 216 Computer Simulation, 61, 180 Computerized axial tomography, 180, 216 Computerized tomography, 40, 180 Conduction, 137, 180 Confounding, 24, 180 Congestive heart failure, 6, 46, 85, 136, 180 Conjunctiva, 180, 196 Connective Tissue, 175, 179, 180, 183, 189, 190, 201, 221 Consciousness, 180, 183, 215 Constriction, 180, 181, 197, 224 Constriction, Pathologic, 181, 224 Contraindications, ii, 181 Control group, 11, 18, 22, 181, 211, 213 Controlled study, 6, 96, 181 Conus, 181, 212 Coronary, 4, 11, 38, 50, 59, 100, 124, 134, 136, 170, 176, 181, 203 Coronary Artery Bypass, 124, 181 Coronary heart disease, 4, 134, 176, 181 Coronary Thrombosis, 181, 203 Cortex, 181 Cortical, 37, 181, 187 Corticosteroid, 21, 41, 53, 69, 76, 77, 181, 210 Cortisone, 181, 210 Cranial, 181, 192, 207, 208 C-Reactive Protein, 53, 181 Cross-Sectional Studies, 181, 187 Curative, 182, 221 Cutaneous, 182, 197, 199 Cyclic, 182, 192, 204, 208, 221

230

Chronic Obstructive Pulmonary Disease

Cysteine, 45, 49, 55, 130, 167, 182, 220 Cystine, 182 Cytochrome, 182, 215 Cytochrome b, 182, 215 Cytokine, 16, 18, 20, 32, 34, 55, 182 Cytoplasm, 172, 173, 177, 182, 187, 199, 202, 221 Cytoskeleton, 37, 182 Cytotoxic, 54, 182 D Data Collection, 14, 51, 182, 189 Deamination, 182, 224 Decompensation, 32, 182 Decompression, 23, 182 Decompression Sickness, 23, 182 Decubitus, 33, 183, 217 Decubitus Ulcer, 33, 183, 217 Degenerative, 181, 183, 193 Deletion, 172, 183 Delivery of Health Care, 183, 192 Dementia, 4, 183 Dendrites, 183, 204 Dendritic, 10, 183 Dental Care, 136, 137, 183 Dental Caries, 23, 183 Dentists, 137, 183 Deoxyribonucleic, 183, 215 Deoxyribonucleic acid, 183, 215 Depolarization, 45, 183 Depressive Disorder, 47, 183 Dermis, 183, 215 Desensitization, 49, 183 Desmosine, 102, 184 Detergents, 184, 217 Deuterium, 184, 193 Diabetes Mellitus, 6, 137, 138, 184, 191, 193 Diagnostic procedure, 184 Diaphragm, 70, 84, 184, 209, 215 Diastolic, 184, 194 Diffusion, 31, 174, 184, 196 Diffusivity, 31, 184 Digestion, 174, 175, 184, 199, 219 Digitalis, 119, 184 Dilated cardiomyopathy, 65, 184 Dilation, 140, 175, 184 Dilution, 25, 184 Direct, iii, 17, 19, 28, 43, 44, 46, 58, 178, 184, 185, 214, 220 Discrete, 19, 184, 221 Disease Susceptibility, 43, 184 Disorientation, 183, 184

Distal, 37, 41, 45, 181, 184, 212 Diuresis, 184, 221 Diuretic, 184, 189 Diverticula, 184, 185 Diverticulitis, 185 Diverticulosis, 152, 185 Dopamine, 72, 185, 204, 208 Dorsum, 185, 190 Double-blind, 42, 51, 185 Double-blinded, 42, 51, 185 Drug Interactions, 137, 185 Drug Tolerance, 185, 222 Dysphoric, 183, 185 Dysplasia, 15, 185 Dyspnoea, 102, 118, 185 E Edema, 182, 185, 189, 203 Effector, 30, 167, 179, 185, 208 Effector cell, 30, 185 Efficacy, 6, 10, 13, 22, 35, 51, 74, 99, 119, 185 Eicosanoids, 25, 185 Elastic, 40, 185, 218, 220 Elastin, 49, 179, 184, 185, 188 Elective, 5, 185 Electrocardiogram, 126, 186 Electrocoagulation, 178, 186 Electrolyte, 181, 186, 202, 218 Electrons, 171, 173, 186, 197, 206, 213 Electrophoresis, 56, 186 Embolus, 186, 195 Embryo, 186, 195 Emergency Treatment, 93, 186 Enamel, 183, 186 Endogenous, 38, 185, 186, 206 Endorphins, 186, 204 Endosomes, 50, 186 Endothelium, 186, 204 Endothelium-derived, 186, 204 Endotoxin, 16, 186, 223 Endotracheal intubation, 92, 186 Energy balance, 119, 186, 198 Enkephalins, 186, 204 Environmental Health, 23, 31, 32, 44, 53, 59, 114, 144, 146, 186 Environmental Pollutants, 32, 43, 187 Environmental tobacco smoke, 24, 55, 187 Enzymatic, 176, 179, 183, 187, 201 Enzyme, 31, 37, 40, 45, 176, 185, 187, 190, 191, 192, 201, 208, 209, 211, 212, 219, 220, 221, 225 Enzyme Inhibitors, 31, 187, 209

231

Eosinophil, 187, 214 Epidemiologic Studies, 51, 53, 187 Epidemiological, 4, 15, 43, 187 Epidemiology, Molecular, 44, 187 Epigastric, 187, 206 Epinephrine, 168, 185, 187, 204, 205, 223 Epithelial, 16, 20, 30, 37, 38, 47, 48, 52, 54, 56, 62, 121, 167, 174, 187, 191, 198 Epithelial Cells, 16, 30, 37, 47, 48, 52, 54, 56, 62, 187, 198 Epithelium, 16, 55, 173, 186, 187 Ergometer, 19, 116, 187 Erythrocytes, 170, 175, 187, 217 Erythromycin, 178, 187 Esophagus, 134, 187, 208, 219 Excitation, 177, 187, 204 Excitatory, 10, 45, 187, 191 Exercise Test, 61, 78, 188 Exercise Therapy, 120, 188 Exercise Tolerance, 18, 23, 89, 96, 132, 188 Exocrine, 188, 206 Exocytosis, 37, 188, 221 Exogenous, 51, 118, 168, 174, 186, 188 Expiration, 175, 188, 214, 215, 225 Expiratory, 83, 100, 188 Extracellular, 37, 38, 170, 180, 188, 200, 218 Extracellular Matrix, 180, 188, 200 Extracellular Matrix Proteins, 188, 200 Extrapyramidal, 185, 188 Extremity, 33, 188 Eye Infections, 167, 188 F Failure to Thrive, 140, 188 Family Planning, 145, 188 Fasciculation, 188, 204 Fat, 68, 140, 168, 172, 174, 175, 181, 183, 186, 188, 198, 210, 220 Fatigue, 76, 96, 189, 192 Fatty acids, 169, 185, 189, 191, 211, 217, 221 Fibrinogen, 32, 45, 53, 189, 209, 221 Fibrosis, 8, 65, 138, 189, 212, 216 Fixation, 189, 217 Flatus, 189, 190 Focus Groups, 9, 189 Fold, 136, 189, 201, 206 Forced Expiratory Volume, 51, 189 Forearm, 174, 189 Free Radicals, 43, 171, 189 Friction, 169, 189 Furosemide, 73, 189

G Galactosides, 173, 189 Ganglia, 36, 167, 190, 204, 207, 208, 220 Ganglion, 10, 36, 190 Gap Junctions, 190, 221 Gas exchange, 108, 190, 212, 215, 224 Gastrin, 190, 193 Gastrointestinal, 175, 187, 190, 198, 217, 218, 219, 223 Gastrointestinal tract, 190, 198, 217, 223 Gelsolin, 37, 190 Gene Expression, 15, 26, 36, 43, 48, 52, 53, 54, 66, 190 Gene Therapy, 167, 190 General practitioner, 60, 190 Generator, 22, 190 Genetic Markers, 16, 49, 190 Genetic Techniques, 7, 12, 27, 28, 30, 35, 191 Genetics, 7, 9, 12, 13, 15, 27, 28, 30, 35, 56, 68, 79, 80, 136, 191, 197 Genomics, 56, 79, 191 Genotype, 7, 11, 12, 27, 28, 29, 35, 101, 191, 208 Geriatric, 14, 57, 115, 117, 191 Gland, 168, 181, 191, 206, 209, 211, 216, 219, 222 Glucans, 44, 191 Glucocorticoid, 18, 175, 191, 210 Glucose, 184, 191, 193, 216 Glucose Intolerance, 184, 191 Glutamic Acid, 191, 204, 211 Glutathione Peroxidase, 15, 43, 191, 216 Glycerol, 191, 208 Glycerophospholipids, 191, 208 Glycine, 191, 204 Glycols, 191, 194 Glycoprotein, 189, 191, 198, 202, 221, 223 Goblet Cells, 52, 191 Gonadal, 191, 219 Governing Board, 191, 210 Graft, 124, 192, 195 Graft Rejection, 192, 195 Grafting, 181, 192 Granule, 37, 55, 192 Granulocyte, 55, 81, 192 Granulomatous Disease, Chronic, 192, 215 Guanylate Cyclase, 192, 204 H Half-Life, 38, 192 Haplotypes, 59, 192 Headache, 192, 196

232

Chronic Obstructive Pulmonary Disease

Health Care Costs, 7, 11, 12, 26, 27, 29, 34, 192 Health Education, 50, 150, 151, 192 Health Expenditures, 192 Health Services, 47, 50, 183, 192 Health Status, 51, 58, 192 Heart attack, 176, 192 Heart failure, 8, 192, 212 Heartbeat, 192, 219 Hemoglobin, 170, 187, 192, 206 Hemorrhage, 186, 192, 193, 219 Hemostasis, 193, 217 Hepatitis, 140, 193 Hepatocellular, 140, 193 Hepatocellular carcinoma, 140, 193 Hepatocyte, 177, 193 Heredity, 190, 191, 193 Histone Deacetylase, 69, 193 Histones, 178, 193 Homeostasis, 10, 193, 207, 218 Homologous, 190, 193, 216, 217, 220, 223 Hormonal, 172, 181, 193 Hormone, 71, 95, 174, 181, 185, 187, 190, 193, 198, 211, 215, 222 Hybrid, 50, 193 Hydrogen, 47, 167, 173, 176, 184, 188, 191, 193, 198, 202, 204, 206, 208, 212, 220 Hydrogen Peroxide, 47, 176, 191, 193, 198, 220 Hydrolysis, 173, 174, 193, 198, 210, 212 Hydrophobic, 184, 191, 194, 199 Hydroxides, 194 Hydroxyl Radical, 47, 194 Hydroxylysine, 179, 194 Hydroxyproline, 179, 194 Hygienic, 194, 217 Hyperbaric, 23, 194 Hyperbaric oxygen, 23, 194 Hyperbilirubinemia, 194, 197 Hypercapnia, 41, 66, 118, 194 Hyperoxia, 14, 194 Hyperplasia, 38, 52, 194 Hypersecretion, 34, 37, 52, 194 Hypersensitivity, 169, 183, 187, 194, 198, 215, 216 Hyperstimulation, 16, 194 Hypertension, 20, 35, 53, 98, 129, 137, 138, 152, 176, 192, 194, 201, 210, 222 Hypertrophy, 38, 194 Hypothalamus, 173, 194, 209 Hypoventilation, 10, 194 Hypoxanthine, 194, 225

Hypoxemia, 20, 22, 46, 194 Hypoxia, 10, 36, 45, 194 I Idiopathic, 56, 65, 194 Imaging procedures, 194, 223 Immersion, 116, 194 Immune system, 7, 11, 12, 16, 27, 29, 35, 185, 195, 198, 200, 208, 224, 225 Immunity, 7, 11, 12, 17, 27, 29, 35, 84, 195 Immunization, 195, 216 Immunocompromised, 137, 195 Immunohistochemistry, 41, 195 Immunologic, 41, 195 Immunology, 56, 62, 86, 168, 195, 197 Immunosuppressive, 191, 195 Immunosuppressive therapy, 195 Immunotherapy, 14, 184, 195 Impairment, 4, 16, 34, 40, 177, 188, 195 In situ, 136, 195 In vitro, 10, 30, 50, 52, 54, 190, 195, 222 In vivo, 10, 16, 52, 85, 190, 195, 206, 222 Incision, 195, 197 Induction, 54, 170, 195 Infarction, 7, 12, 27, 28, 30, 35, 195 Infiltration, 38, 55, 196 Influenza, 73, 196 Infusion, 25, 196 Ingestion, 175, 196 Inhalation, 34, 59, 62, 72, 77, 168, 196, 197 Inhalation Exposure, 34, 196 Initiation, 15, 196 Innervation, 38, 196 Inorganic, 194, 196, 203 Inotropic, 185, 196 Insight, 26, 50, 196 Insomnia, 11, 196 Institutionalization, 33, 196 Intensive Care, 35, 83, 88, 105, 109, 196 Intensive Care Units, 35, 196 Intercostal, 196, 215 Interferon, 25, 49, 54, 196 Interferon-alpha, 196 Interleukins, 45, 196 Intermittent, 10, 197 Interstitial, 19, 56, 197, 201 Intervention Studies, 58, 197 Intracellular, 41, 50, 178, 191, 195, 197, 201, 204, 214, 216 Intracellular Membranes, 197, 201 Intravascular, 35, 197 Intravenous, 108, 196, 197 Intrinsic, 168, 173, 197

233

Intubation, 104, 177, 197 Invasive, 5, 25, 42, 87, 92, 195, 197, 200, 206 Investigative Techniques, 56, 197 Involuntary, 187, 197, 203, 214, 217, 218 Ion Channels, 41, 197, 220 Ionization, 197 Ionizing, 31, 169, 197 Ions, 129, 173, 186, 190, 193, 197 Ipratropium, 70, 108, 129, 197 Irritants, 24, 197 Ischemia, 170, 172, 183, 197 J Jaundice, 140, 194, 197 K Kb, 144, 198 Keratolytic, 183, 198 Kidney Disease, 134, 144, 198 Kinetic, 197, 198 L Laminin, 173, 188, 198 Laryngeal, 136, 198 Laryngectomy, 138, 198 Larynx, 134, 198, 223 Latent, 54, 198 Length of Stay, 57, 94, 198 Lens, 176, 198 Leptin, 71, 88, 198 Lesion, 20, 181, 198, 199, 223 Leukemia, 5, 137, 190, 198 Leukocyte Disorders, 137, 198 Leukotrienes, 172, 185, 198 Ligament, 198, 211 Linkage, 8, 16, 28, 80, 190, 198, 207 Lipid, 13, 42, 171, 191, 198, 199, 206 Lipid Peroxidation, 13, 42, 198, 206 Lipolysis, 65, 198 Lipopolysaccharide, 42, 55, 198 Lipoprotein, 51, 199 Liver, 134, 137, 140, 167, 169, 172, 173, 174, 178, 193, 199, 210, 216, 224 Liver cancer, 140, 199 Liver scan, 199, 216 Lobe, 199, 207 Lobectomy, 31, 104, 199 Localization, 16, 36, 195, 199 Localized, 37, 41, 50, 183, 189, 195, 198, 199, 209, 223 Longitudinal Studies, 13, 182, 199 Longitudinal study, 51, 199 Low-density lipoprotein, 199 Lumbar, 173, 199

Lung Transplantation, 25, 65, 199 Lung volume, 18, 40, 55, 86, 178, 199 Lupus, 199, 221 Lymphatic, 186, 195, 199, 201 Lymphocyte Subsets, 86, 199 Lymphocytes, 53, 54, 171, 195, 199, 200, 214, 225 Lymphocytic, 52, 200 Lymphoid, 171, 199, 200 Lymphoma, 137, 200 Lysine, 184, 193, 194, 200 M Macrophage, 14, 34, 42, 200 Magnetic Resonance Imaging, 31, 200, 216 Major Histocompatibility Complex, 192, 200 Malignant, 167, 171, 199, 200, 203 Malignant tumor, 200, 203 Malnutrition, 122, 169, 172, 200 Mammary, 181, 200 Manifest, 56, 200 Matrix metalloproteinase, 79, 200 Mechanical ventilation, 108, 122, 200 Mediate, 47, 49, 185, 200 Mediator, 200, 217 Medical Staff, 185, 200 MEDLINE, 145, 200 Medullary, 41, 200 Meiosis, 200, 220, 224 Melanin, 201, 208, 223 Membrane Fusion, 37, 201 Membrane Lipids, 201, 208 Memory, 183, 201 Meninges, 177, 201 Menopause, 201, 210 Mental, iv, 4, 14, 144, 146, 177, 179, 183, 184, 189, 201, 205, 212, 214 Mental Health, iv, 4, 14, 144, 146, 201, 205, 212 Mesenchymal, 49, 201 Mesenteric, 201, 210 Meta-Analysis, 86, 89, 90, 97, 98, 201 Metabolic disorder, 140, 201 Metastasis, 200, 201 Metoprolol, 119, 201 Microbe, 201, 222 Microbiology, 51, 64, 167, 201 Microfilaments, 37, 201 Microorganism, 201, 207, 225 Micro-organism, 183, 201 Microscopy, 41, 50, 173, 201 Mineralocorticoids, 168, 181, 202

234

Chronic Obstructive Pulmonary Disease

Mitochondrial Swelling, 202, 203 Mitosis, 172, 202 Mobility, 33, 202 Mobilization, 73, 202 Modeling, 33, 41, 202 Modification, 33, 202, 213 Modulator, 10, 202 Molecule, 13, 40, 171, 173, 179, 185, 186, 187, 193, 202, 206, 214 Monitor, 21, 40, 92, 202, 205 Monoclonal, 20, 44, 202, 213 Monocytes, 202, 214 Mononuclear, 202, 223 Morphological, 45, 186, 202 Motility, 190, 202, 217 Mucinous, 190, 202 Mucins, 47, 191, 202 Mucolytic, 167, 175, 202 Mucosa, 52, 199, 202, 203 Mucus, 20, 34, 45, 47, 52, 202 Multicenter Studies, 20, 203 Multicenter study, 57, 203 Multiple Myeloma, 137, 203 Muscle Hypertonia, 203, 204 Mustard Gas, 197, 203 Myalgia, 196, 203 Mydriatic, 184, 203 Myocardial infarction, 7, 11, 12, 26, 27, 29, 32, 33, 34, 85, 181, 203 Myocarditis, 76, 203 Myocardium, 170, 203 N Naloxone, 108, 203 Nasal Cavity, 38, 203 Nasal Mucosa, 196, 203 Nasal Septum, 203 Nasopharynx, 52, 203 NCI, 1, 133, 143, 203 Necrosis, 55, 172, 195, 203 Neonatal, 35, 203 Nephropathy, 198, 203 Nerve Fibers, 36, 203 Nervous System, 10, 23, 36, 168, 173, 177, 200, 204, 207, 208, 220, 221 Neural, 36, 168, 170, 204 Neuromuscular, 83, 137, 167, 204 Neuromuscular Diseases, 137, 204 Neuromuscular Junction, 167, 204 Neuronal, 36, 41, 78, 204 Neurons, 10, 36, 40, 183, 187, 190, 203, 204, 220 Neuropeptides, 36, 204

Neurophysiology, 37, 183, 204 Neuropsychological Tests, 18, 204 Neurotransmitter, 36, 167, 175, 185, 191, 197, 204, 205, 219, 220 Neutrons, 169, 204, 213 Neutrophil, 14, 47, 55, 66, 204 Nicotine, 28, 204 Nitric Oxide, 25, 32, 35, 40, 42, 54, 204 Nitrogen, 54, 169, 170, 182, 188, 189, 204, 223 Nodose, 10, 205 Nonverbal Communication, 205, 212 Norepinephrine, 168, 185, 204, 205 Nosocomial, 64, 205 Nuclear, 48, 85, 173, 186, 190, 203, 205 Nuclei, 169, 186, 190, 193, 200, 202, 204, 205, 207, 212 Nucleic acid, 194, 205, 213, 215 Nucleus, 10, 172, 173, 178, 182, 184, 199, 200, 202, 204, 205, 211, 212, 218 Nursing Care, 134, 205 Nutritional Status, 87, 205 O Occupational Exposure, 24, 44, 53, 59, 205 Occupational Health, 16, 31, 34, 205 Occupational Medicine, 44, 205 Occupational Therapy, 33, 112, 205 Office Visits, 6, 205 Ointments, 205, 217, 225 Opacity, 176, 205 Opiate, 203, 205 Organ Culture, 205, 222 Osteoporosis, 23, 93, 129, 206 Otitis, 48, 52, 206 Otitis Media, 48, 52, 206 Outpatient, 93, 115, 206 Oxidants, 51, 118, 206 Oxidation, 167, 171, 174, 182, 191, 198, 206, 221 Oxidation-Reduction, 174, 206 Oxidative Stress, 13, 23, 43, 55, 72, 74, 106, 206 Oximetry, 97, 115, 206 Oxygen Consumption, 188, 206, 215 Oxygenation, 183, 194, 206 P Palate, 203, 206 Palliative, 121, 206, 221 Pancreas, 134, 167, 174, 206, 216, 219, 223 Panniculitis, 140, 206 Parasympathetic Nervous System, 36, 207 Parenchyma, 54, 207

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Parietal, 207, 209 Partial remission, 207, 214 Particle, 32, 34, 41, 44, 53, 59, 207, 218 Patch, 41, 181, 207 Pathogen, 52, 84, 207 Pathologic, 15, 31, 47, 172, 174, 181, 194, 207 Pathologic Processes, 172, 207 Pathophysiology, 14, 74, 136, 137, 207 Patient Education, 70, 96, 101, 138, 152, 153, 158, 160, 165, 207 Peak flow, 60, 70, 207 Pedigree, 16, 207 Pelvic, 207, 211 Peptide, 45, 178, 198, 207, 210, 211, 212 Peptide Chain Elongation, 178, 207 Perfusion, 104, 194, 207 Pericardium, 207, 221 Periodontal disease, 64, 68, 207 Perioperative, 137, 207 Peripheral blood, 8, 13, 26, 196, 208 Peripheral Nervous System, 186, 204, 208, 219 Peripheral Nervous System Diseases, 204, 208 Peritoneal, 172, 208 Peritoneal Cavity, 172, 208 Peroxide, 47, 208 PH, 13, 35, 108, 208 Phagocyte, 206, 208 Pharmacokinetic, 208 Pharmacologic, 37, 170, 192, 208, 222 Pharmacotherapy, 57, 62, 65, 77, 123, 208 Pharynx, 196, 203, 208 Phenotype, 7, 12, 13, 25, 27, 28, 30, 35, 52, 208 Phenylalanine, 208, 223 Phosphodiesterase, 63, 74, 208 Phospholipids, 25, 188, 199, 201, 208 Phosphorus, 176, 208, 209 Phosphorylation, 50, 209 Photocoagulation, 178, 209 Physical Examination, 137, 209 Physical Fitness, 136, 188, 209 Physical Therapy, 33, 113, 116, 118, 126, 209 Physiologic, 41, 45, 49, 53, 75, 122, 124, 168, 192, 209, 214, 217 Physiology, 45, 65, 75, 98, 102, 104, 106, 127, 204, 209 Pilot study, 118, 120, 124, 125, 209 Pitch, 209, 225

Pituitary Gland, 181, 209 Plants, 169, 172, 176, 184, 191, 205, 209, 210, 216, 222 Plasma, 37, 42, 50, 51, 76, 84, 169, 171, 177, 178, 181, 189, 191, 193, 201, 202, 203, 209, 216 Plasma cells, 171, 203, 209 Plasma protein, 169, 181, 209 Plasticity, 10, 209 Platelet Aggregation, 204, 209, 222 Platelets, 204, 209, 214 Pleura, 209 Pleural, 67, 209 Pneumococcal Infections, 17, 210 Pneumonia, 57, 64, 95, 181, 210 Polymorphic, 49, 210 Polypeptide, 169, 179, 189, 210, 211, 225 Polysaccharide, 171, 210, 212 Polyunsaturated fat, 25, 117, 210, 222 Population Density, 32, 210 Portal Hypertension, 140, 210 Portal Vein, 140, 210 Positive pressure ventilation, 92, 122, 210 Posterior, 170, 172, 173, 185, 206, 210 Postmenopausal, 95, 206, 210 Postnatal, 10, 38, 210 Postsynaptic, 10, 210, 221 Post-translational, 48, 210 Practice Guidelines, 146, 210 Precancerous, 210 Precursor, 172, 185, 186, 187, 205, 208, 210, 223 Prednisolone, 210 Prednisone, 93, 210 Premalignant, 15, 210 Preoperative, 137, 211 Presynaptic, 204, 211, 220, 221 Prevalence, 15, 18, 25, 33, 42, 63, 134, 211 Primary endpoint, 15, 211 Progesterone, 211, 219 Progression, 25, 31, 55, 86, 170, 211 Progressive, 15, 30, 58, 117, 134, 178, 183, 185, 203, 211, 212, 223 Proline, 179, 194, 211 Prophase, 211, 220, 224 Prophylaxis, 100, 211, 224 Prospective study, 95, 199, 211 Prostaglandins, 172, 185, 211 Prostate, 51, 174, 211, 223 Protease, 49, 179, 211 Protein C, 38, 169, 171, 179, 199, 211, 224 Protein Conformation, 169, 211

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Chronic Obstructive Pulmonary Disease

Protein Isoforms, 5, 169, 211 Protein S, 174, 178, 187, 211 Proteinuria, 203, 212 Proteoglycans, 173, 188, 212 Proteolytic, 179, 189, 212 Protocol, 5, 22, 77, 212 Protons, 169, 193, 197, 212, 213 Proximal, 37, 41, 184, 203, 211, 212 Psychiatric, 23, 57, 212 Psychiatry, 46, 57, 63, 189, 212, 224 Psychic, 201, 212 Psychotherapy, 61, 212 Public Health, 13, 17, 20, 32, 46, 51, 53, 91, 109, 133, 146, 212 Public Policy, 145, 212 Publishing, 60, 113, 136, 137, 212 Pulmonary Alveoli, 194, 212 Pulmonary Artery, 20, 65, 69, 174, 212, 224 Pulmonary Fibrosis, 8, 56, 150, 212 Pulmonary hypertension, 8, 35, 212 Pulmonary Ventilation, 212, 215 Pulse, 31, 115, 202, 206, 212 Pupil, 184, 203, 213 Purifying, 30, 52, 184, 213 Purines, 213, 225 R Race, 33, 169, 213 Racemic, 169, 213 Radiation, 31, 170, 189, 194, 197, 213, 216, 225 Radiation therapy, 194, 213 Radioactive, 175, 192, 193, 197, 199, 205, 213, 216 Radioisotope, 213, 223 Radiopharmaceutical, 190, 213 Random Allocation, 213 Randomization, 19, 20, 213 Randomized, 6, 15, 18, 21, 22, 42, 45, 50, 51, 61, 77, 96, 98, 124, 185, 213 Randomized clinical trial, 18, 21, 51, 213 Randomized Controlled Trials, 98, 213 RANTES, 42, 214 Reactive Oxygen Species, 45, 47, 214 Receptor, 10, 14, 18, 20, 32, 38, 42, 48, 50, 66, 72, 108, 167, 171, 177, 185, 214, 217 Receptors, Serotonin, 214, 217 Recombination, 190, 214 Rectum, 171, 179, 189, 190, 211, 214 Refer, 1, 179, 186, 189, 199, 204, 205, 214, 222 Reflex, 36, 214 Refraction, 214, 218

Regimen, 137, 185, 208, 214 Rehabilitation Centers, 57, 214 Rehabilitative, 57, 83, 214 Reliability, 70, 125, 214 Remission, 47, 214 Residual Volume, 42, 214 Respirable, 34, 44, 214 Respiration, 36, 68, 75, 88, 99, 118, 121, 171, 175, 176, 177, 202, 215 Respirator, 200, 210, 215 Respiratory Burst, 55, 215 Respiratory distress syndrome, 56, 215 Respiratory failure, 64, 74, 92, 98, 108, 115, 215 Respiratory Muscles, 127, 135, 215 Respiratory Physiology, 66, 69, 71, 72, 73, 77, 81, 83, 88, 90, 91, 102, 105, 120, 125, 127, 215, 224 Respiratory System, 37, 168, 215 Respiratory Therapy, 126, 215 Respite Care, 134, 215 Resuscitation, 215 Reticular, 41, 215 Retrospective, 33, 215 Reverberant, 184, 215 Rheumatoid, 137, 206, 215 Rheumatoid arthritis, 137, 215 Rhinitis, 197, 215 Ribonucleic acid, 42, 215 Ribose, 167, 215 Risk factor, 3, 23, 24, 26, 79, 140, 185, 187, 211, 215 Rod, 178, 216 S Saline, 175, 216 Saphenous, 181, 216 Saphenous Vein, 181, 216 Saponins, 216, 219 Scans, 26, 216 Sclerosis, 134, 216 Screening, 31, 99, 100, 101, 102, 103, 140, 178, 216 Sebaceous, 183, 197, 216 Sebaceous gland, 183, 197, 216 Secretion, 30, 36, 37, 49, 65, 181, 194, 196, 202, 216 Secretory, 16, 37, 216, 220 Segregation, 16, 214, 216 Selenium, 51, 216 Selenomethionine, 51, 216 Self Care, 167, 216 Semen, 211, 216

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Semisynthetic, 178, 216 Senile, 206, 216 Sensitization, 38, 216 Sequencing, 7, 12, 27, 28, 29, 30, 35, 217 Serotonin, 41, 204, 208, 214, 217, 223 Serum, 32, 42, 49, 51, 52, 53, 119, 169, 179, 199, 202, 217, 223 Shivering, 217, 221 Side effect, 134, 168, 217, 222 Signs and Symptoms, 99, 136, 150, 153, 214, 217 Skeletal, 23, 75, 76, 91, 170, 178, 203, 217, 218 Skeleton, 167, 217 Skin Care, 134, 217 Sleep apnea, 10, 41, 45, 217 Small intestine, 178, 193, 217 Smoking Cessation, 18, 21, 25, 101, 217 Smooth muscle, 36, 38, 40, 49, 97, 108, 175, 203, 217, 218, 219 Soaps, 217 Social Environment, 213, 217 Social Isolation, 33, 217 Social Security, 214, 218 Social Support, 14, 134, 218, 219 Sodium, 108, 202, 217, 218 Solitary Nucleus, 173, 218 Soma, 218 Somatic, 14, 200, 202, 208, 218 Sound wave, 180, 218 Soybean Oil, 210, 218 Spasm, 204, 218 Specialist, 154, 184, 218 Species, 47, 54, 187, 193, 200, 202, 210, 213, 214, 218, 219, 223, 225 Specificity, 5, 168, 218 Spectroscopic, 25, 218 Spectrum, 9, 13, 26, 58, 140, 218 Sphincter, 198, 218 Spinal cord, 175, 177, 190, 201, 204, 207, 208, 214, 218, 220 Spirometry, 21, 25, 26, 31, 102, 150, 218 Splenic Vein, 210, 219 Sputum, 13, 15, 18, 21, 45, 52, 60, 85, 89, 108, 219 Staging, 216, 219 Steel, 178, 219 Steroid, 14, 17, 18, 41, 181, 216, 219 Stimulus, 185, 187, 196, 197, 214, 219, 221 Stomach, 167, 185, 187, 190, 193, 208, 217, 219

Stress, 11, 13, 14, 38, 55, 93, 164, 173, 177, 206, 215, 219 Stress management, 11, 219 Stroke, 33, 59, 134, 137, 144, 152, 176, 219 Stroma, 207, 219 Subacute, 195, 219 Subclinical, 195, 219 Subcutaneous, 140, 168, 185, 206, 219 Subspecies, 218, 219 Substance P, 187, 216, 219 Substrate, 187, 219 Sudden death, 32, 219 Sulfur, 114, 188, 219, 220 Sulfur Dioxide, 114, 220 Superoxide, 43, 54, 215, 220 Superoxide Dismutase, 43, 54, 220 Supplementation, 51, 94, 118, 119, 123, 220 Support group, 165, 220 Suppression, 181, 220 Surfactant, 45, 220 Survival Rate, 22, 220 Sympathetic Nervous System, 173, 207, 220 Sympathomimetic, 185, 187, 205, 220 Symphysis, 177, 211, 220 Symptomatology, 57, 220 Synapse, 168, 204, 207, 211, 220, 223 Synapsis, 220 Synaptic, 10, 36, 204, 220, 221 Synaptic Transmission, 10, 36, 204, 220 Synaptic Vesicles, 221 Synergistic, 4, 221 Systemic, 17, 21, 32, 34, 42, 53, 87, 89, 100, 106, 137, 171, 174, 187, 195, 210, 213, 221, 224 Systemic disease, 137, 221 Systemic lupus erythematosus, 137, 221 Systolic, 194, 221 T Tachycardia, 108, 122, 164, 173, 221 Tachypnea, 164, 173, 221 Tear Gases, 197, 221 Tendon, 190, 221 Theophylline, 21, 93, 101, 108, 119, 130, 213, 221 Therapeutics, 38, 65, 66, 74, 77, 105, 114, 197, 221 Thermal, 42, 204, 221 Thermogenesis, 65, 221 Thoracic, 9, 42, 65, 68, 69, 75, 85, 88, 95, 99, 100, 118, 121, 173, 184, 209, 221, 225 Threshold, 19, 64, 115, 122, 125, 194, 221

238

Chronic Obstructive Pulmonary Disease

Thrombin, 189, 209, 211, 221 Thrombomodulin, 211, 221 Thrombosis, 7, 12, 27, 28, 30, 32, 35, 212, 219, 221 Thromboxanes, 172, 185, 221 Thyroid, 137, 222, 223 Tinnitus, 206, 222 Tissue Culture, 41, 222 Tolerance, 29, 123, 167, 191, 222 Tomography, 222 Tone, 36, 203, 222 Tonus, 222 Tooth Preparation, 167, 222 Topical, 172, 193, 217, 222, 225 Torsion, 195, 222 Toxic, iv, 23, 42, 55, 172, 176, 184, 195, 204, 216, 220, 222 Toxicity, 23, 34, 35, 185, 222 Toxicokinetics, 222 Toxicology, 23, 44, 62, 64, 108, 134, 146, 222 Toxin, 186, 222 Trace element, 42, 222 Tracer, 32, 223 Trachea, 36, 175, 198, 208, 222, 223 Tracheostomy, 89, 223 Traction, 178, 223 Tractus, 10, 223 Transcutaneous, 125, 223 Transfection, 35, 174, 190, 223 Translating, 15, 101, 223 Translational, 56, 223 Translocate, 34, 223 Translocation, 178, 187, 223 Transmitter, 10, 167, 185, 197, 200, 205, 221, 223 Transplantation, 67, 178, 195, 200, 223 Trauma, 192, 203, 222, 223 Tryptophan, 179, 217, 223 Tuberculosis, 56, 88, 102, 136, 137, 199, 223 Tumor marker, 174, 223 Tumor Necrosis Factor, 13, 18, 25, 42, 89, 223 Tumour, 190, 223 Tunica, 202, 223 Tyrosine, 15, 54, 185, 223 U Ulcer, 183, 223, 224 Ulceration, 183, 224 Univalent, 194, 206, 224 Urea, 98, 224 Urethra, 211, 224

Urinary, 51, 74, 102, 224, 225 Urine, 42, 174, 184, 212, 224 V Vaccination, 73, 151, 224 Vaccine, 17, 212, 224 Valves, 137, 224 Vascular, 13, 19, 35, 45, 67, 170, 183, 186, 195, 204, 224 Vascular endothelial growth factor, 13, 45, 224 Vascular Resistance, 170, 224 Vasoconstriction, 35, 187, 224 Vasodilator, 20, 35, 175, 185, 224 VE, 99, 112, 224 Vein, 170, 197, 205, 210, 216, 219, 224 Venous, 7, 11, 12, 26, 27, 29, 34, 182, 212, 224 Venous Thrombosis, 7, 11, 12, 26, 27, 29, 34, 224 Ventilation, 18, 92, 104, 105, 121, 152, 224 Ventricle, 194, 212, 221, 224 Ventricular, 126, 170, 224 Ventricular Function, 126, 224 Venules, 174, 224 Vertigo, 206, 224 Veterinary Medicine, 145, 225 Viral, 35, 55, 104, 105, 167, 196, 225 Virulence, 52, 173, 222, 225 Virus, 54, 196, 225 Viscera, 218, 225 Visceral, 173, 225 Visceral Afferents, 173, 225 Viscosity, 45, 167, 225 Vital Capacity, 189, 225 Vitro, 10, 225 Vivo, 10, 225 Voice Disorders, 136, 225 W White blood cell, 53, 137, 171, 192, 199, 200, 202, 204, 209, 225 Windpipe, 175, 186, 208, 222, 225 Wound Healing, 200, 225 X Xanthine, 43, 106, 225 Xanthine Oxidase, 43, 225 Xenograft, 170, 225 X-ray, 31, 164, 165, 180, 205, 213, 216, 225 Y Yeasts, 208, 225 Z Zinc Oxide, 34, 225 Zymogen, 211, 225

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Chronic Obstructive Pulmonary Disease