BACTERIAL PNEUMONIA 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., 1960Bacterial Pneumonia: 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: 0-497-00121-7 1. Bacterial Pneumonia-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on bacterial pneumonia. 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 BACTERIAL PNEUMONIA .......................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Bacterial Pneumonia ..................................................................... 4 E-Journals: PubMed Central ....................................................................................................... 46 The National Library of Medicine: PubMed ................................................................................ 46 CHAPTER 2. ALTERNATIVE MEDICINE AND BACTERIAL PNEUMONIA .......................................... 81 Overview...................................................................................................................................... 81 National Center for Complementary and Alternative Medicine.................................................. 81 Additional Web Resources ........................................................................................................... 86 General References ....................................................................................................................... 87 CHAPTER 3. MULTIMEDIA ON BACTERIAL PNEUMONIA ............................................................... 89 Overview...................................................................................................................................... 89 Audio Recordings......................................................................................................................... 89 CHAPTER 4. PERIODICALS AND NEWS ON BACTERIAL PNEUMONIA............................................. 91 Overview...................................................................................................................................... 91 News Services and Press Releases................................................................................................ 91 Academic Periodicals covering Bacterial Pneumonia .................................................................. 93 CHAPTER 5. RESEARCHING MEDICATIONS .................................................................................... 95 Overview...................................................................................................................................... 95 U.S. Pharmacopeia....................................................................................................................... 95 Commercial Databases ................................................................................................................. 96 APPENDIX A. PHYSICIAN RESOURCES ............................................................................................ 99 Overview...................................................................................................................................... 99 NIH Guidelines............................................................................................................................ 99 NIH Databases........................................................................................................................... 101 Other Commercial Databases..................................................................................................... 103 APPENDIX B. PATIENT RESOURCES ............................................................................................... 105 Overview.................................................................................................................................... 105 Patient Guideline Sources.......................................................................................................... 105 Finding Associations.................................................................................................................. 109 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 111 Overview.................................................................................................................................... 111 Preparation................................................................................................................................. 111 Finding a Local Medical Library................................................................................................ 111 Medical Libraries in the U.S. and Canada ................................................................................. 111 ONLINE GLOSSARIES................................................................................................................ 117 Online Dictionary Directories ................................................................................................... 117 BACTERIAL PNEUMONIA DICTIONARY ............................................................................ 119 INDEX .............................................................................................................................................. 175
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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 bacterial pneumonia 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 bacterial pneumonia, 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 bacterial pneumonia, 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 bacterial pneumonia. 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 bacterial pneumonia, 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 bacterial pneumonia. The Editors
1
From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON BACTERIAL PNEUMONIA Overview In this chapter, we will show you how to locate peer-reviewed references and studies on bacterial pneumonia.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and bacterial pneumonia, 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 “bacterial pneumonia” (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: •
Relationship Between Chronic Oral Infectious Diseases and Systemic Diseases Source: Bulletin of the Tokyo Dental College. 39(3): 165-174. August 1998. Contact: Available from Tokyo Dental College. 1-2-2 Masago, Mihama-Ku, Chiba 2618502, Japan. Summary: There are over 300 species of bacteria forming populations of several hundred billion in the human oral cavity. When the mouth is not sufficiently cleaned, the number of bacteria reaches a thousand billion. This article explores the relationship between chronic oral infectious diseases and systemic diseases. The authors explain that oral health care, primarily mouth cleaning, is important for not only oral disease, but also for a healthy life. Topics include oral bacterial endocarditis, the relationship
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Bacterial Pneumonia
between periodontopathic bacteria and cardiovascular diseases, pathogens for bacterial pneumonia in the oral cavity, oral chronic infectious diseases and secondary diseases, heat shock proteins produced by oral bacteria that may induce dermal diseases, gingivitis pathogens and pregnancy disorders, and opportunistic infections and the significance of oral hygiene. 8 figures. 3 tables. 57 references.
Federally Funded Research on Bacterial Pneumonia The U.S. Government supports a variety of research studies relating to bacterial pneumonia. 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 bacterial pneumonia. 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 bacterial pneumonia. The following is typical of the type of information found when searching the CRISP database for bacterial pneumonia: •
Project Title: ALCOHOL EFFECT OPPORTUNISTIC DISEASES
ON
SIV
PRIMARY INFECTION
AND
Principal Investigator & Institution: Nelson, Steve; Louisiana State Univ Hsc New Orleans New Orleans, La 70112 Timing: Fiscal Year 2002 Summary: Bacterial pneumonia substantially contributes to the morbidity and mortality among individuals abusing alcohol. The goal of this project is to elucidate the in vivo events that lead to impaired lung host defense against infection in acute and chronic alcohol-treated rats. We proposed that alcohol disrupts the normal evolution of proinflammatory cytokines elaborated by the alveolar macrophage (AM) during the course of an infectious challenge which leads to an acquired immunodeficient state. Our previous work has shown that alcohol suppresses AM expression of tumor necrosis factor-alpha (TNF), which is known to be a potent stimulus for the AM to produce granulocyte colony-stimulating factor (G- CSF). G-CSF is a cytokine that increases both the number and function of neutrophils (PMN). It is our hypothesis that alcohol-induced inhibition of AM-derived TNF directly contributes to the adverse effects of ethanol on PMN function and host defense by suppressing the normal autocrine amplification pathway responsible for macrophage G-CSF production. This proposal will test this hypothesis in a rat model and has 4 Specific Aims; 1) to characterize the effect of alcohol on cytokine responses to in vivo and ex vivo LPS challenge; 2) to delineate the mechanism(s) of alcohol-induced suppression of TNF and G-CSF; 3) to determine the role of endogenous G-CSF on the antibacterial defenses of the lung and PMN kinetic 2
Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
Studies
5
during an intrapulmonary infectious challenge; 4) to examine whether exogenously administered cytokines can reverse or attenuated the host defense deficits induced by alcohol. To accomplish these aims we will: a) examine the effect of alcohol dose on LPSinduced suppression of TNF and G-CSF both in vivo and ex vivo in isolated AM, the duration of this suppression, and whether depletion of TNF alters the in vivo and ex vivo LPS-induced G-CSF responses; b) determine if alcohol- induced increases in corticosterone contribute to the immunosuppressive effects of alcohol on lung host defense; c) examine the effects of an anti-G CSF antibody on pulmonary antibacterial defense and neutrophil function during an infectious challenge; d) determine if the administration of gamma-interferon and/or G-CSF attenuates the suppressive effects of alcohol on lung host defense. The identification of the basic mechanisms underlying alcohol-induced suppression of lung antibacterial defenses will increase our understanding of the host- cytokine network and may provide the foundation for innovative approaches in the treatment of these infections in susceptible patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ALCOHOL MODULATION OF RECEPTOR SITES FOR HIV AND PRODUCTION OF CHEMOKINES Principal Investigator & Institution: Bautista, Abraham P.; Scientist Administrator; Louisiana State Univ Hsc New Orleans New Orleans, La 70112
Review
Timing: Fiscal Year 2002 Summary: This proposal is based on the overall hypothesis that alcohol modulates the hepatic immune system at the plasma membrane and molecular levels by altering cell surface receptor expression (binding sites for HIV-1) and production of soluble mediators (chemokines) in hepatic non-parenchymal cells [NPC], i.e., Kupffer cells and sinusoidal endothelial cells. Specifically, acute or chronic alcohol regulates the expression of CD4, chemokine receptors and mannose-specific receptors on hepatic NPC as a result of ethanol-induced alteration in plasma membranes on hepatic NPC. This event could also lead to enhanced intracellular production of H2O2 which in turn activates NF-kappaB. The nuclear translocation and activation of NF-kappaB, a transcription factor, enhances the expression of m-RNA and synthesis of alpha and betachemokines. These chemokines could potentially block the binding of HIV-1 or exacerbate its replication in CD4 lymphocytes. The HIV-1 gp120-induced production of beta-chemokines by hepatic NPC may also be modulated by alcohol. The liver is the major organ for microbial clearance and ethanol metabolism. Thus, hepatic cells become susceptible to these agents that could have an impact on the liver itself as well as on the overall homeostasis of the host. For example increased production of pro-inflammatory mediators by hepatic NPC which are the largest contributors of these agents, may also regulate functions of immunocompetent cells in other organs. Thus, based on these considerations, the following specific aims are proposed. Specific aim 1: To determine the effect of acute or chronic alcohol intoxication of hiv-1 GP120 binding, expression of mannose-specific receptors and CD4 on hepatic NPC. The internalization and degradation of HIV-1 gp120 by hepatic NPC will be examined. Specific aim 2: To determine the effect of acute or chronic alcohol intoxication on the intracellular production of H2O2, activation of NF-kappaB, m-RNA expression and secretion of alpha (CINC or IL-8) and beta (Rantes, MIP-1 alpha, MIP-1beta, MCP-1) chemokines in hepatic NPC. The biological activity of HIV-1 gp120 on beta-chemokine production will be assessed, as well as the role of endogenous and exogenous endotoxin on the above parameters (specific aims 1&2). The latter objective will test the hypothesis that chronic alcohol-mediated influx of LPS from the gut to the circulation is responsible, at least in
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Bacterial Pneumonia
part, for the regulation of hepatic NPC functions at the plasma membrane and molecular levels. Specific aim 3: To determine the effect of chronic alcohol intoxication on hepatic NPC functions, i.e., superoxide anion production, phagocytosis, chemokine and cytokine production, chemokine receptor (CXCR4 & CCR5) expression and SIV gp120 binding. This study will also examine chemokine-mediated SIV-1 replication in a simian model of SIV-1/AIDS. The overall regulation of the above processes by alcohol may further comprise susceptible individuals to HIV-1 infections and opportunistic pathogens associated with this viral infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ALVEOLAR FACTORS IN UPTAKE OF LUNG SURFACTANT Principal Investigator & Institution: Wright, Jo Rae; Professor; Cell Biology; Duke University Durham, Nc 27710 Timing: Fiscal Year 2003; Project Start 01-JUL-1994; Project End 30-JUN-2007 Summary: (provided by applicant): Pulmonary surfactant plays important roles in reducing surface tension at the air-liquid interface of the lung and in regulating lung host defense. In order to carry out these roles, a functional pool of adequate surfactant must be maintained by balancing the rates of secretion and clearance. Studies from our and other laboratories have shown that clearance in the normal lung occurs via reuptake and recycling by type II cells, and via degradation by both type II cells and macrophages. Recently we have focused on understanding the factors that affect surfactant metabolism in the injured or inflamed lung and have discerned that inflammatory cells and bacterial products contribute significantly to surfactant degradation. Our recent preliminary data show that Pseudomonas aeruginosa, an important pulmonary pathogen, degrades SP-A and SP-D and we have identified enzymes, including Pseudomonas elastase, that contribute to this process. In addition, our preliminary data suggest that neutrophils and activated macrophages contribute substantially to surfactant degradation. The hypothesis to be tested in this competitive renewal is that infection and inflammation result in release of degradative enzymes from bacteria and from newly recruited inflammatory cells that result in enhanced degradation and decreases in surfactant pool size. The decrease in the pool of functional surfactant leads to altered lung homeostasis, including decreased lung compliance and increased susceptibility to infection and inflammation. Five specific aims are proposed to test this hypothesis. Specific Aim 1 is to determine if bacterial enzymes degrade surfactant lipids and proteins in vitro. Specific Aim 2 is to determine the role of a newly described P. aeruginosa enzyme, Protease IV, in degrading surfactant. Specific Aim 3 is to investigate the functional consequences of degradation of surfactant by bacterial enzymes in vitro. Specific Aim 4 is to determine if surfactant is degraded in vivo. Specific Aim 5 is to investigate the role of activated macrophages and neutrophils in the degradation of surfactant. Results from these studies will help determine if these mechanisms contribute to the alterations in surfactant pool size that are observed patients with acute lung injury. We propose that degradation of surfactant by bacterial enzymes and cells recruited in response to bacterial infection represent a novel mechanism of pathogen adaptation and manipulation of the host response which would contribute to alterations in surfactant pool size and resulting lung injury. Significance: An understanding of the factors that regulate surfactant metabolism in lung injury and infection should contribute to development of therapies targeted at inhibiting surfactant degradation for treatment of surfactant deficiency of diseases such as ARDS and bacterial pneumonia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies
•
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Project Title: ANALYSIS OF ASSOCIATION BETWEEN C. PNEUMONIAE AND MS Principal Investigator & Institution: Sriram, Subramaniam; Professor; Neurology; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2003 Summary: Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system (CNS). Although the etiology of MS is not known, there is considerable indirect evidence to suggest the role of infectious agents in the development of the disease. While a viral agent is still strongly considered, efforts to defect a virus in patients with MS have failed. We present preliminary data which argue that Chlamydiae Pneumoniae may be a candidate pathogen in MS. This inference is based on: a) the presence of PCR products to major outer membrane protein (MOMP) gene of C. pneumoniae in the cerebrospinal fluid (CSF) of patients with secondary progressive MS but not in other neurologic disease controls (OND); b) the presence of antibody to C. pneumonia antigens in the CSF of MS patients; and c) the presence of chlamydial antigens in brain autopsy specimens of patients who have died of MS. C. pneumoniae belongs to a genus of intracellular pathogens that are infectious to humans and other vertebrates. C. pneumoniae are implicated in many chronic diseases, including those presumed to be autoimmune. Chlamydiae cause chronic persistent inflammation in humans and other vertebrate animals and tissue injury in all cases appears to be immune mediated. Immune activation by C. pneumoniae includes induction of T cell response to heat shock proteins and production of pro-inflammatory cytokines. Our proposal sets out to meet the necessary criteria required to attribute a causal association between C. pneumoniae and MS. These would include the ability to detect the organism either directly by culture or by demonstrating the presence of C. pneumoniae DNA and mRNA and evidence of intracytoplasmic or organisms as proven by electron microscopy in the CNS tissue of patients with MS. Also, the presence of an immune response to C. pneumoniae that is contained within the CNS compartment will constitute strong circumstantial evidence of microbial infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ANIMAL TESTING OF A BLOCKING ANTIBODY OF PCRV Principal Investigator & Institution: Sawa, Teiji; Intermune Pharmaceuticals, Inc. 1710 Gilbreth Rd, #301 Burlingame, Ca 94010 Timing: Fiscal Year 2002; Project Start 01-JAN-2002; Project End 30-JUN-2003 Summary: (provided by applicant): This grant will determine the efficacy of a humanized monoclonal antibody in treating a lethal Pseudomonas-induced lung injury. We have shown that the airspace instillation of a strain of Pseudomonas aeruginosa that contains the type Il system predictably causes lung necrosis, sepsis and death (J Clin Invest 1999). We have also shown that the systemic administration of polyclonal antibody raised against recombinant PcrV, a type III bacterial protein involved in translocating the bacterial toxins into eukaryotic cells, prevented lung injury and death in mice pretreated with the antibody (Nature Med 1999). More recently, we have identified a mouse antiPcrV monoclonal antibody that when administered prior to the bacterial instillation, prevented mortality in mice airspace-infected with the virulent Pseudomonas. The proposed experiments will determine whether the systemic or lung administration of a humanized monoclonal antibody after the airspace instillation of the virulent Pseudomonas improves hemodynamics, gas exchange and/or improves the septicemia in airspace-infected, anesthetized rabbits. These results will be critical for
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Bacterial Pneumonia
deciding how to plan a clinical trial; the results will determine whether the antibody should be utilized as a therapy or as a prophylactic treatment. PROPOSED COMMERCIAL APPLICATIONS: Pseudomonas aeruginosa is a major cause of hospital infection, accounting for 20% of nosoconual pneumonias, 10-15% of nosocomial urinary tract infections, and 10% of sepsis. In addition, P. aeruginosa infection is the major cause of mortality in cystic fibrosis. Current treatment is associated with a high rate of antibiotic resistance and a 25-50% failure rate. The proposed treatment provides a novel approach to the prevention of P. aeruginosa infection in patients at high risk for this infection, including patients on ventilators, burn patients, patients with in-dwelling catheters, neutropenic patients, an patients with cystic fibrosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AZITHROMYCIN AND CORONARY EVENTS Principal Investigator & Institution: Cohn, Peter; State University New York Stony Brook Stony Brook, Ny 11794 Timing: Fiscal Year 2003 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: RESPONSE
BACTERIAL
MODULATION
OF
LUNG
INFLAMMATORY
Principal Investigator & Institution: Russo, Thomas A.; Associate Professor; Medicine; State University of New York at Buffalo Suite 211 Ub Commons Buffalo, Ny 14228 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 31-MAY-2005 Summary: (Unedited Applicant's Abstract): Gram-negative bacilli (GNB) are pathogens that are capable of causing severe, life-threatening pneumonia. More than 60 percent of nosocomial pneumonias are caused by GNB and associated mortality rates are often >50 percent. Over the last 10-15 years, there has been little improvement in outcome from this infection. As a result, this syndrome continues to cause significant morbidity and mortality and strongly contributes to the economic burden of our national health care system. The successful use of immune intervention in the treatment or modulation of infections has marked the beginning of a new era in the management of infectious diseases. There exists a delicate balance between an efficacious and injurious host defense response. An understanding of the host response in GNB pneumonia and how bacterial components affect this response will, in turn, lead to the development of rapid diagnostic tests that will enable the clinician to effectively utilize a variety of biologic modulators. It is also necessary to understand the relative role of bacterial components versus host factors in mediating damage to the lungs prior to therapeutic manipulations on which little is known. This information will enable us to appreciate the relative risk benefit ratio of altering the host response. Further, a more precise clarification of which host components are damaged is also needed. This knowledge may identify independent therapeutic interventions. Their global hypothesis is that surface components of GNB and/or secreted proteins differentially alter host antibacterial defenses and directly, and/or indirectly (by inflammatory mechanisms) promote lung injury. Preliminary data supports this hypothesis. These responses will have significant implications when attempting therapeutic immune interventions. The goals of this proposal are to determine the mechanisms by which the bacterial capsule and 0-specific antigen modulate neutrophil recruitment into the lungs in a diametrical manner and extend our evaluations on the relative roles of bacterial factors (e.g. hemolysin) and
Studies
9
bacterially induced host response elements in directly mediating the pathogenesis of lung injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PNEUMONIA
BACTERIAL
PREDICTORS
OF
SEVERE
NOSOCOMIAL
Principal Investigator & Institution: Hauser, Alan R.; Microbiology and Immunology; Northwestern University Office of Sponsored Research Chicago, Il 60611 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 31-DEC-2007 Summary: (provided by applicant): The long-term objective of the proposed study is to better understand the pathogenesis of hospital-acquired pneumonia caused by Pseudomonas aeruginosa. The general strategy is to characterize the role of the P. aeruginosa type III secretion system in hospital-acquired pneumonia. This complex secretion pathway transports and injects four known effector proteins into host cells: ExoS, ExoT, ExoU (also known as PepA), and ExoY. Interestingly, clinical isolates differ in the combination of effector proteins they secrete. Recent studies are beginning to define the role of individual effector proteins in pathogenesis. Preliminary studies using bacterial mutants indicate that ExoS, ExoT, ExoU, and ExoY all have cytotoxic effects on mammalian cells in cell culture systems. ExoT, ExoU, and possibly ExoS contribute to virulence in animal models of pneumonia. In addition, ExoU secretion is associated with worse clinical outcomes in humans with hospital-acquired pneumonia. Together, these findings support an important role for type III effector proteins in the acute pneumonia, although the exact role of each effector protein and the mechanisms by which these proteins lead to the pathophysiological consequences of pneumonia remain to be defined and are the subject of this proposal. Our preliminary data suggest that type III secretion contributes to bacterial persistence, dissemination, and mortality as well as neutrophil killing and suppression of proinflammatory cytokine release in a mouse model of pneumonia. Further defining the role of individual effector proteins in these processes is crucial to our understanding of the pathogenesis of hospital-acquired pneumonia caused by P. aeruginosa. It is hypothesized that specific effector proteins play an important role in the pathogenesis of hospital-acquired pneumonia, including the prevention of bacterial clearance by neutrophils. Furthermore, it is hypothesized that because of these effects secretion of specific effector proteins can be used as markers for strains associated with especially severe hospital-acquired pneumonia in human patients. Studies using both mice and humans will be performed to define the roles of these effector proteins in the pathogenesis of acute pneumonia, including modulation of the inflammatory response and resistance to neutrophil-mediated clearance, and to determine whether secretion of particular effector proteins serves as a marker for strains capable of causing especially severe disease in human patients with hospital-acquired pneumonia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIOLOGY OF CHLAMYDIA PNEUMONIAE CELL ENTRY Principal Investigator & Institution: Li, Erguang; Scripps Research Institute Tpc7 La Jolla, Ca 92037 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2004 Summary: (provided by applicant): Chlymadia pneumoniae is a common respiratory pathogen of human diseases. Virtually everyone is infected at some point in life, and reinfection occurs commonly. Epidemiological and histological studies show that C.
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Bacterial Pneumonia
pneumoniae infection is one of the leading environmental factors of atherosclerosis. C. pneumoniae infects and replicates within macrophage, endothelial, and epithelial cells. Infection of C. pneumoniae induces adhesion molecule up-regulation, increases inflammatory factor release, and causes foam cell formation, although the receptor(s) that mediates bacterial cell attachment, the signaling events that promote bacterial cell entry remain poorly understood. This proposal seeks to identify receptors for C. pneumoniae infection and define the signaling pathways that promote bacterial cell entry and infection-induced gene expression. We will use functional cloning and proteomics to identify the proteins as putative C. pneumoniae attachment receptors. We will define signal transduction pathways controlling C. pneumoniae cell entry and the infection-induced up-regulation of adhesion and inflammation molecules. We will define bacterial outer membrane components for activating these signaling pathways. These studies will further our understanding of chlamydial cell entry mechanisms and may lead to the development of new therapeutics for chlamydial infections. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: C3-BINDING AND -DEGRADING PROTEINS IN S. PNEUMONIAE Principal Investigator & Institution: Hostetter, Margaret K.; Professor and Chair; Pediatrics; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 23-SEP-2002; Project End 22-SEP-2004 Summary: (provided by applicant): Streptococcus pneumoniae remains a leading cause of morbidity and mortality in community acquired respiratory infections. The third component of complement, C3, stands as the central mediator of host defense in susceptible patients who lack anti-capsular antibody. Over the past 5 years, we have identified two C3-degrading enzymes from S. pneumoniae: CppA, which degrades the C3 beta-chain; and PhpA, which cleaves the C3 alpha-chain into previously unrecognized fragments. Neither proteinase has any homolog in the database, and both are expressed by a wide variety of encapsulated clinical isolates. Intranasal immunization of mice with recombinant rCppA reduced nasopharyngeal colonization with a serotype 3 organism. Immunization of mice with rPhpA significantly reduced bacteremia and increased survival; in separate experiments, immunization with rPhpA was more effective than the serotype 3 conjugate vaccine in reducing nasopharyngeal colonization. In addition to the protective effects of CppA and PhpA in vivo, cppA- and phpA- mutants are more susceptible to C3-mediated opsonophagocytosis in vitro than is the isogenic parent. This revised proposal focuses on the mechanisms by which CppA and PhpA enable S. pneumoniae to elude C3-mediated killing in blood and lung. In Specific Aim One, we will characterize the mechanism of proteolysis by which CppA degrades the C3 beta-chain using chromogenic substrates and standard protease inhibitors. Truncation constructs expressed in Lactococcus lactis will be used to map the active site. A cppA- mutant in an encapsulated serotype 4 will be constructed. Specific Aim Two will focus on PhpA, a 79 kDa proteinase that cleaves the C3 alpha-chain into novel fragments of 97 and 83 kDa. Possible biologic activities of these C3 fragments in inhibiting C3 or neutrophils will be assayed. Biochemical techniques will be employed to understand how full-length PhpA liberates an internal 20 kDa polypeptide that appears to account for the majority of C3-cleaving activity. A phpA- mutant in an encapsulated serotype 4 will be constructed. Specific Aim Three will use a standard killing assay and a double mutant to test for additive or synergistic effects of CppA and PhpA. Other opsonins in blood (fibronectin) and lung (surfactant protein A) will be assessed as potential substrates for CppA and PhpA. Specific Aim Four will employ cppA- and phpA- mutants in the encapsulated strain to understand whether the effects
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of CppA and PhpA on C3-mediated killing contribute to virulence in a rabbit model of pneumonia and bacteremia. This revised proposal will define the role of two potent immunogens in pneumococcal pathogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CD-18 DEPENDENT/INDEPENDENT WBC RESPONSES IN THE LUNG Principal Investigator & Institution: Doerschuk, Claire M.; Professor of Pediatrics and Pathology; Pediatrics; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2003; Project Start 01-AUG-1994; Project End 31-MAY-2008 Summary: (provided by applicant): Neutrophil emigration into the lungs can occur through at least two different pathways depending upon the stimulus, one that requires the CD11/CD18 adhesion complex, and one that does not. Our studies provide evidence that mice deficient in the NF-kappaB p65 (Rel A) subunit, mice deficient in both TNF R1 and IL-1R1, or mice with blockade of ICAM-1 have defects in E. coli-induced CD18dependent emigration. In contrast, mice deficient in the leukocyte non-receptor Src tyrosine kinases Lyn, Fgr, and Hck, in the small GTPase Rac2, or in interferon-(IFN-g) have defects in S. pneumoniae-induced CD18-independent but not E. coli-induced CD18-dependent emigration. Moreover, exogenous IFN-( switches CD18-dependent to CD18-independent emigration, whereas genetic deficiency of IFN-( switches CD18independent to CD18-dependent emigration. Studies comparing gene expression during these bacterial pneumonias also provided many new ideas. Our goal is, to understand the mechanisms, through which CD18-dependent and CD18-independent adhesion pathways are elicited and function; and to identify ways of modulating the acute inflammatory process to benefit the host. Our working hypothesis is that neutrophil emigration occurs through CD11/CD18-dependent pathways when early stages of host defense result in nuclear translocation of NF-kappaB, production of TNF-alpha and IL-1, and increased expression of ICAM-1 on pulmonary capillary endothelial cells, while CD11/CD18- independent mechanisms are selected when IFN-( is produced and the leukocyte Src kinases Lyn, Fgr, and Hck and the small GTPase Rac2 are activated. The proposed Aims will test this hypothesis and examine the role of each of these required molecules in the mechanisms of neutrophil emigration. Aim 1 will determine the role of NF-(B -mediated gene transcription and the function of TNF-alpha and IL-1 in CD18dependent and -independent neutrophil emigration. Aim 2 will determine the role of IFN-g in CD18- independent emigration. Aim 3 will determine the role of Lyn, Fgr, and Hck and of Rac2, and the functional relationships between these molecules and IFN-g in neutrophil recruitment and function. Aim 4 will determine the functional role of molecules identified by gene microarray technology to be differentially expressed in S. pneumoniae but not E. coli pneumonia. These studies will help to elucidate the molecular mechanisms of neutrophil recruitment and identify potential targets for therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CELLULAR TUBERCULOSIS
NECROSIS
INDUCED
BY
MYCOBACTERIUM
Principal Investigator & Institution: King, C Harold.; Medicine; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2002; Project Start 15-SEP-2002; Project End 31-DEC-2003
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Bacterial Pneumonia
Summary: (provided by applicant): A key step in the pathogenesis of M tuberculosis is its ability to cause caseating necrosis, parenchymal lung destruction, and cavity formation, which develop into the characteristic necrotizing bronchointerstitial pneumonia and bronchiolitis of tuberculosis. M tuberculosis is cytotoxic to epithelial cells in vitro, and we have shown that this cytotoxicity is associated with cell membrane permeation to lactose dehydrogenase and is mediated by necrosis of lung epithelial cells after infection with virulent mycobacteria (Dobos, K. M., Quinn, F. D. and King, C. H. 2000, Infect. Immun. 68:6300-6310). Interestingly, the attenuated M bovis BCG does not induce necrosis in this epithelial cell model suggesting that necrosis is related to the virulence of mycobacteria. Our working hypothesis is that M tuberculosis possesses factors that cause necrosis. We intend to identify the genes that encode or synthesize such factors and determine their functions. Towards this goal, we have been successful in isolating two such (necrosis-deficient) mutants with insertions into genes that have no known function by screening a transposon library of the Erdman strain of M tuberculosis (TN5370) for mutants that have lost their ability to cause cell membrane permeation and necrosis. Both nec mutants possess extremely interesting phenotypes when grown in mice. The first mutant (necA) appears to be highly attenuated for growth and virulence in SCID mice. This is an important result as it suggests that we have identified a gene whose product either directly causes necrosis or induces necrosis and thus should enhance our understanding of tuberculosis pathogenesis. Interestingly, the second mutant (necB) appears to kill SCID mice more rapidly than the parental strain. We intend to characterize these mutants, characterize the functions of the gene products, and extend this mutant isolation strategy to identify a large battery of mutants defective for necrosis of host cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHIMERIC VIRUS VACCINES FOR P. AERUGINOSA INFECTIONS Principal Investigator & Institution: Staczek, John; Professor; Microbiology and Immunology; Louisiana State Univ Hsc Shreveport P. O. Box 33932 Shreveport, La 71103 Timing: Fiscal Year 2003; Project Start 01-JUL-1998; Project End 31-MAR-2007 Summary: (provided by applicant): Pseudomonas infection is an underappreciated cause of morbidity and mortality. Nosocomial infections can be life-threatening in immunocompromized populations, cancer patients, the elderly, and patients with cystic fibrosis. Physicians try to protect patients with antibiotic therapy, but the bacteria quickly develop antibiotic resistance. A complementary approach to antibiotic therapy is therefore urgently needed, and one such approach is vaccination. Our long-range goal is to develop vaccines that protect against Pseudomonas lung infection. We have developed two effective outer membrane protein F (OprF)-based vaccines that protect against both nonmucoid and mucoid Pseudomonas phenotypes. These vaccines are called F/I and F/HG. The F/I vaccine consists of three biolistic inoculations of naked DNA sequences for the fusion protein OprF/l. The F/HG vaccine uses a prime-boost strategy with two biolistic inoculations of naked DNA-oprF sequences followed by an intramuscular booster containing the chimeric influenza virus HG10-11. Each vaccine appears to induce a polarized immune response. The F/I vaccine induced antibodymediated immunity (AMI) while F/HG induced cell-mediated immunity (CMI). Insufficient information is available regarding the immune mechanisms whereby Pseudomonas infection is controlled or how Pseudomonas vaccines work. AMI in pulmonary Pseudomonas infection is believed to be important, but the definitive mechanism for clearance is unknown. We propose to define the mechanisms of antibody protection by identifying antibody isotypes and serum cytokines in infected and F/I-
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immunized mice that are immune-intact or immune-deficient. Likewise, the role of CMI in Pseudomonas pneumonia is poorly understood. Our F/HG vaccine will allow us to define the mechanism(s) of Pseudomonas-specific, cell-mediated protection in the lungs of infected and immunized mice that are immune-intact or immune-deficient. Defining these mechanisms will allow us to rationally modify immune responses to protect more effectively against pulmonary Pseudomonas infection. As researchers delineate the immune responses to pulmonary Pseudomonas infection in humans, we will be uniquely positioned to modify our vaccines to induce specific Th-1 or Th-2 responses. These rationally designed vaccines tested in a pulmonary chronic infection model will provide guiding principles to prevent and treat more effectively Pseudomonas pneumonia in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHLAMYDIA ATHEROSCLEROSIS
PNEUMONIAE
AND
MACROPHAGES
IN
Principal Investigator & Institution: Byrne, Gerald I.; Professor & Chairman; Medical Microbiol & Immunology; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2002; Project Start 15-FEB-1999; Project End 30-SEP-2002 Summary: (Adapted from the Applicant's Abstract): Chlamydia pneumoniae, a causative agent in human community acquired pneumonia, also has been implicated in a variety of sequelae associated with chronic disease and re-exposure to the organism. One important sequel associated with C. pneumoniae infection is the development of atherosclerotic lesions that define the pathology of cardiovascular disease in people. Cardiovascular disease due to atherogenic processes is a major health problem in most of the world, accounting for about 50% of all deaths. It is clear that vascular injury is crucial in the development and progression of atherosclerosis and that this injury can result from a variety of causes, including infection. Several lines of evidence support the hypothesis that C. pneumoniae infection is linked to the development of atherosclerosis. Initially, seroepidemiological evidence was generated to establish a relationship between C. pneumoniae and cardiovascular disease. Subsequently, evidence for the presence of the organism in atherosclerotic lesions was obtained using either direct antigen detection methods or probes specific for C. pneumoniae nucleic acids. In addition, the organism has been isolated from an aortic lesion and grown in cell culture. Finally, two pilot secondary prevention antibiotic treatment trials have provided evidence to suggest that treatment of C. pneumoniae in individuals with coronary heart disease significantly reduces cardiac events in treated versus placebo administered populations. Thus, although the association of C. pneumoniae and atherosclerosis is well-established, existing data do not prove an etiology or pathogenic role for the organism in disease, although both rabbit and murine animal models have been developed to determine if C. pneumoniae is causally associated with development or progression of atherosclerotic lesions in vivo. Activation and modification of mononuclear phagocyte function is associated with atherosclerotic lesion development. Characteristic changes include development of cholesteryl ester-laden monocytes (foam cells) and oxidation of lipids to form tissue-damaging derivatives. The hypothesis to be tested here is that infection of human monocytes, monocyte-derived macrophages or murine monocyte cell lines with C. pneumoniae results in changes in macrophage morphology and function that are consistent with a role for C. pneumoniae in the pathogenesis of atherosclerosis. This hypothesis will be tested by determining if C. pneumoniae causes mononuclear phagocytes to form foam cells in the presence of low
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Bacterial Pneumonia
density lipoprotein (LDL) or other cholesterol-containing serum lipoprotein complexes. Studies also will be conducted to determine if C. pneumoniae contributes to the oxidative modification of LDL and molecular characterization of C. pneumoniae antigens involved in these processes will be identified. Finally, a murine model will be developed to provide in vivo correlates to cell culture observations. Results will help establish links between C. pneumoniae infection and the atherosclerotic disease process. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHLAMYDIA SIGNIFICANCE
PNEUMONIAE
ANTIGENS
OF
BIOLOGICAL
Principal Investigator & Institution: Campbell, Lee A.; Professor; Pathobiology; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 01-APR-1998; Project End 31-MAR-2007 Summary: (provided by the applicant): Chlamydia pneumoniae is a human respiratory pathogen that causes 5 percent to 10 percent of pneumonia, bronchitis, and sinusitis. Virtually everyone is infected in his or her lifetime and reinfection is common. Infection is difficult to treat even with sensitive antibiotics. Chronic infection is common and has been associated with asthma, reactive airway disease, Reiter's syndrome, erythema nodosum, and sarcoidosis. The potential public health impact of infection with this pathogen is underscored by the association of C. pneumoniae with atherosclerosis and related clinical manifestations such as coronary heart disease, carotid artery stenosis, aortic aneurysm, claudication, and stroke. If C. pneumoniae infection plays a role in atherogenesis, there will be an urgent need to facilitate diagnosis and develop strategies for intervention and prevention. The overall goal of this proposal is two fold. First, C. pneumoniae specific antigens that are recognized during human infection will be exploited to facilitate serodiagnosis and identify putative vaccine candidates. The second goal is to define chlamydial/host cell interactions that lead to entry and survival of C. pneumoniae in host cells relevant to atherosclerosis. The specific focus will be on the interaction of the chlamydial glycan moiety with carbohydrate binding receptors on the host cell. Importantly, infection of epithelial cells can be inhibited with N-linked high mannose type oligosaccharide, the major component of the glycan. The novel hypothesis to be tested is that C. pneumoniae enters through the mannose-6 phosphate receptor by binding to the site involved in transport of phosphomannosylated residues to the lysosome and this differs from C. trachomatis, which utilizes the mannose receptor. The ultimate goals of these studies are to identify C. pneumoniae specific antigens to facilitate laboratory diagnosis and virulence factors playing a role in pathogenesis to guide vaccine development or develop anti-adhesive strategies for prevention of infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE--CLINICAL Principal Investigator & Institution: Shasby, D Michael.; Professor; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2003 Summary: While there are some optimistic reports, the mortality for ARDS remains near 50%. Of the patients who die, one half survive beyond the first three days. In these patients who survive more than 3 days, signs of persistent lung and systemic inflammation are associated with increased mortality. Early autopsy series detected a large number of unsuspected cases of bacterial infection of the lung in persons dying
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with ARDS. In more recent clinical studies culture of bronchoscopic samples from live patients without clinical signs of pneumonia have not yielded a high prevalence of results that meet strict criteria for pneumonia. However, a large fraction of samples did contain bacteria and the prevalence of samples with bacteria increased with time on the ventilator. In addition to bacterial colonization of the lung itself, translocation of bacteria across the intestinal wall occurs in severely ill patients, and especially those with shock. The use of broad spectrum antibiotics in patients with ARDS limits the sensitivity of strict quantitative culture criteria to accurately quantify the bacterial burden in ARDS patients. We hypothesize that a significant portion of the persistent acute inflammation present in the lungs of ARDS patients derives from bacteria which colonize the lung surfaces and/or translocate into the blood stream. In the case of bacteria which translocate into the blood stream the primed lung becomes the subject of a response similar to the Shwartzman phenomenon. Recent studies have not detected high levels of lung colonization or blood stream invasion by bacteria because of the ubiquitous use of broad spectrum antibiotics. We will measure bacterial burden in the lung and blood stream of ARDS patients using PCR for bacterial DNA, the sensitivity of which is not as limited by the presence of antibiotics. We will determine if the bacterial burden in the lung and blood as an independent predictor of mortality and if it correlates with indices of acute inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CYSTEINE PRESENTATION
PROTEASES
IN
MHC
CLASS
II
ANTIGEN
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-JAN-1993; Project End 31-DEC-2002 Summary: (Adapted from the applicant's abstract): Presentation of foreign antigens by MHC class II gene products is a central arm of immunity. The process of MHC class IIdependent antigen presentation involves several discrete steps mediated by proteolytic enzymes: generation of peptides for their subsequent presentation as antigens in peptide complexes with MHC alpha/beta dimers and the stepwise breakdown of the class IIassociated molecular chaperone, the invariant chain (Ii). Degradation of Ii promotes loading of MHC class II alpha/beta with newly formed peptides. A single protease, cathepsin S, was recently found to be essential to the process of Ii breakdown and efficient MHC class II peptide loading. These studies are aimed at elucidating the mechanisms by which cathepsin S promotes antigen presentation and at understanding the consequences of inhibition of cathepsin S on MHC class II function. Toward that end, cellular models of antigen presentation in which the activity of cathepsin S, and other cysteine proteases can be manipulated have been developed. Ii resistant to cleavage of cathepsin S will be generated by site-directed mutagenesis and the function of mutant Ii assessed in vitro and in vivo. The importance of cathepsin S in vivo to MHC class II-dependent immune responses, including allergic pulmonary reactions, will be tested by creating a selective, systemic deficiency of cathepsin S with low molecular weight protease inhibitors. And finally, mice with targeted disruption ("knockout") of the cathepsin S gene are being generated in order to assess the consequences of longstanding cathepsin S deficiency on MHC class II function and to provide a fertile background on which to search for additional proteases important to antigen presentation. These studies should provide new information on the basic events important to MHC class II peptide loading and establish whether there is a clear rationale for therapeutic inhibition of cathepsin S to suppress inflammation in lung
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Bacterial Pneumonia
diseases promoted by MHC class II-dependent immune reactions such as asthma, hypersensitivity pneumonitis, and transplant rejection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEVELOPMENT AND CHARACTERIZATION OF CD14 DEFICIENT MICE Principal Investigator & Institution: Freeman, Mason W.; Chief; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2002; Project Start 15-FEB-2001; Project End 31-JAN-2006 Summary: (Adapted from the applicant's abstract): CD14 is a 55 kDa glycosyl phosphatidylinositol-linked protein that is also present in a soluble form in serum. CD14 binds lipopolysaccharides (LPSs) derived from the outermost layer of Gram-negative bacteria and activates a signaling cascade that results in the production of inflammatory cytokines that include tumor necrosis factor alpha, interleukin-6, and interleukin-1. This response has been shown to be important in the pathogenesis of septic shock following Gram- negative septicemia. Recent data have also suggested that a similar response may play a role in accelerating atherosclerotic plaque development and in enhancing the formation of the macrophage foam cell, the histologic hallmark of the early atheroma. Several lines of evidence also implicate this pathway in the pathogenesis of PID, a leading cause of infertility in the developed world, and in the phagocytosis of apoptotic cells, an essential event in tissue remodeling and development. Investigators working on inflammatory bowel disease, periodontal disease, and a variety of inflammatory pulmonary disorders have also postulated an important role for CD14 in these conditions. Given the widespread interest in understanding the contributions of CD14 to normal physiology and pathologic conditions, the applicant's laboratory has generated homologous recombinant mice lacking this protein. This grant application proposes to generate a breeding colony of these animals and to distribute these mice to the many investigators that have requested them. These investigators, working on diseases supported by a diverse group of NIH Institutes, can then utilize these animals in experiments that explore the biological processes in which CD14 activity has been implicated. In addition to developing the breeding colony of CD14 deficient mice, this application proposes to characterize the utility of these animals as models for diseases that represent major human health problems in which the principal investigators of the grant have established research efforts. Thus, the CD14 deficient animals will be bred into mouse strains that are susceptible to atherosclerosis in order to explore the role of Chlamydial infections in the pathogenesis of cardiovascular disease. In addition, CD14null mice will also be used to explore the role of the endotoxin signaling pathway in mouse models of PID. This work is intended to broaden the applicability of CD14 deficient mice to research involving acute and chronic inflammatory disease and to make a critical animal resource available to the investigative community at large. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EARLY EVENTS IN THE PATHOGENESIS OF PNEUMONIA PLAGUE Principal Investigator & Institution: Goldman, William E.; Professor; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: Pneumonic plague is the deadliest form of disease caused by Yersinia pestis. The rapid progression of pneumonic plague, along with the ability to transmit it by an aersolized form make it a deadly bioterrorism threat. In this project, we will characterize
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the interaction between Yersinia pestis and airway epithelial cells using an in vitro model of infection. Primary cultures of rat pneumocytes will be infected with bacterIa, and we will characterize both the bacterial and host responses to infection using a variety of techniques, including microarray analyses. We will extend these studies to the hamster tracheal organ culture system developed by our laboratory and use these to study Y. pestis wild type organisms, as well as mutants of Yersinia lacking one or more of the three virulence plasmids. These studies will tell us more about how Yersinia interacts with host respiratory cells, and may provide new targets for therapeutics and plague vaccines. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EARLY HOST MICROBIAL INTERACTIONS IN S. AUREUS PNEUMONIA Principal Investigator & Institution: Rubens, Craig E.; Professor; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 30-JUN-2008 Summary: Staphylococcus aureus is the second leading cause of hospital-acquired pneumonia and an important agent of severe community-acquired pneumonia. Pneumonia is both an important preceding event to acute lung injury and the most commonly fatal complication of ARDS. We hypothesize that early host:pathogen interactions in the lung determine whether S. aureus establishes a successful infection or is eliminated by innate defenses. There is a limited understanding of the pathogenesis of pneumonia, especially the initial microbial:host interaction. Using state of the art in vivo model systems and genomic/proteomic technology we will investigate the early microbial and host responses in the first few hours after bacterial entry into the lungs. Four aims will address our hypothesis. In aim 1 we will characterize changes in bacterial gene expression using genomic array analysis in response to the lung environment during the first few hours of infection. Aim 2 will examine the host proteins in airway fluid, which bind to the bacterial surface and correlate these to changes in gene expression examined over the same time frame as observed in aim 1. In addition, we will characterize the mouse airway fluid proteome, which has yet to be characterized. These studies may identify the host proteins which serve as signals to the organism during the initial phases of infection and further define those which serve as innate defenses against infection for the host. Aim 3 will determine the role of Toll-Like Receptors (TLR) on the interaction of S. aureus with the host, using animals deficient in TLR expression; specifically defective for expressing the downstream signaling molecule MyD88. These studies will evaluate the importance of the initial inflammatory response to bacterial survival and host immunity. The final aim will extend the above experiments by further examining the importance of the bacterial surface associated protein genes with antisense gene inhibition technology in our animal model of pneumonia, to identify those genes and their products which are primarily involved in the initial interactions in the airway. These studies will yield novel insights into bacterial pathogenesis in the lower respiratory tract by examining both sides of the host:pathogen interface in the early stages of infection. These insights could have important implications for the mechanisms underlying the initiation of pneumonia, acute lung injury, and its sequelae. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Bacterial Pneumonia
Project Title: EARLY PULMONARY HOST DEFENSE IN M. TUBERCULOSIS INFECTIO Principal Investigator & Institution: Sherman, David R.; Senior Scientist; Pediatrics; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2003; Project Start 30-SEP-1999; Project End 31-JUL-2004 Summary: Although a lung is a portal of entry for this M. tuberculosis and chronic pneumonia is the most common disease caused by M. tuberculosis infection, the specific nature of the pulmonary host response to this pathogen is relatively unknown. The central goal of the studies outlined in this proposal is to determine whether components of the early pulmonary immune response are critical determinants for resistance or susceptibility to disease caused by M. tuberculosis. The specific aims will address the role of TNF-alpha, beta chemokines and the B7/CD28/CTLA4 costimulation pathway in the initiation and amplification of the pulmonary host response to aerosol infection with M. tuberculosis. Preliminary studies using transgenic mice with a local inhibition of TNF-alpha in the lung (SPCTNFRIIFc mice) indicate that blockade of TNF-alpha selectively in the lung results in early deaths, severe lung pathology and an alteration of antigen specific immunity. These studies also indicate that transgenic mice with local inhibition of the immune response in the lung are a useful model to study pulmonary host defense. Further studies are proposed to compare the response that develops in the lung vs. regional lymph nodes in wildtype and SPCTNFRIIFc mice. To investigate the role of beta chemokines in the pulmonary host defense, transgenic mice that secrete a virally encoded inhibitor of all chemokines has been generated. The phenotype of these mice will be determined then used to investigate the role of beta chemokines in the initiation of the pulmonary host response to M. tuberculosis. To investigate the role of the B7/CD28/CTLA4 costimulation pathway in the initiation and amplification of the pulmonary host response to M. tuberculosis, transgenic mice that secrete an inhibitor of the B7/CD28/CTLA4 co stimulation pathway will be generated, characterized then used in experiments examining the immune response to M. tuberculosis. To determine the relative importance of the intrapulmonary component of the immune response vs the systemic immune response, in each of the project specific aims, mice will be included with both local inhibition of the immune response and systemic inhibition. In the studies examining the pulmonary host response to M. tuberculosis, infections will occur via the aerosol route because inhalation is the usual route of infection in humans. The primary endpoints will include bacterial burden, lung histology, survival and the phenotypic and functional characteristics of the immune response. The proposed studies should advance the existing knowledge of the specific nature of the pulmonary immune response to M. tuberculosis, will directly test the role of these mediators in host defense against M. tuberculosis, suggest important targets for novel therapies and elucidate role of specific mediators of the host immune response that are critical for the induction of an antigen specific immune response by candidate vaccines. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ELDERLY POLYSACCHARIDE
IMMUNE
RESPONSE
TO
PNEUMOCOCAL
Principal Investigator & Institution: Westerink, M a J.; Medicine; Medical College of Ohio at Toledo Research & Grants Admin. Toledo, Oh 436145804 Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: Infection is one of the leading causes of morbidity and mortality in the elderly. Streptococcus pneumoniae is the organism most commonly isolated from
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elderly patients with pneumonia. Increased susceptibility to infections that occur in the elderly has been attributed to deteriorating health, decreased pulmonary function and a functional decline of the immune system. The immune system is unique in that it may be manipulated to achieve a desirable response. Studies in aged mice demonstrate both quantitative and qualitative changes in the immune response to T-independent type 2 (TI-2) antigens. Reports indicate age related loss of affinity, fine specificity and protective immunity are associated with a molecular shift in V gene usage and changes in cytokine profile. Studies of the in vivo immune response in elderly have been limited to vaccine efficacy studies and quantitative analysis of the magnitude and duration of the post-vaccination antibody response. The results of these studies suggest that despite adequate quantitative immune response the elderly show decreased vaccine efficacy. Current knowledge concerning the aging immune response to TI-2 antigens is mostly based on animal models and may not be applicable to humans. Human studies are fragmented and address quantitative and qualitative immune response as separate issues. We propose to study and characterize the immune response to S. pneumoniae capsular polysaccharide in the elderly. We will focus on both quantitative and qualitative changes in the immune response on molecular and functional levels. The quantitative immune response, isotype and IgG subclass, will be correlated with opsonophagocytic activity. We hypothesize that the discrepancy between the quantitative and qualitative immune response in the elderly results from altered V region sequence. We will characterize the immunoglobulin gene usage pattern and V-DJ joint diversity of the antibody response to pneumococcal polysaccharides (PPS) of serotypes 4 and 14 in elderly and young adults. This will be accomplished by gene family specific ELISA and by isolating single responding cells and determining the sequence of the V chains. Second, we propose to evaluate the influence of soluble regulatory factors on the aging immune response. The reconstituted SCID mouse model will be used to study the aging human B cell response to PPS 4 and 14 in a controlled cytokine environment allowing us to differentiate altered response intrinsic to the B cells versus altered responses secondary to environmental factors such as cytokines. The results of these studies will form the essential baseline for the rational development of vaccine and adjuvant strategies for the elderly. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ELR-CXC CHEMOKINES IN LUNG ANTIBACTERIAL HOST DEFENSE Principal Investigator & Institution: Standiford, Theodore J.; Professor; Internal Medicine; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 01-DEC-1996; Project End 30-NOV-2005 Summary: (provided by applicant): Bacterial pneumonia is the second most common cause of hospital-acquired infection, and is leading cause of death among all nosocomial infections. Innate, or natural immunity, is the principal pathway for effective elimination of bacterial organisms from the lung. While ELR-CXC chemokines have been shown to be expressed during the generation of Th1 cell-mediated immune responses against intracellular microbial pathogens, the contribution of this family of chemokines to innate immunity against common gram-positive and gram-negative bacterial pathogens is unknown. We have focused this competitive renewal on ELRCXC chemokines, as our preliminary observations indicate that the in-vivo depletion of selected ELR-CXC chemokines substantially impairs bacterial clearance and survival of mice with pneumonia due to Klebsiella pneumoniae. It is the hypothesis of this proposal
20
Bacterial Pneumonia
that ELR-CXC chemokines are integral components of the innate neutrophil-dependent immune response against gram-negative bacterial infection of the lung. A murine model of Klebsiella pneumonia will be employed to achieve the following specific aims: 1) to determine the time course of expression and cellular sources of ELR-CXC chemokines and their common receptor (CXCR3) during the evolution of gram-negative bacterial pneumonia; 2) to determine the contribution of ELR-CXC chemokines and their receptor to leukocyte recruitment, proinflammatory cytokine expression, bacterial clearance, survival in Klebsiella pneumonia using specific neutralizing antibodies or knockout mice; 3) to determine the effect of IP-10 or MIG administration/transgenic expression on proinflammatory cytokine expression, bacterial clearance, and survival in murine Klebsiella pneumonia in-vivo and on alveolar macrophage effector cell function in-vitro; and 4) to identify endogenous signals that regulate the expression of ELR-CXC chemokines during the evolution of Klebsiella pneumonia in-vivo and in isolated lung cells in-vitro. Elucidation of specific cellular and molecular mechanisms of lung antibacterial host defense, in conjunction with the use of novel gene therapy approaches will provide important insights into the treatment of patients with serious multi-drug resistant bacterial infections of the lung. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FILAMENTOUS COLONIZATION
INFLUENZA
VIRUS
AND
MICROBIAL
Principal Investigator & Institution: Roberts, Paul C.; Immunology and Microbiology; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 29-SEP-2005 Summary: (provided by applicant): Individuals recovering from influenza A virus infection demonstrate an increased susceptibility to secondary bacterial pulmonary infections, particularly with the pathogens Streptococcus pyogenes and Streptococcus pneumoniae. Quite often, these secondary bacterial pneumonias are fatal, especially in geriatric and immunocompromized patients. The mechanism(s) behind this increased susceptibility to a secondary streptococcal infection are unknown. We hypothesize that this increased susceptibility to bacterial super-infection is due to a filamentous form of influenza A virus significantly facilitating the adhesion of pathogenic streptococci to respiratory mucosa. Experiments in this application will determine if filamentous influenza A virus can directly serve as a receptor for bacterial binding or if the respiratory mucosa is altered by infection with influenza virus to promote increased bacterial adherence. In parallel, we will also determine whether prior bacterial colonization can affect influenza virus replication in respiratory epithelium. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENOME ANALYSIS OF STREPTOCOCCUS AGALACTIAE Principal Investigator & Institution: Tettelin, Herve S.; Associate Investigator; Institute for Genomic Research Rockville, Md 20850 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 29-SEP-2004 Summary: (provided by applicant): Group B streptococci (GBS) or Streptococcus agalactiae are weakly beta-hemolytic, facultatively anaerobic Gram-positive cocci, which have emerged over the past 50 years as the most significant bacterial cause of neonatal sepsis, pneumonia, and meningitis. GBS account for 30-50 percent of neonatal bacterial infections and increases in adult GBS infections have also been noted. This demonstrates that GBS infections remain an important public health problem. We propose to sequence
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the 2.1 Mb genome of S. agalactiae serotype Ia strain A909 using a genome-wide random shotgun approach. We will then use the final assembled sequence and its complete annotation to perform detailed comparative genomics analyses between serotype Ia and other organisms causing pneumonia and meningitis. These analyses will allow to identify virulence determinants shared by all organisms or specific to individual ones. These determinants will be related to Drs. Jones and Rubens? experiments on signature tagged mutagenesis and TnphoZ translational fusion (identification of secreted proteins) mutant libraries constructed through transposon insertions in strain A909. Regions where transposons inserted will be aligned to the genome sequence to identify the genes affected. A subset of the mutants conserved across serotypes will be analyzed in the rat sepsis model to evaluate their virulence. This collaborative effort will provide extensive preliminary data for future proposals relevant to understanding the pathogenesis of S. agalactiae infections. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HIV SURVEILLANCE AFFECTS MACROPHAGE FUNCTION Principal Investigator & Institution: Wewers, Mark D.; Professor; Internal Medicine; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2002; Project Start 30-SEP-1998; Project End 31-AUG-2003 Summary: Bacterial pneumonia remains one of the most common complications of HIV infections. In spite of our growing understanding of the pathogenesis of the immune deficiency associated with HIV infection, the factors that predispose HIV+ individuals to pneumonia remain obscure. For example, the risk of pneumonia for HIV infected individuals is 6 fold higher than for HIV-individuals. This risk can only partially be explained by lower blood CD4 counts. Our preliminary experiments demonstrate that the lung CD4 counts remain normal in the face of falling peripheral counts when compared to HIV uninfected subjects. However, CD8+ lymphocytes are markedly increased in the lung, a hallmark of HIV infection. These cytotoxic CD8+ lymphocytes (CTLs) are believed to function to suppress viral replication. In this context, the primary defense against bacterial infections in the lung is provided by alveolar macrophages which are also the prime source of HIV in the lung. Since macrophage HIV infection is enhanced by inflammatory events, we have hypothesized that 1) initiation of antibacterial function by lung macrophages induces local HIV replication, and 2) as a consequence of this increase in viral burden, lung CTLs may be signaled to suppress this viral replication. This suppression of virus may in the process suppress macrophage antibacterial function. We therefore, propose to test these hypotheses by studying the macrophage's ability to phagocytose opsonized particles. We will evaluate lung macrophages from HIV infected individuals and normal controls to test whether opsonized phagocytosis induces viral replication in the macrophage. As a corollary we will determine whether CTLs can impair macrophage phagocytosis. These in vitro experiments will be corroborated by studies of lung macrophages taken at the time of bacterial pneumonia. Together these experiments will improve our understanding of how the innate immune defense against bacteria is affected by attempts to suppress HIV in macrophages. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HOST CELL DETERMINANTS IN PSEUDOMONAS PNEUMONIA Principal Investigator & Institution: Mostov, Keith E.; Professor; Anatomy; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747
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Bacterial Pneumonia
Timing: Fiscal Year 2002; Project Start 30-SEP-1995; Project End 31-MAR-2004 Summary: (Adapted from the Applicant's Abstract): In immunocompromised and other severely ill patients, Pseudomonas aeruginosa (PA) causes an acute pneumonitis, which has an extremely high fatality rate. Improved methods for prevention and therapy are urgently needed. An in vitro model of PA infection using polarized Madin-Darby canine kidney (MDCK) cells or cultured lung epithelial cells mimics many important features of in vivo pneumonia. Live Pseudomonas organisms added to the apical surface of these cultures attach to and kill the cells. These foci of infection spread centripetally. The current proposal will study the host cell factors that determine susceptibility to Pseudomonas pneumonia using these in vitro model systems. There are four aims in this study: to investigate how modification of cell polarity affects virulence; to identify the receptors for PA and how their regulation affects bacterial interaction; to determine the pathway for internalization of PA organisms; and to examine the role of the actin cytoskeleton in interaction of PA with cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HOST RESPONSE TO POST-OPERATIVE PNEUMONIA Principal Investigator & Institution: Knight, Paul R.; Professor and Vice Chairman; Anesthesiology; State University of New York at Buffalo Suite 211 Ub Commons Buffalo, Ny 14228 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 31-MAY-2006 Summary: (Verbatim from the Applicant's Abstract): Anesthesia/surgery predisposes the patient to develop nosocomial pneumonia by mechanisms that are not completely defined. The presence of a viral respiratory tract infection (RTI) during anesthesia/surgery further complicates the host antibacterial response. Evidence from our laboratory has demonstrated anesthesia/surgery induces changes in cytokine response (e.g., TNFalpha, MIP-2, IFNgamma), leukocyte recruitment, and lung injury to influenza RTI. These responses are also critical to innate host defenses against bacterial pathogens. Our focus is to examine cellular mechanisms during a viral RTI that predispose the host to a post-surgical bacterial pneumonia. We hypothesize that anesthesia/surgery will change host responses differently during distinct periods in the course of a viral RTI by altering expression of pro- and antiinflammatory cytokines, thereby decreasing antibacterial defenses. Aim #1 will assess the effects of anesthesia/surgery during influenza on bacterial clearance, inflammatory cell influx, and cytokine expression an Escherichia coli challenge. We predict that laparotomy during influenza will promote the relative expression of MCP-1 and IL-10 over TNFalpha, MIP-2, and IFNgamma. Aim #2: will assess ex vivo the combined effect of laparotomy and influenza on a) LPS stimulated aMphi cytokine expression and phagocytic activity, and b) the ability of in vitro antiMCP-1, antiIL-10, or IFNgamma administration to improve M dysfunction. We postulate that laparotomy during influenza will alter aMphi regulatory functions and decrease effector functions as a result of selective enhancement of expression anti-compared to proinflammatory cytokines. Finally, in Aim #3, we will examine the contribution of endogenous cytokines in the suppression of antibacterial defenses following laparotomy during influenza by selective cytokine manipulations. Bacterial clearance, inflammatory cell influx, and cytokine levels will be assessed. We anticipate that neutralization of IL-10 or MCP-1, administration of IFNgamma, or increased TNFalphaexpression will improve antibacterial host defenses following laparotomy during physical signs of influenza. These studies will examine mechanisms that lead to alterations in bacterial clearance post-surgically following a viral RTI, assess the pathogenesis of post-surgical
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pneumonia in general, and suggest immune adjuvant strategies to prevent this complication. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IL-17 AND KLEBSIELLA PNEUMONIA Principal Investigator & Institution: Shellito, Judd E.; Professor; Medicine; Louisiana State Univ Hsc New Orleans New Orleans, La 70112 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 30-APR-2007 Summary: The long-term objective of this project is to understand interactions between cellular and soluble factors in host defense against bacterial pneumonia. Preliminary data from our laboratory indicate that deposition of bacteria (Klebsiella pneumoniae) into the lungs of mice stimulates the release of one such soluble factor- the lymphocytederived cytokine, Interleukin-17 (IL-17). Additional experiments in IL- 17 receptor "knock-out" mice show increased mortality and impaired neutrophil recruitment after K. Pneumoniae challenge. In this project, we will test the experimental hypothesis that IL17 released from lung T-lymphocytes amplifies the host response to bacterial infection through stimulated release of C-X-C chemokines for neutrophils and enhanced release of other proinflammatory cytokines. In Specific Aim 1, we will localize IL-17 to CD4+ and CD8+ T- lymphocytes in the interstitium or alveolar space at serial intervals after bacterial challenge using flow cytometry and laser capture microdissection. In Specific Aim 2, we will show that IL-17 enhances host release of CXC chemokines and recruitment of neutrophils in response to K. Pneumoniae. We will utilize IL-17 receptor knock-out mice and mice administered a neutralizing IL-17 receptor/FC fusion construct by gene transfer. In Specific Aim 3, we will investigate the interactions between IL-17 and other pro-inflammatory and anti-inflammatory cytokines released into lung tissue in response to K. Pneumoniae. These experiments will focus on TNFalpha, IL-12, IFN-gamma, and IL-10. In Specific Aim 4, we will upregulate IL-17 in lung tissue with gene transfer of the murine IL-17 gene using an adenoviral vector and demonstrate increased bacterial clearance and enhanced recruitment of neutrophils. The results of these experiments will provide new information on how IL-17 participates in host defense against bacterial pneumonia and may lead to novel approaches to augment immune function in the immunocompromised host. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IMMUNOLOGY OF BACTERIAL PNEUMONIA IN HTLV-II INFECTION Principal Investigator & Institution: Jarvis, Gary A.; Northern California Institute Res & Educ 4150 Clement Street (151-Nc) San Francisco, Ca 941211545 Timing: Fiscal Year 2002; Project Start 01-MAR-2000; Project End 28-FEB-2004 Summary: (Adapted from the Applicant's Abstract): This projects seeks to understand the immunologic basis for the epidemiological outcome observation of an increased incidence of bacterial pneumonia in HTLV-II-infected blood donors. In a study of persons with both HTLV-II seropositivity and intravenous drug use, an increased risk for bacterial pneumonia compared to patients with neither risk was found. A similar finding of increased risk for bacterial pneumonia in HTLV-II-infected individuals was observed in a clinical outcome analysis of blood donors who participated in a Retroviral Epidemiological Donors Study. Since the cell tropism of HTLV-II infection includes CD4+ and CD8+ T cells, B cells and monocytes, the investigators will determine whether HTLV-II infection predisposes to bacterial pneumonia by creating immune dysfunction
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Bacterial Pneumonia
in these cells which are known to be critical for natural protection against pneumococcal pneumonia, the most common cause of bacterial pneumonia in individuals with immune dysfunction. Studies planned for the next five years address the immune status of HTLV-II-infected persons. HTLV-II-infected and -uninfected individuals will be vaccinated with the pneumococcal 23-valent polysaccharide vaccine, and their qualitative and quantitative antibody responses will be investigated by determining the isotype and IgG subclass distribution, concentration, avidity and opsonic function of specific pneumococcal capsular antibodies. The same individuals will also be vaccinated with tetanus toxoid protein antigen as a control for antibody response to a separate class of antigen, and their antibody responses measured. The effect of HTLV-II infection of T cells on the proliferative and antibody-secreting functions of B lymphocytes will be tested. CD4+ and CD8+ T cells will be isolated from HTLV-II-infected persons using immunobeads, co-cultivated with normal B lymphocytes, and the functional activity of the B cells assessed using mitogen stimulation and ELISA antibody quantitation assays. Levels of B cell regulatory cytokines produced by infected and uninfected T cells will be measured by ELISA. Levels of immune response markers IL2 receptor on CD8+ T cells, and CD21 and CD35 on B cells will be determined by flow cytometry. The phagocytic and bactericidal function of PMN and of human macrophages derived from the monocytes from HTLV-II-infected individuals will be tested and compared to the function of those cells from uninfected persons. Human CD4+ and CD8+ T cells will be isolated using immunobeads and quantities of macrophage and PMN regulatory cytokines produced by HTLV-II-infected and -uninfected T Cells will be measured by ELISA. The effect of HTLV-II infection of human T cells on cytokine-dependent activation of macrophages and PMN will be studied using functional assays of pneumococcal phagocytic killing. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INHALED PARTICLES AND HOST DEFENSE IN THE PRIMED LUNG Principal Investigator & Institution: Kobzik, Lester; Associate Professor; Environmental Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 07-JUL-2003; Project End 31-MAY-2008 Summary: (provided by applicant): The Problem: Hospital admissions for pneumonia are increased by elevated air particle levels. The mechanism(s) underlying particle effects on lung infection are unknown, but may reflect increased incidence of infection, increased severity of infection, or both. Hypothesis: The pathogenesis of the pneumococcal pneumonia (the most common variety and the disease we will study) suggests three possible mechanisms for particle effects: enhancement of lung cell 'receptors' used by bacteria for initial adhesion, damage to antimicrobial function of host cells (AMs and PMNs), and exaggerated inflammation in established infection leading to worse signs and symptoms. Hence, the central thesis of this research is that oxidant components of air particles mediate 1) dysfunction of host defenses against infection (incidence) and 2) increased inflammation in extant pneumonia (severity). Experimental Plan: Aim 1 will measure expression and function of pneumococcal 'receptors' (e.g., PAF receptor) used by pneumococcal for initial adhesion after exposure to concentrated ambient particles (CAPs) or control particles. Aim 2 will determine effects of air particles on pulmonary inflammation before and after onset of pneumococcal pneumonia. The hypothesis to be tested is that particles cause enhanced release of cytokine mediators by primed AMs, leading to increased inflammation and ultimately oxidant damage to both
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AM and PMN In vivo and in vitro studies will measure release of pro-inflammatory cytokines, cell influx and viability and severity of pneumonic inflammation. Aim 3 will test the hypothesis that particle exposure inhibits bacterial clearance via oxidantdependent damage of anti-microbial functions of AMs and PMNs. Component analysis will be performed using a panel of CAPs samples to provide links of particle constituents (e.g., metals, organics, endotoxin) with biologic effects. Rotated factor analysis will be used to correlate source types with CAPs toxicity. Specific intracellular oxidant pathways will be identified by measurement of oxidant production, intracellular levels of antioxidants, and the effect of a panel of anti-oxidants and other inhibitors. Significance: This research is relevant to the public health question of how inhaled particles cause pulmonary health effects and to the pathophysiology of lung host defense against environmental agents. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INNATE MECHANISMS OF MYCOPLASMAL KILLING BY ALVEOLAR MAC Principal Investigator & Institution: Hickman-Davis, Judy M.; Anesthesiology; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2002; Project Start 01-JUL-1999; Project End 30-JUN-2004 Summary: I graduated from Emory University in 1987 and then spent 2 years as a research assistant in the Department of Pediatric Biochemistry at Emory Hospital. My research experience at Emory prompted me to study animal medicine and I received the D.V.M., cum laude from the University of GA in 1993. At UAB I have received excellent training in laboratory animal medicine, and molecular and Cellular Pathology (Ph.D. December 1998; mentor, Dr. Lindsey). My dissertation research has produced a number of important advances in understanding pulmonary antimycoplasmal defenses applicable to human disease. This SERCA provides the ideal setting for my desired maturation into an independent comparative medicine scientist. Mycoplasma pneumoniae is a leading cause of pneumonia and extrapulmonary disease in humans. C57BL mice are highly resistant and C3H mice are highly susceptible to Mycoplasma pulmonis and are excellent models of the human disease. I have shown that the alveolar macrophage (AM) is the key cell in resistance of C57BL mice, and surfactant protein A (SP-A) mediates the killing of mycoplasmas by C57BL AMs in vitro through the production of reactive oxygen-nitrogen species. Furthermore, my results suggest for the first time that AM nitric oxide derived species, but not reactive oxygen species, are essential for killing mycoplasmas in vivo and in vitro. My aims for the 01-03 years are: (1) Determine the molecular mechanism(s) responsible for SP-A mediate mycoplasmal killing by C57BL AMs in vivo and in vitro, and (2) Identify the mechanism responsible for the defect in SP-A mediated killing by susceptible C3H AMs in vivo and in vitro. My tentative plan for the 04-05 years is to investigate the mechanism by which reactive species damage and effect killing of mycoplasmas, and the pathophysiologic sequelae of mycoplasmal injury to alveolar epithelium in vivo. My career will emphasize the development of models and the investigation of immunologic mechanisms for resistance/susceptibility to bacterial pneumonias, utilizing transgenic and other methodologies. Thus, I plan to perform experiments in vivo, to show the relevance of my findings in human disease, and in vitro to identify the basic mechanisms. This SERCA with Dr. Matalon (lung physiology, biochemistry) as advisor and Drs. Lindsey (mycoplasmal diseases, lung defenses) and Wood (molecular genetics, transgenics) as co-advisors provides a unique and extremely stimulating environment, ideal for my
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Bacterial Pneumonia
desired maturation into an independent scientist focused on the development of models for pneumonic processes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MACROPHAGE ELASTASE IN HOST DEFENSE Principal Investigator & Institution: Shapiro, Steven D.; Chief; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2006 Summary: (provided by applicant): Matrix metalloproteinases (MMPs) are a group of matrix degrading enzymes whose aberrant or excessive expression can lead to a variety of tissue destructive diseases. Less is known about the normal physiologic functions of MMPs. We present data that macrophage elastase (MMP-12) is the only MMP that has direct antimicrobial activity. MMP-12 acts within the lung macrophage as the first line of defense against microbes within the alveolar space. MMPs are well known for their roles in promoting tumor progression. However, with the discovery of angiostatin, an antiangiogenic proteolytic fragment of plasminogen, it became clear that proteinases can be involved in limiting tumor growth. We present evidence that MMP-12 plays a major role in limiting tumor growth within the lung. This property might have clinical importance since at least 6 phase 3 trials using MMP inhibitors for cancer therapy and two for arthritis were stopped last year related to this under-appreciated property of certain MMPs to limit tumor growth. To further define the role of macrophages and MMP-12 in host defense against bacteria and tumors in the lung, we propose to: 1. Test the hypothesis that MMP-12 represents a novel macrophage-mediated intracellular antimicrobial agent. We provide preliminary data that MMP-12-/- mice have a poorer outcome in response to S. aureus pneumonia, MMP-12-/- macrophages have impaired intracellular killing of S. aureus, and show that MMP-12 has direct antimicrobial capacity. This activity is independent of catalytic capacity and involves the non-catalytic C-terminal domain. Studies are proposed to define the spectrum of bacteria influenced by MMP-12. We will also define the structural components of MMP-12 responsible for this activity. 2. We will extend the hypothesis that MMP-12 interferes with tumor growth via inhibition of angiogenesis and further define potential mechanisms of action. We provide preliminary data that MMP-12 is required to maintain dormancy of Lewis lung cell carcinoma (LLC) metastases. This activity appears related to inhibition of angiogenesis. This is not merely due to generation of angiostatin. Additional antiangiogenic protein fragments play a role, and we postulate that MMP-12 also interferes with MMP-2-mediated promotion of tumor growth. MMP-12 might do this by cleavage of MMP-2 as well as by competition with MMP-2 for endothelial cell and tumor cell binding through its C-terminal domain. 3. We will determine the role of macrophages in lung development, bacterial infection, and tumor progression. We will take advantage of MMP-12 macrophage specific expression and complete generation of diphtheria toxin (DT) "knock-in" to the MMP-12 locus. We hypothesize that this will result in mice deficient in lung (and peritoneal) macrophages, and that these mice will undergo normal lung development. If this hypothesis is correct, then the mice will be used to study the requirement of macrophages in host defense and inflammation. If the mutation is lethal or not fully deficient in pulmonary macrophages, then lung-specific transgenic mice will be used to inducibly express DT in lungs of mature mice. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OF BACTERIAL INDUCED LUNG INJURY Principal Investigator & Institution: Wiener-Kronish, Jeanine P.; Professor; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 30-JUN-2008 Summary: Pneumonia is the most common cause of sepsis and the most common cause of acute lung injury (ALI). The overall objective of this project is to investigate the contribution of human genetic abnormalities and bacterial virulence genes to the development of clinical lung injury and pneumonia. We have chosen a specific human genetic abnormality and a group of bacterial virulence genes (type III secretion system) to investigate because of their potential importance in lung infections, particularly lung infections in critically ill patients, and in patients at risk for ALI. Mannose binding lectin (MBL) deficiency is one of the most common immunodeficiencies and has been associated with severe lung disease due to mucosally-acquired pathogens. P.aeruginosa is the most frequent Gram negative pathogen associated with ventilator-associated pneumonia (VAP). The products of Type III secretion system genes in P.aeruginosa cause acute lung injury in experimental animals and P.aeruginosa strains isolated from critically ill patients produce type III secretion proteins. We will establish a prospective cohort investigation to test the hypothesis that genetic abnormalities in MBL are associated with an increased risk of severe ALI (Aim 1). We will also establish a prospective cohort investigation of the molecular characteristics of P.aeruginosa strains and the genetic expression of virulence genes in ventilated patients who are colonized with P.aeruginosa (Aim 2). Patients with P. aeruginosa colonization (established by surveillance cultures of tracheal aspirates) will undergo periodic BAL to determine whether colonization can be distinguished from VAP by a biochemical marker of lung epithelial injury. BAL will also be done on patients with VAP and/or ALI due to P.aeruginosa; the results of these BAL fluids will be compared to the BAL obtained from colonized patients. This aim will test the hypothesis that transformation from colonization to lung infection is associated with the expression of the Type III secretion virulence genes. We will then compare the P.aeruginosa strains obtained from patients with VAP and/or ALI to the strains obtained from patients who are only colonized with P.aeruginosa and quantify the lung injury caused by the airspace instillation of the strains into mice (Aim 3). This final aim will allow us to utilize animals to answer a clinical question; whether the colonizing strains and the strains found in patients with VAP differ in terms of their biologic effects. BAL fluids from patients and from the mice will be utilized in other projects (l&3) to evaluate the procoagulant pathway and the antifibrinolytic pathway in the distal airspaces. The fluids will also be evaluated in the proteomics core to determine whether bacterial virulence proteins can be measured in BAL fluids from patients with VAP and/or ALI and whether markers of epithelial injury can also be found in the BAL fluids of these patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OF SURFACTANT INHIBITION Principal Investigator & Institution: Walther, Frans J.; Professor; Harbor-Ucla Research & Educ Inst 1124 W Carson St Torrance, Ca 905022052 Timing: Fiscal Year 2002; Project Start 01-FEB-1996; Project End 31-JAN-2006 Summary: (Applicant's Abstract): Lung surfactant is a surface-active material that lines the alveolar surface of the lung and is composed of -90 percent lipids and 5-10 percent surfactant proteins (SF-A, B, C, and D). SF-A and SP-D are complex, lung-specific glycoproteins which modulate surfactant metabolism and lung immunological defense.
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Bacterial Pneumonia
SP-B and SP-C are short hydrophobic proteins, responsible for the surface activity of clinical surfactants derived from bovine and porcine lungs. Because natural surfactant preparations vary considerably in protein composition and may expose recipients to immunogenic proteins and viral contamination, we have focused on the structural and functional characteristics of synthetic mimics of human SP-B and SP-C and the design of a standardized, reproducible surfactant preparation of controlled composition. Premature infants with respiratory distress syndrome (RDS) are surfactant deficient due to lung immaturity, but functional surfactant deficiency due to inhibition of lung surfactant in the alveolar space predominates in adult respiratory distress syndrome (ARDS). Our objective is to design synthetic surfactants that will resist various types of inhibition associated with ARDS. The proposed studies include the design, synthesis, structural characterization, and in vitro and in vivo surface activity testing of synthetic lung surfactant formulations composed of phospholipids and SP-B and SP-C mimic peptides for use in the treatment of lung surfactant deficiency, surfactant inhibition, and bacterial pneumonia. We propose to extend these synthetic peptide design efforts to the synthesis of disulfide linked SP-B and SF-C homodimers that are similar to native hydrophobic surfactant proteins. Since SP-B and SF-C interact in vitro and in vivo and SP-A decreases the inhibition sensitivity of surfactant preparations, we will assess the surface activity of formulations with synthetic SF-B and SP-C mimic peptides and native SF-A. Overall, these studies will facilitate the identification and development of novel, peptide containing lung surfactant formulations that should be useful for treating surfactant deficiency and surfactant inhibition in neonatal RDS and ARDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MENTORED DEVELOPMENT AW
PATIENT-ORIENTED
RESEARCH
CAREER
Principal Investigator & Institution: Moses, Harold L.; Director, Vanderbilt-Ingram Comprehensiv; Neurology; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2002; Project Start 30-SEP-2000; Project End 31-AUG-2005 Summary: It is estimated to affect between one million and one and a quarter million people worldwide and over 350,000 persons in North America. Disease susceptibility appears to be influenced by genetic determinants, location of residence through adolescence, and possibly age of exposure to certain infectious agents. Recent work in the MS laboratory at Vanderbilt University has found an association between CNS infection with Chlamydia pneumoniae and MS. The objectives of this application are to examine the role antibiotic therapy has on C. pneumoniae infection in the cerebrospinal fluid (CSF) of MS patients. We hypothesize that appropriate antibiotic therapy will markedly reduce or eradicate C. pneumoniae infection in the CSF of MS patients and that the clinical course of their disease will improve following treatment. A randomized clinical trial to examine the efficacy of two different antibiotic regimens versus placebo will be done over a six-month period of time in C. pneumoniae positive MS patients. Efficacy will be determined by eradication of C. pneumoniae in a culture system and a 90% reduction of DNA products using a quantitative polymerase chain reaction (PCR) assay. After an effective anti-chlamydial regimen has been found, a second randomized clinical trial will examine clinical outcome measures in a cohort of secondary progressive multiple sclerosis (SPMS) patients. Half of these patients will receive antibiotics and interferon-?1b and the other half interferon-?1b alone. These patients will be followed for two years and the primary outcome measure will be measures of sustained progression or disability. These studies will determine both the optimal
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antibiotic treatment of CNS C. pneumoniae infection in MS patients and if antibiotic therapy favorable alters the natural history of MS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MICROARRAY DETERMINANTS IN COMMUNITY-ACQUIRED PNEUMONIA Principal Investigator & Institution: Wood, Kelly; Critical Care Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-APR-2008 Summary: (provided by applicant): I am a junior faculty member in the Department of Critical Care Medicine at the University of Pittsburgh. I am trained in Pulmonary and Critical Care Medicine and have a Masters of Health Science degree in clinical research. My short-term goal is to become expertly trained in clinical research of the critically ill, specifically focusing on the integration of emerging knowledge of the biology of critical illness with advances in clinical research, biostatistics, and data management. My longterm goal is to bring a new level to critical care medicine where an individual's pathophysiologic response to illness is used to predict outcome and guide care. Under the tutelage and mentorship of Dr. Angus (sponsor) and key consultants, I have developed a set of formal coursework, directed reading and tutorials that will form the educational and training core necessary to achieve my goals. This training and education will take place in the Department of Critical Care Medicine, the Department of Biostatistics in the Graduate School of Public Health, the Center for Human Genetics and integrative Biology at the University of Pittsburgh Medical Center, and at the adjacent Carnegie Mellon University. My research project, "Microarray Determinants in Community-Acquired Pneumonia (CAP)" is designed to both provide important new information and provide an important educational opportunity complimenting the other components of my training and education. CAP is a major public health problem, frequently fatal in the elderly. The proposed study will perform a high throughput genetic analysis of elderly Caucasian males with pneumococcal CAP using microarray technology. Two substudies will occur. The first substudy is designed to develop a mortality risk prediction that distinguishes survivors and non-survivors, who are phenotypically similar, from a pre-existing database of stored whole blood samples (n=50). The second substudy involves the recruitment of a prospective inception cohort (n=50) of elderly white males with pneumococcal pneumonia. The value that provocation testing (with pneumococcal vaccine) has in providing additional information with regard to predicting clinical outcome will be explored. This second substudy will also serve as a validation cohort for the model developed in the first substudy. This proposed study will generate a new predictive tool of clinical outcome based on gene expression analysis in the narrowly defined, homogeneous cohort of elderly Caucasian males with CAP and potentially identify genes not previously known to be involved in the immune response to infection. Information will also be generated regarding the pathophysiology of infection and possible points of early intervention with medical therapy that may alter the course of the disease process. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MK-0826 VS CEFTRIAXONE FOR PNEUMONIA Principal Investigator & Institution: Dunbar, Lala; Tulane University of Louisiana New Orleans, La New Orleans, La 70112 Timing: Fiscal Year 2003
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Bacterial Pneumonia
Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOTIVATION AND PATCH TREATMENT FOR HIV POSITIVE SMOKERS Principal Investigator & Institution: Niaura, Raymond S.; Director of Research; Miriam Hospital Providence, Ri 029062853 Timing: Fiscal Year 2002; Project Start 01-JAN-1999; Project End 31-DEC-2003 Summary: Treatments for persons who are infected with the Human Immunodeficiency virus (HIV) or who have developed AIDS have advanced to there point where death is no longer the most likely outcome of a diagnosis. Combination anti-retroviral therapies and treatments with protease inhibitors have made HIV-infection a manageable, chronic conditions. Efforts to improve the health and quality of life of persons living with AIDS or who are HIV- positive is therefore a high priority. Cigarette smoking posses several health risks that are unique to the HIV-positive population, including increased risk of bacterial pneumonia, oral candidiasis, and perhaps even increased risk for progression to full-blown AIDS. Clearly, quitting smoking would help to improve these risk profiles. However, to date, no clinical research studies have been conducted to evaluate the effectiveness of stop smoking treatments specifically tailored to the HIV- positive population of smokers. In a additive design, this proposal will evaluate two treatments for smoking cessation in four outpatient clinics which treat HIV-infected persons. The goal is to enroll all eligible smokers, regardless of their motivation to quit smoking, into the study. Patients randomized into the Brief Treatment condition will receive from their physician a stop smoking intervention, following NCI guidelines from brief smoking cessation counseling. They will also receive a prescription for the nicotine patch. One follow-up visit will be scheduled between the physician and patient to check on their progress at quitting smoking. Patients randomized into the Motivational Enhancement condition will receive on their progress in quitting smoking. Patient randomized into the Motivational Enhancement condition will receive the above, in addition to two inperson visits (over a two month period, to coincide with the patient's regular clinic visits) with a trained Health Educator who will tailor the cessation intervention to the patient's level of motivation to quit smoking. All patients will be followed for a 2-, 4-, and 6-month follow-up. Point prevalence smoking status (7-day, CO verified) at the 6month point will be the primary outcome of interest. We hypothesize that 9% of the Motivational Enhancement patients will have quit smoking at this point, compared to 3% to patients in the Brief treatment condition. A number of important mediators of treatment outcome (e.g., self-efficacy, motivation decisional balance) also will be examined and the cost effectiveness of the treatments will be evaluated. This study will be the first to examine different smoking cessation treatments in an HIV-positive population and the results will have implications for important cost effective cessation interventions into clinical care settings. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MUNC18 PROTEINS IN AIRWAY MUCUS HYPERSECRETION Principal Investigator & Institution: Dickey, Burton F.; Professor and Chairman; Medicine; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Airway mucus forms a protective layer against inhaled particles and pathogens. However, excessive mucus secretion in response to
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inflammatory stimuli can lead to airflow obstruction. Mucus hypersecretion can be divided into two distinct stages: metaplasia of an epithelial layer that consists predominantly of ciliated and Clara cells into a layer that consists predominantly of mucus-secreting goblet cells; this is followed by regulated secretion of mucus from the metaplastic epithelium. At a molecular level, secretory metaplasia involves expression of genes encoding three sets of proteins: secretory products; components of an exocytic machinery; and signal transduction pathways connecting extracellular secretory signals to exocytic membrane fusion. Secreted macromolecules and signal transduction pathways are subjects of intensive study, but little is known about the exocytic machinery. Munc18 proteins are ubiquitous components of the exocytic machinery of secretory cells. Their absence leads to a complete failure of secretion, and their overexpression also impairs secretion. Together, these data indicate the critical role played by Munc18 proteins and suggest that their expression is tightly regulated. We have found that Munc18B is highly upregulated in metaplastic airway epithelium of mice, and that its promoter region contains elements known to respond to inflammatory stimuli. We propose to suppress expression of Munc18B to test the protective and pathophysiologic roles of mucus secretion in models of allergic and infectious lung inflammation in mice, and to analyze the control of Munc18B expression in mice and humans to gain insight into the molecular pathogenesis of mucus metaplasia. Aim 1: Further characterize the cellular biology of Munc18 proteins in the regulation of airway mucus secretion in murine and human cells. Aim 2: Analyze the protective and pathophysiologic roles of mucus hypersecretion in murine models of allergic asthma and bacterial pneumonia by reducing the capability of airway goblet cells to secrete mucus through reduction of Munc18B expression. Aim 3: Identify critical cis-acting DNA elements and transcription factors that control expression of the Munc18B gene in metaplastic airway epithelium of mice. Aim 4: Confirm the importance of cis-acting DNA elements and transcription factors that control expression of the Munc18B gene in airway secretory metaplasia of humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEONATAL INHALED NITRIC OXIDE Principal Investigator & Institution: Ehrenkranz, Richard A.; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ORAL CARE AND RESPIRATORY PATHOGEN COLONIZATION Principal Investigator & Institution: Akca, Ozan; Anesthesiology; University of Louisville Jouett Hall, Belknap Campus Louisville, Ky 40292 Timing: Fiscal Year 2003; Project Start 15-JUL-2003; Project End 30-APR-2005 Summary: (provided by applicant): Ventilator-associated pneumonia (VAP) causes significant morbidity and increases health care cost. Identical bacteria have been cultured from the mouth and sputum of VAP patients suggesting that the oropharynx of critically ill patients becomes colonized with respiratory pathogens that are aspirated into the lungs. Antimicrobial rinsing reduces surface bacteria in the oropharynx, but does not remove plaque, which can serve as a reservoir of bacteria for recolonizing the entire oropharynx. Removing dental plaque may thus reduce recolonization following antibacterial rinse. A national survey of oral care practices in American intensive care
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Bacterial Pneumonia
units indicates that usual oral care consists primarily of swabbing the teeth and mouth with foam toothettes and rinsing with alcohol-free mouthwash. Foam swabbing is not effective in plaque removal and may not remove respiratory pathogens. Plaque removal with manual toothbrushing is effective but is performed once a day or less often by approximately 80% of ICU nurses. We will therefore test the hypothesis that mechanical removal of dental plaque combined with antimicrobial oral rinse significantly reduces respiratory pathogen colonization when compared usual to oral care plus swabbing with a placebo solution or the antimicrobial agent chlorhexidine. Seventy-five patients expected to be on a ventilator for more than 48 hours will be recruited for this study. Patients will be randomly assigned to: 1) Control: twice daily swabbing of the oropharynx with placebo in addition to usual oral care; 2) Chlorhexidine: twice daily swabbing of the oropharynx with chlorhexidine in addition to usual oral care; 3) Chlorhexidine/brushing: twice daily swabbing of the oropharynx with chlorhexidine followed by brushing of the teeth with a powered toothbrush with simultaneous suctioning and finally another swabbing with chlorhexidine. Research personnel who are unaware of patient assignment will collect plaque scores and microbial samples from all patients at baseline and every three days until extubation or day 15. The primary outcome will be the colonization by respiratory pathogens of microbiological samples taken from the teeth, mucosa, and sputum, Secondary outcomes will be dental plaque scores, endotracheal tube colonization and development of VAP. Data and confounding factors will be quantitatively analyzed. This study will serve as a basis for future multi-site clinical trials that will: 1) validate the effectiveness of dental hygiene as another measure to prevent VAP; 2) evaluate cost effectiveness; and 3) evaluate mortality. Reducing respiratory pathogen colonization in the mouth could significantly reduce the morbidity and cost of VAP. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ORAL CARE INTERVENTION IN MECHANICALLY VENTILATED ADULTS Principal Investigator & Institution: Munro, Cindy L.; Associate Professor; Adult Health Nursing; Virginia Commonwealth University Richmond, Va 232980568 Timing: Fiscal Year 2002; Project Start 01-MAR-2002; Project End 28-FEB-2007 Summary: (provided by applicant) Pneumonia is the leading cause of death from nosocomial infections. Intubation and mechanical ventilation greatly increase the risk of bacterial ventilator-associated pneumonia (VAP). Growth of potentially pathogenic bacteria in dental plaque of critically ill patients provides a nidus of infection for microorganisms that have been shown to be responsible for the development of VAP. Since these organisms are concentrated in dental plaque, removal of organisms form the oral cavity by oral care interventions is a theoretically attractive method to reduce the risk of development of VAP. However, evidence-based protocols for oral care of mechanically ventilated patients are not available. Thus, we propose a prospective, randomized clinical trial to test the effects of three oral care interventions (mechanical, MECHI; pharmacologic, PHARMI; and combination, mechanical plus pharmacologic, COMBI) in reducing the risk of developing VAP. The primary aim of this study is to test the effects of mechanical, pharmacologic and combination (mechanical plus pharmacologic) oral care interventions on dental plaque, oral microbial flora and oral immunity in critically ill mechanically ventilated adults. Secondary aims are to1) examine the effects of mechanical, pharmacologic and combination (mechanical plus pharmacologic) oral care interventions on development of VAP in critically ill mechanically ventilated adults; and 2) describe any differential effects of mechanical and
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pharmacologic oral care interventions on the development of VAP in specific patient populations (medical, surgical, and neurologic critically ill patients). A total of 456 subjects will be randomly assigned to 4 groups (control, MECHI, PHARMI, COMBI) in order to attain an adequate sample size of 300 subjects. The effects of interventions will be examined using a between-subjects 22 factorial design. A two-factor analysis of variance will be used to conduct significance tests, including tests of the effect of each intervention (MECHI, PHARMI, and COMBI) on the outcomes of dental plaque (UMOHI score), oral immunity (salivary IgA and lactoferrin), oral flora (semi-quantitative culture), and development of VAP (CPIS score). Results of the study have the potential to positively affect patient well-being, morbidity, mortality and health care costs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PATHOGENESIS OF KLEBSIELLA AIRWAY INFECTIONS Principal Investigator & Institution: Clegg, Steven; Professor; Microbiology; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): The opportunistic pathogen, Klebsiella pneumoniae, is responsible for a significant number of pulmonary infections in compromised individuals. The ubiquity of antibiotic resistant strains, particularly those producing extended-spectrum beta-lactamases, presents a serious clinical problem among groups such as hospitalized individuals and chronic alcoholics. The pathogenesis of Klebsiella airway infections has not been studied to any great extent and the investigation of the production of virulence determinants has essentially focused upon the role of capsules as antiphagocytic factors. The mouse has been extensively used as a model of airway infections due to K. pneumoniae primarily to investigate host cell responses. Also, epidemiologic observations suggest that specific capsular serotypes (e.g. K2) are most frequently associated with pulmonary infections. However, our preliminary data indicate that not all K2-positive isolates are virulent in the mouse model of infection. Therefore, although the capsule is most likely to be an antiphagocytic factor and prevent efficient killing of the bacteria in vivo, additional factors are necessary to establish airway infections with subsequent invasion of the bloodstream. We propose to identify and confirm the role of previously unknown virulence factors that mediate airway infections due to K. pneumoniae. Three techniques; signature-tagged mutagenesis, subtractive hybridization and in vivo gene expression technology will identify these determinants. The murine model of Klebsiella infection will be used to demonstrate the role of putative virulence factors during infection. The three approaches are complementary and have been used to investigate virulence in many different types of pathogens. Since very little is known about the virulence factors of K. pneumoniae, it is anticipated that these studies will provide information on new and novel virulence factors produced by these bacteria. Fundamental to devising new therapeutic approaches to opportunistic infections will be an understanding of the virulence factors produced by this group of organisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PATHOGENESIS OF LUNG INJURY IN LUNG AND PERITONEAL SEPSIS Principal Investigator & Institution: Martin, Thomas; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002
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Bacterial Pneumonia
Summary: Problem. This project will investigate the cellular and molecular events that link local infection in a primary body space with systemic consequences and injury to distant organs. The major hypothesis is that a three compartment model best explains the responses of humans to bacteria and their products. In this model, bacteria enter an initial compartment (e.g., lungs or abdominal cavity), and local interactions between bacteria and host effector systems govern whether bacteria are effectively eliminated. When first compartment responses are ineffective, responses occur in the second "systemic" compartment. When the second compartment responses are severe, responses occur in the third compartment (distant organs). In the lungs these responses include injury to the epithelial barrier and sustained loss of function. We will investigate important questions that relate to understanding this model. The major long-term goal is to understand how responses in the second and third compartments can be minimized without adversely affecting bacterial elimination in the first compartment. Specific Aims. 1) to investigate the "first compartment" responses in the lungs and the peritoneal cavity, in order to determine why the "first compartment" responses differ in each of these two sites; 2) to investigate the critical inter-relationships between the first compartment and the second compartment inflammatory responses; 3) to investigate the mechanisms by which injury occurs to the lung epithelium in the third compartment; 4) to investigate strategies that will protect the third compartment without adversely affecting antibacterial responses in the first compartment. Experimental approach. We will study rabbits with pneumonia or peritonitis due to E. coli, and follow them for up to 24 hours after infection. Responses in the first compartment will be compared with systemic physiologic and inflammatory response variables, and measurements of functional and anatomic integrity of the third compartment (lungs). New strategies to protect the third compartment without compromising antibacterial defenses in the first compartment will be investigated. Significance. These studies will provide information about the relationship between local and systemic responses and lung injury in sepsis, and will help to determine whether the best approach to prevention and treatment of septic complications is to focus on the specific organism (e.g., better antibiotics), or on interfering with the host response (e.g., better anti-inflammatory therapy), or both. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PLATELET CELL ADHESION MOLECULES Principal Investigator & Institution: Furie, Bruce; Chief, Coagulation Unit; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2002; Project Start 01-DEC-1994; Project End 30-NOV-2003 Summary: P-selectin is a cell adhesion molecule that resides in the storage granules of platelets and endothelial cells. Upon cell stimulation, the protein is translocated to the plasma membrane where it functions as a leukocyte receptor for PSGL-1 on neutrophils and monocytes. The current application represents a continuation of studies of the biology of P-selectin and PSGL-1. Since PSGL-1 has been shown to bind to all selectins, the kinetic and equilibrium binding of soluble PSGL-1 to soluble P-selectin, E-selectin and L-selectin will be analyzed by fluorescence spectroscopy. During the past grant period, we have prepared a PSGL-1 deficient mouse by homologous recombination and have completed the initial characterization. Cells from this mouse will be used to establish the physiologic role of PSGL-1 in selectin function by comparing the interaction of PSGL-1 (-/-), (+/-) and (+/+) leukocytes with P-selectin, E- selectin and Lselectin under rolling conditions in a parallel plate ex vivo assay using neutrophils and T lymphocytes. The PSGL-1 deficient mouse and double knockout mice including PSGL1 null/P-selectin null mice, PSGL-1 null/E-selectin null mice and PSGL-1 null/L-
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selectin null mice will be employed in model systems to determine the physiologic function of PSGL-1. Pathologic processes to be studied include models of non- immune mediated and T-cell mediated skin inflammation, leukocyte rolling following trauma and TNF, experimental glomerulonephritis, chemical peritonitis, bacterial pneumonitis, thrombosis, atherosclerosis, wound healing and platelet rolling. To understand the molecular basis of signal transduction and effector function induced by platelet activation or P-selectin binding to the P-selectin ligand on leukocytes, the induction of Ca2+ flux in platelets by PSGL-1 via P-selectin will be analyzed. Furthermore, binding of cytoplasmic tails of P-selectin and PSGL-1 to cytoplasmic signalling proteins in platelets and monocytes respectively will be examined using dimer constructs of cytoplasmic tails. If these studies indicate that PSGL-1 and ESL-1 are not physiologically critical counterreceptors for E-selectin or that there is evidence for another P- selectin ligand, we propose to expression clone a novel E-selectin ligand from a leukocyte library prepared from WEHI cells and a novel P-selectin ligand from a library prepared from neutrophils isolated from the PSGL-1 null mouse. The putative ligands will undergo characterization of their full length cDNAs and comparison of their predicted amino acid sequences with that of the PSGL-1, ESL-1 and GlyCAM-1. These studies will contribute to our understanding of the physiologically relevant receptors and counterreceptors that define cell-cell interaction during inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PPARGAMMA IN SEPSIS-INDUCED IMMUNOSUPPRESSION Principal Investigator & Institution: Reddy, Raju C.; Internal Medicine; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Patients with sepsis are highly susceptible to the development of nosocomial infection, particularly bacterial infection of the lung. While the exact mechanism(s) that contribute to sepsis-mediated immunosuppression remains unclear, dysregulation of monocyte/macrophage function is believed to play an important role in these phenomena. Recently, peroxisome proliferator-activated receptor-gamma (PPARy), a member of the nuclear receptor superfamily of liganddependent transcription factors, has been shown to inhibit the expression of inflammatory mediators from monocytes/macrophages and other leukocyte populations. The hypothesis of this proposal is that sepsis induced immunosuppression is mediated, in part, by PPARy. Furthermore, we postulate that inhibition of this ligand dependent transcription factor will reverse sepsis-induced changes in alveolar macrophage function, resulting in augmented lung antibacterial host defense. A murine model of cecal ligation and puncture (resulting in an abdominal sepsis syndrome) will be utilized to assess the following Specific Aims: I) to determine the time course and magnitude of PPARy expression in lung during the evolution of murine abdominal sepsis; II) to determine the functional significance of PPARy activation on effector cell functions of primary murine alveolar macrophages or murine alveolar macrophage cell lines; III) to identify the endogenous signals that regulate PPARy expression during the evolution of murine abdominal sepsis; and IV) to determine the effect of inhibition of PPARy on sepsis- induced alterations in alveolar macrophage function ex-vivo and susceptibility to Pseudomonas pneumonia in-vivo. Performance of the studies outlined will help define the role of PPARy as a mediator of sepsis-induced alveolar macrophage dysfunction, and may lead to the development of novel therapies to be employed in the treatment of patients with sepsis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Bacterial Pneumonia
Project Title: PREVENTION OF INFECTION IN INDIAN NEONATES Principal Investigator & Institution: Panigrahi, Pinaki; Pediatrics; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2002; Project Start 03-SEP-2001; Project End 30-APR-2006 Summary: (Provided by applicant): India, with one of the world's largest populations, continues to struggle with extremely high infant and neonatal mortality rates. Sepsis now accounts for 50% of deaths among community-born (and 20% of mortality among hospital-born) infants. Closely linked with this is a burgeoning problem with antimicrobial resistance, which is increasingly restricting the therapeutic options for medical care providers. To deal with these critical issues, the investigators propose to establish a Research Unit for the study of MCH in India, based on strong, existing collaborations between investigators in the Department of Pediatrics and Epidemiology and Preventive Medicine at the UMSM, Baltimore, and the AIIMS, New Delhi, and hospitals and the Ministry of Health in the state of Orissa, India. The applicant will initially develop an infrastructure to monitor occurrence of neonatal sepsis in community- and hospital-born infants. This will include: 1) identification of all hospitalized children, and children brought to hospital, with the diagnosis of sepsis; 2) obtaining blood cultures from these children; 3) screening of all bacterial strains isolated from blood cultures for antimicrobial resistance; 4) collecting basic demographic, risk factor, and treatment data on each case; and 5) development of a computer-based system and network for data management. In villages of Orissa State, the applicants will set up a village-level surveillance system to identify women during their pregnancy, monitor pregnancy outcomes, and establish a mechanism for referral of all potentially septic infants to participating clinics or hospitals for evaluation, including collection of blood cultures. Subsequent studies will identify potential sources of bacterial isolates causing sepsis. To this end, the applicants will screen skin, nares, and stool cultures from infants (and skin, nares, and vaginal cultures from their mothers), and seek to match blood isolates with these colonizing isolates, using molecular epidemiologic techniques. In the latter years of the grant period, and with these data collection systems in place, the applicants will initiate a series of interventions, including implementation of a hospital- and community-based system of "preferred" antimicrobials, use of probiotics to reduce the risk of neonatal sepsis, and implement alcohol-based handwashing products in hospital and community-based healthcare settings to minimize pathogen transmission. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROPHYLAXIS FOR MAC, PNEUMONIA, AND HIV INFECTION Principal Investigator & Institution: Muschatt, David M.; Tulane University of Louisiana New Orleans, La New Orleans, La 70112 Timing: Fiscal Year 2003 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INFECTION
PULMONARY
HUMORAL
IMMUNE
RESPONSES
IN
HIV
Principal Investigator & Institution: Twigg, Homer L.; Associate Professor; Medicine; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167
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Timing: Fiscal Year 2002; Project Start 30-SEP-1998; Project End 31-AUG-2004 Summary: While infection with the human immunodeficiency virus (HIV) is classically associated with impaired cell mediated immune responses, perturbations in humoral, or B cell, immunity is also common but much less studied. Impairment of humoral immunity is especially important in the lung. The incidence of bacterial pneumonia, typically controlled by humoral immunity, is increased in HIV-infected patients. Preliminary data demonstrates very low levels of opsonizing IgG in BAL of infected patients and little evidence of local production of IgG. The generation of pulmonary immune responses can be viewed as a multi step process involving antigen uptake by accessory cells and transport to regional lymphoid tissue where the primary immune response occurs, antigen presentation to T cells leading to generation of "effector" T cells capable of providing B cell help, activation and differentiation of B cells stimulated by T cells resulting in immunoglobulin production, trafficking of B cells back to the lung to the site of initial infection, and finally expansion of the immune response in the alveolar environment. In HIV infection defects can occur at any of these steps leading to an impaired ability to generate local opsonizing antibody. In this proposal we will explore each of the steps involved in the generation of a humoral response using cells from HIV infected subjects as well as cells infected in vitro with HIV. In this proposal we will (1) determine the ability of alveolar macrophages, lung macrophages, monocytes, lung dendritic cells, and B cells to induce an antibody response and if HIV infection of accessory cells alters this ability, (2) determine the ability of normal and HIV-infected antigen-activated T cells to provide B cell help by measuring T cell activation markers, cytokine secretion, and longevity, (3) determine the ability of B cells to respond to normal and HIV-infected antigen-activated T cells by measuring T cell-B cell conjugate formation, B cell proliferation, expression of activation markers, immunoglobulin secretion, and premature B cell death, (4) determine if activated immunoglobulin secreting B cells express receptors which will allow them to traffic back to the lung, and (5) determine the ability of antibody specific B cells to proliferate and secrete immunoglobulin in an alveolar environment. Understanding mechanisms behind the impairment in humoral immunity in the lungs of HIV-infected individuals will contribute substantially to our understanding of pulmonary morbidity in this disease and offer suggestions on novel immune based therapeutic strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PULMONARY IMMUNE DEFENCES AGAINST M. BOVIS-BCG INFECTION Principal Investigator & Institution: Fulton, Scott A.; Medicine; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 01-SEP-2000; Project End 31-JUL-2005 Summary: Dr. Fulton is an Instructor at Case Western Reserve University School of Medicine in the Division of Infectious Diseases. As a fellow, Dr. Fulton was supported by an institutional training grant supported by the NIAID and a training grant from the American Lung Association. He has been responsible for setting up a new animal model to study the immune response to tuberculosis and chosen to continue studying tuberculosis at CWRU because of its long and productive interest in in immunity to tuberculosis. The scholarly environment was initiated by Dr. J. Ellner who is the current PI for a multi-center collaborative Tuberculosis Research Unit. Dr. Fulton's mentors, Drs. W. H. Boom and F. P. Heinzel are interested in cellular immune responses to complex intracellular pathogens and have had significant success in training physician scientists. Other members include Dr. Z. Toossi, Dr. R. Wallis, Dr. C. Hirsch and Dr. R. Silver who
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Bacterial Pneumonia
contribute to the intellectual environment. Additional formal and informal interactions with scientists in Geographic Medicine (Dr. J. Kazura, Dr. C. King, Dr. E. Pearlman) will foster Dr. Fulton's training environment. Dr. Fulton now proposes addditional specialized training with the goal of becoming an independent physician scientist. He has set up a mouse model of aerogenic M. bovis-BCG infection as a model of human disease since M. bovis-BCG grows in the lung and elicits protective T cell responses that eradicate 99 percent of the bacteria. 1 percent of bacteria persist in a steady state infection characterized by granuloma formation and immune surveillance. In contrast, viulent M. tuberculosis leads to progressive infection. Since human pulmonary immune responses can be only partially and indirectly studied, animal models have provided a means for studying the unique susceptibilty of the lung. To analyze immune responses that characterize the susceptibility of the lung to mycobacteria, three aims are proposed: Aim 1. To characterize the expression of chemokines and cytokines within the bronchoalveolar and lung microenvironments during early, maximal, and late immune activation phases of aerogenic M. bovis-BCG and M. tuberculosis infection. Aim 2. To characterize mycobacterial antigen presentation and T cell activation within the bronchoalveolar and lung microenvironments during early, maximal and late immune activation phases of aerogenic M. bovis-BCG and M. tuberculosis infection. Aim 3. To characterize the early pulmonary immune responses to aerogenic M. bovis-BCG and M. tuberculosis during local and systemic immunomodulation of cytokine and chemokine expression. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RISK FACTORS FOR DRUG RESISTANT PNEUMOCOCCAL PNEUMONIA Principal Investigator & Institution: Metlay, Joshua P.; Assistant Professor of Medicine & Epidem; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2004 Summary: Adapted from the Applicant's Abstract): The emergence of antimicrobial drug resistance among isolates of S. pneumoniae threatens to have a major impact on the management of patients with community-acquired pneumonia (CAP). S. pneumoniae is the most common cause of CAP and adequate pneumococcal coverage is at the center of empirical guidelines for the management of this disease. Yet, risk factors for infection with drug-resistant vs. drug-susceptible S. pneumoniae are controversial and the clinical impact of in vitro levels of resistance is poorly understood. This study will focus on resistance to penicillin because penicillin and related ,8-lactam antimicrobials are a major component of current empirical treatment options for patients with CAP. Thus, understanding the risk factors for penicillin resistance can make a major contribution to the empirical management of these patients. The primary aim of this study is to identify risk factors for penicillin drug resistance in patients with bacteremic pneumococcal pneumonia. The primary study hypothesis is that both individual and community risk factors independently predict infection with penicillin resistant S. pneumoniae in patients with bacteremic pneumococcal pneumonia. A secondary hypothesis is that the duration of prior antibiotic use is a strong independent predictor of penicillin resistance in these patients. The secondary aims of this study are (1) to develop a prediction rule for penicillin resistance in patients with bacteremic pneumococcal pneumonia and (2) to measure the impact of different levels of penicillin resistance on medical outcomes in these patients. The hypotheses for these secondary aims are that (1) a prediction rule can be developed which accurately categorizes
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patients into high and low risk groups in order to improve the empirical selection of antimicrobial therapy for patients with CAP and (2) the in vitro level of penicillin resistance, alone, is a poor predictor of medical outcomes, but categorization of the adequacy of antimicrobial drug coverage, based on drug susceptibility profiles and pharmacodynamic drug considerations, will be a strong predictor of medical outcomes. This study is a population-based, case-control study, enrolling all hospitalized patients diagnosed with bacteremic pneumococcal pneumonia within the Pennsylvania Delaware Valley. Risk factors will be identified through patient interview and outpatient and inpatient medical record review. Pneumococcal drug resistance will be categorized at our microbiology laboratory with standardized susceptibility testing of all pneumococcal blood isolates. Finally, a cohort study will be completed within the study design, by examining outcomes for all patients, stratifying by pneumococcal drug susceptibility and adequacy of antimicrobial drug coverage. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE INFLAMMATION
OF
ENDOTHELIAL
DUFFY
ANTIGEN
IN
LUNG
Principal Investigator & Institution: Lee, Janet S.; Medicine; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2007 Summary: (provided by applicant): The major goal of this proposal is to determine the role of Duffy Antigen/ Receptor for Chemokines (DARC) in endothelial cells during lung inflammation. DARC binds multiple CXC and CC chemokines and is expressed on post-capillary venular endothelial cells, the site where leukocytes traverse the endothelium in response to inflammatory signals released from a site of tissue injury. Although endothelial DARC is upregulated during inflammation, its biological function remains unknown. It's focal location at the site of leukocyte emigration, its upregulation during inflammation, and preservation of expression on endothelial cells in all individuals suggest that it may participate in the regulation of inflammatory cell recruitment at the bloodtissue interface. The specific aims will explore the following : (1)endothelial DARC's role in chemokine transport, (2) its ability to modify neutrophil transendothelial migration, (3) its in vivo expression in the lung during suppurative pneumonia, (4) and DARC's contribution to neutrophil recruitment in a mouse model of pneumonia. A human endothelial cell line stably expressing DARC cDNA has been developed to study its ability to modify the biological activity of chemokines in vitro. Immunohistochemical analysis of human lungs will define the expression pattern of endothelial DARC during suppurative pneumonia. Finally, DARC's role will be examined in an animal model of bacterial pneumonia using DARC knockout mice. These studies are important, as they will determine endothelial DARC's contribution to the pulmonary recruitment of neutrophils during lung inflammation. Understanding endothelial DARC's function may provide novel strategies in modifying the inflammatory component of specific diseases such as bacterial pneumonia. These studies will further the candidate's research training in cell and molecular biology and provide the foundation for a career as a physicianscientist. The proposed studies will be conducted at the Pulmonary VA Research laboratories under the guidance of the sponsor and co-sponsor. Interactions with consultants throughout the University of Washington research community will enrich the candidate's training and ensure the success of the proposal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Bacterial Pneumonia
Project Title: SCCOR IN TRANSLATIONAL RESEARCH IN ACUTE LUNG INJURY Principal Investigator & Institution: Matthay, Michael A.; Professor; Cardiovascular Research Inst; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 30-JUN-2008 Summary: (provided by applicant): This is an Acute Lung Injury SCCOR application designed to study the pathogenesis and treatment of early acute lung injury. Although considerable progress has been made in selected areas of research and treatment of clinical acute lung injury, the pathogenesis of clinical lung injury is incompletely understood and mortality remains too high. Clinical and basic research is needed to provide new knowledge regarding fundamental mechanisms of lung injury as well as to test new therapies for acute lung injury (ALl), an important cause of acute respiratory failure in critically ill patients. Project 1 proposes a randomized, double-blind, phase II clinical trial to evaluate the potential efficacy of activated protein C (APC) for the treatment of acute lung injury. This project will also explore mechanistically the contribution of coagulation and inflammation dependent mechanisms to clinical lung injury. Project 2 is a clinical project to investigate the interactions among human genetics, bacterial genetics, and host events in the development of acute lung injury from bacterial pneumonia. This project will test the potential contribution of Mannose Binding Lectin genetic abnormalities as a cause of severe pneumonia and acute lung injury. This project will also test the hypothesis that P.aeruginosa colonization transforms to lung infection (ventilator-associated pneumonia) when the P.aeruginosa strains express type III virulence genes. Project 3 will examine the contribution of coagulation dependent mechanisms in experimental lung injury in mice by studying genetically modified mice as well as testing the impact of recombinant mouse AP C as therapy for experimental lung injury. Project 4 will examine the role of transforming growth factor-beta1 as a pathogenetic mechanism for early experimental acute lung injury, evaluating the mechanisms for TGF-beta1 activation, and also will identify the mechanisms for responsible for the TGF-beta1 induced alterations in alveolar epithelial fluid transport. The administrative and clinical cores (Cores A & B) will support the scientific objective of the projects. The proteomics core (Core C) will provide innovative methods for identifying novel proteins in the bronchoalveolar lavage fluid from patients and animals with acute lung injury, both before and after several treatment strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SMOKING AND ETHANOL-INDUCED DEFECTS IN PNEUMONIA DEFENSE Principal Investigator & Institution: Gentry-Nielsen, Martha J.; Medicine; Creighton University 2500 California Plaza Omaha, Ne 68178 Timing: Fiscal Year 2002; Project Start 01-DEC-2001; Project End 30-NOV-2004 Summary: (provided by applicant): The goal of this application is to use a novel rat model to study the compounding effects of cigarette smoke and alcohol abuse on susceptibility to severe pneumococcal pneumonia. Pneumonia is a major cause of morbidity and mortality in alcoholics, and the pneumococcus is the most common bacterial cause. Alcoholics have a higher incidence of pneumococcal pneumonia and they have a greater likelihood of developing bacteremia, which increases their mortality rate. Although scientists have studied the deleterious effects of ethanol ingestion on resistance to infectious diseases for years, the concurrent effects of smoking have been ignored. Because 80-90% of alcoholics smoke and >50% of multi-pack/day smokers are
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alcohol dependent, it is imperative to consider the additional effects of smoking when studying alcohol-induced defects in host defense against respiratory infections. Our hypothesis is that smoking exacerbates the detrimental effects of ethanol ingestion on host defense mechanisms critical for protection against lethal pneumococcal pneumonia. To test this hypothesis, rats will be exposed twice daily to cigarette smoke or room air in whole body chambers. Half of the rats also will be fed ethanol in a liquid diet. In Specific Aim 1, the rats will be infected intranasally, and the numbers of pneumococci reaching their lungs will be quantified by plate-counts. Movement of the organisms into the lungs will be correlated with alterations in the ciliary beat frequency of the rats' tracheal epithelial cells. In Specific Aim 2, novel in vitro assays will be used to determine the effects of ethanol ingestion, with and without smoke exposure, on the ability of the rats' pulmonary neutrophils to phagocytose and kill pneumococci. In Specific Aim 3, quantitative blood cultures will be used to determine the separate and combined effects of smoke exposure and ethanol ingestion on bacteremia development after establishment of pneumonia. Bacteremia will be correlated with mortality for 10-days post-infection with the use of a hypothermia model to predict death and determine the appropriate time for euthanasia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SUFACTANT PROTEIN-A AND LUNG DEFENSE Principal Investigator & Institution: Korfhagen, Thomas R.; Professor of Pediatrics; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 452293039 Timing: Fiscal Year 2004; Project Start 01-APR-1998; Project End 31-JAN-2009 Summary: (provided by applicant): Pulmonary inflammatory processes due to bacterial pneumonia impose a considerable clinical burden of morbidity and mortality in the US and other countries. A number of microbes considered as potential bioterrorist threats cause severe pulmonary inflammation. During the previous funding period, studies using transgenic mice, demonstrated that surfactant protein-A (SP-A) reduces inflammation caused by microbes and microbial products. Studies from patients with pneumonia or cystic fibrosis (CF) demonstrated reduced concentrations of SP-A suggesting that SP-A modulates the extent of microbial induced pulmonary inflammation. The goal of the present application is to determine mechanisms whereby SP-A regulates pulmonary inflammatory responses. Recent studies have demonstrated important roles for toll-like receptors (TLR) in inducing inflammatory responses. TLR4 is a major receptor for LPS and gram-negative bacteria. LPS binds to CD14 and LPS/CD14 interacts with MD-2/TLR4 forming a cell surface tripartite receptor complex that transduces intracellular signals leading to activation of cytokines and other inflammatory modulators. SP-A does not bind smooth forms of LPS but SP-A blocks smooth LPS induced cytokine production in vivo and in vitro. The lack of binding to smooth LPS suggests that SP-A cannot simply be sequestering LPS from interactions with the TLR complex. TLR4, CD14, and MD-2 RNA are present in alveolar macrophages and mouse lung epithelial cells supporting the central hypothesis that SPA alters inflammatory responses in the lung by reducing smooth LPS signaling through TLR-4 components. This hypothesis will be tested using smooth LPS mediated induction of NF-kappaB in cell transfections or LPS and gram-negative infection in mouse models to complete the following aims: (1) The SP-A structures and LPS receptor components that functionally interact to cause SP-A inhibition of LPS mediated signaling will be identified in vitro; (2) Mechanisms by which SP-A inhibits LPS mediated signaling will be determined by testing if SP-A alters interactions between TLR4 components necessary for LPS signaling in vitro; and (3) Structural domains of SP-
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Bacterial Pneumonia
A required for SP-A inhibition of LPS or gram-negative bacterial mediated signaling in vivo will be identified. The present application seeks to identify novel mechanisms of SP-A regulation of pulmonary inflammatory responses with the goal of identifying novel approaches to reducing pulmonary inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SURFACTANT PROTEIN A IN PULMONARY HOST DEFENSE Principal Investigator & Institution: Mccormack, Francis X.; Internal Medicine; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2002; Project Start 01-DEC-1998; Project End 30-NOV-2003 Summary: Bacterial pneumonia is a leading cause of morbidity and mortality in the United States. Infection is initiated by inhaled microorganisms that are deposited in the aqueous lining film which coats the alveolar epithelium. This compartment contains pulmonary surfactant, a mixture of phospholipids and proteins that maintains alveolar patency by reducing surface tension forces at the dir-liquid interface. Recent data suggests that surfactant protein A (SP-A), an abundant oligomeric glycoprotein in the distal airspaces, is also an acute phase reactant that functions as a major preimmune opsonin and lipopolysaccharide (LPs)-binding protein in the lung. The response of the alveolar macrophage (AM), the predominant inflammatory cell in the alveolar lumen, to microbes and microbial products must be tightly regulated to promote effective clearance while avoiding inappropriate inflammatory responses that may compromise gas exchange. Preliminary data presented herein suggests that SP-A enhances the clearance of pulmonary bacterial infections in mice and regulates the interaction of LPS with macrophages. Using recombinant SP-As with targeted mutations in critical structural domains and transgenic mice that overexpress rat and mutant of SP-A, we will test the hypothesis that SP-A modulates the inflammatory response of the lung to LPS and pathogenic microorganisms in the lung, and in the clearance of LPS and microbial infection from the airspace. Specific aim #2 will examine the structural domains of SP- A that mediate binding to LPS and bacterial microorganisms, the production of proinflammatory mediators and nitric oxide, and the clearance of LPS and microorganisms from the airspace. These studies will elucidate the role of SP-A in the innate immune defense of the lung, and may assist in the design of optimal antimicrobial strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SURFACTANT PROTEIN SP-R -- A KEY IN INNATE IMMUNITY Principal Investigator & Institution: Strange, Charlton B.; Medical University of South Carolina P O Box 250854 Charleston, Sc 29425 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THE FASTFASL SYSTEM IN LUNG INJURY Principal Investigator & Institution: Matute-Bello, Gustavo; Medicine; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 06-AUG-2002; Project End 30-JUN-2007 Summary: (provided by applicant): My main career goal is to become an independent investigator performing translational and integrative research in the field of acute lung
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injury. Acute lung injury (ALI) is characterized by severe neutrophilic alvelitis and extensive injury to the alveolar epithelium, both of unclear cause. My main scientific goal is to determine the specific contributions of the pro-apoptotic and proinflammatory functions of the Fas/FasL system to the pathogenesis of ALI. The main hypothesis is that early in the course of ALI, activated alveolar macrophages (AM) and bronchial epithelial cells release soluble Fas-ligand (sFasL). Binding of sFasL to Fas (CD95) in alveolar epithelial cells results in apoptosis and epithelial damage. In contrast, activation of Fas in AM does not result in apoptosis, but instead leads to release of inflammatory cytokines. This hypothesis is derived from our preliminary data and the literature. Aim 1 investigates the cellular sources of sFasLin the airspaces of the lung and the mechanisms that control its release. Aim 2 investigates the specific role of the proapoptotic function of Fas in the development of alveolar permeability changes during bacterial pneumonia. Aim 3 investigates the specific role of the proinflammatory function of Fas, by generating chimeric mice lacking either Fas or FasL in key target cells, then evaluating the inflammatory response to either intratracheal FasL or aerosolized LPS. Clarifying the role of the Fas/FasL system in the pathogenesis of ALI is important because it could lead to the development of therapeutic strategies for the Acute Respiratory Distress Syndrome (ARDS). These studies will be performed at the laboratory of Dr. Thomas R. Martin at the University of Washington (UW). This career development proposal includes a customized training program consisting of an advisory committee composed of six experts in the field, a didactic component including several graduate courses at the UW, and active participation in the Respiratory Cell and Molecular Biology Study Group at the Pulmonary Division of the UW. The proposed studies will allow for the acquisition of new techniques and further scientific development of the trainee into an independent investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THERAPEUTIC SCFV ANTIBODY FOR HUMAN PERIODONTITIS Principal Investigator & Institution: Teng, Yen-Tung A.; Associate Professor; Eastman Dentistry; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 31-MAR-2006 Summary: Human periodontal (gum) disease (i.e., gingivitis, and periodontitis - a more severe form of gingivitis) is the result of infections associated with specific oral bacteria below the gum lines. Chronic inflammatory periodontitis is the leading cause of tooth loss in adults (prevalence, >80 percent worldwide). Approximately $15 billion dollars per year are spent on its diagnosis, professional cleaning and treatment including the replacement of affected teeth in the United States. Recently, severe periodontal disease has been shown to be associated with an increased risk for coronary heart disease, stroke, bacterial pneumonia, diabetes and undesired pregnant outcomes. Conventional periodontal treatment relies on mechanical debridement of the affected teeth and gums by scaling, root planning and surgeries, sometimes combined with antibiotic usage, which suffers from nonspecific removal of the target microorganisms, high costs, time consuming, emergence of antibiotic resistance strains, re-infection of the gums etc. Therefore, human periodontal disease is a significant health and healthcare issue. In the current application, the applicant proposed to develop a new generation of neutralizing human single-chain Fv monoclonal antibodies (called: scFv-MoAbs) against a recently defined critical microbial target involved in human periodontitis, CagE homologue: a death-inducing protein of an etiological human periodontal pathogen, Actinobacillus actinomycetemcmomitans, from infected gum tissues. Importantly, the resulting neutralizing monoclonal antibodies will be tested in a "humanized" mouse model
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Bacterial Pneumonia
established by the applicant to validate the efficacy of the scFv-MoAbs being assessed before approaching human clinical studies. This combined new technology and specifically targeted approach by applying scFv-MoAbs to modulate or treat periodontal infections, if successful, will likely to become the new therapy for gum diseases and infections in the 21st century. Therefore, the patients' periodontal health will be improved and, eventually, this new treatment modality will also alleviate the chronic or/and long-term exposure of periodontal infections to systemic complications or risks; thereby, reducing the health-care burden and the associated socio-economical costs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INFECTION
TYPE
II
SECRETION
AND
LEGIONELLA
PNEUMOPHILA
Principal Investigator & Institution: Cianciotto, Nicholas P.; Professor; Microbiology and Immunology; Northwestern University Office of Sponsored Research Chicago, Il 60611 Timing: Fiscal Year 2004; Project Start 01-DEC-1998; Project End 30-NOV-2008 Summary: (provided by applicant): Legionella pneumophila (Lp) is the agent of Legionnaires' disease pneumonia. In its aquatic habitat, Lp survives as an intracellular parasite of protozoans, and after inoculation into the lung, it flourishes within alveolar macrophages. Previously, we discovered an Lp gene (pilD) whose product is homologous with PilD, which, in other Gram-negatives, mediates pilus biogenesis and type II protein secretion. Indeed, an Lp pilD mutant lacked pili. More importantly, the pilD mutant, but not a pilin mutant, was defective for infection of amoebae and macrophages, suggesting that Lp has a type II secretion system that promotes infection. During this last grant period, we confirmed Lp has a type II system (lsp) that mediates secretion of many proteins, including novel enzymes, and is critical for infection of both protozoa and human cells. Some of our other data suggested that the Lp peptidyl-prolyl isomerase Mip and SurA have a role in the secretion process. Presently, Lp is the only known system for studying type II secretion in an intracellular pathogen. In the last grant period, we also demonstrated that lsp mutants are greatly impaired for survival in the lungs of A/J mice, with the severity of their defect indicating that Lp type II secretion is a key virulence determinant that may be involved in more than just macrophage infection. Finally, we made the novel observation that lsp is required for growth at 12-25 degrees C. Thus, Lp type II secretion is uniquely critical for intracellular infection, virulence, and low-temperature growth. In the current proposal, we aim to identify the type II exoproteins that are critical for intracellular infection, confirm the role of Mip and SurA in secretion, and determine how type II secretion promotes in vivo survival as well as low-temperature growth in water and amoebae. The results of these studies will i) increase our understanding of Lp physiology and pathogenesis, ii) provide new insight into bacterial protein secretion, intracellular infection, and lowtemperature growth, and iii) have implications for other important human pathogens, including both other intracellular parasites and extracellular pathogens, such as Vibrio, Pseudomonas, and Burkholderia that survive at low-temperature and have type II systems. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TYPE PNEUMONIA
III
SECRETION
IN
PSEUDOMONAS
AERUGINOSA
Principal Investigator & Institution: Martin, Ciara G.; Microbiology and Immunology; Northwestern University Office of Sponsored Research Chicago, Il 60611
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Timing: Fiscal Year 2004; Project Start 01-MAY-2004; Project End 30-APR-2006 Summary: (provided by applicant): Pseudomonas aeruginosa is a bacterium that commonly inhabits natural locations such as rivers, lakes, and soil, and may secondarily colonize man-made surfaces like sinks and medical devices. Because of its prevalence, humans are frequently exposed to P. aeruginosa; however, most encounters in nature do not result in disease development. Rather, extremely severe disease, with a mortality of up to 70%, rapidly develops when exposure is coupled with another insult, such as chronic disease like emphysema, hospitalization, or immune suppression. In fact, current research suggests that P. aeruginosa pneumonia among hospitalized patients most frequently originates from previous environmental exposure. The long-term objective of this proposal is to better understand the pathogenesis of P. aeruginosa pneumonia. In particular, the roles of several effector proteins, secreted by a type III secretion system, will be investigated using isogenic bacterial mutants. The work will characterize the relative roles of three effectors proteins in causing acute pulmonary disease, focusing on their functions in the development of pneumonia and in modulating the innate immune response to infection. These experiments will yield a greater understanding of the pathogenesis of acute P. aeruginosa pneumonia and may present potential targets for clinical treatment of these severe infections. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: VITAMIN A/ZINC - PREVENTION OF PNEUMONIA (VAZPOP) STUDY Principal Investigator & Institution: Griffiths, Jeffrey K.; Associate Professor; Family Medicine & Cmty Health; Tufts University Boston Boston, Ma 02111 Timing: Fiscal Year 2002; Project Start 18-JAN-2000; Project End 31-DEC-2004 Summary: (Adapted from applicant's description): The Vitamin A and Zinc - Prevention of Pneumonia (VAZPOP) Study. Linking Vitamin A and Zinc Deficiencies, Immunity, Growth, and the Prevention of the Leading Cause of Childhood Death. The objective is to delineate how vitamin A and zinc supplementation interact in improving immunity, fostering growth, and preventing infection, in populations at risk for malnutrition and vitamin A and zinc deficiency. Malnutrition is involved in half of the global deaths in children less than 5. Acute respiratory infection (ARI), especially acute lower respiratory infection (ALRI) or pneumonia, is the leading cause of death in children. The investigators propose to conduct a randomized, placebo controlled, double blind, nutritionally stratified study of low dose vitamin A, 10 mg/day elemental zinc, both, or placebo in 2,400 children in Quito Ecuador. They will test the hypotheses that: a) lowdose vitamin A has paradoxically positive and negative effects on ALRI in underweight and well nourished children; b) zinc will protect against ALRI and diarrhea while boosting cell mediated immunity; c) growth will be fostered by zinc (and potentially by vitamin A) in deficient children; and d) misclassification of ALRI cases can mask the benefits or risks of vitamin A. The investigators will use state-of- the-art field techniques to assess body composition and growth, and utilize sophisticated techniques to assess vitamin A and zinc deficiency. In addition, they will use rigorous definitions of ALRI/pneumoma to avoid misclassification and ascertainment bias, which may have affected prior studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Bacterial Pneumonia
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 “bacterial pneumonia” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for bacterial pneumonia in the PubMed Central database: •
Automatic Detection of Acute Bacterial Pneumonia from Chest X-ray Reports. by Fiszman M, Chapman WW, Aronsky D, Evans RS, Haug PJ.; 2000 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129668
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 bacterial pneumonia, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “bacterial pneumonia” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for bacterial pneumonia (hyperlinks lead to article summaries): •
3 4
(Another) new technique for an old disease: the protected brush catheter and bacterial pneumonia. Author(s): Wallace RJ Jr. Source: Chest. 1982 May; 81(5): 532-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7075271
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. 6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A clinical pharmacy-oriented drug surveillance network: results of a nationwide antibiotic utilization review of bacterial pneumonia--1987. Author(s): Grasela TH Jr, Schentag JJ, Boekenoogen SJ, Crist KD, Lowes WL, Lum BL. Source: Dicp. 1989 February; 23(2): 162-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2728507
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A clinical profile of chronic bacterial pneumonia. Report of 115 cases. Author(s): Kirtland SH, Winterbauer RH, Dreis DF, Pardee NE, Springmeyer SC. Source: Chest. 1994 July; 106(1): 15-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8020263
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A comparative study of dirithromycin and erythromycin in bacterial pneumonia. Author(s): Liippo K, Tala E, Puolijoki H, Bruckner OJ, Rodrig J, Smits JP. Source: The Journal of Infection. 1994 March; 28(2): 131-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8034992
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A comparative study of the effects of almitrine bismesylate and lateral position during unilateral bacterial pneumonia with severe hypoxemia. Author(s): Dreyfuss D, Djedaini K, Lanore JJ, Mier L, Froidevaux R, Coste F. Source: Am Rev Respir Dis. 1992 August; 146(2): 295-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1489115
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A comparison of three severity score indexes in an evaluation of serious bacterial pneumonia. Author(s): Durocher A, Saulnier F, Beuscart R, Dievart F, Bart F, Deturck R, Wattel F. Source: Intensive Care Medicine. 1988; 14(1): 39-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3125234
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A nationwide survey of antibiotic prescribing patterns and clinical outcomes in patients with bacterial pneumonia. Author(s): Grasela TH Jr, Welage LS, Walawander CA, Timm EG, Pelter MA, Poirier TI, Walters JK. Source: Dicp. 1990 December; 24(12): 1220-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2089835
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A new bronchoscopic technique for the diagnosis of bacterial pneumonia in HIVpositive patients. Author(s): Sauleda J, Maimo A, Riera M, Ramirez J, Togores B, Pons S, Payeras A, Agusti AG. Source: Respiratory Medicine. 1997 October; 91(9): 530-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9415353
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A study of HIV RNA viral load in AIDS patients with bacterial pneumonia. Author(s): Bush CE, Donovan RM, Markowitz NP, Kvale P, Saravolatz LD. Source: Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology : Official Publication of the International Retrovirology Association. 1996 September; 13(1): 23-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8797682
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A study of the agglutinin response in 40 cases of bacterial pneumonia. Author(s): Nicholls AC, Pease PE, Green ID. Source: Journal of Clinical Pathology. 1975 June; 28(6): 453-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=806611
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A year's review of bacterial pneumonia at the central hospital of Lucerne, Switzerland. Author(s): Hug B, Rossi M. Source: Swiss Medical Weekly : Official Journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology. 2001 December 22; 131(47-48): 687-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11875753
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Accuracy of delayed (24 hours) processing of bronchoalveolar lavage for diagnosing bacterial pneumonia. Author(s): de Lassence A, Joly-Guillou ML, Salah A, Martin-Lefevre L, Hidri N, Ricard JD, Bouvry D, de Castro N, Dreyfuss D. Source: Critical Care Medicine. 2004 March; 32(3): 680-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15090947
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Accuracy of delayed cultures of plugged telescoping catheter samples for diagnosing bacterial pneumonia. Author(s): de Lassence A, Joly-Guillou ML, Martin-Lefevre L, Le Miere E, Lasry S, Morelot C, Coste F, Dreyfuss D. Source: Critical Care Medicine. 2001 July; 29(7): 1311-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11445676
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Acute community-acquired bacterial pneumonia in Human Immunodeficiency Virus (HIV) infected and non-HIV-infected adult patients in Cameroon: aetiology and outcome. Author(s): Koulla-Shiro S, Kuaban C, Belec L. Source: Tubercle and Lung Disease : the Official Journal of the International Union against Tuberculosis and Lung Disease. 1996 February; 77(1): 47-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8733414
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Acute pulmonary coccidioidomycosis mimicking bacterial pneumonia and septic shock: a report of two cases. Author(s): Lopez AM, Williams PL, Ampel NM. Source: The American Journal of Medicine. 1993 August; 95(2): 236-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8356990
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Aetiology and clinical presentation of mild community-acquired bacterial pneumonia. Author(s): Beovic B, Bonac B, Kese D, Avsic-Zupanc T, Kreft S, Lesnicar G, GorisekRebersek J, Rezar L, Letonja S. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2003 October; 22(10): 58491. Epub 2003 September 12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13680399
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An open, comparative evaluation of amoxycillin and amoxycillin plus clavulanic acid ('Augmentin') in the treatment of bacterial pneumonia in children. Author(s): Jibril HB, Ifere OA, Odumah DU. Source: Current Medical Research and Opinion. 1989; 11(9): 585-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2612203
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Anaerobic bacterial pneumonia in an otherwise healthy young adult. Author(s): Swartz MA, Marino PL. Source: Postgraduate Medicine. 1985 January; 77(1): 87-8, 90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3966068
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Antimicrobial susceptibility in community-acquired bacterial pneumonia in adults. Author(s): Kariuki S, Muyodi J, Mirza B, Mwatu W, Daniels JJ. Source: East Afr Med J. 2003 April; 80(4): 213-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12918806
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Aortic valve endocarditis after bacterial pneumonia. Author(s): Fonseca N, Santos J, Rodrigues S, Caetano F, Cardoso P, Segurado F, Bernardino L, Silvestre I, Fera M, Calquinha J, Martins AP, Ines L. Source: Rev Port Cardiol. 2003 May; 22(5): 707-11. English, Portuguese. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12940182
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Are HTLV-II-seropositive injection drug users at increased risk of bacterial pneumonia, abscess, and lymphadenopathy? Author(s): Modahl LE, Young KC, Varney KF, Khayam-Bashi H, Murphy EL. Source: Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology : Official Publication of the International Retrovirology Association. 1997 November 1; 16(3): 169-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9390568
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Association of low mannose-binding lectin serum concentrations and bacterial pneumonia in HIV infetion. Author(s): Hundt M, Heiken H, Schmidt RE. Source: Aids (London, England). 2000 August 18; 14(12): 1853-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10985324
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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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Atypical distribution of bacterial pneumonia after thoracic radiation therapy. Author(s): Fujita J, Bungo M, Nakamura H, Yamaji Y, Hata Y, Shiotani T, Irino S. Source: Ajr. American Journal of Roentgenology. 1990 November; 155(5): 1135. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2120949
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Automatic detection of acute bacterial pneumonia from chest X-ray reports. Author(s): Fiszman M, Chapman WW, Aronsky D, Evans RS, Haug PJ. Source: Journal of the American Medical Informatics Association : Jamia. 2000 November-December; 7(6): 593-604. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11062233
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Azithromycin versus cefaclor in the treatment of acute bacterial pneumonia. Author(s): Kinasewitz G, Wood RG. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 1991 October; 10(10): 8727. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1662636
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Bacterial pneumonia as a suprainfection in young adults with measles. Author(s): Loukides S, Panagou P, Kolokouris D, Kalogeropoulos N. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1999 February; 13(2): 356-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10065681
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Bacterial pneumonia associated with HIV-1 infection. Author(s): Noskin GA, Glassroth J. Source: Clinics in Chest Medicine. 1996 December; 17(4): 713-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9016373
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Bacterial pneumonia can increase serum concentration of clozapine. Author(s): Raaska K, Raitasuo V, Arstila M, Neuvonen PJ. Source: European Journal of Clinical Pharmacology. 2002 August; 58(5): 321-2. Epub 2002 June 25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12185555
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Bacterial pneumonia causes augmented expression of the secretory leukoprotease inhibitor gene in the murine lung. Author(s): Abe T, Tominaga Y, Kikuchi T, Watanabe A, Satoh K, Watanabe Y, Nukiwa T. Source: American Journal of Respiratory and Critical Care Medicine. 1997 October; 156(4 Pt 1): 1235-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9351627
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Bacterial pneumonia complicating adenoviral pneumonia. A comparison of respiratory tract bacterial culture sources and effectiveness of chemoprophylaxis against bacterial pneumonia. Author(s): Ellenbogen C, Graybill JR, Silva J Jr, Homme PJ. Source: The American Journal of Medicine. 1974 February; 56(2): 169-78. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4359823
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Bacterial pneumonia due to Bordetella bronchiseptica in a patient with acute leukemia. Author(s): Gomez L, Grazziutti M, Sumoza D, Beran M, Rolston K. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1998 April; 26(4): 1002-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9564496
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Bacterial pneumonia during the Hong Kong influenza epidemic of 1968-1969. Author(s): Schwarzmann SW, Adler JL, Sullivan RJ Jr, Marine WM. Source: Archives of Internal Medicine. 1971 June; 127(6): 1037-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5578560
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Bacterial pneumonia following surgery for chronic osteomyelitis. Author(s): Oni OO. Source: Clinical Orthopaedics and Related Research. 1984 January-February; (182): 3101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6692624
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Bacterial pneumonia in adult patients with HIV infection. Author(s): Moroni M, Franzetti F. Source: J Chemother. 1995 August; 7(4): 292-306. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8568541
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Bacterial pneumonia in adult populations with human immunodeficiency virus (HIV) infection. Author(s): Caiaffa WT, Graham NM, Vlahov D. Source: American Journal of Epidemiology. 1993 December 1; 138(11): 909-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8256779
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Bacterial pneumonia in HIV. Author(s): Cohen JI. Source: The New England Journal of Medicine. 1996 January 18; 334(3): 195. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8531989
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Bacterial pneumonia in HIV-infected patients. Author(s): Daley CL. Source: Seminars in Respiratory Infections. 1993 June; 8(2): 104-15. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8278678
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Bacterial pneumonia in HIV-infected patients: a prospective study of 68 episodes. Author(s): Falco V, Fernandez de Sevilla T, Alegre J, Barbe J, Ferrer A, Ocana I, Ribera E, Martinez-Vazquez JM. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1994 February; 7(2): 235-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8162975
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Bacterial pneumonia in HIV-infected patients: analysis of risk factors and prognostic indicators. Author(s): Tumbarello M, Tacconelli E, de Gaetano K, Ardito F, Pirronti T, Cauda R, Ortona L. Source: Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology : Official Publication of the International Retrovirology Association. 1998 May 1; 18(1): 3945. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9593456
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Bacterial pneumonia in hospitalized patients with HIV infection: the Pulmonary Complications, ICU Support, and Prognostic Factors of Hospitalized Patients with HIV (PIP) Study. Author(s): Afessa B, Green B. Source: Chest. 2000 April; 117(4): 1017-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10767233
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Bacterial pneumonia in immunocompromised patients. Author(s): Conces DJ Jr. Source: Journal of Thoracic Imaging. 1998 October; 13(4): 261-70. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9799134
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Bacterial pneumonia in patients with human immunodeficiency virus infection. Author(s): Chaisson RE. Source: Seminars in Respiratory Infections. 1989 June; 4(2): 133-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2501846
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Bacterial pneumonia in patients with the acquired immunodeficiency syndrome. Author(s): Polsky B, Gold JW, Whimbey E, Dryjanski J, Brown AE, Schiffman G, Armstrong D. Source: Annals of Internal Medicine. 1986 January; 104(1): 38-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3484420
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Bacterial pneumonia in persons infected with the human immunodeficiency virus. Pulmonary Complications of HIV Infection Study Group. Author(s): Hirschtick RE, Glassroth J, Jordan MC, Wilcosky TC, Wallace JM, Kvale PA, Markowitz N, Rosen MJ, Mangura BT, Hopewell PC. Source: The New England Journal of Medicine. 1995 September 28; 333(13): 845-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7651475
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Bacterial pneumonia in recipients of bone marrow transplantation. A five-year prospective study. Author(s): Lossos IS, Breuer R, Or R, Strauss N, Elishoov H, Naparstek E, Aker M, Nagler A, Moses AE, Shapiro M, et al. Source: Transplantation. 1995 October 15; 60(7): 672-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7570975
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Bacterial pneumonia in solid organ transplantation. Author(s): Mermel LA, Maki DG. Source: Seminars in Respiratory Infections. 1990 March; 5(1): 10-29. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2188317
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Bacterial pneumonia in the elderly. Author(s): Limthongkul S, Charoenlap P, Wongthim S, Udompanich V, Nuchprayoon C. Source: J Med Assoc Thai. 1994 April; 77(4): 169-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7844490
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Bacterial pneumonia in the elderly. Author(s): Sims RV. Source: Emergency Medicine Clinics of North America. 1990 May; 8(2): 207-20. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2187678
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Bacterial pneumonia in the elderly. Author(s): Bentley DW. Source: Hosp Pract (Off Ed). 1988 December 15; 23(12): 99-104, 107-9, 114-6. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3142909
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Bacterial pneumonia in the elderly. Author(s): Verghese A, Berk SL. Source: Medicine; Analytical Reviews of General Medicine, Neurology, Psychiatry, Dermatology, and Pediatrics. 1983 September; 62(5): 271-85. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6353130
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Bacterial pneumonia in the elderly. Author(s): Ebright JR, Rytel MW. Source: Journal of the American Geriatrics Society. 1980 May; 28(5): 220-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7365185
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Bacterial pneumonia in the elderly: a reappraisal of conventional therapy, with a note on cefamandole. Author(s): Gleckman RA, Esposito AL. Source: Journal of the American Geriatrics Society. 1979 August; 27(8): 345-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=458085
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Bacterial pneumonia in the elderly: clinical features, diagnosis, etiology, and treatment. Author(s): Bentley DW. Source: Gerontology. 1984; 30(5): 297-307. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6386609
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Bacterial pneumonia in the elderly: the observations of Sir William Osler in retrospect. Author(s): Berk SL. Source: Journal of the American Geriatrics Society. 1984 September; 32(9): 683-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6381576
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Bacterial pneumonia in the HIV-infected patient. Author(s): Cohn DL. Source: Infectious Disease Clinics of North America. 1991 September; 5(3): 485-507. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1955696
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Bacterial pneumonia or pulmonary infarction? Author(s): Fred HL. Source: Dis Chest. 1969 May; 55(5): 422-5. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4888992
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Bacterial pneumonia. Author(s): Schneider RF. Source: Seminars in Respiratory Infections. 1999 December; 14(4): 327-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10638512
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Bacterial pneumonia. Managing a deadly complication of influenza in older adults with comorbid disease. Author(s): Sethi S. Source: Geriatrics. 2002 March; 57(3): 56-61. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11899549
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Bacterial pneumonia. S pneumoniae and H influenzae are the villains. Author(s): Wisinger D. Source: Postgraduate Medicine. 1993 May 15; 93(7): 43-6, 49-52. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8493197
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Bacterial pneumonia. Teaching your patient how to fight it. Author(s): Moreno MM. Source: Nursing. 1993 September; 23(9): 32C-32D. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8371854
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Bacterial pneumonia: aids in diagnosis and management. Author(s): Leonard J. Source: J Tenn Med Assoc. 1975 December; 68(12): 975-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1207126
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Bacterial pneumonia: commoner than perceived. Author(s): Shann F. Source: Lancet. 2001 June 30; 357(9274): 2070-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11445094
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Bacterial pneumonia: comparison between diabetics and non-diabetics. Author(s): Akbar DH. Source: Acta Diabetologica. 2001; 38(2): 77-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11757805
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Bacterial pneumonia: specific diagnosis and treatment of the elderly. Author(s): Gleckman RA, Bergman MM. Source: Geriatrics. 1987 September; 42(9): 29-36, 41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3497844
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Blood culture: specificity in childhood bacterial pneumonia. Author(s): Ejzenberg B, Rodrigues JC, Vieira VS, Brandileone MC, Baldacci ER, Okay Y. Source: Revista Do Instituto De Medicina Tropical De Sao Paulo. 1995 NovemberDecember; 37(6): 541-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8731269
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Bronchoalveolar lavage for diagnosing acute bacterial pneumonia. Author(s): Thorpe JE, Baughman RP, Frame PT, Wesseler TA, Staneck JL. Source: The Journal of Infectious Diseases. 1987 May; 155(5): 855-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3559289
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Bronchoalveolar lavage for diagnosing bacterial pneumonia in mechanically ventilated patients. Author(s): Aubas S, Aubas P, Capdevila X, Darbas H, Roustan JP, Du Cailar J. Source: American Journal of Respiratory and Critical Care Medicine. 1994 April; 149(4 Pt 1): 860-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8143047
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Bronchoscopic protected specimen brush and bronchoalveolar lavage in the diagnosis of bacterial pneumonia. Author(s): Broughton WA, Middleton RM 3rd, Kirkpatrick MB, Bass JB Jr. Source: Infectious Disease Clinics of North America. 1991 September; 5(3): 437-52. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1955692
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CD14 expression on monocytes and TNF alpha production in patients with septic shock, cardiogenic shock or bacterial pneumonia. Author(s): de Werra I, Zanetti G, Jaccard C, Chiolero R, Schaller MD, Yersin B, Glauser MP, Calandra T, Heumann D. Source: Swiss Medical Weekly : Official Journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology. 2001 January 27; 131(3-4): 35-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11219189
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Cefaclor versus amoxicillin in the treatment of bacterial pneumonia: a comparative double-blind study. Author(s): Leuenberger P, Vrantchev S. Source: European Journal of Clinical Microbiology. 1983 February; 2(1): 11-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6341045
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Cefazolin in the treatment of bacterial pneumonia. Author(s): Turck M, Clark RA, Beaty HN, Holmes KK, Karney WW, Reller LB. Source: The Journal of Infectious Diseases. 1973 October; 128: Suppl: S382-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4147579
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Cefepime versus cefotaxime for empirical treatment of bacterial pneumonia in HIVinfected patients: an open, randomized trial. Author(s): Cordero E, Bouza E, Ruiz I, Pachon J. Source: The Journal of Antimicrobial Chemotherapy. 2001 October; 48(4): 527-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11581232
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Ceforanide (BL-S786) in the treatment of community-acquired bacterial pneumonia. Author(s): Wallace RJ Jr, Martin RR, Greenberg SB. Source: Infection. 1979; 7(4): 176-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=315929
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Cefotaxime in the treatment of severe bacterial pneumonia in paediatric patients. Author(s): Rusconi F, Rancilio L, Cerri MA, Parizzi F, Pietrogrande MC, Razon S, Rogari P, Serafini L, Torti G, Vaggi D, et al. Source: Drugs. 1988; 35 Suppl 2: 203-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3293976
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Cephacetrile in the treatment of acute bacterial pneumonia. Author(s): Fee WH Jr, Winter LW, Bright TP, Smith JW, Farber MO, Bartram CE. Source: Curr Ther Res Clin Exp. 1975 May; 17(5): 419-26. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=236153
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Cephradine and cephalexin in the treatment of children with bacterial pneumonia. Author(s): Alban J, Caloza DL Jr. Source: Curr Ther Res Clin Exp. 1975 October; 18(4): 539-45. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=241608
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Changes in fatty acids in phospholipids of the bronchoalveolar fluid in bacterial pneumonia and in adult respiratory distress syndrome. Author(s): Baughman RP, Stein E, MacGee J, Rashkin M, Sahebjami H. Source: Clinical Chemistry. 1984 April; 30(4): 521-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6705194
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Changes in pulmonary surfactant during bacterial pneumonia. Author(s): Brogden KA. Source: Antonie Van Leeuwenhoek. 1991 May; 59(4): 215-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1883227
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Changing patterns in the etiology of HIV-associated bacterial pneumonia in the era of highly active antiretroviral therapy. Author(s): Boumis E, Petrosillo N, Girardi E, De Carli G, Armignacco O, Visca P, Ippolito G. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2001 January; 20(1): 71-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11245332
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Chest radiograph interpretation of Pneumocystis carinii pneumonia, bacterial pneumonia, and pulmonary tuberculosis in HIV-positive patients: accuracy, distinguishing features, and mimics. Author(s): Boiselle PM, Tocino I, Hooley RJ, Pumerantz AS, Selwyn PA, Neklesa VP, Lange RC. Source: Journal of Thoracic Imaging. 1997 January; 12(1): 47-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8989759
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Cigarette smoking, bacterial pneumonia, and other clinical outcomes in HIV-1 infection. Terry Beirn Community Programs for Clinical Research on AIDS. Author(s): Burns DN, Hillman D, Neaton JD, Sherer R, Mitchell T, Capps L, Vallier WG, Thurnherr MD, Gordin FM. Source: Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology : Official Publication of the International Retrovirology Association. 1996 December 1; 13(4): 374-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8948377
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Clindamycin (Cleocin) in bacterial pneumonia. Author(s): Quintiliani R, McGreevy MJ. Source: Curr Ther Res Clin Exp. 1970 November; 12(11): 701-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4993122
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Clinical and experimental studies on fibronectin in bacterial pneumonia and adhesiveness of bacteria to fibronectin. Author(s): Oshitani H, Kobayashi H. Source: Kansenshogaku Zasshi. 1988 March; 62 Suppl: 151-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3138340
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Clinical predictors of Pneumocystis carinii pneumonia, bacterial pneumonia and tuberculosis in HIV-infected patients. Author(s): Selwyn PA, Pumerantz AS, Durante A, Alcabes PG, Gourevitch MN, Boiselle PM, Elmore JG. Source: Aids (London, England). 1998 May 28; 12(8): 885-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9631142
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Community-acquired bacterial pneumonia in human immunodeficiency virusinfected patients: validation of severity criteria. The Grupo Andaluz para el Estudio de las Enfermedades Infecciosas. Author(s): Cordero E, Pachon J, Rivero A, Giron JA, Gomez-Mateos J, Merino MD, Torres-Tortosa M, Gonzalez-Serrano M, Aliaga L, Collado A, Hernandez-Quero J, Barrera A, Nuno E. Source: American Journal of Respiratory and Critical Care Medicine. 2000 December; 162(6): 2063-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11112115
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Community-acquired bacterial pneumonia in the elderly. Author(s): Gleckman RA, Roth RM. Source: Pharmacotherapy. 1984 March-April; 4(2): 81-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6371723
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Community-acquired bacterial pneumonia requiring admission to hospital. Author(s): Klimek JJ, Ajemian E, Fontecchio S, Gracewski J, Klemas B, Jimenez L. Source: American Journal of Infection Control. 1983 June; 11(3): 79-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6349427
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Community-acquired pneumonia in Ugandan adults: short-term parenteral ampicillin therapy for bacterial pneumonia. Author(s): Yoshimine H, Oishi K, Mubiru F, Nalwoga H, Takahashi H, Amano H, Ombasi P, Watanabe K, Joloba M, Aisu T, Ahmed K, Shimada M, Mugerwa R, Nagatake T. Source: The American Journal of Tropical Medicine and Hygiene. 2001 March-April; 64(3-4): 172-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11442214
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Comparative efficacy and safety of ceftizoxime, cefotaxime and latamoxef in the treatment of bacterial pneumonia in high risk patients. Author(s): Yangco BG, Baird I, Lorber B, Noble R, Bermudez R, Silverblatt F, Vasquez G. Source: The Journal of Antimicrobial Chemotherapy. 1987 February; 19(2): 239-48. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3553135
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Congenital bacterial pneumonia with intact fetal membranes. Author(s): Monif GR. Source: Pediatrics. 1970 May; 45(5): 865-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5462811
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Consensus: management of presumed bacterial pneumonia in ambulatory children. Author(s): Grossman M, Klein JO, McCarthy PL, Schwartz RH, McCracken GH Jr, Nelson JD. Source: Pediatr Infect Dis. 1984 November-December; 3(6): 497-500. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6334843
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Correlation of leucocyte count and erythrocyte sedimentation rate with the day of illness in presumed bacterial pneumonia of childhood. Author(s): Triga MG, Syrogiannopoulos GA, Thoma KD, Fezoulidis IB, Pastromas VG, Beratis NG. Source: The Journal of Infection. 1998 January; 36(1): 63-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9515671
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Countercurrent immunoelectrophoresis for diagnosis of acute bacterial pneumonia in Chinese children. Author(s): Yang YH, Jiang ZF, Chen XN, Jiang QB, Zhang GR, Shen XZ, Peng H, Schneerson R, Robbins JB. Source: Chinese Medical Journal. 1993 February; 106(2): 105-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8504692
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Counterimmunoelectrophoresis and latex particle agglutination in the etiologic diagnosis of presumed bacterial pneumonia in pediatric patients. Author(s): Rusconi F, Rancilio L, Assael BM, Bonora G, Cerri M, Pietrogrande MC, Razon S, Serafini L, Torti G, Vaggi D, et al. Source: The Pediatric Infectious Disease Journal. 1988 November; 7(11): 781-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3266006
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Counterimmunoelectrophoresis of urine for diagnosis of bacterial pneumonia in pediatric outpatients. Author(s): Turner RB, Hayden FG, Hendley JO. Source: Pediatrics. 1983 May; 71(5): 780-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6601259
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Culture from epipharynx of little value in bacterial pneumonia. Author(s): Steinum O, Alestig K, Brorson JE. Source: Scandinavian Journal of Infectious Diseases. 1987; 19(3): 309-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3303304
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Current status of bacterial pneumonia with special reference to pneumococcal infection. Author(s): Austrian R. Source: J Clin Pathol Suppl (R Coll Pathol). 1968; 2: 93-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5271933
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Cytokine immunotherapy during bacterial pneumonia: from benchtop to bedside. Author(s): Moore TA, Standiford TJ. Source: Seminars in Respiratory Infections. 2001 March; 16(1): 27-37. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11309710
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Cytokine treatment of bacterial pneumonia. Author(s): Nelson S, Bagby GJ, Dale D. Source: Seminars in Respiratory Infections. 2001 March; 16(1): 38-46. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11309711
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Cytokines as targets of immunotherapy in bacterial pneumonia. Author(s): Standiford TJ, Tsai WC, Mehrad B, Moore TA. Source: The Journal of Laboratory and Clinical Medicine. 2000 February; 135(2): 129-38. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10695657
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Cytokines, nitrite/nitrate, soluble tumor necrosis factor receptors, and procalcitonin concentrations: comparisons in patients with septic shock, cardiogenic shock, and bacterial pneumonia. Author(s): de Werra I, Jaccard C, Corradin SB, Chiolero R, Yersin B, Gallati H, Assicot M, Bohuon C, Baumgartner JD, Glauser MP, Heumann D. Source: Critical Care Medicine. 1997 April; 25(4): 607-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9142024
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Cytology of bronchoalveolar lavage fluid in bacterial pneumonia. Author(s): Castella X, Artigas A. Source: Chest. 1990 June; 97(6): 1500-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2393418
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Decreased apoptosis and increased activation of alveolar neutrophils in bacterial pneumonia. Author(s): Droemann D, Aries SP, Hansen F, Moellers M, Braun J, Katus HA, Dalhoff K. Source: Chest. 2000 June; 117(6): 1679-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10858402
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Decreased surfactant protein A in patients with bacterial pneumonia. Author(s): Baughman RP, Sternberg RI, Hull W, Buchsbaum JA, Whitsett J. Source: Am Rev Respir Dis. 1993 March; 147(3): 653-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8442601
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Detection of Pneumocystis DNA in samples from patients suspected of bacterial pneumonia--a case-control study. Author(s): Helweg-Larsen J, Jensen JS, Dohn B, Benfield TL, Lundgren B. Source: Bmc Infectious Diseases [electronic Resource]. 2002 November 25; 2(1): 28. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12445330
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Diagnosis and treatment of bacterial pneumonia in Korea. Author(s): Han YC, Woo JH. Source: Respirology (Carlton, Vic.). 1996 June; 1(2): 115-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9434326
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Diagnosis of acute bacterial pneumonia in Nigerian children. Value of needle aspiration of lung of countercurrent immunoelectrophoresis. Author(s): Silverman M, Stratton D, Diallo A, Egler LJ. Source: Archives of Disease in Childhood. 1977 December; 52(12): 925-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=343723
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Diagnosis of bacterial pneumonia with fiberoptic bronchoscopy. Author(s): Winterbauer RH. Source: European Journal of Clinical Microbiology. 1985 April; 4(2): 95-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4006936
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Diagnosis of nosocomial bacterial pneumonia in acute, diffuse lung injury. Author(s): Andrews CP, Coalson JJ, Smith JD, Johanson WG Jr. Source: Chest. 1981 September; 80(3): 254-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7273874
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Diagnosis of nosocomial bacterial pneumonia in intubated patients undergoing ventilation: comparison of the usefulness of bronchoalveolar lavage and the protected specimen brush. Author(s): Chastre J, Fagon JY, Soler P, Bornet M, Domart Y, Trouillet JL, Gibert C, Hance AJ. Source: The American Journal of Medicine. 1988 October; 85(4): 499-506. Erratum In: Am J Med 1989 February; 86(2): 258. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3177397
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Diagnostic accuracy of protected catheter sampling in ventilator-associated bacterial pneumonia. Author(s): Bregeon F, Papazian L, Thomas P, Carret V, Garbe L, Saux P, Drancourt M, Auffray JP. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2000 November; 16(5): 969-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11153601
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Diagnostic and therapeutic advantages of serial quantitative cultures of fresh sputum in acute bacterial pneumonia. Author(s): Pirtle JK, Monroe PW, Smalley TK, Mohr JA, Rhoades ER. Source: Am Rev Respir Dis. 1969 December; 100(6): 831-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4390935
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Diagnostic efficacy of a nasotracheal protected specimen brush in patients with suspected bacterial pneumonia. Author(s): Gong H Jr, Soffer MJ, Ertle AR, Inderlied CB, Bruckner DA. Source: Diagnostic Microbiology and Infectious Disease. 1988 October; 11(2): 87-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3229099
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Diagnostic value of bronchoalveolar lavage in patients with opportunistic and nonopportunistic bacterial pneumonia. Author(s): Dalhoff K, Braun J, Hollandt H, Lipp R, Wiessmann KJ, Marre R. Source: Infection. 1993 September-October; 21(5): 291-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8300244
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Diagnostic value of quantitative cultures of bronchoalveolar lavage and telescoping plugged catheters in mechanically ventilated patients with bacterial pneumonia. Author(s): Torres A, Puig de la Bellacasa J, Xaubet A, Gonzalez J, Rodriguez-Roisin R, Jimenez de Anta MT, Agusti Vidal A. Source: Am Rev Respir Dis. 1989 August; 140(2): 306-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2764366
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Diagnostic value of telescoping plugged catheters in mechanically ventilated patients with bacterial pneumonia using the Metras catheter. Author(s): Torres A, Puig de la Bellacasa J, Rodriguez-Roisin R, Jimenez de Anta MT, Agusti-Vidal A. Source: Am Rev Respir Dis. 1988 July; 138(1): 117-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3202391
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Double-blind study of endotracheal tobramycin in the treatment of gram-negative bacterial pneumonia. The Endotracheal Tobramycin Study Group. Author(s): Brown RB, Kruse JA, Counts GW, Russell JA, Christou NV, Sands ML. Source: Antimicrobial Agents and Chemotherapy. 1990 February; 34(2): 269-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2183716
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Early-onset bacterial pneumonia: a comparison with severe hyaline membrane disease. Author(s): Leslie GI, Scurr RD, Barr PA. Source: Aust Paediatr J. 1981 September; 17(3): 202-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7325903
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Editorial response: do bacterial pneumonia and Pneumocystis carinii pneumonia accelerate progression of human immunodeficiency virus disease? Author(s): Kaplan JE, Janoff EN, Masur H. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1999 September; 29(3): 544-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10530444
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Effect of antiretroviral therapy on the incidence of bacterial pneumonia in patients with advanced HIV infection. Author(s): Sullivan JH, Moore RD, Keruly JC, Chaisson RE. Source: American Journal of Respiratory and Critical Care Medicine. 2000 July; 162(1): 64-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10903221
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Effect of highly active antiretroviral therapy on the incidence of bacterial pneumonia in HIV-infected subjects. Author(s): de Gaetano Donati K, Bertagnolio S, Tumbarello M, Tacconelli E, Cataldo M, Longo B, Cauda R. Source: International Journal of Antimicrobial Agents. 2000 November; 16(3): 357-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11091063
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Effect of indomethacin on arterial oxygenation in critically ill patients with severe bacterial pneumonia. Author(s): Hanly PJ, Roberts D, Dobson K, Light RB. Source: Lancet. 1987 February 14; 1(8529): 351-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2880162
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Efficacy and safety of clarithromycin versus josamycin in the treatment of hospitalized patients with bacterial pneumonia. Author(s): Straneo G, Scarpazza G. Source: J Int Med Res. 1990 March-April; 18(2): 164-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2140330
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Efficacy and safety of high dose intravenous ciprofloxacin in the treatment of bacterial pneumonia. Italian Ciprofloxacin Study Group. Author(s): Periti P, Mazzei T, Curti ME. Source: International Journal of Antimicrobial Agents. 1998 August; 10(3): 215-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9832282
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Elastin fibers and the diagnosis of bacterial pneumonia in the adult respiratory distress syndrome. Author(s): Shepherd KE, Lynch KE, Wain JC, Brown EN, Wilson RS. Source: Critical Care Medicine. 1995 November; 23(11): 1829-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7587258
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Etiological diagnosis of bacterial pneumonia by gram stain and quantitative culture of expectorates. Leukocytes or alveolar macrophages as indicators of sample representativity. Author(s): Kalin M, Lindberg AA, Tunevall G. Source: Scandinavian Journal of Infectious Diseases. 1983; 15(2): 153-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6192493
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Evaluation of bronchoalveolar lavage for the diagnosis of bacterial pneumonia in ventilated patients. Author(s): Roger-Moreau I, de Barbeyrac B, Ducoudre M, Hilbert G, Gbikpi-Benissan G, Cardinaud JP, Bebear C. Source: Annales De Biologie Clinique. 1992; 50(8): 587-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1294014
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Expression and regulation of chemokines in bacterial pneumonia. Author(s): Standiford TJ, Kunkel SL, Greenberger MJ, Laichalk LL, Strieter RM. Source: Journal of Leukocyte Biology. 1996 January; 59(1): 24-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8558063
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Gas exchange and hemodynamics in patients with bacterial pneumonia ventilated with high PEEP levels. Author(s): Raimondi GA, Raimondi AC. Source: Medicina (B Aires). 1986; 46(2): 147-56. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3553837
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G-CSF application in patients with severe bacterial pneumonia increases IL-10 expression in neutrophils. Author(s): Spuck S, Schaaf B, Wiedorn KH, Hansen F, Vollmer E, Dalhoff K, Braun J. Source: Respiratory Medicine. 2003 January; 97(1): 51-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12556011
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Gram stain and culture of sputum to diagnose bacterial pneumonia. Author(s): Musher DM. Source: The Journal of Infectious Diseases. 1985 November; 152(5): 1096. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2413144
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Gram-negative bacterial pneumonia in the immunocompromised host. Author(s): Pennington JE. Source: Seminars in Respiratory Infections. 1986 September; 1(3): 145-50. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3317607
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Gram-negative bacterial pneumonia with secondary aspergillosis in an AIDS patient. Author(s): Bonatz K, Weiss A, Hehlmann R, Assmus HP, Heine M. Source: Klin Wochenschr. 1991 November 15; 69(18): 853-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1770754
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GRO alpha and interleukin-8 in Pneumocystis carinii or bacterial pneumonia and adult respiratory distress syndrome. Author(s): Villard J, Dayer-Pastore F, Hamacher J, Aubert JD, Schlegel-Haueter S, Nicod LP. Source: American Journal of Respiratory and Critical Care Medicine. 1995 November; 152(5 Pt 1): 1549-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7582292
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HIV infection and chronic chest disease as risk factors for bacterial pneumonia: a case-control study. Author(s): Charalambous S, Day JH, Fielding K, De Cock KM, Churchyard GJ, Corbett EL. Source: Aids (London, England). 2003 July 4; 17(10): 1531-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12824791
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HIV-associated bacterial pneumonia in the era of highly active antiretroviral therapy. Author(s): Tumbarello M, Tacconelli E, de Gaetano Donati K, Cauda R. Source: Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology : Official Publication of the International Retrovirology Association. 1999 February 1; 20(2): 208-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10048911
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Hospitalizations for bacterial pneumonia after renal transplantation in the United States. Author(s): Tveit DJ, Hypolite IO, Poropatich RK, Hshieh P, Cruess D, Hawkes CA, Agodoa LY, Abbott KC. Source: Journal of Nephrology. 2002 May-June; 15(3): 255-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12113596
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Identification of human beta-defensin-2 in respiratory tract and plasma and its increase in bacterial pneumonia. Author(s): Hiratsuka T, Nakazato M, Date Y, Ashitani J, Minematsu T, Chino N, Matsukura S. Source: Biochemical and Biophysical Research Communications. 1998 August 28; 249(3): 943-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9731241
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Impact of bacterial pneumonia and Pneumocystis carinii pneumonia on human immunodeficiency virus disease progression. Pulmonary Complications of HIV Study Group. Author(s): Osmond DH, Chin DP, Glassroth J, Kvale PA, Wallace JM, Rosen MJ, Reichman LB, Poole WK, Hopewell PC. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1999 September; 29(3): 536-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10530443
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Increased risk of bacterial pneumonia in HIV-infected intravenous drug users without AIDS. Author(s): Selwyn PA, Feingold AR, Hartel D, Schoenbaum EE, Alderman MH, Klein RS, Friedland GH. Source: Aids (London, England). 1988 August; 2(4): 267-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3140832
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Indomethacin and arterial oxygenation in critically ill patients with severe bacterial pneumonia. Author(s): Bihari DJ. Source: Lancet. 1987 March 28; 1(8535): 755. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2882177
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Infection due to Pneumocystis carinii simulating lobar bacterial pneumonia. Author(s): Byrd RB, Horn BR. Source: Chest. 1976 July; 70(1): 91-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1084255
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Interleukin-10 gene therapy-mediated amelioration of bacterial pneumonia. Author(s): Morrison DF, Foss DL, Murtaugh MP. Source: Infection and Immunity. 2000 August; 68(8): 4752-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10899882
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Interleukin-8 and granulocyte colony-stimulating factor in bronchoalveolar lavage fluid and plasma of human immunodeficiency virus-infected patients with Pneumocystis carinii pneumonia, bacterial pneumonia, or tuberculosis. Author(s): Grunewald T, Schuler-Maue W, Ruf B. Source: The Journal of Infectious Diseases. 1993 October; 168(4): 1077-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7690822
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Interleukin-8 and leukotriene B4 in bronchoalveolar lavage fluid from HIV-infected patients with bacterial pneumonia. Author(s): Krarup E, Vestbo J, Benfield TL, Lundgren JD. Source: Respiratory Medicine. 1997 May; 91(5): 317-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9176651
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Invasive techniques in the diagnosis of bacterial pneumonia in the intensive care unit. Author(s): Chauncey JB, Lynch JP 3rd, Hyzy RC, Toews GB. Source: Seminars in Respiratory Infections. 1990 September; 5(3): 215-25. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2255805
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Journal Club. HIV-associated bacterial pneumonia. Author(s): Sanders A. Source: Aids Read. 1999 November; 9(8): 580-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11082736
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Laboratory abnormalities in patients with bacterial pneumonia. Author(s): Sankaran RT, Mattana J, Pollack S, Bhat P, Ahuja T, Patel A, Singhal PC. Source: Chest. 1997 March; 111(3): 595-600. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9118693
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Legionnaires' disease and other newly recognized Legionella-like causes of bacterial pneumonia. Author(s): Myerowitz RL. Source: J Med. 1980; 11(4): 293-302. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6943261
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Letter: Fulminating bacterial pneumonia complicating influenza. Author(s): Price TM. Source: British Medical Journal. 1976 February 28; 1(6008): 520. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1252826
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Letter: N. B. T. test in pulmonary embolism and bacterial pneumonia. Author(s): Hellum KB, Solberg CO. Source: Lancet. 1974 December 28; 2(7896): 1575-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4141015
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Life-threatening bacterial pneumonia in male homosexuals with laboratory features of the acquired immunodeficiency syndrome. Author(s): White S, Tsou E, Waldhorn RE, Katz P. Source: Chest. 1985 April; 87(4): 486-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3979135
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Lobar pneumonia. Author(s): Hammerschmidt DE. Source: The Journal of Laboratory and Clinical Medicine. 2004 May; 143(5): 327. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15152620
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Low specificity of the bacterial index for the diagnosis of bacterial pneumonia by bronchoalveolar lavage. Author(s): Speich R, Hauser M, Hess T, Wust J, Grebski E, Kayser FH, Russi EW. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 1998 February; 17(2): 7884. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9629970
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Management of bacterial pneumonia in ventilated patients. Protected bronchoalveolar lavage as a diagnostic tool. Author(s): Meduri GU, Wunderink RG, Leeper KV, Beals DH. Source: Chest. 1992 February; 101(2): 500-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1735280
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Management of community-acquired bacterial pneumonia in hospitalized children. Author(s): Schutze GE, Jacobs RF. Source: The Pediatric Infectious Disease Journal. 1992 February; 11(2): 160-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1741196
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Mechanical ventilation with 100% oxygen does not increase intrapulmonary shunt in patients with severe bacterial pneumonia. Author(s): Lampron N, Lemaire F, Teisseire B, Harf A, Palot M, Matamis D, Lorino AM. Source: Am Rev Respir Dis. 1985 March; 131(3): 409-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3977178
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Microbiology of community-acquired bacterial pneumonia in persons with and at risk for human immunodeficiency virus type 1 infection. Implications for rational empiric antibiotic therapy. Author(s): Burack JH, Hahn JA, Saint-Maurice D, Jacobson MA. Source: Archives of Internal Medicine. 1994 November 28; 154(22): 2589-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7979856
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Mode of presentation and diagnosis of bacterial pneumonia in human immunodeficiency virus-infected patients. Author(s): Magnenat JL, Nicod LP, Auckenthaler R, Junod AF. Source: Am Rev Respir Dis. 1991 October; 144(4): 917-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1928971
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Moxalactam therapy for bacterial pneumonia. Author(s): Perlino CA. Source: Reviews of Infectious Diseases. 1982 November-December; 4 Suppl: S617-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6218574
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Neutrophil chemotactic factors in bacterial pneumonia. Author(s): Hopkins H, Stull T, Von Essen SG, Robbins RA, Rennard SI. Source: Chest. 1989 May; 95(5): 1021-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2539955
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Nosocomial bacterial pneumonia in human immunodeficiency virus infected subjects: incidence, risk factors and outcome. Author(s): Tumbarello M, Tacconelli E, de Gaetano Donati K, Bertagnolio S, Cataldo M, Pirronti T, Ardito F, Cauda R. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 2001 April; 17(4): 636-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11401057
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Nosocomial bacterial pneumonia in ventilated children: clinical significance of culture-positive peripheral bronchial aspirates. Author(s): Barzilay Z, Mandel M, Keren G, Davidson S. Source: The Journal of Pediatrics. 1988 March; 112(3): 421-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3346781
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Nosocomial bacterial pneumonia: an overview. Author(s): Pugliese G, Lichtenberg DA. Source: American Journal of Infection Control. 1987 December; 15(6): 249-65. Review. Erratum In: Am J Infect Control 1988 June; 16(3): 122. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3326432
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Oral ciprofloxacin in the treatment of 14 patients with bacterial pneumonia. Author(s): Wollschlager CM, Raoof S, Khan FA. Source: N Y State J Med. 1987 June; 87(6): 330-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3475610
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Oral ofloxacin for the treatment of acute bacterial pneumonia: use of a nontraditional protocol to compare experimental therapy with "usual care" in a multicenter clinical trial. Author(s): Sanders WE Jr, Morris JF, Alessi P, Makris AT, McCloskey RV, Trenholme GM, Iannini P, Bittner MJ. Source: The American Journal of Medicine. 1991 September; 91(3): 261-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1892146
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Outbreak of pneumonia in a long-term care facility: antecedent human parainfluenza virus 1 infection may predispose to bacterial pneumonia. Author(s): Fiore AE, Iverson C, Messmer T, Erdman D, Lett SM, Talkington DF, Anderson LJ, Fields B, Carlone GM, Breiman RF, Cetron MS. Source: Journal of the American Geriatrics Society. 1998 September; 46(9): 1112-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9736104
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Parapneumonic effusions secondary to community-acquired bacterial pneumonia in human immunodeficiency virus-infected patients. Author(s): Gil Suay V, Cordero PJ, Martinez E, Soler JJ, Perpina M, Greses JV, Sanchis J. Source: The European Respiratory Journal : Official Journal of the European Society for Clinical Respiratory Physiology. 1995 November; 8(11): 1934-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8620965
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Penicillins in the treatment of bacterial pneumonia. Author(s): Bunn P. Source: Clin Notes Respir Dis. 1966 Fall; 5(2): 3-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5914379
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Pharmacokinetic parameters of ciprofloxacin (500 mg/5 mL) oral suspension in critically ill patients with severe bacterial pneumonia: a comparison of two dosages. Author(s): Debon R, Breilh D, Boselli E, Saux MC, Duflo F, Chassard D, Allaouchiche B. Source: J Chemother. 2002 April; 14(2): 175-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12017373
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Prevention of nosocomial bacterial pneumonia. Author(s): Vincent JL. Source: Thorax. 1999 June; 54(6): 544-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10335011
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Primaxin in the treatment of acute bacterial pneumonia in adults. Author(s): Gebhart RJ, Duma RJ, Patterson PM, Bagett JW, Williams DS. Source: The Journal of Antimicrobial Chemotherapy. 1985 February; 15(2): 233-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3980311
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Prospective study of the aetiology of adult community acquired bacterial pneumonia needing hospitalisation in Singapore. Author(s): Hui KP, Chin NK, Chow K, Brownlee A, Yeo TC, Kumarasinghe G, Chan TB, Tan WC. Source: Singapore Med J. 1993 August; 34(4): 329-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8266206
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Protected specimen brush versus transtracheal aspiration. A comparative study in bacterial pneumonia. Author(s): Torres A, Estopa R, Marin A, Agusti-Vidal A. Source: Am Rev Respir Dis. 1982 August; 126(2): 368-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7103269
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Protein 1 (Clara cell protein) serum levels in healthy subjects and patients with bacterial pneumonia. Author(s): Nomori H, Horio H, Fuyuno G, Kobayashi R, Morinaga S, Hirabayashi Y. Source: American Journal of Respiratory and Critical Care Medicine. 1995 August; 152(2): 746-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7633737
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Proteinase inhibitory function in inflammatory lung disease. I. Acute bacterial pneumonia. Author(s): Abrams WR, Fein AM, Kucich U, Kueppers F, Yamada H, Kuzmowycz T, Morgan L, Lippmann M, Goldberg SK, Weinbaum G. Source: Am Rev Respir Dis. 1984 May; 129(5): 735-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6609652
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Pulmonary gangrene complicating bacterial pneumonia. Author(s): Kothari PR, Jiwane A, Kulkarni B. Source: Indian Pediatrics. 2003 August; 40(8): 784-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12951383
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Pulmonary gangrene. A complication of bacterial pneumonia. Author(s): Penner C, Maycher B, Long R. Source: Chest. 1994 February; 105(2): 567-73. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8306765
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Pyogenic bacterial pneumonia in human immunodeficiency virus-infected inpatients: a clinical, radiological, microbiological, and epidemiological study. Author(s): Baril L, Astagneau P, Nguyen J, Similowski T, Mengual X, Beigelman C, Caumes E, Katlama C, Bricaire F. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1998 April; 26(4): 964-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9564484
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Pyogenic bacterial pneumonia in the acquired immunodeficiency syndrome. Author(s): Daley CL. Source: Journal of Thoracic Imaging. 1991 September; 6(4): 36-42. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1942196
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Quantitative culture of bronchoalveolar lavage fluid for the diagnosis of bacterial pneumonia. Author(s): Cantral DE, Tape TG, Reed EC, Spurzem JR, Rennard SI, Thompson AB. Source: The American Journal of Medicine. 1993 December; 95(6): 601-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8259777
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Radiographic resolution of community-acquired bacterial pneumonia in the elderly. Author(s): El Solh AA, Aquilina AT, Gunen H, Ramadan F. Source: Journal of the American Geriatrics Society. 2004 February; 52(2): 224-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14728631
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Rapid diagnosis of community-acquired bacterial pneumonia. Author(s): Guzzetta P, Toews GB, Robertson KJ, Pierce AK. Source: Am Rev Respir Dis. 1983 September; 128(3): 461-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6412607
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Re: "Bacterial pneumonia in adult populations with human immunodeficiency virus (HIV) infection". Author(s): Clark R, Kissinger P. Source: American Journal of Epidemiology. 1995 January 15; 141(2): 176-7. Erratum In: Am J Epidemiol 1995 April 1; 141(7): 697. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7817975
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Recurrent bacterial pneumonia: a contemporary perspective. Author(s): Roth RM, Gleckman RA. Source: Southern Medical Journal. 1985 May; 78(5): 573-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3887578
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Relationships between periodontal disease and bacterial pneumonia. Author(s): Scannapieco FA, Mylotte JM. Source: J Periodontol. 1996 October; 67(10 Suppl): 1114-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8910830
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Responses to bacterial pneumonia. Author(s): Rozas CJ, Goldman AL. Source: Geriatrics. 1982 December; 37(12): 61-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7141228
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Rhabdomyolysis and bacterial pneumonia. Author(s): Byrd RP Jr, Roy TM. Source: Respiratory Medicine. 1998 February; 92(2): 359-62. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9616540
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Risk factors for acute renal insufficiency in patients with suspected or documented bacterial pneumonia. Author(s): Welage LS, Walawander CA, Timm EG, Grasela TH. Source: The Annals of Pharmacotherapy. 1994 April; 28(4): 515-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8038478
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Secondary Pneumocystis carinii pneumonia prophylaxis with trimethoprimsulphamethoxazole does not prevent bacterial pneumonia in HIV-infected persons. Author(s): Tumbarello M, Tacconelli E, Cauda R, Ortona L. Source: Aids (London, England). 1996 November; 10(13): 1603-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8931803
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Secondary pulmonary infections following antibiotic therapy for primary bacterial pneumonia. Author(s): Tillotson JR, Finland M. Source: Antimicrobial Agents Chemother. 1968; 8: 326-30. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5735377
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Serum adenosine deaminase in viral and bacterial pneumonia. Author(s): Klockars M, Kleemola M, Leinonen M, Koskela M. Source: Chest. 1991 March; 99(3): 623-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1899819
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Serum lactate dehydrogenase (LDH) in Pneumocystis carinii pneumonia, tuberculosis, and bacterial pneumonia. Author(s): Quist J, Hill AR. Source: Chest. 1995 August; 108(2): 415-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7634877
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Serum level monitoring of aminoglycoside antibiotics. Limitations in intensive care unit-related bacterial pneumonia. Author(s): Flint LM, Gott J, Short L, Richardson JD, Polk HC Jr. Source: Archives of Surgery (Chicago, Ill. : 1960). 1985 January; 120(1): 99-103. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3966875
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Serum procalcitonin concentrations in bacterial pneumonia in children: a negative result in primary healthcare settings. Author(s): Korppi M, Remes S, Heiskanen-Kosma T. Source: Pediatric Pulmonology. 2003 January; 35(1): 56-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12461740
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Severe Pneumocystis carinii pneumonia produces a hyperdynamic profile similar to bacterial pneumonia with sepsis. Author(s): Parker MM, Ognibene FP, Rogers P, Shelhamer JH, Masur H, Parrillo JE. Source: Critical Care Medicine. 1994 January; 22(1): 50-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8124974
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Significance of isolated increases in total lactate dehydrogenase and its isoenzymes in serum of patients with bacterial pneumonia. Author(s): Rotenberg Z, Weinberger I, Davidson E, Fuchs J, Sperling O, Agmon J. Source: Clinical Chemistry. 1988 July; 34(7): 1503-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3390929
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Spontaneous release of granulocyte colony-stimulating factor (G-CSF) by alveolar macrophages in the course of bacterial pneumonia and sarcoidosis: endotoxindependent and endotoxin-independent G-CSF release by cells recovered by bronchoalveolar lavage. Author(s): Tazi A, Nioche S, Chastre J, Smiejan JM, Hance AJ. Source: American Journal of Respiratory Cell and Molecular Biology. 1991 February; 4(2): 140-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1703767
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The comparative value of sputum and blood cultures in the diagnosis of acute bacterial pneumonia. Author(s): Shinwarie MN. Source: J Indiana State Med Assoc. 1977 March; 70(3): 139-41. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=864269
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The continuing problem of community-acquired bacterial pneumonia. Author(s): Feldman C. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1992 February 1; 81(3): 129-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1734547
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The etiology of bacterial pneumonia and meningitis in Vietnam. Author(s): Tran TT, Le QT, Tran TN, Nguyen NT, Pedersen FK, Schlumberger M. Source: The Pediatric Infectious Disease Journal. 1998 September; 17(9 Suppl): S192-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9781761
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The patient with acute bacterial pneumonia: a therapeutic approach. Author(s): Conley RL. Source: J Am Osteopath Assoc. 1971 November; 71(3): 67-73. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5211339
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The problem of diagnosing bacterial pneumonia in patients with chronic bronchitis. Bacteria in sputum and bronchial washings from patients with chronic bronchitis are antibody coated. Author(s): Yoo OH, Donath J, Desmond E, Lesser M. Source: The Mount Sinai Journal of Medicine, New York. 1988 October; 55(5): 395-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3265180
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The role of bronchoalveolar lavage in diagnosing nonopportunistic bacterial pneumonia. Author(s): Meduri GU, Baselski V. Source: Chest. 1991 July; 100(1): 179-90. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2060341
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The role of bronchoalveolar lavage in the diagnosis of bacterial pneumonia. Author(s): Sanchez Nieto JM, Carillo Alcaraz A. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 1995 October; 14(10): 83950. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8605896
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The role of cytokines in bacterial pneumonia: an inflammatory balancing act. Author(s): Moore TA, Standiford TJ. Source: Proceedings of the Association of American Physicians. 1998 July-August; 110(4): 297-305. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9686677
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The serodiagnosis of nonpneumococcal bacterial pneumonia. Author(s): Campbell JF, Spika JS. Source: Seminars in Respiratory Infections. 1988 June; 3(2): 123-30. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3041513
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The spontaneous reduction of nitroblue tetrazolium as a test of sensitivity to antibiotics in patients with bacterial pneumonia. Author(s): Kruszewski J, Markiewicz K, Jedrzejczak W. Source: Med Interne. 1979 July-September; 17(3): 279-83. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=504932
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The use of ceftriaxone for bacterial pneumonia in pediatric patients. Author(s): Congeni B. Source: Clinical Pediatrics. 1990 November; 29(11): 640-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2265515
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The use of quantitative cultures and antibody coating of bacteria to diagnose bacterial pneumonia by fiberoptic bronchoscopy. Author(s): Winterbauer RH, Hutchinson JF, Reinhardt GN, Sumida SE, Dearden B, Thomas CA, Schneider PW, Pardee NE, Morgan EH, Little JW. Source: Am Rev Respir Dis. 1983 July; 128(1): 98-103. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6346980
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Transtracheal aspiration in the severely ill elderly patient with bacterial pneumonia. Author(s): Berk SL, Holtsclaw SA, Kahn A, Smith JK. Source: Journal of the American Geriatrics Society. 1981 May; 29(5): 228-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7229234
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Treatment of bacterial pneumonia. Author(s): Marks MI. Source: Pediatr Infect Dis. 1985 March-April; 4(2): 213. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3982988
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Treatment of presumed bacterial pneumonia in ambulatory children. Author(s): Calderon E, Gatica R, Echaniz G, Conde C, Salinas L, Olvera G, Zorrilla E, Velazquez ME. Source: Clinical Therapeutics. 1991 November-December; 13(6): 699-706. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1790545
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Trovafloxacin versus high-dose amoxicillin (1 g three times daily) in the treatment of community-acquired bacterial pneumonia. Author(s): Tremolieres F, de Kock F, Pluck N, Daniel R. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 1998 June; 17(6): 447-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9758291
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Tuberculosis mimicking acute pyogenic bacterial pneumonia. Author(s): Padmanabhan K, Dhar SR, Bhatt B. Source: N Y State J Med. 1987 July; 87(7): 404-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3476870
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Type-specific vs. cross-protective vaccination for gram-negative bacterial pneumonia. Author(s): Pennington JE, Menkes E. Source: The Journal of Infectious Diseases. 1981 December; 144(6): 599-603. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6799587
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Use of bronchoalveolar lavage to diagnose bacterial pneumonia in mechanically ventilated patients. Author(s): Guerra LF, Baughman RP. Source: Critical Care Medicine. 1990 February; 18(2): 169-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2298009
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Usefulness of sputum culture for diagnosis of bacterial pneumonia in HIV-infected patients. Author(s): Cordero E, Pachon J, Rivero A, Giron-Gonzalez JA, Gomez-Mateos J, Merino MD, Torres-Tortosa M, Gonzalez-Serrano M, Aliaga L, Collado A, Hernandez-Quero J, Barrera A, Nuno E. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2002 May; 21(5): 362-7. Epub 2002 May 07. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12072920
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Ventilator-associated bacterial pneumonia: challenges in diagnosis, treatment, and prevention. Author(s): Craven DE, Steger KA. Source: New Horiz. 1998 May; 6(2 Suppl): S30-45. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9654310
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Virulent course of bacterial pneumonia in a male homosexual. Author(s): Promisloff RA, Lenchner GS. Source: Chest. 1985 December; 88(6): 935. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3877618
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CHAPTER 2. ALTERNATIVE MEDICINE AND BACTERIAL PNEUMONIA Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to bacterial pneumonia. 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 bacterial pneumonia 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 “bacterial pneumonia” (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 bacterial pneumonia: •
A novel type of metastatically spreading subcutaneous aspergillosis without epidermal lesions following allogeneic stem cell transplantation. Author(s): Cornely OA, Pels H, Bethe U, Seibold M, Toepelt K, Soehngen D, Ritzkowsky A. Source: Bone Marrow Transplantation. 2001 November; 28(9): 899-901. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11781653
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Aetiology, outcome, and risk factors for mortality among adults with acute pneumonia in Kenya. Author(s): Scott JA, Hall AJ, Muyodi C, Lowe B, Ross M, Chohan B, Mandaliya K, Getambu E, Gleeson F, Drobniewski F, Marsh K. Source: Lancet. 2000 April 8; 355(9211): 1225-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10770305
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Allogeneic stem-cell transplantation for lymphoproliferative disorders using BEAMCAMPATH (+/- fludarabine) conditioning combined with post-transplant donorlymphocyte infusion. Author(s): Lush RJ, Haynes AP, Byrne J, Cull GM, Carter GI, Pagliuca A, Parker JE, Mufti G, Mahendra P, Craddock CF, Lui Yin JA, Garg M, Prentice HG, Potter MN, Russell NH. Source: Cytotherapy. 2001; 3(3): 203-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12171727
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Ascorbate modulates antibacterial mechanisms in experimental pneumococcal pneumonia. Author(s): Esposito AL. Source: Am Rev Respir Dis. 1986 April; 133(4): 643-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3516039
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Assessment of vitamin A status with the relative-dose-response test in Peruvian children recovering from pneumonia. Author(s): Stephensen CB, Franchi LM, Hernandez H, Campos M, Colarossi A, Gilman RH, Alvarez JO. Source: The American Journal of Clinical Nutrition. 2002 December; 76(6): 1351-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12450903
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Cystic fibrosis. Author(s): Morony T. Source: Prog Phys Ther. 1970; 1(3): 220-31. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5523596
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Detection of Mycoplasma pneumoniae in spiked clinical samples by nucleic acid sequence-based amplification. Author(s): Loens K, Ursi D, Ieven M, van Aarle P, Sillekens P, Oudshoorn P, Goossens H. Source: Journal of Clinical Microbiology. 2002 April; 40(4): 1339-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11923354
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Differential selection of multidrug efflux mutants by trovafloxacin and ciprofloxacin in an experimental model of Pseudomonas aeruginosa acute pneumonia in rats. Author(s): Join-Lambert OF, Michea-Hamzehpour M, Kohler T, Chau F, Faurisson F, Dautrey S, Vissuzaine C, Carbon C, Pechere J. Source: Antimicrobial Agents and Chemotherapy. 2001 February; 45(2): 571-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11158756
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Diffuse pulmonary disease caused by nontuberculous mycobacteria immunocompetent people (hot tub lung). Author(s): Khoor A, Leslie KO, Tazelaar HD, Helmers RA, Colby TV.
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Source: American Journal of Clinical Pathology. 2001 May; 115(5): 755-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11345841 •
Dot-enzyme-linked immunosorbent assay (Dot-ELISA) for detection of pneumococcal polysaccharide antigens in pleural fluid effusion samples. Comparison with bacterial culture, counterimmunoelectrophoresis and latex agglutination. Author(s): Requejo HI, Alkmin M das G, Almeida RG, Casagrande ST, Cocozza AM, Lotufo JP, Waetge AR, Rodrigues JC. Source: Revista Do Instituto De Medicina Tropical De Sao Paulo. 1994 NovemberDecember; 36(6): 531-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7569628
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Drug smoking, Pneumocystis carinii pneumonia, and immunosuppression increase risk of bacterial pneumonia in human immunodeficiency virus-seropositive injection drug users. Author(s): Caiaffa WT, Vlahov D, Graham NM, Astemborski J, Solomon L, Nelson KE, Munoz A. Source: American Journal of Respiratory and Critical Care Medicine. 1994 December; 150(6 Pt 1): 1493-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7952605
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Drugs of abuse and infectious diseases. Author(s): Specter S. Source: J Fla Med Assoc. 1994 July; 81(7): 485-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7964576
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Effect of half the standard dose of Mao-bushi-saishin-to in two MRSA patients and one decubitus ulcer patient. Author(s): Kamei T, Nagura S, Toriumi Y, Kumano H, Kondoh T, Tomioka H. Source: The American Journal of Chinese Medicine. 2000; 28(2): 301-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10999449
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Effects of ginseng treatment on neutrophil chemiluminescence and immunoglobulin G subclasses in a rat model of chronic Pseudomonas aeruginosa pneumonia. Author(s): Song Z, Kharazmi A, Wu H, Faber V, Moser C, Krogh HK, Rygaard J, Hoiby N. Source: Clinical and Diagnostic Laboratory Immunology. 1998 November; 5(6): 882-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9801351
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Effects of qing fei tang (TJ-90) on aspiration pneumonia in mice. Author(s): Iwasaki K, Wang Q, Satoh N, Yoshida S, Akaike T, Sekizawa K, Maeda H, Sasaki H.
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Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 1999 May; 6(2): 95-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10374247 •
Effects of Radix Angelicae sinensis and shuanghuanglian on a rat model of chronic Pseudomonas aeruginosa pneumonia. Author(s): Song ZJ, Johansen HK, Moser C, Faber V, Kharazmi A, Rygaard J, Hoiby N. Source: Chinese Medical Sciences Journal = Chung-Kuo I Hsueh K'o Hsueh Tsa Chih / Chinese Academy of Medical Sciences. 2000 June; 15(2): 83-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12901629
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Enzyme linked immunosorbent assay for lactoferrin. Plasma and tissue measurements. Author(s): Bezwoda WR, Baynes RD, Khan Q, Mansoor N. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1985 September 16; 151(1): 61-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3930100
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Ethnographic studies of ARI in Bolivia and their use by the national ARI programme. Author(s): Hudelson P, Huanca T, Charaly D, Cirpa V. Source: Social Science & Medicine (1982). 1995 December; 41(12): 1677-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8746867
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From the Food and Drug Administration. Author(s): Henney JE. Source: Jama : the Journal of the American Medical Association. 1999 October 6; 282(13): 1218. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10517411
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Gerimax ginseng regulates both humoral and cellular immunity during chronic Pseudomonas aeruginosa lung infection. Author(s): Song Z, Wu H, Mathee K, Hoiby N, Kharazmi A. Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 August; 8(4): 459-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12230906
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Ginseng treatment enhances bacterial clearance and decreases lung pathology in athymic rats with chronic P. aeruginosa pneumonia. Author(s): Song ZJ, Johansen HK, Faber V, Hoiby N. Source: Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica. 1997 June; 105(6): 438-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9236860
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Ginseng treatment reduces bacterial load and lung pathology in chronic Pseudomonas aeruginosa pneumonia in rats. Author(s): Song Z, Johansen HK, Faber V, Moser C, Kharazmi A, Rygaard J, Hoiby N. Source: Antimicrobial Agents and Chemotherapy. 1997 May; 41(5): 961-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9145852
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Hemorrhagic pleural effusion as a complication of chronic lymphocytic leukemia. Author(s): Zeidman A, Yarmolovsky A, Djaldetti M, Mittelman M. Source: Haematologia. 1995; 26(3): 173-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7797147
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High-resolution computed tomography appearance of pulmonary Mycobacterium avium complex infection after exposure to hot tub: case of hot-tub lung. Author(s): Pham RV, Vydareny KH, Gal AA. Source: Journal of Thoracic Imaging. 2003 January; 18(1): 48-52. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12544748
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Immunodiagnoses of community-acquired pneumonia in childhood. Author(s): Requejo HI, Guerra ML, Dos Santos M, Cocozza AM. Source: Journal of Tropical Pediatrics. 1997 August; 43(4): 208-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9283122
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Increased gut permeability and bacterial translocation in Pseudomonas pneumoniainduced sepsis. Author(s): Yu P, Martin CM. Source: Critical Care Medicine. 2000 July; 28(7): 2573-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10921597
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Inhibitory effects of combined administration of antibiotics and anti-inflammatory drugs on lung tumor development initiated by N-nitrosobis(2-hydroxypropyl)amine in rats. Author(s): Tsutsumi M, Kitada H, Shiraiwa K, Takahama M, Tsujiuchi T, Sakitani H, Sasaki Y, Murakawa K, Yoshimoto M, Konishi Y. Source: Carcinogenesis. 2000 February; 21(2): 251-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10657965
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Integrating allopathic and alternative therapies in the treatment of a patient with multiple myeloma and vancomycin-resistant Staphylococcus aureus pneumonia. Author(s): Scheinbart EA. Source: Alternative Therapies in Health and Medicine. 2001 May-June; 7(3): 160, 158-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11347281
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Interleukin-1 alpha (IL-1 alpha) production by alveolar macrophages in patients with acute lung diseases: the influence of zinc supplementation. Author(s): Abul HT, Abul AT, al-Athary EA, Behbehani AE, Khadadah ME, Dashti HM. Source: Molecular and Cellular Biochemistry. 1995 May 24; 146(2): 139-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7565643
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Investigation on the antibacterial properties of garlic (Allium sativum) on pneumonia causing bacteria. Author(s): Dikasso D, Lemma H, Urga K, Debella A, Addis G, Tadele A, Yirsaw K. Source: Ethiop Med J. 2002 July; 40(3): 241-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12602248
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Latex agglutination test for diagnosing pneumococcal pneumonia in children in developing countries. Author(s): O'Neill KP, Lloyd-Evans N, Campbell H, Forgie IM, Sabally S, Greenwood BM. Source: Bmj (Clinical Research Ed.). 1989 April 22; 298(6680): 1061-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2497890
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Microvascular perfusion deficits are not a prerequisite for mucosal injury in septic rats. Author(s): Neviere RR, Pitt-Hyde ML, Piper RD, Sibbald WJ, Potter RF. Source: The American Journal of Physiology. 1999 April; 276(4 Pt 1): G933-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10198337
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Nutritional effects on host response to lung infections with mucoid Pseudomonas aeruginosa in mice. Author(s): van Heeckeren AM, Schluchter M, Xue L, Alvarez J, Freedman S, St George J, Davis PB. Source: Infection and Immunity. 2004 March; 72(3): 1479-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14977953
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Pulmonary bone marrow embolism following external cardiac massage. Author(s): Carstens PH. Source: Acta Pathol Microbiol Scand. 1969; 76(4): 510-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5351207
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to bacterial pneumonia; 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 Flu Source: Integrative Medicine Communications; www.drkoop.com Influenza Source: Integrative Medicine Communications; www.drkoop.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 3. MULTIMEDIA ON BACTERIAL PNEUMONIA Overview In this chapter, we show you how to keep current on multimedia sources of information on bacterial pneumonia. 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.
Audio Recordings The Combined Health Information Database contains abstracts on audio productions. To search CHID, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find audio 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 “Sound Recordings.” Type “bacterial pneumonia” (or synonyms) into the “For these words:” box. The following is a typical result when searching for sound recordings on bacterial pneumonia: •
What's New With AIDS? Contact: California Medical Association, Audio Digest Foundation, 1577 E Chevy Chase Dr, Glendale, CA, 91206, (213) 245-8505. Summary: This sound recording contains the transcripts of speeches given by three physicians that discuss HIV infection. The first speaker, Dr. Mitchell Katz, traces the scope of HIV infection in the United States and examines the consequences or the new definition of AIDS. He then poses epidemiologic considerations, factors affecting CD4 staging, and the drugs approved for treating HIV infection, AZT and ddI. Other drugs that inhibit reverse transcriptase are also included, as well as the efficacy of antiviral combination therapy. The second speaker, Dr. Neil Flynn, expands on the management of HIV and opportunistic infections. He discusses herpes, bacterial pneumonia, mycobacterium infection, cryptococcal meningitis, PCP, toxoplasmosis, and Kaposi's sarcoma. The concluding speaker, Dr. Faith Fitzgerald, shares some thoughts on the epidemic, including the public perceptions of AIDS and the differing response to this epidemic as opposed to previous ones.
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Infectious Diseases and HIV Drug Abusers Contact: Audio Visual, Incorporated, 5542 Tuxedo Rd, Cheverly, MD, 20781, (301) 3225600. Summary: This sound recording of a National Institute on Drug Abuse Conference presents a panel discussion held January 15, 1991 of a variety of infectious diseases which affect people with Human immunodeficiency virus (HIV) infection or Acquired immunodeficiency syndrome (AIDS). The first speaker describes the diseases, besides HIV, which he found in a cohort of 800 Intravenous drug users (IVDU's) in the Bronx. Tuberculosis (TB), bacterial pneumonia, and pneumocystis carinii pneumonia (PCP) were among the most common ones found. The second speaker examines vaccines which HIV-positive people may take without ill effects. These include hepatitis, pneumococcal, and various influenza vaccines. Oral polio vaccine should never be given. The third speaker discusses results of examining the death certificates of drug addicts.
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CHAPTER 4. PERIODICALS AND NEWS ON BACTERIAL PNEUMONIA Overview In this chapter, we suggest a number of news sources and present various periodicals that cover bacterial pneumonia.
News Services and Press Releases One of the simplest ways of tracking press releases on bacterial pneumonia is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “bacterial pneumonia” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to bacterial pneumonia. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “bacterial pneumonia” (or synonyms). The following was recently listed in this archive for bacterial pneumonia: •
Vapor biosensor identifies patients with bacterial pneumonia or sinusitis Source: Reuters Industry Breifing Date: April 28, 2004
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Minimal increase in risk of bacterial pneumonia after TMP/SMX withdrawal Source: Reuters Medical News Date: May 05, 2003
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Tests do not reliably differentiate viral and bacterial pneumonia in children Source: Reuters Medical News Date: May 14, 2002 The NIH
Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “bacterial pneumonia” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “bacterial pneumonia” (or synonyms). If you know the name of a company that is relevant to bacterial pneumonia, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/.
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BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “bacterial pneumonia” (or synonyms).
Academic Periodicals covering Bacterial Pneumonia Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to bacterial pneumonia. In addition to these sources, you can search for articles covering bacterial pneumonia that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 5. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for bacterial pneumonia. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a non-profit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with bacterial pneumonia. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.).
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The following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to bacterial pneumonia: Enfuvirtide •
Systemic - U.S. Brands: Fuzeon http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500467.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute7: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
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National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
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These publications are typically written by one or more of the various NIH Institutes.
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National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.8 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:9 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
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NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
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Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
8
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 9 See http://www.nlm.nih.gov/databases/databases.html.
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•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM Gateway10 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.11 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “bacterial pneumonia” (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 9731 9 980 247 56 11023
HSTAT12 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.13 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.14 Simply search by “bacterial pneumonia” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
10
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
11
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 12 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 13 14
The HSTAT URL is http://hstat.nlm.nih.gov/.
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.
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Coffee Break: Tutorials for Biologists15 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.16 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.17 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
15 Adapted 16
from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 17 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on bacterial pneumonia 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 bacterial pneumonia. 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 bacterial pneumonia. 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 “bacterial pneumonia”:
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Bacterial Infections http://www.nlm.nih.gov/medlineplus/bacterialinfections.html Childhood Immunization http://www.nlm.nih.gov/medlineplus/childhoodimmunization.html Influenza http://www.nlm.nih.gov/medlineplus/influenza.html Legionnaires' Disease http://www.nlm.nih.gov/medlineplus/legionnairesdisease.html Meningitis http://www.nlm.nih.gov/medlineplus/meningitis.html Plague http://www.nlm.nih.gov/medlineplus/plague.html Pneumonia http://www.nlm.nih.gov/medlineplus/pneumonia.html Syphilis http://www.nlm.nih.gov/medlineplus/syphilis.html You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on bacterial pneumonia. 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: •
Special Health Issues for Women: Put Yourself First : Life Is What You Make It Contact: Agouron Pharmaceuticals Inc, 10350 N Torrey Pines Rd, La Jolla, CA, 92307, (619) 622-3000, http://www.agouron.com. Summary: This brochure, written for women with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS), provides information about special health issues related to their treatment. HIV is a virus that replicates in the immune system, weakens it, and eventually develops in to AIDS. The brochure discusses how to tell partners and children of a positive HIV status, stress management techniques, and safer sex for woman with HIV/AIDS. HIV is likely to affect a woman's period and make her more vulnerable to contracting the human papillomavirus (HPV), which puts women at greater risk for cervical cancer. A Pap smear, a test that should be
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performed every six months on women with HIV, can detect HPV and cervical cancer. Women with HIV are more likely than men with HIV to develop wasting syndrome and are more likely than persons without HIV to develop an opportunistic infection (IO) such as bacterial pneumonia, pneumocystis carinii pneumonia (PCP), candidiasis, and mycobacterium avium complex (MAC). The brochure briefly discusses these OIs and their symptoms. The brochure provides information on the special considerations regarding HIV-positive women who are or who want to become pregnant and the effectiveness of the therapeutic drug zidovudine (AZT) on the prevention of perinatal transmission. The brochure discusses treatment regimen adherence and provides contact information for services from which individuals can learn more about HIV/AIDS. •
HIV Infection in Persons Using Injection Drugs Contact: National AIDS Treatment Information Project, Beth Israel Deaconess Medical Center, Beth Israel Hospital, 330 Brookline Ave Libby Bldg 317, Boston, MA, 02215, (617) 667-5520, http://www.natip.org. Summary: This fact sheet is for individuals with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS) who are also injection drug users (IDUs). IDUs often experience viral and bacterial health problems not directly related to HIV (e.g., infections from contaminated materials, from close personal contact with others, and sexually transmitted diseases (STDs) from unprotected sex). Examples of bacterial and viral infections include skin infections, bone infections, heart valve infections, hepatitis B virus (HBV), hepatitis C virus (HCV), bacterial pneumonia, tuberculosis (TB), syphilis, gonorrhea, chlamydia, and herpes simplex virus. Bacterial pneumonias, TB , chronic HBV and HCV, and Kaposi's sarcoma (KS) are more frequent among IDUs with HIV/AIDS. Medical care is important for IDUs with HIV/AIDS so that problems associated with injection drug use and HIV/AIDS can be monitored and treated. Some of the symptoms often associated with withdrawal from injection drug use includes fever, chills, weight loss, shortness of breath, cough, chest pain, abdominal pain, nausea, vomiting, diarrhea, confusion, stiff neck, and localized weakness or numbness. People experiencing these symptoms should see a doctor immediately. IDUs with HIV/AIDS can help to take care of their health by ceasing to use drugs, making regular visits to their primary care provider, adhering to HIV/AIDS regimens, and seeing a mental health provider. A table is provided that identifies some of the medical complication of IDUs.
•
Preventing Periodontal Disease Source: JADA. Journal of the American Dental Association. 132(9): 1339. September 2001. Contact: Available from American Dental Association. ADA Publishing Co, Inc., 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2867. Website: www.ada.org. Summary: This fact sheet on preventing periodontal disease is designed to be photocopied and distributed by dentists and dental care providers. The fact sheet notes that many adults develop some type of periodontal (the gums and other structures that hold the teeth) disease. There is some evidence that links periodontal diseases with other health concerns such as cardiovascular problems, stroke, bacterial pneumonia, and increased risk during pregnancy. The fact sheet reviews the known causes of gum disease, emphasizing the importance of daily removal of plaque (the sticky film of bacteria that constantly forms on teeth). If plaque is not removed with thorough daily
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brushing and cleaning between teeth, gums become irritated and inflamed (gingivitis). The irritated gum tissue can separate from the teeth and form spaces called pockets. Bacteria move into the pockets, where they continue to promote irritation. Left untreated, the process can continue until the bone and other tooth supporting tissues are destroyed. The early stage of periodontal disease is called gingivitis; this stage is usually reversible. The fact sheet emphasizes the importance of prevention through regular check ups and daily dental care. The fact sheet concludes with a list of the warning signs of gum disease, which include gums that bleed during brushing, red or swollen gums, gums that have pulled away from the teeth, persistent bad breath, pus between the teeth and gums, loose or separating teeth, a change in the way the teeth fit together when they are closed, a change in the fit of partial dentures. •
Respiratory Problems Contact: National AIDS Treatment Information Project, Beth Israel Deaconess Medical Center, Beth Israel Hospital, 330 Brookline Ave Libby Bldg 317, Boston, MA, 02215, (617) 667-5520, http://www.natip.org. Summary: This fact sheet, written for persons with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS), discusses various opportunistic respiratory infections and diseases. Respiratory problems are common in individuals with HIV/AIDS. Disorders of the lower tract include bronchitis, pneumonia, and lung tumors. Other disorders include bacterial pneumonia, tuberculosis, pneumocystis pneumonia, mycobacterium avium complex (MAC), cytomegalovirus (CMV), Kaposi's sarcoma, and lymphoma. The symptoms of bronchitis include chest cough that produces phlegm, chest discomfort, severe chest pain, and shortness of breath. The symptoms of pneumonia are a sudden onset of fever, pleuritic chest pain, shortness of breath, cough with pus-like phlegm, fatigue, a dry non-productive cough, and weight loss. Respiratory problems are often diagnosed through a physical examination, a chest x-ray, expectorated or induced sputum, oximetry or arterial blood gases, bronchoscopy with biopsy, and a lung biopsy. The fact sheet identifies the treatments available to HIVpositive individuals for bronchitis and bacterial pneumonia. 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 bacterial pneumonia. 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.
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Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMDHealth: http://my.webmd.com/health_topics
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to bacterial pneumonia. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with bacterial pneumonia. 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 bacterial pneumonia. 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 “bacterial pneumonia” (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
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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 “bacterial pneumonia”. 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 “bacterial pneumonia” (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 “bacterial pneumonia” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.18
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
18
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)19: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
•
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
•
Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
•
California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
•
California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
•
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
•
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
•
California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
•
California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
•
Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
•
Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
•
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
19
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
•
Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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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
•
Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
•
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
•
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
•
Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
•
Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
•
Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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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
•
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
•
Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
•
Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
•
Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
•
Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
•
Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
•
Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
•
Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
•
Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
•
Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
•
Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
•
Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
•
Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
•
Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
•
Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
•
Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
•
National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
•
National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
•
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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•
Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
•
New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
•
New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
•
New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
•
New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
•
New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
•
New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
•
New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
•
Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
•
Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
•
Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
•
Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
•
Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
•
Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
•
Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
•
Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
•
Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
•
Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
•
Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
•
Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
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Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).
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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BACTERIAL PNEUMONIA DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abscess: A localized, circumscribed collection of pus. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] 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] Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acute leukemia: A rapidly progressing cancer of the blood-forming tissue (bone marrow). [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] 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] Adenosine Deaminase: An enzyme that catalyzes the hydrolysis of adenosine to inosine with the elimination of ammonia. Since there are wide tissue and species variations in the
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enzyme, it has been used as a tool in the study of human and animal genetics and in medical diagnosis. EC 3.5.4.4. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] 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]
Aetiology: Study of the causes of disease. [EU] 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] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Agarose: A polysaccharide complex, free of nitrogen and prepared from agar-agar which is produced by certain seaweeds (red algae). It dissolves in warm water to form a viscid solution. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] 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] Allantois: An embryonic diverticulum of the hindgut of reptiles, birds, and mammals; in man its blood vessels give rise to those of the umbilical cord. [NIH]
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Allogeneic: Taken from different individuals of the same species. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] Almitrine: A respiratory stimulant that enhances respiration by acting as an agonist of peripheral chemoreceptors located on the carotid bodies. The drug increases arterial oxygen tension while decreasing arterial carbon dioxide tension in patients with chronic obstructive pulmonary disease. It may also prove useful in the treatment of nocturnal oxygen desaturation without impairing the quality of sleep. [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] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amnion: The extraembryonic membrane which contains the embryo and amniotic fluid. [NIH]
Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to ampicillin except that its resistance to gastric acid permits higher serum levels with oral administration. [NIH] Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broadspectrum antibiotic. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of
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pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable. [NIH] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] 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] 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] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anode: Electrode held at a positive potential with respect to a cathode. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Antecedent: Existing or occurring before in time or order often with consequential effects. [EU]
Antiangiogenic: Having to do with reducing the growth of new blood vessels. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antifibrinolytic: Inhibiting fibrinolysis. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with
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specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Aorta: The main trunk of the systemic arteries. [NIH] Aortic Aneurysm: Aneurysm of the aorta. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is
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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] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Aqueous: Having to do with water. [NIH] Archaea: One of the three domains of life (the others being bacteria and Eucarya), formerly called Archaebacteria under the taxon Bacteria, but now considered separate and distinct. They are characterized by: 1) the presence of characteristic tRNAs and ribosomal RNAs; 2) the absence of peptidoglycan cell walls; 3) the presence of ether-linked lipids built from branched-chain subunits; and 4) their occurrence in unusual habitats. While archaea resemble bacteria in morphology and genomic organization, they resemble eukarya in their method of genomic replication. The domain contains at least three kingdoms: crenarchaeota, euryarchaeota, and korarchaeota. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] 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] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Aspergillosis: Infections with fungi of the genus Aspergillus. [NIH] Aspiration: The act of inhaling. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Atherogenic: Causing the formation of plaque in the lining of the arteries. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Autacoids: A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autopsy: Postmortem examination of the body. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Bacillus: A genus of Bacillaceae that are spore-forming, rod-shaped cells. Most species are saprophytic soil forms with only a few species being pathogenic. [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
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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] Bacterial toxin: A toxic substance, made by bacteria, that can be modified to kill specific tumor cells without harming normal cells. [NIH] Bacterial Translocation: The passage of viable bacteria from the gastrointestinal tract to extra-intestinal sites, such as the mesenteric lymph node complex, liver, spleen, kidney, and blood. Factors that promote bacterial translocation include overgrowth with gram-negative enteric bacilli, impaired host immune defenses, and injury to the intestinal mucosa resulting in increased intestinal permeability. These mechanisms can act in concert to promote synergistically the systemic spread of indigenous translocating bacteria to cause lethal sepsis. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] 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] 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] Beta-Lactamases: Enzymes found in many bacteria which catalyze the hydrolysis of the amide bond in the beta-lactam ring. Well known antibiotics destroyed by these enzymes are penicillins and cephalosporins. EC 3.5.2.6. [NIH] Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bewilderment: Impairment or loss of will power. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biogenesis: The origin of life. It includes studies of the potential basis for life in organic
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compounds but excludes studies of the development of altered forms of life through mutation and natural selection, which is evolution. [NIH] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Bioterrorism: The use of biological agents in terrorism. This includes the malevolent use of bacteria, viruses, or toxins against people, animals, or plants. [NIH] Bladder: The organ that stores urine. [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] 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 Marrow Transplantation: The transference of bone marrow from one human or animal to another. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH]
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Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchioles: The tiny branches of air tubes in the lungs. [NIH] Bronchiolitis: Inflammation of the bronchioles. [NIH] Bronchiseptica: A small, gram-negative, motile bacillus. A normal inhabitant of the respiratory tract in man, dogs, and pigs, but is also associated with canine infectious tracheobronchitis and atrophic rhinitis in pigs. [NIH] Bronchitis: Inflammation (swelling and reddening) of the bronchi. [NIH] Bronchoalveolar Lavage: Washing out of the lungs with saline or mucolytic agents for diagnostic or therapeutic purposes. It is very useful in the diagnosis of diffuse pulmonary infiltrates in immunosuppressed patients. [NIH] Bronchoalveolar Lavage Fluid: Fluid obtained by washout of the alveolar compartment of the lung. It is used to assess biochemical and inflammatory changes in and effects of therapy on the interstitial lung tissue. [NIH] Bronchoscopy: Endoscopic examination, therapy or surgery of the bronchi. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Candidiasis: Infection with a fungus of the genus Candida. It is usually a superficial infection of the moist cutaneous areas of the body, and is generally caused by C. albicans; it most commonly involves the skin (dermatocandidiasis), oral mucous membranes (thrush, def. 1), respiratory tract (bronchocandidiasis), and vagina (vaginitis). Rarely there is a systemic infection or endocarditis. Called also moniliasis, candidosis, oidiomycosis, and formerly blastodendriosis. [EU] Candidosis: An infection caused by an opportunistic yeasts that tends to proliferate and become pathologic when the environment is favorable and the host resistance is weakened. [NIH]
Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [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] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both
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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 Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume (volume per beat). [NIH] 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] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [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] Cefamandole: Semisynthetic wide-spectrum cephalosporin with prolonged action, probably due to beta-lactamase resistance. It is used also as the nafate. [NIH] Cefotaxime: Semisynthetic broad-spectrum cephalosporin. [NIH] Ceftizoxime: A semisynthetic cephalosporin antibiotic which can be administered intravenously or by suppository. The drug is highly resistant to a broad spectrum of betalactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative organisms. It has few side effects and is reported to be safe and effective in aged patients and in patients with hematologic disorders. [NIH] Ceftriaxone: Broad-spectrum cephalosporin antibiotic with a very long half-life and high penetrability to usually inaccessible infections, including those involving the meninges, eyes, inner ears, and urinary tract. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell Polarity: Orientation of intracellular structures especially with respect to the apical and basolateral domains of the plasma membrane. Polarized cells must direct proteins from the
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Golgi apparatus to the appropriate domain since tight junctions prevent proteins from diffusing between the two domains. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Cephalexin: A semisynthetic cephalosporin antibiotic with antimicrobial activity similar to that of cephaloridine or cephalothin, but somewhat less potent. It is effective against both gram-positive and gram-negative organisms. [NIH] Cephaloridine: A cephalosporin antibiotic. [NIH] Cephalosporins: A group of broad-spectrum antibiotics first isolated from the Mediterranean fungus Acremonium (Cephalosporium acremonium). They contain the betalactam moiety thia-azabicyclo-octenecarboxylic acid also called 7-aminocephalosporanic acid. [NIH] Cephalothin: A cephalosporin antibiotic. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemoreceptors: Cells specialized to detect chemical substances and relay that information centrally in the nervous system. Chemoreceptors may monitor external stimuli, as in taste and olfaction, or internal stimuli, such as the concentrations of oxygen and carbon dioxide in the blood. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chest Pain: Pressure, burning, or numbness in the chest. [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]
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Chlamydia: A genus of the family Chlamydiaceae whose species cause a variety of diseases in vertebrates including humans, mice, and swine. Chlamydia species are gram-negative and produce glycogen. The type species is Chlamydia trachomatis. [NIH] Chlorhexidine: Disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque. [NIH] Cholera: An acute diarrheal disease endemic in India and Southeast Asia whose causative agent is vibrio cholerae. This condition can lead to severe dehydration in a matter of hours unless quickly treated. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chorion: The outermost extraembryonic membrane. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic Obstructive Pulmonary Disease: Collective term for chronic bronchitis and emphysema. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciprofloxacin: A carboxyfluoroquinoline antimicrobial agent that is effective against a wide range of microorganisms. It has been successfully and safely used in the treatment of resistant respiratory, skin, bone, joint, gastrointestinal, urinary, and genital infections. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clarithromycin: A semisynthetic macrolide antibiotic derived from erythromycin that is active against a variety of microorganisms. It can inhibit protein synthesis in bacteria by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation. [NIH] Claudication: Limping or lameness. [EU] Clavulanic Acid: Clavulanic acid (C8H9O5N) and its salts and esters. The acid is a suicide inhibitor of bacterial beta-lactamase enzymes from Streptomyces clavuligerus. Administered alone, it has only weak antibacterial activity against most organisms, but given in combination with beta-lactam antibiotics prevents antibiotic inactivation by microbial lactamase. [NIH]
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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] Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent. [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] Coccidioidomycosis: An infectious disease caused by a fungus, Coccidioides immitis, that is prevalent in the western United States and is acquired by inhalation of dust containing the spores. [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognitive restructuring: A method of identifying and replacing fear-promoting, irrational beliefs with more realistic and functional ones. [NIH] Colitis: Inflammation of the colon. [NIH] 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] Colony-Stimulating Factors: Glycoproteins found in a subfraction of normal mammalian plasma and urine. They stimulate the proliferation of bone marrow cells in agar cultures and the formation of colonies of granulocytes and/or macrophages. The factors include interleukin-3 (IL-3), granulocyte colony-stimulating factor (G-CSF), macrophage colonystimulating factor (M-CSF), and granulocyte-macrophage colony-stimulating factor (GMCSF). [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
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C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH]
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Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] 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] Constipation: Infrequent or difficult evacuation of feces. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] 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] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [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 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] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Counterimmunoelectrophoresis: Immunoelectrophoresis in which immunoprecipitation occurs when antigen at the cathode is caused to migrate in an electric field through a suitable medium of diffusion against a stream of antibody migrating from the anode as a result of endosmotic flow. [NIH] Critical Care: Health care provided to a critically ill patient during a medical emergency or crisis. [NIH] Critical Illness: A disease or state in which death is possible or imminent. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Crowns: A prosthetic restoration that reproduces the entire surface anatomy of the visible natural crown of a tooth. It may be partial (covering three or more surfaces of a tooth) or complete (covering all surfaces). It is made of gold or other metal, porcelain, or resin. [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]
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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]
Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [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] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [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] Death Certificates: Official records of individual deaths including the cause of death certified by a physician, and any other required identifying information. [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] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] 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] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH]
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Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
Dental Abutments: Natural teeth or teeth roots used as anchorage for a fixed or removable denture or other prosthesis (such as an implant) serving the same purpose. [NIH] Dental Care: The total of dental diagnostic, preventive, and restorative services provided to meet the needs of a patient (from Illustrated Dictionary of Dentistry, 1982). [NIH] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
Dental Plaque: A film that attaches to teeth, often causing dental caries and gingivitis. It is composed of mucins, secreted from salivary glands, and microorganisms. [NIH] Dentists: Individuals licensed to practice dentistry. [NIH] Dentures: An appliance used as an artificial or prosthetic replacement for missing teeth and adjacent tissues. It does not include crowns, dental abutments, nor artificial teeth. [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] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Developing Countries: Countries in the process of change directed toward economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diaphragm: The musculofibrous partition that separates the thoracic cavity from the abdominal cavity. Contraction of the diaphragm increases the volume of the thoracic cavity aiding inspiration. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Diphtheria: A localized infection of mucous membranes or skin caused by toxigenic strains of Corynebacterium diphtheriae. It is characterized by the presence of a pseudomembrane at the site of infection. Diphtheria toxin, produced by C. diphtheriae, can cause myocarditis, polyneuritis, and other systemic toxic effects. [NIH] Diphtheria Toxin: A 60 kD single chain protein elaborated by Corynebacterium diphtheriae that causes the sign and symptoms of diphtheria; it can be broken into two unequal fragments, the smaller (A fragment) inhibits protein synthesis and is the lethal moiety that needs the larger (B fragment) for entry into cells. [NIH]
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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 Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] 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] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dormancy: The period when an organism (i. e., a virus or a bacterium) is in the body but not producing any ill effects. [NIH] Dose-dependent: Refers to the effects of treatment with a drug. If the effects change when the dose of the drug is changed, the effects are said to be dose dependent. [NIH] 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] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration. [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]
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Duct: A tube through which body fluids pass. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyspnea: Difficult or labored breathing. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] 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] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] 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]
Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH] Embolism: Blocking of a blood vessel by a blood clot or foreign matter that has been transported from a distant site by the blood stream. [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] Embryo Transfer: Removal of a mammalian embryo from one environment and replacement in the same or a new environment. The embryo is usually in the pre-nidation phase, i.e., a blastocyst. The process includes embryo or blastocyst transplantation or transfer after in vitro fertilization and transfer of the inner cell mass of the blastocyst. It is not used for transfer of differentiated embryonic tissue, e.g., germ layer cells. [NIH] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Empiric: Empirical; depending upon experience or observation alone, without using scientific method or theory. [EU] Empirical: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium,
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characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endocardium: The innermost layer of the heart, comprised of endothelial cells. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed. [NIH] Eosinophils: Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU]
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Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythema Nodosum: An erythematous eruption commonly associated with drug reactions or infection and characterized by inflammatory nodules that are usually tender, multiple, and bilateral. These nodules are located predominantly on the shins with less common occurrence on the thighs and forearms. They undergo characteristic color changes ending in temporary bruise-like areas. This condition usually subsides in 3-6 weeks without scarring or atrophy. [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] Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Euthanasia: The act or practice of putting to death people or animals suffering from incurable conditions or diseases. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [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] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH]
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Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Fertilization in Vitro: Fertilization of an egg outside the body when the egg is normally fertilized in the body. [NIH] Fetal Membranes: Thin layers of tissue which surround the embryo or fetus and provide for its nutrition, respiration, excretion and protection; they are the yolk sac, allantois, amnion, and chorion. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinolysis: The natural enzymatic dissolution of fibrin. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibronectin: An adhesive glycoprotein. One form circulates in plasma, acting as an opsonin; another is a cell-surface protein which mediates cellular adhesive interactions. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Flatus: Gas passed through the rectum. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fludarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells. [NIH] Fold: A plication or doubling of various parts of the body. [NIH]
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Foramen: A natural hole of perforation, especially one in a bone. [NIH] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gamma Rays: Very powerful and penetrating, high-energy electromagnetic radiation of shorter wavelength than that of x-rays. They are emitted by a decaying nucleus, usually between 0.01 and 10 MeV. They are also called nuclear x-rays. [NIH] Gamma-interferon: Interferon produced by T-lymphocytes in response to various mitogens and antigens. Gamma interferon appears to have potent antineoplastic, immunoregulatory and antiviral activity. [NIH] Gangrene: Death and putrefaction of tissue usually due to a loss of blood supply. [NIH] Gangrenous: A circumscribed, deep-seated, suppurative inflammation of the subcutaneous tissue of the eyelid discharging pus from several points. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by
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such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] 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] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gingivitis: Inflammation of the gingivae. Gingivitis associated with bony changes is referred to as periodontitis. Called also oulitis and ulitis. [EU] Ginseng: An araliaceous genus of plants that contains a number of pharmacologically active agents used as stimulants, sedatives, and tonics, especially in traditional medicine. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [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] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Goblet Cells: Cells of the epithelial lining that produce and secrete mucins. [NIH] Gonorrhea: Acute infectious disease characterized by primary invasion of the urogenital tract. The etiologic agent, Neisseria gonorrhoeae, was isolated by Neisser in 1879. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Gp120: 120-kD HIV envelope glycoprotein which is involved in the binding of the virus to its membrane receptor, the CD4 molecule, found on the surface of certain cells in the body. [NIH]
Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to
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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] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Granulocyte: A type of white blood cell that fights bacterial infection. Neutrophils, eosinophils, and basophils are granulocytes. [NIH] Granulocyte Colony-Stimulating Factor: A glycoprotein of MW 25 kDa containing internal disulfide bonds. It induces the survival, proliferation, and differentiation of neutrophilic granulocyte precursor cells and functionally activates mature blood neutrophils. Among the family of colony-stimulating factors, G-CSF is the most potent inducer of terminal differentiation to granulocytes and macrophages of leukemic myeloid cell lines. [NIH] Granuloma: A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents. [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] Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [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] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Care Costs: The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from health expenditures, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost. [NIH] Health 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] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Hemodynamics: The movements of the blood and the forces involved in systemic or regional blood circulation. [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] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes simplex or to herpes zoster. [EU] Herpes Zoster: Acute vesicular inflammation. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Histology: The study of tissues and cells under a microscope. [NIH] HIV: Human immunodeficiency virus. Species of lentivirus, subgenus primate lentiviruses, formerly designated T-cell lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV). It is acknowledged to be the agent responsible for the acute infectious manifestations, neurologic disorders, and immunologic abnormalities linked to the acquired immunodeficiency syndrome. [NIH] HIV-1: The type species of Lentivirus and widely recognized as the etiologic agent of acquired immunodeficiency syndrome (AIDS). It is characterized by its cytopathic effect and affinity for the T4-lymphocyte. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU]
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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] Horseradish Peroxidase: An enzyme isolated from horseradish which is able to act as an antigen. It is frequently used as a histochemical tracer for light and electron microscopy. Its antigenicity has permitted its use as a combined antigen and marker in experimental immunology. [NIH] Human papillomavirus: HPV. A virus that causes abnormal tissue growth (warts) and is often associated with some types of cancer. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hyaline membrane disease: A respiratory disease of newborns, especially premature infants, in which a membrane composed of proteins and dead cells forms and lines the alveoli making gas exchange difficult or impossible. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hyperreflexia: Exaggeration of reflexes. [EU] Hypersecretion: Excessive secretion. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals; in man usually accidental or unintentional. [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]
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Idiopathic: Describes a disease of unknown cause. [NIH] Immaturity: The state or quality of being unripe or not fully developed. [EU] Immune adjuvant: A drug that stimulates the immune system to respond to disease. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] 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] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunocompromised Host: A human or animal whose immunologic mechanism is deficient because of an immunodeficiency disorder or other disease or as the result of the administration of immunosuppressive drugs or radiation. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodeficiency syndrome: The inability of the body to produce an immune response. [NIH]
Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction. [NIH]
Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] 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] Immunosuppression: Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several
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mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes. [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. [EU]
Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] 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] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and
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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] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inner ear: The labyrinth, comprising the vestibule, cochlea, and semicircular canals. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Inpatients: Persons admitted to health facilities which provide board and room, for the purpose of observation, care, diagnosis or treatment. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Instillation: . [EU] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [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] 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] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus. IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to
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platelet factor 4. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestinal Mucosa: The surface lining of the intestines where the cells absorb nutrients. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracellular Membranes: Membranes of subcellular structures. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Isoenzymes: One of various structurally related forms of an enzyme, each having the same mechanism but with differing chemical, physical, or immunological characteristics. [NIH] Josamycin: A macrolide antibiotic from Streptomyces narbonensis. The drug has antimicrobial activity against a wide spectrum of pathogens. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Laceration: 1. The act of tearing. 2. A torn, ragged, mangled wound. [EU] Lactate Dehydrogenase: A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of lactate and pyruvate. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist. [NIH] Laparotomy: A surgical incision made in the wall of the abdomen. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH]
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Lentivirus: A genus of the family Retroviridae consisting of non-oncogenic retroviruses that produce multi-organ diseases characterized by long incubation periods and persistent infection. Lentiviruses are unique in that they contain open reading frames (ORFs) between the pol and env genes and in the 3' env region. Five serogroups are recognized, reflecting the mammalian hosts with which they are associated. HIV-1 is the type species. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leukemia: Cancer of blood-forming tissue. [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood is reduced. [NIH] Ligaments: Shiny, flexible bands of fibrous tissue connecting together articular extremities of bones. They are pliant, tough, and inextensile. [NIH] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Linkages: 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] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Liquor: 1. A liquid, especially an aqueous solution containing a medicinal substance. 2. A general term used in anatomical nomenclature for certain fluids of the body. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Long-Term Care: Care over an extended period, usually for a chronic condition or disability, requiring periodic, intermittent, or continuous care. [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] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphadenitis: Inflammation of the lymph nodes. [NIH]
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Lymphadenopathy: Disease or swelling of the lymph nodes. [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] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation. [NIH] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale 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] 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] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lymphoproliferative Disorders: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lysosome: A sac-like compartment inside a cell that has enzymes that can break down cellular components that need to be destroyed. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] 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] 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]
Man-made: Ionizing radiation emitted by artificial or concentrated natural, radioactive material or resulting from the operation of high voltage apparatus, such as X-ray apparatus or particle accelerators, of nuclear reactors, or from nuclear explosions. [NIH] Mastitis: Inflammatory disease of the breast, or mammary gland. [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
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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] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Melanin: The substance that gives the skin its color. [NIH] 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] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] 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] Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenteric: Pertaining to the mesentery : a membranous fold attaching various organs to the body wall. [EU] Metaplasia: A condition in which there is a change of one adult cell type to another similar adult cell type. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiological: Pertaining to microbiology : the science that deals with microorganisms, including algae, bacteria, fungi, protozoa and viruses. [EU] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [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] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH]
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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] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucociliary: Pertaining to or affecting the mucus membrane and hairs (including eyelashes, nose hair, .): mucociliary clearing: the clearance of mucus by ciliary movement ( particularly in the respiratory system). [EU] 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, water, inorganic salts, and exfoliated cells. [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] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's
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immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multivalent: Pertaining to a group of 5 or more homologous or partly homologous chromosomes during the zygotene stage of prophase to first metaphasis in meiosis. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myalgia: Pain in a muscle or muscles. [EU] Mycobacteriosis: Any disease caused by Mycobacterium other than M. tuberculosis, M. bovis, and M. avium. [NIH] Mycobacterium: A genus of gram-positive, aerobic bacteria. Most species are free-living in soil and water, but the major habitat for some is the diseased tissue of warm-blooded hosts. [NIH]
Mycobacterium avium: A bacterium causing tuberculosis in domestic fowl and other birds. In pigs, it may cause localized and sometimes disseminated disease. The organism occurs occasionally in sheep and cattle. It should be distinguished from the M. avium complex, which infects primarily humans. [NIH] Mycobacterium avium Complex: A complex that includes several strains of M. avium. M. intracellulare is not easily distinguished from M. avium and therefore is included in the complex. These organisms are most frequently found in pulmonary secretions from persons with a tuberculous-like mycobacteriosis. Strains of this complex have also been associated with childhood lymphadenitis and AIDS. M. avium alone causes tuberculosis in a variety of birds and other animals, including pigs. [NIH] Mycoplasma: A genus of gram-negative, facultatively anaerobic bacteria bounded by a plasma membrane only. Its organisms are parasites and pathogens, found on the mucous membranes of humans, animals, and birds. [NIH] Myelin: The fatty substance that covers and protects nerves. [NIH] Myocarditis: Inflammation of the myocardium; inflammation of the muscular walls of the heart. [EU] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Natural selection: A part of the evolutionary process resulting in the survival and reproduction of the best adapted individuals. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] 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] Nebramycin: A complex of antibiotic substances produced by Streptomyces tenebrarius. [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]
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Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasm: A new growth of benign or malignant tissue. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neuroleptic: A term coined to refer to the effects on cognition and behaviour of antipsychotic drugs, which produce a state of apathy, lack of initiative, and limited range of emotion and in psychotic patients cause a reduction in confusion and agitation and normalization of psychomotor activity. [EU] Neurologic: Having to do with nerves or the nervous system. [NIH] 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] 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] Neutralization: An act or process of neutralizing. [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]
Nitroblue Tetrazolium: Colorless to yellow dye that is reducible to blue or black formazan crystals by certain cells; formerly used to distinguish between nonbacterial and bacterial diseases, the latter causing neutrophils to reduce the dye; used to confirm diagnosis of chronic granulomatous disease. [NIH] Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nosocomial: Pertaining to or originating in the hospital, said of an infection not present or
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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] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Ofloxacin: An orally administered broad-spectrum quinolone antibacterial drug active against most gram-negative and gram-positive bacteria. [NIH] Oncology: The study of cancer. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] Oral Hygiene: The practice of personal hygiene of the mouth. It includes the maintenance of oral cleanliness, tissue tone, and general preservation of oral health. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [NIH] Oropharynx: Oral part of the pharynx. [NIH] Osteomyelitis: Inflammation of bone caused by a pyogenic organism. It may remain localized or may spread through the bone to involve the marrow, cortex, cancellous tissue, and periosteum. [EU] 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] Overexpress: An excess of a particular protein on the surface of a cell. [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
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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] 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] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Paediatric: Of or relating to the care and medical treatment of children; belonging to or concerned with paediatrics. [EU] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Papillomavirus: A genus of Papovaviridae causing proliferation of the epithelium, which may lead to malignancy. A wide range of animals are infected including humans, chimpanzees, cattle, rabbits, dogs, and horses. [NIH] Paranasal Sinuses: Air-filled extensions of the respiratory part of the nasal cavity into the frontal, ethmoid, sphenoid, and maxillary cranial bones. They vary in size and form in different individuals and are lined by the ciliated mucous membranes of the nasal cavity. [NIH]
Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] 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] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. [NIH]
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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]
Penicillin: An antibiotic drug used to treat infection. [NIH] Penicillin Resistance: Nonsusceptibility of an organism to the action of penicillins. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Chain Elongation: The process whereby an amino acid is joined through a substituted amide linkage to a chain of peptides. [NIH] 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] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] 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] Periodontitis: Inflammation of the periodontal membrane; also called periodontitis simplex. [NIH]
Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness, constipation, vomiting, and moderate fever. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by
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phagocytic cells. [NIH] Pharmacodynamic: Is concerned with the response of living tissues to chemical stimuli, that is, the action of drugs on the living organism in the absence of disease. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] 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] 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] Plague: An acute infectious disease caused by Yersinia pestis that affects humans, wild rodents, and their ectoparasites. This condition persists due to its firm entrenchment in sylvatic rodent-flea ecosystems throughout the world. Bubonic plague is the most common form. [NIH] Plague Vaccine: A suspension of killed Yersinia pestis used for immunizing people in enzootic plague areas. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasmids: Any extrachromosomal hereditary determinant. Plasmids are self-replicating
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circular molecules of DNA that are found in a variety of bacterial, archaeal, fungal, algal, and plant species. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelet Factor 4: A high-molecular-weight proteoglycan-platelet factor complex which is released from blood platelets by thrombin. It acts as a mediator in the heparin-neutralizing capacity of the blood and plays a role in platelet aggregation. At high ionic strength (I=0.75), the complex dissociates into the active component (molecular weight 29,000) and the proteoglycan carrier (chondroitin 4-sulfate, molecular weight 350,000). The molecule exists in the form of a dimer consisting of 8 moles of platelet factor 4 and 2 moles of proteoglycan. [NIH]
Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] 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] Pleural cavity: A space enclosed by the pleura (thin tissue covering the lungs and lining the interior wall of the chest cavity). It is bound by thin membranes. [NIH] Pleural Effusion: Presence of fluid in the pleural cavity resulting from excessive transudation or exudation from the pleural surfaces. It is a sign of disease and not a diagnosis in itself. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Pneumonia, Bacterial: Pneumonia caused by various species of bacteria. Bacterial pneumonia commonly results from bronchogenic spread of infection following microaspiration of secretions. The largest category of this disease arises from communityacquired pneumonias. [NIH] Pneumonia, Pneumocystis carinii: A pulmonary disease occurring in immunodeficient or malnourished patients or infants, characterized by dyspnea, tachypnea, and hypoxemia. Pneumocystis carinii pneumonia is a frequently seen opportunistic infection in AIDS. It is caused by the fungus Pneumocystis carinii. [NIH] Pneumonitis: A disease caused by inhaling a wide variety of substances such as dusts and molds. Also called "farmer's disease". [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their
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complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polyneuritis: Inflammation of several peripheral nerves at the same time. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [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] 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] Pregnancy Outcome: Results of conception and ensuing pregnancy, including live birth, stillbirth, spontaneous abortion, induced abortion. The outcome may follow natural or artificial insemination or any of the various reproduction techniques, such as embryo transfer or fertilization in vitro. [NIH] 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] 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] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promotor: In an operon, a nucleotide sequence located at the operator end which contains all the signals for the correct initiation of genetic transcription by the RNA polymerase holoenzyme and determines the maximal rate of RNA synthesis. [NIH]
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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] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Proteome: The protein complement of an organism coded for by its genome. [NIH] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU]
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Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Embolism: Embolism in the pulmonary artery or one of its branches. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Putrefaction: The process of decomposition of animal and vegetable matter by living organisms. [NIH] Pyogenic: Producing pus; pyopoietic (= liquid inflammation product made up of cells and a thin fluid called liquor puris). [EU] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH]
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Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] 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] 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] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regional lymph node: In oncology, a lymph node that drains lymph from the region around a tumor. [NIH] Reinfection: A second infection by the same pathogenic agent, or a second infection of an organ such as the kidney by a different pathogenic agent. [EU] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary,
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4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respirator: A mechanical device that helps a patient breathe; a mechanical ventilator. [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [NIH] Respiratory Physiology: Functions and activities of the respiratory tract as a whole or of any of its parts. [NIH] Response Elements: Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promotor and enhancer regions. [NIH]
Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rhinitis: Inflammation of the mucous membrane of the nose. [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 developing a disease. [NIH] Risk patient: Patient who is at risk, because of his/her behaviour or because of the type of person he/she is. [EU] Ristocetin: An antibiotic mixture of two components, A and B, obtained from Nocardia lurida (or the same substance produced by any other means). It is no longer used clinically because of its toxicity. It causes platelet agglutination and blood coagulation and is used to assay those functions in vitro. [NIH] Rod: A reception for vision, located in the retina. [NIH] Saline: A solution of salt and water. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to
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characterize schizophrenia. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] 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] Sediment: A precipitate, especially one that is formed spontaneously. [EU] Sedimentation: The act of causing the deposit of sediment, especially by the use of a centrifugal machine. [EU] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Septicaemia: A term originally used to denote a putrefactive process in the body, but now usually referring to infection with pyogenic micro-organisms; a genus of Diptera; the severe type of infection in which the blood stream is invaded by large numbers of the causal. [NIH] Septicemia: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Called also blood poisoning. [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] Serotypes: A cause of haemorrhagic septicaemia (in cattle, sheep and pigs), fowl cholera of birds, pasteurellosis of rabbits, and gangrenous mastitis of ewes. It is also commonly found in atrophic rhinitis of pigs. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sexually Transmitted Diseases: Diseases due to or propagated by sexual contact. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Shock, Cardiogenic: Shock resulting from diminution of cardiac output in heart disease. [NIH]
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Shunt: A surgically created diversion of fluid (e.g., blood or cerebrospinal fluid) from one area of the body to another area of the body. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Sinusitis: An inflammatory process of the mucous membranes of the paranasal sinuses that occurs in three stages: acute, subacute, and chronic. Sinusitis results from any condition causing ostial obstruction or from pathophysiologic changes in the mucociliary transport mechanism. [NIH] 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] 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]
Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] 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
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distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] 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] Spirochete: Lyme disease. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH] Spores: The reproductive elements of lower organisms, such as protozoa, fungi, and cryptogamic plants. [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]
Steady state: Dynamic equilibrium. [EU] Stenosis: Narrowing or stricture of a duct or canal. [EU] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Stillbirth: The birth of a dead fetus or baby. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococci: A genus of spherical Gram-positive bacteria occurring in chains or pairs. They are widely distributed in nature, being important pathogens but often found as normal commensals in the mouth, skin, and intestine of humans and other animals. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs
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or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] 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] Stricture: The abnormal narrowing of a body opening. Also called stenosis. [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] 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] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Suppository: A medicated mass adapted for introduction into the rectal, vaginal, or urethral orifice of the body, suppository bases are solid at room temperature but melt or dissolve at body temperature. Commonly used bases are cocoa butter, glycerinated gelatin, hydrogenated vegetable oils, polyethylene glycols of various molecular weights, and fatty acid esters of polyethylene glycol. [EU] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppressive: Tending to suppress : effecting suppression; specifically : serving to suppress activity, function, symptoms. [EU] Suppurative: Consisting of, containing, associated with, or identified by the formation of pus. [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]
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
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homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]
Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tachypnea: Rapid breathing. [NIH] Teichoic Acids: Bacterial polysaccharides that are rich in phosphodiester linkages. They are the major components of the cell walls and membranes of many bacteria. [NIH] Terminator: A DNA sequence sited at the end of a transcriptional unit that signals the end of transcription. [NIH] Tetani: Causal agent of tetanus. [NIH] Tetanic: Having the characteristics of, or relating to tetanus. [NIH] Tetanus: A disease caused by tetanospasmin, a powerful protein toxin produced by Clostridium tetani. Tetanus usually occurs after an acute injury, such as a puncture wound or laceration. Generalized tetanus, the most common form, is characterized by tetanic muscular contractions and hyperreflexia. Localized tetanus presents itself as a mild condition with manifestations restricted to muscles near the wound. It may progress to the generalized form. [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] Thoracic: Having to do with the chest. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [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] Thrush: A disease due to infection with species of fungi of the genus Candida. [NIH] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH]
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Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tobramycin: An aminoglycoside, broad-spectrum antibiotic produced by Streptomyces tenebrarius. It is effective against gram-negative bacteria, especially the Pseudomonas species. It is a 10% component of the antibiotic complex, nebramycin, produced by the same species. [NIH] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tooth Loss: The failure to retain teeth as a result of disease or injury. [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] 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] Toxoid: The material resulting from the treatment of toxin in such a way that the toxic properties are inactivated whilst the antigenic potency remains intact. [NIH] Toxoplasmosis: The acquired form of infection by Toxoplasma gondii in animals and man. [NIH]
Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a
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protein. It occurs on the ribosome and is unidirectional. [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] Translocating: 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] Transposons: Discrete genetic elements capable of inserting, in a non-permuted fashion, into the chromosomes of many bacteria. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]
Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [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] 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] Ulceration: 1. The formation or development of an ulcer. 2. An ulcer. [EU] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [NIH]
Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH]
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Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Utilization Review: An organized procedure carried out through committees to review admissions, duration of stay, professional services furnished, and to evaluate the medical necessity of those services and promote their most efficient use. [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] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginal: Of or having to do with the vagina, the birth canal. [NIH] Vaginitis: Inflammation of the vagina characterized by pain and a purulent discharge. [NIH] Vancomycin: Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasodilators: Any nerve or agent which induces dilatation of the blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venous: Of or pertaining to the veins. [EU] 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] Ventricles: Fluid-filled cavities in the heart or brain. [NIH] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] 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] Viral Load: The quantity of measurable virus in the blood. Change in viral load, measured in plasma, is used as a surrogate marker in HIV disease progression. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virulent: A virus or bacteriophage capable only of lytic growth, as opposed to temperate phages establishing the lysogenic response. [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
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kill, tumor cells. [NIH] Virus Replication: The process of intracellular viral multiplication, consisting of the synthesis of proteins, nucleic acids, and sometimes lipids, and their assembly into a new infectious particle. [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] Warts: Benign epidermal proliferations or tumors; some are viral in origin. [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]
Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Yolk Sac: An embryonic membrane formed from endoderm and mesoderm. In reptiles and birds it incorporates the yolk into the digestive tract for nourishing the embryo. In placental mammals its nutritional function is vestigial; however, it is the source of most of the intestinal mucosa and the site of formation of the germ cells. It is sometimes called the vitelline sac, which should not be confused with the vitelline membrane of the egg. [NIH] Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIVinduced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia. [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]
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INDEX A Abdominal, 34, 35, 107, 119, 135, 157, 158 Abdominal Pain, 107, 119, 158 Aberrant, 26, 119 Abscess, 50, 119 Acceptor, 119, 157 Acetylcholine, 119, 130, 155 Acquired Immunodeficiency Syndrome, 53, 70, 74, 119, 144 Actin, 22, 119 Acute leukemia, 51, 119 Acute renal, 75, 119, 144 Adaptability, 119, 128 Adaptation, 6, 119 Adenine, 119 Adenosine, 75, 119 Adenosine Deaminase, 75, 119 Adjustment, 119, 120 Adjuvant, 19, 120 Adolescence, 28, 120 Adverse Effect, 4, 120, 131, 167 Aerobic, 120, 128, 154 Aerosol, 18, 120 Aetiology, 48, 49, 73, 81, 120 Affinity, 19, 120, 131, 144 Agar, 120, 131, 146, 159 Agarose, 120, 146 Agonist, 120, 121, 136, 155 Airway, 14, 17, 30, 33, 120 Algorithms, 120, 126 Alimentary, 120, 157 Alkaloid, 120, 155 Allantois, 120, 140 Allogeneic, 81, 82, 121, 143 Allylamine, 121 Almitrine, 47, 121 Alpha Particles, 121, 163 Alternative medicine, 92, 121 Alveoli, 121, 145, 173 Amine, 85, 121 Amino Acid Sequence, 35, 121, 122, 141 Amino Acids, 121, 139, 141, 158, 161, 162, 171 Ammonia, 119, 121 Amnion, 121, 140 Amoxicillin, 57, 79, 121 Ampicillin, 60, 121 Amplification, 4, 18, 82, 121
Anaerobic, 20, 49, 121, 128, 154 Anaesthesia, 121, 147 Analysis of Variance, 33, 122 Anaphylatoxins, 122, 132 Anatomical, 122, 129, 147, 150, 166 Anemia, 122, 153, 174 Anesthesia, 22, 120, 122 Animal model, 9, 13, 17, 19, 37, 39, 122 Annealing, 122, 160 Anode, 122, 133 Antagonism, 122, 131 Antecedent, 72, 122 Antiangiogenic, 26, 122 Antibacterial, 4, 8, 20, 21, 22, 31, 34, 35, 82, 86, 122, 130, 156, 168, 173 Antibodies, 20, 24, 43, 122, 123, 143, 145, 146, 153, 159 Anticoagulant, 122, 162 Antifibrinolytic, 27, 122 Antigen, 8, 13, 15, 18, 24, 37, 38, 39, 120, 122, 123, 124, 132, 133, 135, 138, 144, 145, 146, 147, 152 Antigen-Antibody Complex, 123, 132 Antigen-presenting cell, 123, 135 Anti-infective, 123, 130 Anti-inflammatory, 23, 34, 85, 123, 147 Antimicrobial, 24, 26, 31, 36, 38, 42, 49, 57, 60, 64, 65, 72, 75, 82, 85, 123, 129, 130, 149 Antineoplastic, 123, 141 Antioxidant, 123, 157 Antipsychotic, 123, 131, 155 Antiserum, 123, 124 Antiviral, 89, 123, 141, 148 Aorta, 123 Aortic Aneurysm, 14, 123 Apolipoproteins, 123, 150 Apoptosis, 43, 62, 123 Applicability, 16, 124 Aqueous, 42, 124, 125, 134, 150 Archaea, 124, 152 Arginine, 122, 124, 155 Arterial, 65, 68, 108, 121, 124, 130, 145, 162 Arteries, 123, 124, 126, 133, 150 Arterioles, 124, 126, 127 Artery, 14, 124, 137, 157, 163 Aseptic, 124, 156, 168 Aspergillosis, 67, 81, 124
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Aspiration, 62, 73, 78, 83, 124 Assay, 10, 28, 34, 84, 124, 146, 165 Atherogenic, 13, 124 Atrophy, 124, 139 Attenuated, 5, 12, 124 Atypical, 50, 124, 131 Autacoids, 124, 147 Autoimmune disease, 124, 153 Autopsy, 7, 14, 124 Avidity, 24, 124 B Bacillus, 124, 127 Bacteremia, 10, 40, 124 Bacterial Infections, 20, 21, 42, 106, 125 Bacterial Physiology, 119, 125 Bacterial toxin, 7, 125 Bacterial Translocation, 85, 125 Bactericidal, 24, 125, 139 Bacteriostatic, 125, 139 Bacterium, 45, 125, 136, 144, 154 Base, 119, 125, 141, 149 Basophils, 125, 143 Beta-Lactamases, 33, 125, 128 Beta-Thromboglobulin, 125, 148 Bewilderment, 125, 133 Bilateral, 125, 139 Bile, 125, 141, 145, 150 Binding Sites, 5, 125 Biochemical, 10, 27, 67, 125, 127, 140, 149, 166 Biogenesis, 44, 125 Biological response modifier, 126, 148 Biopsy, 108, 126 Biosynthesis, 126, 162 Biotechnology, 46, 92, 101, 126 Bioterrorism, 16, 126 Bladder, 126, 132, 153, 172 Blood pressure, 126, 128, 145, 153 Body Composition, 45, 126 Bone Marrow, 53, 81, 86, 119, 126, 131, 141, 146, 151, 153, 174 Bone Marrow Transplantation, 53, 81, 126 Bowel, 126, 147, 149, 158, 168 Bowel Movement, 126, 168 Brachytherapy, 126, 149, 163 Bradykinin, 126, 155 Breeding, 16, 126 Broad-spectrum, 121, 127, 128, 129, 156, 171 Bronchi, 127, 139 Bronchial, 43, 71, 77, 127 Bronchioles, 121, 127
Bronchiolitis, 12, 127 Bronchiseptica, 51, 127 Bronchitis, 14, 77, 108, 127, 130 Bronchoalveolar Lavage, 40, 48, 56, 62, 63, 64, 66, 68, 69, 70, 74, 76, 77, 79, 127 Bronchoalveolar Lavage Fluid, 40, 62, 68, 69, 74, 127 Bronchoscopy, 63, 78, 108, 127 C Calcium, 127, 131, 167 Candidiasis, 30, 107, 127 Candidosis, 127 Capillary, 11, 39, 126, 127, 173 Capsules, 33, 127 Carbohydrate, 14, 127, 142, 161 Carbon Dioxide, 121, 127, 129, 141, 164 Carcinogenic, 127, 148, 161 Carcinogens, 127, 157 Carcinoma, 26, 127, 128 Cardiac, 13, 86, 121, 128, 138, 139, 166 Cardiac Output, 128, 166 Cardiovascular, 4, 13, 16, 40, 107, 128, 166 Cardiovascular disease, 4, 13, 16, 128 Catheter, 46, 48, 63, 64, 128 Cathode, 122, 128, 133, 137 Causal, 7, 128, 166, 170 Cause of Death, 19, 32, 45, 128, 134 Cefamandole, 54, 128 Cefotaxime, 57, 60, 128 Ceftizoxime, 60, 128 Ceftriaxone, 78, 128 Cell Adhesion, 34, 128 Cell Death, 37, 123, 128, 154 Cell Differentiation, 128, 167 Cell Division, 125, 128, 129, 153, 159, 166 Cell membrane, 12, 128, 135, 152, 159 Cell Polarity, 22, 128 Cell proliferation, 37, 129, 167 Cell Size, 129, 140 Cell Transplantation, 81, 82, 129 Central Nervous System, 7, 119, 129, 131, 143, 153, 166 Cephalexin, 58, 129 Cephaloridine, 129 Cephalosporins, 125, 129 Cephalothin, 129 Cerebrospinal, 7, 28, 129, 167 Cerebrospinal fluid, 7, 28, 129, 167 Cerebrovascular, 128, 129 Cervical, 106, 129 Cervix, 129 Chemokines, 5, 18, 19, 23, 38, 39, 66, 129
177
Chemoreceptors, 121, 129 Chemotactic Factors, 71, 129, 132 Chest Pain, 107, 108, 129 Chin, 68, 73, 129, 152 Chlamydia, 13, 14, 28, 107, 130 Chlorhexidine, 32, 130 Cholera, 130, 166 Cholesterol, 14, 125, 130, 133, 150, 152 Cholesterol Esters, 130, 150 Cholinergic, 123, 130, 155 Chorion, 130, 140 Chromatin, 124, 130, 138, 151 Chromosomal, 121, 130 Chromosome, 130, 150, 166, 172 Chronic Disease, 7, 13, 45, 130 Chronic Obstructive Pulmonary Disease, 50, 121, 130 Chylomicrons, 130, 150 Ciliary, 41, 130, 153 Ciprofloxacin, 65, 71, 72, 82, 130 CIS, 31, 130 Clarithromycin, 65, 130 Claudication, 14, 130 Clavulanic Acid, 49, 130 Clinical trial, 4, 8, 28, 32, 40, 72, 101, 131, 133, 136, 162, 164 Cloning, 10, 126, 131 Clozapine, 51, 131 Coagulation, 34, 40, 127, 131, 165, 170 Coccidioidomycosis, 49, 131 Coenzyme, 131, 149 Cofactor, 131, 162, 170 Cognitive restructuring, 131, 169 Colitis, 131, 147 Colon, 131, 147 Colony-Stimulating Factors, 131, 143 Combination Therapy, 89, 131 Complement, 10, 122, 131, 132, 141 Complementary and alternative medicine, 81, 87, 132 Complementary medicine, 81, 132 Compliance, 6, 132 Computational Biology, 101, 132 Computed tomography, 85, 132 Computerized axial tomography, 132 Computerized tomography, 132 Conception, 132, 140, 161, 168 Confounding, 32, 132 Confusion, 107, 133, 136, 155 Congestion, 123, 133, 139 Conjunctiva, 133, 147 Connective Tissue, 126, 133, 140, 150, 165
Constipation, 123, 133, 158 Contamination, 28, 133 Contraindications, ii, 133 Control group, 133, 161 Coordination, 133, 153 Coronary, 13, 14, 43, 128, 133 Coronary heart disease, 13, 14, 43, 128, 133 Cortex, 133, 139, 156 Counterimmunoelectrophoresis, 61, 83, 133 Critical Care, 29, 48, 51, 56, 59, 62, 65, 67, 73, 76, 79, 83, 85, 133 Critical Illness, 29, 133 Crossing-over, 133, 164 Crowns, 133, 135 Curative, 133, 170 Cutaneous, 127, 133 Cyclic, 133, 143, 155 Cysteine, 15, 129, 134 Cystine, 134 Cytokine, 4, 6, 9, 19, 20, 22, 23, 24, 37, 38, 41, 61, 134, 148 Cytomegalovirus, 108, 134 Cytoplasm, 124, 125, 128, 134, 138, 151 Cytoskeleton, 22, 134 Cytotoxic, 9, 12, 21, 134, 147, 164, 167 Cytotoxicity, 12, 121, 134 D Data Collection, 36, 134 Death Certificates, 90, 134 Decubitus, 83, 134 Decubitus Ulcer, 83, 134 Defense Mechanisms, 41, 134 Degenerative, 134, 144 Deletion, 123, 134 Delivery of Health Care, 134, 143 Dementia, 119, 123, 134 Denaturation, 134, 160 Dendrites, 134, 135, 155 Dendritic, 37, 135 Dendritic cell, 37, 135 Dental Abutments, 135 Dental Care, 107, 135 Dental Caries, 135 Dental Plaque, 31, 32, 135 Dentists, 107, 135 Dentures, 108, 135 Depolarization, 135, 167 Desensitization, 135, 146 Developing Countries, 86, 135 Diagnostic procedure, 92, 135
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Diaphragm, 135, 160 Diarrhea, 45, 107, 135 Diffusion, 133, 135, 146, 147 Digestion, 120, 125, 126, 135, 149, 150, 168 Diphtheria, 26, 135 Diphtheria Toxin, 26, 135 Direct, iii, 13, 26, 95, 128, 136, 164 Discrete, 15, 136, 172 Disease Progression, 68, 136, 173 Disinfectant, 130, 136, 139 Disorientation, 133, 136 Dissociation, 120, 136 Distal, 27, 42, 136, 162 Dopamine, 123, 131, 136, 155, 159 Dormancy, 26, 136 Dose-dependent, 136, 174 Double-blind, 40, 57, 64, 136 Drug Interactions, 96, 136 Drug Resistance, 38, 136 Drug Tolerance, 136 Duct, 137, 151, 165, 168 Dura mater, 137, 152, 157 Dyspnea, 137, 160 E Effector, 9, 20, 22, 34, 35, 37, 45, 119, 131, 137 Effector cell, 20, 35, 137 Efficacy, 7, 19, 28, 30, 40, 44, 60, 63, 65, 89, 137, 172 Effusion, 83, 137 Elastic, 137, 169 Electrocoagulation, 131, 137 Electrons, 123, 125, 128, 137, 149, 156, 157, 163, 164 Electrophoresis, 137, 146 Emaciation, 119, 137 Embolism, 86, 137, 163 Embolus, 137, 147 Embryo, 121, 128, 137, 140, 147, 161, 168, 174 Embryo Transfer, 137, 161 Emphysema, 45, 130, 137 Empiric, 70, 137 Empirical, 38, 57, 137 Encapsulated, 10, 137 Endocarditis, 3, 49, 127, 137 Endocardium, 137, 138 Endogenous, 4, 5, 20, 22, 35, 136, 138, 157, 171 Endothelial cell, 5, 11, 26, 34, 39, 138, 148, 170 Endothelium, 39, 138, 155
Endothelium, Lymphatic, 138 Endothelium, Vascular, 138 Endothelium-derived, 138, 155 Endotoxin, 5, 16, 25, 76, 138, 172 Enhancer, 138, 165 Environmental Exposure, 45, 138 Environmental Health, 24, 100, 102, 138 Enzymatic, 127, 132, 135, 138, 140, 152, 161 Enzyme-Linked Immunosorbent Assay, 83, 138 Eosinophils, 138, 143 Epidemic, 51, 89, 138 Epidemiological, 9, 23, 74, 138 Epidermal, 81, 138, 149, 174 Epidermis, 138, 139, 149 Epinephrine, 136, 139, 155, 172 Epithelial, 10, 12, 14, 17, 22, 27, 31, 34, 40, 41, 43, 139, 142, 144 Epithelial Cells, 10, 12, 14, 17, 22, 41, 43, 139, 144 Epithelium, 20, 25, 31, 34, 42, 43, 138, 139, 157 Erythema, 14, 139 Erythema Nodosum, 14, 139 Erythrocytes, 122, 126, 139, 164 Erythromycin, 47, 130, 139 Ethanol, 4, 5, 40, 139 Eukaryotic Cells, 7, 139 Euthanasia, 41, 139 Evoke, 139, 168 Excitation, 139, 140, 155 Exogenous, 5, 11, 138, 139 External-beam radiation, 139, 163 Extracellular, 31, 44, 133, 139, 140 F Family Planning, 101, 139 Fat, 126, 133, 134, 137, 140, 150, 154, 167, 169 Fatigue, 108, 140 Fatty acids, 58, 140, 142, 162 Feces, 133, 140, 168 Fertilization in Vitro, 140, 161 Fetal Membranes, 60, 140 Fetus, 140, 168, 173 Fibrin, 140, 158, 170 Fibrinolysis, 122, 140 Fibroblasts, 140, 148 Fibronectin, 10, 59, 140 Fibrosis, 8, 12, 41, 82, 121, 140, 165, 166 Flatus, 140, 141 Flow Cytometry, 23, 24, 140 Fludarabine, 82, 140
179
Fluorescence, 34, 140 Fluorescent Dyes, 140 Foam Cells, 13, 140 Fold, 14, 21, 140, 152, 157 Foramen, 129, 141, 158 Fungus, 127, 129, 131, 141, 160 G Gallbladder, 119, 141 Gamma Rays, 141, 163, 164 Gamma-interferon, 5, 141 Gangrene, 73, 141 Gangrenous, 141, 166 Gas, 7, 42, 66, 121, 127, 135, 140, 141, 145, 155, 165, 173 Gas exchange, 7, 42, 66, 141, 145, 165, 173 Gastric, 121, 141 Gastric Acid, 121, 141 Gastrointestinal, 125, 126, 130, 139, 141, 166, 169 Gastrointestinal tract, 125, 139, 141, 166 Gene, 7, 10, 11, 12, 15, 17, 19, 20, 23, 29, 31, 33, 44, 51, 68, 126, 141, 165, 166 Gene Expression, 10, 11, 17, 29, 33, 141 Gene Therapy, 20, 68, 141 Genetic Code, 141, 156 Genetic Engineering, 126, 131, 141 Genetic testing, 142, 161 Genetics, 25, 29, 40, 120, 142 Genital, 130, 142, 173 Genomics, 21, 142 Genotype, 142, 159 Geriatric, 20, 142 Gestation, 142, 158, 168 Gingivitis, 4, 43, 108, 135, 142 Ginseng, 83, 84, 85, 142 Gland, 142, 150, 151, 157, 166, 168, 170 Glomerular, 142 Glomeruli, 142 Glomerulonephritis, 35, 142 Glycerol, 142, 159 Glycerophospholipids, 142, 159 Glycogen, 130, 142 Glycoprotein, 42, 140, 142, 143, 153, 170, 172 Goblet Cells, 31, 142 Gonorrhea, 107, 142 Governing Board, 142, 161 Gp120, 5, 142 Graft, 142, 143, 147 Graft Rejection, 143, 147
Gram-negative, 8, 16, 19, 41, 44, 64, 66, 67, 79, 125, 127, 128, 129, 130, 143, 154, 156, 171 Gram-positive, 19, 20, 128, 129, 143, 154, 156, 168 Granulocyte, 4, 68, 76, 131, 143 Granulocyte Colony-Stimulating Factor, 4, 68, 76, 131, 143 Granuloma, 38, 143 Guanylate Cyclase, 143, 155 H Habitat, 44, 143, 154 Half-Life, 128, 143 Haptens, 120, 143 Headache, 143, 147 Health Care Costs, 33, 143 Health Expenditures, 143 Heart attack, 128, 143 Hemodynamics, 7, 66, 143 Hemoglobin, 122, 139, 143, 144, 157 Hemoglobinopathies, 141, 144 Hemolytic, 20, 144 Hemorrhage, 137, 143, 144, 169 Hepatic, 5, 144 Hepatitis, 90, 107, 144 Hepatocytes, 144 Hereditary, 144, 159 Heredity, 141, 142, 144 Herpes, 89, 107, 144 Herpes Zoster, 144 Heterogeneity, 120, 144 Histology, 18, 144 HIV-1, 5, 51, 58, 144, 150 Homeostasis, 5, 6, 144 Homogeneous, 29, 144 Homologous, 16, 34, 44, 133, 141, 144, 154, 166, 170, 172 Hormone, 139, 145, 167, 170 Horseradish Peroxidase, 138, 145 Human papillomavirus, 106, 145 Humoral, 37, 84, 143, 145 Humour, 145 Hyaline membrane disease, 64, 145 Hybrid, 145 Hybridization, 33, 145 Hybridomas, 145, 148 Hydrogen, 119, 121, 125, 127, 134, 145, 153, 155, 156, 157, 162 Hydrolysis, 119, 125, 145, 159, 161, 162 Hydrophobic, 28, 142, 145, 150 Hyperreflexia, 145, 170 Hypersecretion, 31, 145
180
Bacterial Pneumonia
Hypersensitivity, 16, 135, 145 Hypertension, 128, 143, 145 Hypothermia, 41, 145 Hypoxemia, 47, 145, 160 Hypoxia, 145 I Idiopathic, 146, 165 Immaturity, 28, 146 Immune adjuvant, 23, 146 Immune Sera, 146 Immune system, 5, 19, 106, 123, 137, 146, 147, 151, 154, 158, 173, 174 Immunity, 12, 15, 17, 18, 19, 32, 37, 45, 68, 84, 86, 119, 146, 171 Immunization, 10, 106, 146, 147 Immunoassay, 138, 146 Immunocompromised, 22, 23, 53, 66, 146 Immunocompromised Host, 23, 66, 146 Immunodeficiency, 30, 37, 48, 52, 53, 59, 64, 68, 70, 71, 72, 74, 83, 90, 106, 107, 108, 119, 144, 146 Immunodeficiency syndrome, 90, 146 Immunodiffusion, 120, 146 Immunoelectrophoresis, 60, 62, 120, 133, 146 Immunogenic, 28, 146 Immunologic, 23, 25, 129, 144, 146, 164, 174 Immunology, 9, 12, 13, 20, 44, 83, 120, 140, 145, 146 Immunosuppression, 35, 83, 146, 147, 151, 156 Immunosuppressive, 5, 146, 147 Immunosuppressive Agents, 146 Immunosuppressive therapy, 147 Immunotherapy, 61, 135, 147 Impairment, 37, 125, 147 Implant radiation, 147, 149, 163 In vitro, 6, 10, 12, 15, 17, 21, 22, 25, 28, 37, 38, 39, 41, 137, 141, 147, 160, 165 In vivo, 4, 6, 10, 13, 15, 17, 19, 22, 25, 28, 33, 39, 41, 44, 141, 147, 151, 156 Incision, 147, 149 Indomethacin, 65, 68, 147 Induction, 7, 18, 35, 41, 123, 147 Infarction, 55, 125, 147 Infertility, 16, 147 Infiltration, 142, 147 Inflammatory bowel disease, 16, 147 Influenza, 12, 20, 22, 51, 55, 69, 87, 90, 106, 147 Infusion, 82, 148
Ingestion, 40, 148, 160 Inhalation, 18, 120, 131, 148, 160 Initiation, 17, 18, 21, 148, 161, 171 Inner ear, 128, 148, 173 Inorganic, 148, 153 Inpatients, 74, 148 Insight, 31, 44, 148 Instillation, 7, 27, 148 Insulator, 148, 154 Intensive Care, 31, 47, 69, 76, 148 Intensive Care Units, 32, 148 Interferon, 11, 28, 141, 148 Interferon-alpha, 148 Interleukin-1, 16, 23, 68, 86, 148 Interleukin-2, 148 Interleukin-6, 16, 148 Interleukin-8, 67, 68, 69, 148 Intermittent, 149, 150 Internal radiation, 149, 163 Interstitial, 126, 127, 149, 152 Intestinal, 15, 125, 149, 174 Intestinal Mucosa, 125, 149, 174 Intestine, 126, 145, 149, 164, 168 Intoxication, 5, 149, 174 Intracellular, 5, 7, 19, 25, 26, 37, 41, 44, 128, 147, 149, 152, 155, 167, 174 Intracellular Membranes, 149, 152 Intramuscular, 12, 149, 157 Intravenous, 23, 65, 68, 90, 148, 149, 157 Intrinsic, 19, 120, 149 Invasive, 69, 146, 149, 157 Ionizing, 121, 138, 149, 151, 164 Ischemia, 124, 134, 149 Isoenzymes, 76, 149 J Josamycin, 65, 149 K Kb, 100, 149 Keratinocytes, 148, 149 Kinetic, 4, 34, 149 L Labile, 131, 149 Laceration, 149, 170 Lactate Dehydrogenase, 76, 149 Laparotomy, 22, 149 Lectin, 27, 40, 50, 149 Lentivirus, 144, 150 Lesion, 13, 143, 150, 172 Lethal, 7, 26, 41, 125, 135, 150 Leucocyte, 60, 150 Leukemia, 85, 141, 150 Leukopenia, 150, 174
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Ligaments, 133, 150 Ligands, 35, 150 Ligation, 35, 150 Linkages, 144, 150, 170, 174 Lipid, 123, 140, 142, 150, 154 Lipopolysaccharide, 42, 143, 150 Lipoprotein, 14, 143, 150 Liquor, 150, 163 Liver, 5, 119, 125, 134, 140, 141, 142, 144, 150, 165 Localized, 107, 119, 135, 137, 147, 150, 154, 156, 159, 170, 172 Long-Term Care, 72, 150 Low-density lipoprotein, 150 Lymph, 50, 125, 129, 138, 144, 145, 150, 151, 164, 165 Lymph node, 125, 129, 150, 151, 164, 165 Lymphadenitis, 150, 154 Lymphadenopathy, 50, 144, 151 Lymphatic, 138, 147, 150, 151, 168, 170 Lymphatic system, 150, 151, 168, 170 Lymphocyte Count, 119, 151 Lymphocyte Depletion, 146, 151 Lymphocytes, 5, 21, 23, 24, 34, 119, 123, 135, 141, 145, 146, 148, 150, 151, 168, 170, 174 Lymphocytic, 85, 151 Lymphoid, 37, 122, 150, 151 Lymphoma, 108, 151 Lymphoproliferative, 82, 151 Lymphoproliferative Disorders, 82, 151 Lysosome, 14, 151 Lytic, 151, 173 M Macrophage, 4, 10, 13, 16, 20, 21, 24, 25, 26, 35, 42, 44, 131, 148, 151 Malignant, 119, 123, 151, 153, 155, 164, 165 Malignant tumor, 151, 153 Malnutrition, 45, 124, 151 Man-made, 45, 151 Mastitis, 151, 166 Mechanical ventilation, 32, 70, 151 Mediate, 24, 25, 33, 42, 136, 151 Mediator, 10, 35, 148, 151, 160, 166 MEDLINE, 101, 152 Melanin, 152, 159, 172 Membrane Fusion, 31, 152 Membrane Lipids, 152, 159 Meninges, 128, 129, 137, 152 Meningitis, 20, 77, 89, 106, 152 Mental, iv, 4, 100, 102, 107, 129, 133, 134, 136, 140, 152, 163, 165
Mental Health, iv, 4, 100, 102, 107, 152, 163 Mentors, 37, 152 Mercury, 140, 152 Mesenteric, 125, 152 Metaplasia, 31, 152 Microbe, 152, 171 Microbiological, 32, 74, 152 Microbiology, 9, 12, 20, 33, 39, 44, 49, 50, 57, 58, 63, 70, 77, 79, 82, 119, 124, 152 Microorganism, 131, 152, 158, 174 Microscopy, 7, 145, 152 Migration, 39, 152 Mitochondrial Swelling, 153, 154 Mitosis, 124, 153 Modification, 13, 22, 141, 153, 163, 174 Molecule, 10, 17, 34, 123, 125, 131, 132, 136, 137, 138, 139, 142, 144, 145, 149, 153, 156, 157, 160, 164, 167, 171, 173 Monitor, 36, 129, 153, 156 Monoclonal, 7, 43, 145, 153, 163 Monoclonal antibodies, 43, 153 Monocyte, 13, 35, 153 Mononuclear, 13, 143, 153, 172 Morphology, 13, 124, 153 Motility, 147, 153, 166 Motion Sickness, 153, 154 Mucins, 135, 142, 153, 165 Mucociliary, 153, 167 Mucolytic, 127, 153 Mucosa, 20, 32, 153 Mucus, 30, 153 Multiple Myeloma, 85, 153 Multiple sclerosis, 7, 28, 153 Multivalent, 124, 154 Mutagenesis, 15, 21, 33, 154 Mutagens, 154 Myalgia, 148, 154 Mycobacteriosis, 154 Mycobacterium, 85, 89, 107, 108, 154, 172 Mycobacterium avium, 85, 107, 108, 154 Mycobacterium avium Complex, 107, 108, 154 Mycoplasma, 25, 82, 154 Myelin, 154 Myocarditis, 135, 154 N Nasal Mucosa, 147, 154 Natural selection, 126, 154 Nausea, 107, 123, 154 NCI, 1, 30, 99, 130, 154 Nebramycin, 154, 171
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Bacterial Pneumonia
Necrosis, 7, 12, 123, 147, 154, 165 Neonatal, 20, 28, 36, 155 Neoplasm, 155, 165 Nervous System, 129, 151, 155, 169, 170 Neural, 145, 155 Neuroleptic, 123, 131, 155 Neurologic, 7, 33, 144, 155 Neurons, 134, 155, 169 Neurotransmitter, 119, 126, 136, 155, 167, 169, 170 Neutralization, 22, 155 Neutrons, 121, 155, 163 Neutrophil, 5, 8, 9, 11, 20, 23, 39, 71, 83, 155 Nicotine, 30, 155 Nitric Oxide, 25, 42, 155 Nitroblue Tetrazolium, 78, 155 Nitrogen, 25, 120, 121, 155 Nosocomial, 8, 12, 19, 22, 32, 35, 50, 63, 71, 72, 155 Nuclear, 5, 11, 35, 137, 139, 141, 151, 154, 156 Nuclei, 121, 137, 141, 142, 153, 155, 156, 162 Nucleic acid, 13, 82, 141, 145, 154, 155, 156, 174 Nucleic Acid Hybridization, 145, 156 Nucleus, 124, 125, 130, 133, 134, 138, 139, 141, 151, 153, 155, 156, 162, 168 O Odds Ratio, 156, 164 Ofloxacin, 72, 156 Oncology, 156, 164 Opportunistic Infections, 4, 33, 89, 119, 156 Oral Health, 3, 156 Oral Hygiene, 4, 156 Organ Culture, 17, 156 Organ Transplantation, 53, 156 Oropharynx, 31, 156 Osteomyelitis, 52, 156 Outpatient, 30, 39, 156 Overexpress, 42, 156 Oxidants, 25, 156 Oxidation, 13, 119, 123, 134, 156, 157 Oxidation-Reduction, 156, 157 Oximetry, 108, 157 Oxygenation, 65, 68, 145, 157 P Pachymeningitis, 152, 157 Paediatric, 57, 157 Palliative, 157, 170
Pancreas, 119, 157 Papillomavirus, 157 Paranasal Sinuses, 157, 167 Parasite, 44, 157 Parenteral, 60, 157 Parietal, 157, 158, 160 Parotid, 157, 165 Particle, 24, 61, 151, 158, 171, 174 Patch, 30, 158 Pathogen, 6, 7, 9, 14, 17, 18, 27, 32, 33, 36, 43, 44, 158 Pathologic, 16, 35, 124, 126, 127, 133, 145, 158 Pathologic Processes, 124, 158 Pathophysiology, 25, 29, 158 Patient Education, 106, 112, 114, 117, 158 Penicillin, 38, 121, 122, 158 Penicillin Resistance, 38, 158 Peptide, 15, 28, 130, 158, 161, 162 Peptide Chain Elongation, 130, 158 Perfusion, 86, 145, 158 Perinatal, 107, 158 Periodontal disease, 16, 43, 50, 75, 107, 158 Periodontitis, 43, 142, 158 Peritoneal, 26, 34, 158 Peritoneal Cavity, 34, 158 Peritoneum, 158 Peritonitis, 34, 35, 158 Phagocyte, 13, 157, 158 Phagocytosis, 6, 16, 21, 158 Pharmacodynamic, 39, 159 Pharmacologic, 32, 122, 124, 143, 159, 171 Pharynx, 147, 156, 159 Phenotype, 18, 159 Phenylalanine, 159, 172 Phospholipases, 159, 167 Phospholipids, 28, 42, 58, 140, 150, 152, 159 Photocoagulation, 131, 159 Physical Examination, 108, 159 Physiologic, 26, 34, 120, 126, 143, 159, 164 Physiology, 16, 25, 44, 86, 159 Plague, 16, 106, 159 Plague Vaccine, 17, 159 Plants, 120, 126, 127, 142, 149, 153, 159, 168, 171, 172 Plaque, 16, 31, 32, 107, 124, 130, 159 Plasma, 5, 34, 67, 68, 84, 122, 125, 128, 130, 131, 138, 140, 144, 153, 154, 159, 173 Plasma cells, 122, 153, 159 Plasmids, 17, 159 Platelet Activation, 35, 160, 167
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Platelet Aggregation, 122, 155, 160 Platelet Factor 4, 149, 160 Platelets, 34, 125, 155, 160, 166, 170 Pleura, 160 Pleural, 83, 85, 160 Pleural cavity, 160 Pleural Effusion, 85, 160 Pneumonia, Bacterial, 58, 59, 68, 160 Pneumonia, Pneumocystis carinii, 107, 160 Pneumonitis, 16, 22, 35, 160 Poisoning, 149, 152, 154, 160, 166 Polymerase, 28, 160, 161 Polymerase Chain Reaction, 28, 160 Polyneuritis, 135, 161 Polypeptide, 10, 121, 145, 161, 162, 174 Polysaccharide, 19, 24, 83, 120, 123, 161 Postsynaptic, 161, 167, 170 Potentiates, 148, 161 Potentiation, 161, 167 Practicability, 161, 172 Practice Guidelines, 102, 161 Precursor, 136, 137, 138, 143, 159, 161, 172 Pregnancy Outcome, 36, 161 Prevalence, 15, 30, 43, 45, 156, 161 Primary endpoint, 18, 161 Progression, 13, 16, 26, 28, 30, 64, 122, 161 Progressive, 7, 28, 38, 128, 134, 136, 154, 160, 161 Projection, 134, 161 Promoter, 31, 161 Promotor, 161, 165 Prophylaxis, 75, 162, 173 Prospective study, 52, 53, 73, 162 Prostaglandins, 147, 162 Prostaglandins A, 147, 162 Protease, 6, 10, 15, 30, 131, 162 Protease Inhibitors, 10, 15, 30, 162 Protein C, 28, 121, 123, 150, 162 Protein Conformation, 121, 162 Protein S, 44, 126, 130, 135, 139, 141, 162 Proteins, 4, 6, 7, 8, 9, 10, 17, 21, 27, 31, 35, 40, 42, 44, 45, 121, 123, 128, 130, 131, 138, 139, 145, 146, 148, 152, 153, 155, 158, 159, 162, 164, 166, 171, 174 Proteinuria, 153, 162 Proteolytic, 15, 26, 132, 162 Proteome, 17, 162 Protocol, 72, 162 Protons, 121, 145, 149, 162, 163 Protozoa, 44, 152, 162, 168 Proximal, 136, 162
Psychiatry, 54, 163, 173 Psychic, 152, 163 Psychoactive, 163, 174 Public Health, 14, 20, 24, 25, 29, 102, 163 Public Policy, 101, 163 Publishing, 46, 107, 163 Pulmonary Artery, 126, 163 Pulmonary Embolism, 69, 163 Pulse, 153, 157, 163 Putrefaction, 141, 163 Pyogenic, 74, 79, 156, 163, 166 Q Quality of Life, 30, 163 R Race, 152, 163 Radiation, 50, 138, 139, 140, 141, 146, 149, 151, 163, 164, 174 Radiation therapy, 50, 139, 149, 163 Radioactive, 143, 145, 147, 149, 151, 153, 156, 163 Radiolabeled, 163 Radiological, 74, 163 Radiology, 163 Radiotherapy, 126, 163, 164 Randomized, 28, 30, 32, 40, 45, 57, 137, 164 Randomized clinical trial, 28, 32, 164 Reactive Oxygen Species, 25, 164 Receptor, 5, 10, 11, 14, 20, 23, 24, 34, 35, 39, 41, 119, 123, 131, 136, 142, 164, 166, 167 Recombinant, 7, 10, 16, 40, 42, 164, 173 Recombination, 34, 141, 164 Rectum, 126, 131, 140, 141, 147, 164 Red blood cells, 139, 144, 164 Refer, 1, 131, 144, 155, 156, 164, 171 Refraction, 164, 168 Regimen, 28, 107, 137, 164 Regional lymph node, 18, 164 Reinfection, 14, 164 Relative risk, 8, 164 Respiration, 121, 127, 140, 153, 164 Respirator, 151, 165 Respiratory distress syndrome, 28, 58, 65, 67, 165 Respiratory failure, 40, 165 Respiratory Physiology, 50, 52, 63, 71, 72, 165, 173 Response Elements, 9, 165 Retroviral vector, 141, 165 Rheumatoid, 157, 165 Rhinitis, 127, 165, 166 Ribose, 119, 165
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Bacterial Pneumonia
Risk factor, 36, 38, 52, 67, 71, 75, 81, 162, 164, 165 Risk patient, 60, 165 Ristocetin, 165, 173 Rod, 124, 125, 165 S Saline, 127, 165 Saliva, 165 Salivary, 33, 134, 135, 165 Salivary glands, 134, 135, 165 Sarcoidosis, 14, 76, 165 Sarcoma, 89, 107, 108, 165 Schizoid, 165, 174 Schizophrenia, 165, 166, 174 Schizotypal Personality Disorder, 165, 174 Sclerosis, 153, 166 Screening, 12, 36, 131, 166 Secretion, 5, 6, 9, 27, 30, 37, 44, 45, 145, 153, 166 Secretory, 31, 51, 166, 170 Sediment, 166 Sedimentation, 60, 166 Segregation, 164, 166 Semisynthetic, 121, 128, 129, 130, 166 Sepsis, 7, 20, 27, 34, 35, 36, 76, 85, 125, 166 Septic, 16, 34, 36, 49, 57, 62, 86, 124, 166 Septicaemia, 166 Septicemia, 7, 16, 166 Sequencing, 161, 166 Serotonin, 123, 131, 155, 166 Serotypes, 19, 21, 33, 166 Serous, 138, 160, 166 Serum, 12, 14, 16, 50, 51, 73, 75, 76, 121, 122, 123, 131, 146, 150, 151, 158, 166, 172 Sex Characteristics, 120, 166 Sexually Transmitted Diseases, 107, 166 Shock, 4, 7, 15, 16, 49, 57, 62, 166, 172 Shock, Cardiogenic, 57, 62, 166 Shunt, 70, 167 Side effect, 95, 120, 123, 128, 167, 171 Signal Transduction, 10, 31, 35, 167 Signs and Symptoms, 24, 167 Sinusitis, 14, 91, 167 Skeletal, 153, 167 Skeleton, 119, 167 Smoking Cessation, 30, 167 Smooth muscle, 121, 122, 124, 140, 167, 169 Social Environment, 163, 167 Social Support, 167, 169 Soft tissue, 126, 167 Solvent, 139, 142, 167
Somatic, 120, 145, 153, 167 Specialist, 109, 167 Specificity, 19, 56, 70, 120, 168 Spectrum, 15, 26, 33, 128, 149, 168 Spinal cord, 129, 130, 137, 152, 155, 157, 168 Spirochete, 168, 170 Spleen, 125, 134, 151, 165, 168 Spontaneous Abortion, 161, 168 Spores, 131, 168 Sputum, 31, 63, 66, 77, 79, 108, 168 Staging, 89, 168 Steady state, 38, 168 Stenosis, 14, 168, 169 Sterility, 147, 168 Stillbirth, 161, 168 Stimulant, 121, 168 Stimulus, 4, 11, 137, 139, 148, 168 Stomach, 119, 141, 145, 154, 158, 159, 168 Stool, 36, 131, 168 Strand, 160, 168 Streptococcal, 20, 168 Streptococci, 20, 168 Streptococcus, 10, 18, 20, 168 Stress, 106, 154, 169 Stress management, 106, 169 Stricture, 168, 169 Stroke, 14, 43, 100, 107, 128, 169 Subacute, 147, 167, 169 Subclinical, 147, 169 Subcutaneous, 81, 141, 157, 169 Subspecies, 167, 169 Substance P, 139, 165, 166, 169 Substrate, 138, 169 Superoxide, 6, 169 Supplementation, 45, 86, 169 Suppository, 128, 169 Suppression, 4, 9, 21, 22, 45, 169, 174 Suppressive, 5, 169 Suppurative, 39, 141, 169 Surfactant, 6, 10, 25, 27, 41, 42, 58, 62, 169 Synaptic, 155, 167, 169, 170 Synaptic Transmission, 155, 170 Synergistic, 10, 170 Syphilis, 106, 107, 170 Systemic disease, 3, 166, 170 T Tachycardia, 124, 170 Tachypnea, 124, 160, 170 Teichoic Acids, 143, 170 Terminator, 170, 174 Tetani, 170
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Tetanic, 170 Tetanus, 24, 170 Therapeutics, 10, 17, 79, 96, 170 Thermal, 136, 155, 160, 170 Thoracic, 50, 53, 58, 74, 85, 135, 151, 160, 170 Thrombin, 140, 160, 162, 170 Thrombocytes, 160, 170 Thrombomodulin, 162, 170 Thrombosis, 35, 125, 162, 169, 170 Thrush, 127, 170 Thymus, 146, 151, 170 Thyroid, 170, 172 Tobramycin, 64, 171 Tomography, 171 Tone, 156, 171 Tooth Loss, 43, 171 Tooth Preparation, 119, 171 Topical, 130, 139, 171 Torsion, 147, 171 Toxic, iv, 125, 134, 135, 138, 146, 155, 171, 173, 174 Toxicity, 25, 136, 152, 165, 171 Toxicology, 102, 171 Toxin, 135, 138, 170, 171 Toxoid, 24, 171 Toxoplasmosis, 89, 171 Transcriptase, 89, 171 Transcription Factors, 31, 35, 165, 171 Transduction, 31, 167, 171 Transfection, 126, 141, 171 Transfer Factor, 146, 171 Translation, 139, 171 Translational, 21, 42, 172 Translocate, 15, 172 Translocating, 7, 125, 172 Translocation, 5, 11, 15, 125, 130, 139, 172 Transmitter, 119, 136, 151, 172 Transplantation, 53, 67, 137, 146, 151, 172 Transposons, 21, 172 Trauma, 35, 143, 154, 172 Treatment Outcome, 30, 172 Tropism, 23, 172 Tuberculosis, 12, 18, 37, 48, 58, 59, 68, 76, 79, 90, 107, 108, 154, 172 Tumor Necrosis Factor, 4, 16, 62, 172 Tunica, 153, 172 Tyrosine, 11, 136, 172 U Ulcer, 134, 172 Ulceration, 134, 172 Ureters, 172
Urethra, 172 Urinary, 8, 128, 130, 172, 173 Urinary tract, 8, 128, 172 Urinary tract infection, 8, 172 Urine, 61, 126, 131, 162, 172 Urogenital, 142, 173 Uterus, 129, 173 Utilization Review, 47, 173 V Vaccination, 12, 19, 79, 173 Vaccine, 10, 12, 14, 19, 24, 29, 90, 120, 162, 173 Vagina, 127, 129, 173 Vaginal, 36, 169, 173 Vaginitis, 127, 173 Vancomycin, 85, 173 Vascular, 13, 121, 138, 147, 155, 173 Vasodilators, 155, 173 Vector, 23, 171, 173 Vein, 149, 156, 157, 173 Venereal, 170, 173 Venous, 125, 162, 173 Ventilation, 63, 173 Ventricles, 129, 173 Venules, 126, 127, 138, 173 Veterinary Medicine, 101, 173 Viral, 6, 7, 18, 21, 22, 28, 48, 75, 92, 107, 147, 171, 173, 174 Viral Load, 48, 173 Virulence, 9, 11, 12, 14, 17, 21, 22, 27, 33, 40, 44, 124, 171, 173 Virulent, 7, 12, 33, 80, 173 Virus Replication, 20, 174 Vitro, 6, 20, 22, 25, 28, 39, 41, 174 Vivo, 4, 14, 15, 19, 22, 25, 28, 33, 34, 35, 42, 151, 174 W Warts, 145, 174 White blood cell, 122, 143, 150, 151, 153, 155, 159, 174 Withdrawal, 92, 107, 174 Wound Healing, 35, 174 X Xenograft, 122, 174 X-ray, 46, 50, 108, 128, 132, 140, 141, 151, 156, 163, 164, 174 Y Yeasts, 127, 141, 159, 174 Yolk Sac, 140, 174 Z Zidovudine, 107, 174 Zymogen, 162, 174
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Bacterial Pneumonia
