NOXIA 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
ii
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., 1960Anoxia: 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: 0-497-00075-X 1. Anoxia-Popular works. I. Title.
iii
Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail:
[email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International, Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.
iv
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 anoxia. 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.
v
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.
vi
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
vii
Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON ANOXIA..................................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Anoxia........................................................................................... 4 E-Journals: PubMed Central ....................................................................................................... 32 The National Library of Medicine: PubMed ................................................................................ 33 CHAPTER 2. ALTERNATIVE MEDICINE AND ANOXIA..................................................................... 65 Overview...................................................................................................................................... 65 National Center for Complementary and Alternative Medicine.................................................. 65 Additional Web Resources ........................................................................................................... 68 General References ....................................................................................................................... 69 CHAPTER 3. DISSERTATIONS ON ANOXIA ...................................................................................... 71 Overview...................................................................................................................................... 71 Dissertations on Anoxia .............................................................................................................. 71 Keeping Current .......................................................................................................................... 71 CHAPTER 4. PATENTS ON ANOXIA ................................................................................................. 73 Overview...................................................................................................................................... 73 Patents on Anoxia........................................................................................................................ 73 Patent Applications on Anoxia .................................................................................................... 82 Keeping Current .......................................................................................................................... 85 CHAPTER 5. BOOKS ON ANOXIA ..................................................................................................... 87 Overview...................................................................................................................................... 87 Book Summaries: Federal Agencies.............................................................................................. 87 Chapters on Anoxia...................................................................................................................... 88 CHAPTER 6. PERIODICALS AND NEWS ON ANOXIA ....................................................................... 89 Overview...................................................................................................................................... 89 News Services and Press Releases................................................................................................ 89 Academic Periodicals covering Anoxia ........................................................................................ 90 APPENDIX A. PHYSICIAN RESOURCES ............................................................................................ 95 Overview...................................................................................................................................... 95 NIH Guidelines............................................................................................................................ 95 NIH Databases............................................................................................................................. 97 Other Commercial Databases....................................................................................................... 99 APPENDIX B. PATIENT RESOURCES ............................................................................................... 101 Overview.................................................................................................................................... 101 Patient Guideline Sources.......................................................................................................... 101 Finding Associations.................................................................................................................. 103 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 105 Overview.................................................................................................................................... 105 Preparation................................................................................................................................. 105 Finding a Local Medical Library................................................................................................ 105 Medical Libraries in the U.S. and Canada ................................................................................. 105 ONLINE GLOSSARIES................................................................................................................ 111 Online Dictionary Directories ................................................................................................... 111 ANOXIA DICTIONARY .............................................................................................................. 113 INDEX .............................................................................................................................................. 179
1
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 anoxia is indexed in search engines, such as www.google.com or others, a nonsystematic 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 anoxia, 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 anoxia, 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 anoxia. 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 anoxia, 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 anoxia. The Editors
1
From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
3
CHAPTER 1. STUDIES ON ANOXIA Overview In this chapter, we will show you how to locate peer-reviewed references and studies on anoxia.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and anoxia, 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 “anoxia” (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: •
Sensorineural Hearing Loss in Children Source: Pediatric Clinics in North America. 43(6): 1195-1216. December 1996. Summary: This article reviews the epidemiology, etiology, diagnosis, and treatment of sensorineural hearing loss (SNHL) in children. The article begins with a brief discussion of the social and educational impact of an undetected hearing loss in infants and young children, then reviews the goals of universal screening and hearing loss detection. The author notes that an optimal protocol for universal screening would permit infants with normal hearing to be accurately segregated from those with true positive results who need expensive follow up and would help identify neonates with transient conducive hearing losses, sparing them the necessity of follow-ups. The article goes on to discuss the causes of SNHL, the use of a multidisciplinary team evaluation, the measurement of hearing (using evoked otacoustic emissions, or OAE, and other methods), and the
4
Anoxia
advances in understanding the genetics of hearing loss. The remainder of the article considers the nongenetic causes of hearing loss, including congenital cytomegalovirus infection, congenital toxoplasmosis, congenital syphilis, rubella, measles and mumps, herpes simplex encephalitis, bacterial meningitis, toxic drugs and chemicals, hypoxia and anoxia, hyperbilirubinemia, recurrent otitis media, neonatal intensive care, ear or temporal bone trauma, perilymph fistula, and noise-induced hearing loss. 3 tables. 79 references. (AA-M). •
Risk Factor and Behavioral Differences Between Vascular and Alzheimer's Dementia: The Pathway to End-Stage Disease Source: Journal of Geriatric Psychiatry and Neurology. 6(1): 29-33. January-March 1993. Summary: This journal article describes a study that examined differences in risk factors and behavioral characteristics in 502 persons with vascular dementia and 810 persons with probable Alzheimer's disease. With respect to risk factors, subjects with vascular dementia were significantly more likely to have a history of general anesthesia, stroke, transient ischemic attacks, and hypertension. There were no differences between the groups in history of closed head trauma, anoxia, diabetes, chronic obstructive pulmonary disease, cigarette smoking, or family history of dementia. With respect to behaviors, subjects with vascular dementia were significantly more likely to exhibit depression in all stages of dementia whereas subjects with Alzheimer's disease were significantly more likely to exhibit wandering in the middle and late stages. The two groups did not differ in the prevalence of agitation or anger, personality change, hallucinations, delusions, and insomnia in any stage of dementia. 18 references.
Federally Funded Research on Anoxia The U.S. Government supports a variety of research studies relating to anoxia. 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 anoxia. 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 anoxia. The following is typical of the type of information found when searching the CRISP database for anoxia: •
Project Title: AAV VECTORS EXPRESSING ANGIOGENIC FACTORS FOR CHD Principal Investigator & Institution: Kan, Yuet W.; Professor of Medicine; Stanford University Stanford, Ca 94305
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
Timing: Fiscal Year 2002 Summary: Intramuscular injection of AAV vectors is an efficient way of delivering secretory proteins such as erythropoietin and Factor IX. It appears, therefore, that this vector could be useful for delivering angiogenic factors for the treatment of coronary heart disease. Preliminary experiments indicate that this model of administration may indeed by useful. VEGF delivered by AAV vectors into the myocardium by intracardiac injection was compared in mice with or without coronary artery ligation. In mice with ligated coronary arteries, ne blood vessel formation was seen, whereas in the mice with intact coronary, very few blood vessels were seen. (1) The first aim of this project is to extend these studies to a larger number of animals. Because the pathophysiological changes associated with ligation of the coronary artery are much better established in rats, these studies will be performed on rats. The animals will be examined by electrophysiology and echocardiography before they are sacrificed for histological examination for pathology and blood vessel formation. Also, a new method for three dimensional imaging of cardiac blood vessels will be used. (2) A second aim of this project is to investigate methods of regulating angiogenic factors of expression in the myocardium. As it has been shown that high level of expression of VEGF in the myocardium may result in hemangioma formation, it is important to control the expression of angiogenic factors. The first may result in hemangioma formation, it is important to control the expression of angiogenic factors. The first mode of regulation that we will investigate that we will investigate is to use the hypoxia responsive element from the erythropoietin gene. Preliminary data showed several copies of this element arranged in tandem could increase the expression of genes in response to anoxia. Other inducible promoters such as the tetracycline or the progesterone receptor system will be tested. (3) A third aim is to improve the quality and quantity of new blood vessel formation. The angiopoietin and fibroblast growth factor, alone and in combination with VEGF will be investigated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIOSYNTHESIS PLASMALOGENS
AND
FUNCTIONS
OF
ANIMAL
CELL
Principal Investigator & Institution: Zoeller, Raphael A.; Biophysics; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 01-DEC-1993; Project End 30-JUN-2004 Summary: Our long-term goals are to understand how animal cells regulate their phospholipid makeup and the importance of this in cell function and in human health. Our main focus has been on plasmalogens; a class of phospholipid that constitutes 18 percent of the phospholipid mass in humans and are found in very high levels in heart, muscle and brain (one-third of heart phospholipid is plasmalogen). We have generated mutants from well characterized somatic cell lines, that are defective in plasmalogen biosynthesis. These plasmalogen-deficient cells are hypersensitive to chemical hypoxia (a chemical model for ischemia/ reperfusion), as well as anoxia/reoxygenation. These and other data suggest a role for plasmalogens, as endogenous antioxidants, in the protection of cells and tissues during episodes of ischemia/reperfusion such as heart attack and stroke. In another area of interest, we have attempted to isolate mutants with general defects in, glycerolipid biosynthesis, particularly in the biosynthesis and initial metabolism of phosphatidic acid. We have recently isolated a putative mutant in phosphatidate phosphohydrolase, a key regulatory enzyme in triglyceride synthesis. Our specific aims for the near future are: 1. To isolate mutants in the first step in diacylglycerolipid biosynthesis, sn-glycero-3-phosphate acyltransferase. 2. To isolate the
6
Anoxia
gene(s) involved in the first step in plasmalogen biosynthesis (dihydroxyacetonephosphate acyltransferase), and in overall glycerolipid biosynthesis (phosphatidate phosphohydrolase), using existing mutants that are deficient in these steps. 3. To define the mechanism by which plasmalogens protect cells during chemical hypoxia and anoxia/reperfusion. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BRAIN ION CHANNEL REGULATION IN ANOXIA AND ANESTHESIA Principal Investigator & Institution: Bickler, Philip E.; Anesthesia & Perioperative Care; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2002; Project Start 01-AUG-1994; Project End 30-JUN-2005 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: CALCIUM CHEMORECEPTORS
SIGNALING
IN
DEVELOPING
CAROTID
Principal Investigator & Institution: Sterni, Laura M.; Pediatrics; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 01-JAN-1998; Project End 31-DEC-2002 Summary: (Adapted from applicants' abstract) Dr. Laura Sterni, the PI, is an assistant professor who completed her pediatric pulmonary fellowship in 1996. In this application she outlines a program to study proposed mechanisms by which the carotid chemoreceptors increase their sensitivity in early postnatal life. The carotid chemoreceptors are oxygen sensors which are almost entirely responsible for driving the ventilatory response to hypoxia. Their sensitivity is weak at birth and requires the first few days to weeks of life to reset, increase their sensitivity to hypoxia, and assume the role of defending the infant from hypoxic stress. An understanding of the mechanisms involved in this postnatal resetting is likely to be important in understanding the pathogenesis of many disorders of neonatal respiratory control, including the Sudden Infant Death Syndrome (SIDS), the number one killer of infants over one month of age in the United States. The PI's fellowship project demonstrated that maturation of carotid chemoreceptor sensitivity to oxygen is due, at least in part, to changes within the chemosensory type I cell. These cells respond to stimuli with an increase in cytoplasmic calcium ([Ca2+]c) which then triggers neurotransmitter release. Type I cells isolated from mature animals had a significantly greater [Ca2+]c response to hypoxia and anoxia than cells isolated from newborns. These studies will investigate the role of intracellular Ca2+ stores in maturation of the [Ca2+]c response of type I cells to hypoxia. The hypotheses that will be tested are: (1) in the mature carotid chemoreceptor cell, intracellular Ca2+ stores modulate the rise in [Ca2+]c produced by voltage gated calcium entry; (2) the effect of the intracellular Ca2+ stores on the type I cell's hypoxia response changes during postnatal maturation; and (3) carotid chemoreceptor resetting is mediated partly by withdrawal of dopaminergic stimulation on Ca2+ influx and Ca2+ stores. The PI will take advantage of the strong mentoring, significant protected research time and the outstanding academic resources of the Johns Hopkins Medical Institutions to reach her goal of becoming an independent investigator in this important field. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies
•
7
Project Title: CAN MICROGLIAL CELLS PREVENT NEURONAL INJURY? Principal Investigator & Institution: Bruce-Keller, Annadora J.; Assistant Professor; Sanders-Brown Ky Res Ctr/Aging; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506 Timing: Fiscal Year 2002; Project Start 15-DEC-1999; Project End 30-NOV-2003 Summary: The nervous and immune systems of man are made up of complex networks of cells that monitor specific body signals and respond appropriately. While effects of the brain on the immune system are well characterized, modulation of brain cell function by immunocompetent cells, especially under conditions of brain injury, is not well characterized. These studies seek to identify and characterize endogenous inflammatory pathways that both increase neuronal resistance to brain injury, and increase synaptic recovery following brain injury. Additionally, pharmacological agents that could mimic these neuroprotective pathways will be evaluated. This proposal, therefore, will determine the role of microglial cells, brain resident immunologic cells, in the development of brain injury. Using a well characterized in slice culture model that preserves the physiological, three-dimensional architecture of the brain, this propose will employ well-characterized pharmacological agents to modulate microglial activation in models of excitotoxicity (i.e., seizure-induced damage), anoxia (i.e., stroke), and amyloid- dependent (i.e., Alzheimer s like pathology). Specific Aim 1 tests the general hypothesis that activation of microglial cells is neuroprotective in these models. Specific Aim 2 tests the hypothesis that microglia protect neuronal systems by channeling death pathways towards apoptosis rather than necrosis, and then isolating/removing the apoptotic cells. Specific Aim 3 tests a hypothesis that microglial activation increases both neuronal to injury and neuronal recovery following injury by selective targeting and removal of white matter (myelin) debris. It is especially important to understand the specific contributions of inflammatory mediators to brain injury because under most clinical settings the first priority is to stop immune and inflammatory processes. The possibility therefore exists that new pharmacological interventions could be devised based on studies such as these that lead to increased efficacy in the treatment and therapeutic recovery of victims of traumatic spinal or brain injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: ENDOTHELIAL CELL INJURY: QUANTIFYING ITS ROLE IN ISCHEMIC ACUTE RENAL FAILURE Principal Investigator & Institution: Molitoris, Bruce A.; Professor of Medicine and Chief,; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: (Taken directly from the application) Ischemia/reperfusion injury (IRI) is a major contributor to the organ damage that results in acute renal failure, one of the major causes of morbidity and mortality in hospitalized patients in the United States. We propose endothelial cell injury during the initiation phase of ARF (anoxia resulting from decreased vascular perfusion of the organ) occurs and is compounded thereafter by continued hypoxia in the cortical medullary region of the kidney. This results in further endothelial cell injury mediating epithelial cell injury and worsening organ dysfunction. Many factors are known to be involved in ischemia/reperfusion injury, but considerable data point to an important role for endothelial cells, as agents of injury in the kidney as well as other organs. Furthermore there is evidence that actin cytoskeletal
8
Anoxia
alterations, occurring during cellular ATP depletion, mediate many of the structural and functional changes known to occur in ischemic cells. However, documentation of endothelial damage in the kidney is lacking. Therefore, we propose to test our hypothesis using an experimental model of ischemia/reperfusion injury in the mouse, and to determine the extent of initial and subsequent ischemia-induced endothelial injury and endothelial actin alterations. We will exploit recent advances in gene therapy and imaging technologies to image endothelial cell dynamics in live animals whose endothelial cells have been labeled with green fluorescent protein (GFP). We will also use this system to investigate the effect of ischemia/reperfusion on the dynamics of renal microvascular blood flow. Finally we will isolate GFP labeled microvascular endothelial cells and study the effects of ATP depletion on the actin cytoskeleton, actin depolymerizing factor (ADF) and expression of ADF using an adenoviral system to express a GFP-ADF chimera in cultured endothelial cells and in in vivo studies. These studies will provide a better understanding of the clinically important phenomenon of ischemia/reperfusion injury, and provide new methods for testing potential therapeutic approaches. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENDOTHELIAL GENERATION OF ROS IN LUNG ISCHEMIA Principal Investigator & Institution: Fisher, Aron B.; Professor and Director; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002 Summary: This project will evaluate mechanisms for generation of partially reduced oxygen species (ROS) by pulmonary endothelium during lung ischemia. The studies are currently supported by an R-01 grant which will be relinquished if the SCOR is funded. Our primary experimental model is the isolated, perfused rat lung that is continuously ventilated in order to maintain tissue oxygenation and ATP during global ischemia +/reperfusion. Additional studies utilize cultured endothelial cell preparations. During our present period of grant support, we have demonstrated generation of ROS and oxidative injury to lung that occurs during the ischemic period and have provided evidence for a new mechanism of ROS production, i.e., ROS production in association with endothelial cell membrane depolarization. ROS generation also was demonstrated in cultured bovine pulmonary artery endothelial cells and in the perfused lung in the presence of membrane depolarizing solutions (high K+) and with anoxia/reoxygenation produced by ventilating lungs with N2 and then 02. Studies with metabolic inhibitors indicated that ROS production with lung ischemia and with anoxia/reoxygenation occurred through different pathways and indicated a role for NADPH oxidase in lung ischemic injury. The specific aims of the present proposal are to: 1) evaluate endothelial generation of ROS through the use of fluorescence imaging in situ and to determine the temporal sequence between endothelial depolarization, changes in intracellular Ca++ and FE2+/3+ and ROS generation; 2) develop an artificial capillary system for the in vitro evaluation of the role of shear stress and shear stress adaptation on endothelial ROS generation with ischemia; and 3) evaluate the role of the NADPH oxidase pathway as the source of ROS and endothelium using inhibitors, a knock-out mouse model, and antisense technology. This project will provide new information concerning a mechanism for initiation of lung oxidative injury and will document the presence of NADPH oxidase in endothelium and a possible pathophysiologic role in lung ischemia injury. This mechanism is of potential importance in ARDS as a source of ROS generation in association with focal capillary obstruction. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies
•
9
Project Title: EXERCISE TRAINING AND MYOCARDIAL K-ATP CHANNEL FUNCTION Principal Investigator & Institution: Moore, Russell L.; Professor; Integrative Physiology; University of Colorado at Boulder Boulder, Co 80309 Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 31-MAR-2008 Summary: (provided by applicant): It is well known that endurance exercise training (Tr) renders the heart more resistant to ischemia and reperfusion injury. To date, the cellular basis for these adaptations has not been clearly identified. In the heart, ATPsensitive K channels exist on the sarcolemma (sI-KATP) and in mitochondria (mitoKATP) and both have been implicated in protecting the heart against ischemic injury. We recently found that Tr elicits a marked reduction in the magnitude of an anoxiainducible, glibenclamide-sensitive outward K current (IK,ATP) in single rat ventricular cardiocytes. In Specific Aim 1, we will use electrophysiological (whole cell and excised patch) and immunoblotting techniques to determine the cellular basis for this finding. We will examine the effect of training on (1) the sensitivity of sI-KATP to inhibition by ATP and ADP, (2) the protein expression of sI-KATP channel subunits (Kit6.2 and SUR2A), and (3) mitochondrial ATP production in the face of ischemic stress. We also found that following severe zonal ischemia elicited by coronary artery occlusion and then reperfusion, Tr produced infarct sparing and augmented mechanical function in isolated perfused hearts. We also observed a marked Tr-induced hyperemia that was apparent throughout the ischemia reperfusion protocol. In Specific Aim 2, we will use KATP antagonists that are selective for sl- and mito-KATP channels to identify the involvement of these specific channels in Tr-induced infarct sparing and preservation of mechanical function. Indomethacin and L-NAME will be used in studies to determine the cellular basis for the hyperemia that was exhibited during post-ischemic reperfusion, and the extent to which the Tr-induced hyperemia contributed to infarct sparing and the preservation of mechanical function in the heart. The experiments in Aim 2 include a comprehensive battery of LV function, metabolite, biochemical, and coronary flow measurements. Exercise training is known to be effective in the prevention and treatment of a wide variety of cardiopathologic conditions. Elucidation of the cellular changes that underlie these positive adaptations may be of particular importance in the design, development, and implementation of molecular and pharmacological heart disease treatment and prevention strategies. This is particularly significant in view of the fact that heart disease claims more North American lives than any other disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: GROWTH FACTORS INFLUENCE STROKE RECOVERY Principal Investigator & Institution: Finklestein, Seth; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2002 Summary: Recent data indicate that focal cerebral ischemia causes neural death, at least in part, through initiation of a "lethal cascade," which includes release of excitatory amino acids (EAAs) with consequent massive Ca2+ entry into cells, and resulting activation of intracellular proteases and nucleases, and generation of toxic free radicals and nitric oxide (NO). Basic fibroblast growth factor (bFGF) is a neuronotrophic polypeptide that promotes neuronal survival in vitro, and protects cultured neurons against a number of insults and toxins, including anoxia, hypoglycemia, EAAs, Ca2+ ionophore, free radicals, and NO. In preliminary studies, we found that exogenouslyadministered bFGF reduced infarct volume in models of focal cerebral ischemia in
10
Anoxia
mature and neonatal rats in vivo. In the proposed studies, we will further explore the phenomenon and mechanism of bFGF neuroprotection in focal ischemia. These studies include: (1) further study of the dose, timing, and route of administration of bFGF in models of ischemia in mature and neonatal rats, as well as comparison of the effects of bFGF to other characterized growth factors, (2) studies of the biodistribution of exogenously- administered bFGF, and the density and localization of bFGF receptors after ischemia, (3) studies of regulation of candidate "neuroprotective" genes by exogenous bFGF, and (4) studies of the effects of bFGF on the cerebral vasculature. It is expected that these studies will shed new light on molecular mechanisms supporting neuronal survival after focal ischemia. P50NS108280032 This proposal utilizes a molecular genetics approach to generate and characterize animal models that lack the neuronal nitric oxide synthase (NOS) gene. Nitric oxide (NO) is a gas that is made by neurons, endothelial cells, glial cells, and other cells in the body. It has unusual properties that make it well suited to be a spatial messenger in cell-cell interactions. As a gas, it is freely diffusible across membranes. It binds to and is inactivated by heme, limiting its half- life to seconds. In the nervous system, NO has been implicated in establishing synaptic plasticity, in the physiologic and toxic response to excitatory neurotransmitters, and may play a role in ischemic damage from cerebrovascular disease. In the vasculature, NO is responsible for endothelial-derived relaxing factor (EDRF) activity, and is likely to be involved in resting blood vessel tone, as well as responses to vascular mediators and endothelial injury, in the cerebrovasculature as well as in the peripheral vasculature. We propose to develop and characterize mice in which the neuronal NOS gene has been selectively disrupted or "knocked-out," herein referred to as KN mice (knock-out, neuronal NOS). Ongoing work in our laboratory is devoted to the parallel development of mice in which the vascular NOS gene is knocked-out, KV mice (knock-out, vascular NOS). We propose to characterize the phenotype of the KN and KV mice, in terms of neuroanatomy and cerebral circulation. We hope to learn about the compensatory mechanisms that allow KN and KV mice to develop and survive in the absence of the endogenous neuronal and vascular NOS genes. This project will also maintain breeding colonies of KN and KV mice, in order to provide sufficient numbers of mice for project #1B. It is hoped that these experiments will contribute to our understanding of the molecular mechanisms involved in cerebrovascular tone in health and disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GUANINE NUCLEOTIDES IN ISCHEMIC RENAL INJURY Principal Investigator & Institution: Dagher, Pierre C.; Medicine; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 31-MAY-2007 Summary: (provided by applicant): lschemic renal disease remains a major cause of mortality and morbidity in this country. It is an important etiologic factor in many cases of renal failure in patients with vascular disease. While the pathophysiology of ischemic tissue damage is complex and multifactorial, several mediators of injury have been identified. Among these, ATP depletion is generally viewed as the hallmark of acute ischemia in many settings. Indeed, mush has been learned using in vitro models of chemical anoxia- induced ATP depletion in cell culture systems. However, the dynamics of cellular GTP pools during ischemia/reperIusion or chemical anoxia/recovery have not been investigated systematically. Thus, there remains a big gap in our understanding of the role of guanine nucleotide depletion in ischemia. Such a role for guanine nucleotides is suggested by the importance of the cellular GTP/GDP ratio in
Studies
11
the functioning of a variety of signaling GTPases that control trafficking, polarity, the cytoskeleton and cell death in epithelia. In particular, the small GTPases Rho, Rac and Cdc42 are emerging as central participants in the injury-repair cycles observed in ischemia/reperfusion. The central hypothesis to be tested in this proposal is that GTP depletion during ischemia/reperfusion is an important and independent variable in determining the form of cell death observed. Apoptosis is increasingly recognized as a significant mode of cell loss during ischemia. Our hypothesis postulates a major role for GTP depletion in modulating this form of cell death, possibly via an effect on Rho family GTPases. We propose to develop models of selective GTP and ATP depletion and correlate them with cell survival and apoptotic death in culture systems. We will also investigate the role of Rho GTPases in modulating apoptosis using cells transfected with constitutively active and dominant negative forms of the GTPases Rho, Rac and Cdc42. Finally, we will examine the role of GTP in renal ischemia in vivo using control and HPRT-null mice that cannot salvage guanosine to GTP. The effects of enhanced GTP levels on morphology, apoptosis and renal function will be determined. These studies will establish GTP as a key. modulator of ischemic injury and might lead to new therapeutic options for this devastating disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HEME OXYGENASE-1 IN LUNG ISCHEMIA-REPERFUSION INJURY Principal Investigator & Institution: Lee, Patty J.; Internal Medicine; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 29-FEB-2008 Summary: (provided by applicant): Oxidant injury is a major contributor to the pathogenesis of many disease processes including acute lung injury. Anoxiareoxygenation (A-R) In cells and ilschemia-reperfusion (I-R) in lungs are common models of oxidant injury. Lung I-R is likely the inciting injury during lung transplantation/surgery, thromboembolectomy, pulmonary embolism, and reexpansion pulmonary edema. These disorders have high mortalities with limited therapeutic options. This is largely due to our limited knowledge of underlying pathogenesis. We also lack appreciation of the degree to which regulatory events in vitro (A-R) are predictive of the events in vivo (I-R). Heme oxygenase (HO) catalyzes the initial and rate-limiting step in the oxidative degradation of heme to biliverdin with generation of carbon monoxide (CO) and iron. A variety of oxidant stressors strongly induce expression of HO-1, an inducible isoform of HO. Studies from our laboratory and others have demonstrated that HO-1 can protect against oxidant-induced lung injury. However, the ability of HO-1 to confer protection and the processes regulating its production in this setting has not been adequately addressed. In addition, the pivotal cell-type responsible for HO-1-mediated protection against oxidant lung injury is unknown. To begin to understand the processes that regulate A-R/I-R we examined the effects of HO-1 in these injury models. We have demonstrated that HO-1 is markedly induced in endothelial cells and mouse lung after A-R/I-R. In addition, the mitogenactivated protein kinases (MAPKs) are responsible for A-R-induced HO-1 expression. We now show that HO-1 overexpression significantly diminishes A-R/I-R-induced apoptosis in cultured lung endothelial cells and in mouse lung. Our data has led us to propose the following hypotheses: 1) in A-R, HO-1 is induced via novel activation pathways that involve MAPKs and cooperative transcription factor interactions; 2) in IR, similar pathways are activated and are cytoprotective; and 3) in I-R, p38 MAPK activation of endothelial cell HO-1 is a critical event in cytoprotection. To test these hypotheses we will: 1) characterize the cis- and trans-acting elements that mediate HO-1
12
Anoxia
induction and define the consequences in vitro; 2) determine whether A-R regulates the relevant transcription factors via p38 or JNK MAPKs and define the consequences in vitro; 3) determine whether the processes identified in Aims I and 2 are important in vivo; and 4) define the role of endothelial cell p38 MAPK and HO-1 in HO-1-mediated cytoprotection in vivo. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HYPOXIC EFFECTS ON MAMMALIAN RESPIRATORY NEURAL NETWORK Principal Investigator & Institution: Ramirez, Jan M.; Associate Professor; None; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2002; Project Start 07-DEC-1998; Project End 30-NOV-2002 Summary: (Adapted from the applicant's abstract): Every year numerous victims suffer brain damage from hypoxic and anoxic insults. To understand the underlying cellular mechanisms this project examines the anoxic effects on the central respiratory network of mice. This network can be isolated in a brainstem slice preparation which generates spontaneously respiratory rhythmic activity. Slices obtained from mice older than one week respond to anoxia in a very similar way as the chemoafferent-denervated but otherwise intact respiratory system. Therefore this preparation will be employed as a model to study the anoxic response of the central respiratory network. The research plan bridges the network, cellular and molecular level using various electrophysiological and pharmacological techniques. Extra and intracellular recording techniques as well as mapping and lesion experiments are performed to identify and characterize different portions of the respiratory system: a network in the so called pre- Boetzinger complex (pBC) which is responsible for generating normal respiration and its anoxia-induced interaction with a neural network which may be responsible for gasping. A model is proposed how the interaction between these neuronal networks leads to the biphasic response to anoxia, which includes an initial augmentation, depression, apnea and then gasping. To understand the neural mechanisms underlying this biphasic response, whole cell, cell attached, outside-out and inside-out patch clamp recording techniques are used. The planned experiments aim at characterizing in great detail the direct anoxic effects on different calcium and potassium channel subtypes. However, this characterization will be supplemented with an analysis of how these direct cellular changes affect indirectly the activation of other cellular properties that are involved in the generation of the respiratory rhythm. Thus, it is only possible to understand the biphasic response in an integrated multi-level approach. A hypothetical model is proposed as to how a suppression of the N-type calcium channel leads indirectly to changes in synaptic transmission and the open probability of calcium-dependent potassium channels. In this model, these alterations result in a decreased activation of the Ih current which will alter the mechanisms of respiratory rhythm generation. To examine this hypothesis, the cascade of these cellular and network events will be analyzed. A better understanding of these neural mechanisms will provide an important foundation for a more rational treatment of various breathing disorders that result in a cessation of breathing such as sleep apnea, recurrent apnea of the newborn and sudden infant death syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies
•
13
Project Title: MECHANISM OF PHAGOCYTE MEDIATED ISCHEMIC RENAL INJURY Principal Investigator & Institution: Simon, Atkinson; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: (Taken directly from the application) Ischemia/reperfusion injury (IRI) is a major contributor to the organ damage that results in acute renal failure, one of the major causes of morbidity and mortality in hospitalized patients in the United States. IRI results in part from an inflammatory response in tissue following a period of ischemia (anoxia resulting from decreased vascular perfusion of the organ). Many factors are involved in ischemia/reperfusion injury, but considerable data points to an important role for phagocytes, and particularly neutrophils, as agents of injury in the kidney as well as other organs. The Rac2 GTPase is an important transducer of signals from cell surface receptors in neutrophils, and mice deficient in Rac2 exhibit numerous defects in neutrophil functions, including chemotaxis, adhesion and production of reactive oxygen species. We therefore propose that Rac2 deficient mice, as a consequence of defective phagocyte function, will be protected against ischemia/reperfusion injury. We propose to test this hypothesis using an experimental model of ischemia/reperfusion injury in the mouse, and to test the relative contribution of reactive oxygen species to injury using mice that lack NADPH-dependent phagocyte oxidase activity. We will exploit recent advances in gene therapy and imaging technologies to image neutrophil dynamics in live animals whose myeloid cells have been labeled with green fluorescent protein. We will use this system to investigate the effect of ischemia/reperfusion on leukocyte trafficking and apply this method to understanding alterations in neutrophil dynamics that result in attenuated ischemia/reperfusion injury in several knockout mouse models. These studies will provide a better understanding of the clinically important phenomenon of ischemia/reperfusion injury, and provide new methods for testing potential therapeutic approaches. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: MECHANISMS OF ANOXIA-REOXYGENATION-INDUCED SINUSOIDAL ENDOTHELIAL CELL DYSFUNCTIO Principal Investigator & Institution: Aw, Tak Yee.; Professor; Louisiana State Univ Hsc Shreveport P. O. Box 33932 Shreveport, La 71103 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2007 Summary: (Provided by the applicant) Ischemia/reperfusion (I/R) injury is an important pathologic problem in liver resection and liver transplantation. Studies in animal models have implicated liver macrophages (Kupffer cells) and neutrophils in the pathogenesis of I/R liver injury wherein Kupffer cell-derived reactive oxygen species (ROS) in hepatic sinusoids contribute to vascular and parenchymal cell injury and the recruitment of neutrophils into the liver. Due to the complexity of in vivo models, the role of ROS in signaling and the cellular and molecular mechanisms of reperfusioninduced hepatic endothelial injury remain unresolved, as are the specific contribution of Kupffer cells and hepatocytes to this injury process. The current project proposes to (a) establish in vitro models of sinusoidal endothelial cell monolayers that are cocultured with either Kupffer cells and/or hepatocytes to simulate the cellular hierarchy in vivo, and (b) employ these models of cellular complexity to delineate the molecular basis for reoxygenation-induced hepatic vascular injury. Our central working hypothesis is that anoxia/reoxygenation (A/R) induces an imbalance in sinusoidal endothelial ROS and
14
Anoxia
nitric oxide (NO) that leads to activation of NFkB and enhanced neutrophil-endothelial cell interaction. We further hypothesize that this inflammatory response is potentiated by mediators derived from Kupffer cells and hepatocytes. The aims address 3 specific hypothesis. Aim 1. To test the hypothesis that A/R induces sinusoidal endothelial ROS/NO imbalance that leads to activation of NFkB, expression of inflammatory cytokines, upregulation of adhesion molecules and enhanced neutrophil-endothelial cell interactions. Aim 2. To test the hypothesis that inflammatory mediators derived from Kupffer cells potentiate A/R-induced sinusoidal endothelial dysfunction during early reoxygenation. Aim 3. To test the hypothesis that hepatocyte-derived mediators contribute to late phase A/R-induced sinusoidal endothelial cell inflammatory response and vascular dysfunction. The results will provide important insights into the mechanism of vascular I/R injury in the liver and will identify potential targets for therapeutic intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS OF NEURONAL INJURY AND SURVIVAL IN HYPOXIA Principal Investigator & Institution: Haddad, Gabriel G.; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002 Summary: In the past several years, one main focus of our laboratory has been to examine the response of central neurons in a number of brain regions to acute and chronic O2 deprivation. We are particularly interested in the mechanisms that can led to neuronal injury and those that, when activated, can prevent or delay injury. Recently, we have made interesting observations regarding membrane ionic events that link metabolism to excitability. One of these observations pertains to the voltage-sensitive Na+ channels in central neurons. An early event during anoxia in mature (adult) neocortical neurons seems to be a profound inhibition of the steady-state availability of these channels with a major reduction in Na+ current (iNa) and a decrease in neuronal excitability. This observation is important because this may be an adaptive strategy in the adult in that the decrease in excitability will lessen O2 consumption and minimize the mismatch between demand and supply. We are not sure how the immature neocortical cells will respond in terms of INa. We therefore focus in this proposal on the study of the Na+ current in neocortical neurons during graded hypoxia and examine 4 separate hypotheses: 1+ Neocortical neurons decrease their excitability during graded hypoxia by inhibiting INa in a graded manner in the mature but not in the immature; 2) the alterations in INa kinetics during O2 deprivation in neocortical neurons are due to changes in specific cytosolic factors and these are more pronounced in the mature than in the immature; 3) O2 deprivation alters INa via mechanisms that are either membranedelimited or dependent on phosphorylation and 4) long term hypoxia modulates the expression of Na+ channels. These experiments will involve the use of the in-vitro slice and microelectrode technique as well as patch clamp with whole-cell and single channel recordings in freshly dissociated neurons. Optical measurements of Ca++ i and H+ i using confocal microscopy will also be performed. All techniques are available and routinely performed in the PI's laboratory. Our long term view and efforts are focussed on understanding the events that occur during anoxia in central neurons so that we can manipulate cell behavior and possibly render mammalian neurons more tolerant to lack of O2. This will have major implications on a vast number of diseases or conditions that span the age spectrum from the fetus to old age. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies
•
15
Project Title: MECHANISMS OF RENAL ADAPTATION TO ANOXIA Principal Investigator & Institution: Siegel, Norman J.; Professor; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002 Summary: The overall objective of this PPG is to advance our understanding of the cellular adaption to oxygen deprivation. The kidney offers a unique opportunity to investigate fundamental mechanisms which respond to limitation in oxygen. The impact of renal development on cellular respiration and susceptibility to oxygen deprivation is the primary focus of our proposed studies. It is often stated that the young kidney is more resistant to the development of acute failure that the adult kidney. However, the mechanism of tolerance have not been investigated formally. To study this problem, we propose: a) To determine the metabolic factors which contribute to the tolerance of the developing tubule to anoxia. This will entail studies of cellular energy distribution between transport and non-transport functions; the glycolytic pathway, as well as intracellular pH in the tolerance of the immature tubules. b) To evaluate polarity and cytoskeletal changes during development and after anoxia by determining the alterations in intracellular localization of Na/K-ATPase subunits, and fodrin. c) To define the adaptive response to anoxia by investigating the expression and localization of heat shock proteins during and following anoia. To accomplish these specific aims we will use an integrated approach to study the mechanisms of tolerance of the immature tubules to anoxia. Studies will utilize a suspension of tubules obtained after collagenase digestion from immature rats (age 8-10 days old) and mature rate (8-10 weeks old). Techniques that will be used include measurement of O2 consumption rates during reperfusion, Northern and Western analysis, gel retardation assay and immunocytochemical localization. Based on these proposed studies, new information concerning the structural and functional adaptation to oxygen deprivation will be defined and the basic mechanisms involved will be relevant to an understanding of adaptive processes in renal epithelial cells and other organs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: MITOCHONDRIA PROTECTION /DYSFUNCTION
&
CEREBRAL
ANOXIA/ISCHEMIA--
Principal Investigator & Institution: Perez-Pinzon, Miguel A.; Associate Professor; University of Miami-Medical Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MITOCHONDRIA AND CARDIAC CELL DEATH Principal Investigator & Institution: Weiss, James N.; Kawata Professor Med. & Physiol.; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2004; Project Start 05-JUN-2004; Project End 31-MAY-2008 Summary: (provided by applicant): A central mechanism leading to necrosis and apoptosis during ischemia/reperfusion is believed to be the mitochondrial permeability transition (MPT), due to permeability transition pore (PTP) opening in the inner mitochondrial membrane. Based on our recent work, we hypothesize. In this revised application that two separable components predispose mitochondria to injury during
16
Anoxia
anoxia/reoxygenation. The MPT threshold component is most relevant to the anoxic or ischemic period, and sets the threshold for MPT during reperfusion. It is manifested as progressive MPT-independent cytochrome c loss and inner membrane leakiness, which can be attributed to accumulation of long chain fatty acids (FA) and reactive oxygen species (ROS). The MPT trigger component is most relevant to reperfusion. Whether MPT occurs during reperfusion is determined by the interplay between MPT inducers/inhibitors present during rexoygenation (particularly matrix free Ca levels) and electron transport capacity for regenerating mitochondrial membrane potential (deltapsim),which in turn depends on cytochrome c content and inner membrane leak. Consistent with its known cardioprotective role, we find that mitoKATP channel agonist diazoxide protects against both the MPT threshold and MPT trigger components, and that this protection is blocked by mitoKATP antagonist 5-HD. In addition, PKC epsilon, a key signaling component in cardioprotection, protects against the MPT trigger component. The objective of this proposal is to further explore the signal transduction pathways protecting mitochondria from the MPT threshold and MPT trigger components under conditions generally relevant to ischemia/reperfusion. Our strategy is to integrate functional studies with proteomics analysis. Functional studies will use spectrofluorometric, imaging (fluorescent, confocal and high voltage electron microscopy), and adenoviral gene transfer techniques to study mitochondria and cardioprotection at three levels: isolated mitochondria, in situ mitochondria in permeabilized myocytes, and isolated myocytes. Proteomic analysis will dissect mitochondrial protein complexes associated with PKCepsilon and PTP components in protected and unprotected intact hearts. Using this integrated approach, we will 1) further characterize the mechanisms by which ischemic/reperfusion elements promote the MPT threshold and trigger components, and how mitoKATP channel agonists are protective; 2) define the roles of isoform-specific PKC signaling in protection against the MPT threshold and trigger components; 3) examine whether other signaling pathways implicated in cardioprotection modulate susceptibility to the MPT threshold and MPT trigger components. 4) identify, using functional proteomics, the proteins forming multiprotein signaling complexes with PKCepsilon and known PTP components in unprotected and protected hearts, and 5) characterize deltapsim depolarization waves induced by anoxia/reoxygenation to define their association with cytochrome c release and MPT and their responsive to mitoKATP activation and cardioprotective signaling pathways Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR MECHANISMS OF PHYTOCHROME SIGNALING Principal Investigator & Institution: Lagarias, John C.; Molecular and Cellular Biology; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 956165200 Timing: Fiscal Year 2003; Project Start 05-AUG-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Phytochromes are biliprotein light sensors that enable photosynthetic organisms to adapt to positive and negative light environments. The recent discovery of phytochromes in nonphotosynthetic bacteria and fungi document that phytochrome ancestors and their ancient signaling partners have evolved into components of signaling systems found in higher eukaryotes. These studies seek to define how tetrapyrrole and light signals are perceived by and propagated within the phytochrome molecule and transduced to downstream target molecules, specifically addressing the hypothesis that phytochromes function as sensors of linear tetrapyrrole (bilins) and light via regulation of their intrinsic protein kinase activities. Ubiquitous to
Studies
17
aerobic organisms, bilins appear to play important signaling roles in metazoans, their levels being linked to anoxia, xenobiotic-induced oxidative stress and vascular damage. The mechanism of this ancient signaling pathway is therefore of fundamental importance for understanding and regulating analogous signaling systems in other eukaryotes, including humans. In addition to leading to new approaches to regulate light responsiveness and productivity of plants, our primary food source, another long term consequence of these studies is the development of phytochrome-based approaches for new light-based therapies. The long term goal is to define the structural basis for the regulatory functions of each member of the extended phytochrome family at the molecular level. This understanding will not only enable the design of new approaches for regulation of light-mediated growth and development of agronomically important crop species, but will facilitate development of phytochrome-based technologies for regulation of important biochemical processes (e.g., transcription, protein stability and/or protein localization) within living cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEURONAL BASIS OF COURTSHIP SPECIFICITY AND PLASTICITY Principal Investigator & Institution: Kitamoto, Toshihiro; City of Hope National Medical Center Duarte, Ca 91010 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2003 Summary: (provided by applicant): The long-term goal of this proposed project is to understand fundamental neuronal mechanisms underlying higher brain functions that control complex behaviors. Disruption of higher brain functions, such as learning and memory, can occur for a number of reasons including brain surgery, chronic alcohol abuse, head injury, anoxia, and various neurodegenerative disorders such as Alzheimer's disease. A basic understanding of how anatomically distinct neurons in the brain communicate with one another to manipulate complex behavior is essential for the prevention and treatment of many disorders affecting higher brain functions. Recent studies indicate that molecules and cellular mechanisms responsible for important biological processes, including learning and memory, are well conserved among distantly related species. In this project, Drosophila male courtship, which consists of a highly stereotypical sequence of activities and also shows considerable experiencedependent plasticity, will be used as a physiological model of higher-order brain functions. Specific aims of the project are to identify the neuronal subsets involved in the learning/memory process of the courtship plasticity and to determine the temporal requirements of neuronal activity during different phases of the memory formation. To accomplish these aims, a novel molecular genetic approach has been established. In this approach a temperature-sensitive allele of the Drosophila shibire gene (shi") is expressed in restricted neuronal subsets using the GAL4IUAS system. Then, synaptic transmission of the targeted neurons is blocked rapidly and reversibly by a mild temperature-shift in intact animals. By taking advantage of the large collection of available GAL4 lines that are specific to restricted brain regions, the significance of particular neuronal subsets in the courtship plasticity will be determined. A combination of genetic and morphological analysis will be applied to further investigate the neuronal subsets whose functional significance is revealed. The neuronal subsets involved in the genetically determined, stereotypical aspects of male courtship will be also identified using the same approach. The anticipated results, together with the accumulated information of Drosophila behavioral genetics, will provide new insight into the neuronal mechanisms of higherbrain functions in flies, and will contribute to the development of conceptual frameworks for the study of complex behaviors in higher vertebrates including humans.
18
Anoxia
Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEURONAL PATHWAYS UNDERLYING IN VITRO MOTOR LEARNING Principal Investigator & Institution: Keifer, Joyce N.; Associate Professor; Anatomy; University of South Dakota 414 E Clark St Vermillion, Sd 57069 Timing: Fiscal Year 2002; Project Start 01-APR-1999; Project End 31-MAR-2004 Summary: Insights into the processes of learning and memory have fundamental implications for understanding memory disorders such as occur during amnesia and Alzheimer's disease. Conditioned response learning is a simple form of associative learning. A promising model to study the neural mechanisms underlying associative learning is the classically conditioned eye-blink reflex. The classically conditioned eyeblink reflex has been widely adopted for physiologic studies of the mechanisms of associative learning. Simple in vitro model systems of associative learning have been established in several species of marine mollusks. These preparations have greatly facilitated our understanding of the neural mechanisms of learning and memory. Similar model systems of learning in vertebrates have previously been hampered by the technical limitations of maintaining the viability of large portions of intact neural tissue in isolation. This problem was recently overcome by the development of an in vitro brainstem-cerebellum preparation from the turtle which takes advantage of this species' extraordinary resistance to anoxia. Using this preparation, conditioning of reflex pathways was undertaken simply by using electrical stimulation of sensory nerves rather than more natural stimuli such as a tone or airpuff. Preliminary data show that a neural correlate of the conditioned eye-blink reflex, the abducens nerve response, can be generated entirely in vitro. Using this model, studies of the neural mechanisms underlying this form of motor learning will complement those studies using whole animal preparations. The goals of the present project are to elucidate the synaptic organization of the abducens eye-blink reflex circuitry and the mechanisms that may underlie associative learning in this in vitro preparation. The Specific Aims are: to evaluate whether NMDA receptors are required for classical conditioning by training the preparation in the presence or absence of the NMDA receptor antagonist APV, to examine the morphological distribution of synaptic inputs from nerves V (US) and pVIII (CS) onto abducens motoneurons using anterograde transport of Fluoro-Ruby and intracellular Lucifer yellow fills in fixed slices, to examine the morphological distribution of NMDA and non-NMDA glutamate receptors on LY-filled abducens motoneurons using immunocytochemistry, to identify the premotor pathways afferent to the abducens motoneurons using retrograde and anterograde tract tracing methods, and to determine the behavioral correlate of the abducens nerve CR by recording EMGs in a reduced preparation and by classical conditioning of the eye-blink reflex in alert turtles. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: NEURONS AND GLIA IN VITRO Principal Investigator & Institution: Ransom, Bruce R.; Neurology; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 01-SEP-1987; Project End 30-JUN-2004 Summary: More than a century ago, Golgi suggested that glial cells provide nutrients to neurons. This idea gained credibility when astrocytes, but not neurons, were discovered to contain glycogen, the main energy reserve in the brain. Recent observations on the
Studies
19
retinas of the honeybee and rabbit, have provided modem experimental evidence that glial cells can provide fuel to neurons. The role of glycogen, however, remains a mystery. The experiments proposed in this application will critically address the role of glycogen in glial- neuronal interactions during brain energy metabolism. These experiments will be carried out using an advantageous preparation of central nervous system (CNS) white matter, the isolated rat optic nerve. The long term goals of this research are: 1) to learn more about the physiology and function of glial cells, and 2) to understand the mechanisms of CNS white matter injury as occurs with stroke, hypoglycemia, anoxia or trauma, and to devise better ways of minimizing this injury. Broadly stated, the specific aims of this proposal are to learn how glial cells and axons in the CNS interact when deprived of glucose and to understand how glucose deprivation injures central axons. Two hypotheses will be tested: 1) During hypoglycemia in the CNS, astrocytes supply energy substrate to axons in the form of lactate derived from glycogen. Axon function and survival depend on glycogen in the absence of glucose. 2) Axon injury caused by glucose deprivation is Ca2+- dependent and is due to Ca2+ entry mediated by reverse Na+/Ca2+ exchange and Ca channels. The role of astrocytes in supplying energy substrate to axons will be studied using the in vitro rat optic nerve preparation, quantitative electrophysiological techniques to monitor optic nerve function, chemical measurement of glycogen content, and pH, glucose-sensitive, and lactate sensitive microelectrodes. The mechanisms of hypoglycemia-induced axon injury will be studied using quantitative measures of optic nerve function in conjunction with measurement of [Ca2+ ]o using Ca2+-sensitive microelectrodes. These studies will provide useful new information about the manner in which glial cells and neurons interact in the context of brain energy metabolism. They will also assess the importance of astrocytic glycogen for neural function during and for recovery after periods of hypoglycemia, and may suggest novel strategies to stave off neural injury under these conditions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEUROSTEROIDS AND SCHIZOPHRENIA Principal Investigator & Institution: Marx, Christine E.; Psychiatry; Duke University Durham, Nc 27710 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 30-JUN-2006 Summary: (Adapted from applicant's abstract) My career goal is to become an academic psychiatrist and independent investigator in the areas of schizophrenia focusing on its neurobiology and therapeutics, applying molecular mechanism-based research to prospective clinical studies. Specifically, I propose to investigate the importance of neurosteroids in schizophrenia. Neurosteroids are differentially expressed in males and females, modulate GABAA and NMDA receptors, regulate neuronal cytoarchitecture, demonstrate neuroprotective effects, play a role in neurodevelopment, and possess memory-enhancing effects. Neurosteroids are therefore logical candidates of investigation to elucidate schizophrenia pathophysiology, since they are potential modulators of schizophrenia gender differences, GABAergic and glutamatergic dysregulation, neurodevelopmental insults associated with increased schizophrenia risk, cytoarchitectural abnormalities in postmortem specimens from patients with schizophrenia, and cognitive disturbances in the disorder. The laboratory has demonstrated that neurosteroids protect embryonic cerebral cortical neurons against anoxia, a neurodevelopmental insult associated with increased schizophrenia risk. We have also demonstrated that acute olanzapine and clozapine administration alters cerebral cortical neurosteroids in rodents. The investigators hypothesize that
20
Anoxia
neurosteroids are important modulators of schizophrenia pathophysiology (including the pronounced gender differences of the disorder) and antipsychotic drug action. We also propose that compounds affecting neurosteroid expression or neurosteroids themselves may be developed as novel therapeutic agents in the treatment of schizophrenia. To test this hypothesis, three investigational strategies are proposed: 1.) A preclinical study examining the effects of antipsychotics on cerebral cortical and serum neurosteroid levels in rodents, 2.) A postmortem study determining neurosteroid levels in parietal cortex and posterior cingulate specimens provided by the Stanley Foundation from patients with schizophrenia compared to control subjects, and 3.) A clinical study examining neurosteroid levels in subjects with schizophrenia from two UNC clinical trials (Dr. Lieberman, PI) to determine if serum or CSF neurosteroid alterations are correlated with antipsychotic efficacy, neurocognitive changes, and/or structural changes on MRI. Results from these preliminary investigations will inform the design of future prospective clinical studies to confirm initial findings and target neurosteroids as therapeutic agents in schizophrenia. To achieve these goals, the candidate will receive training through formal coursework in neuropharmacology, clinical trials design, drug development, and biostatistics. She will also learn highly sensitive and specific gas chromatography mass spectrometry (GC/MS) and other stateof-the-art neurosteroid detection methods. The mentorship of Drs. Jeffrey Lieberman and Leslie Morrow will be critical to the overarching goal of this proposal, the successful translation of exciting preclinical neurosteroid findings to prospective clinical studies examining neurosteroids in schizophrenia pathophysiology and therapeutics. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PATHOGENESIS OF LIVER CELL NECROSIS Principal Investigator & Institution: Farber, John L.; Professor; Pathology, Anat/Cell Biology; Thomas Jefferson University Office of Research Administration Philadelphia, Pa 191075587 Timing: Fiscal Year 2002; Project Start 01-JUL-1986; Project End 30-JUN-2006 Summary: (PROVIDED BY APPLICANT) The overall objective of the studies proposed in this competing continuation application remains the elucidation of the biochemical mechanisms whereby cells are lethally injured. Having addressed previously (19921997) the mechanisms of liver cell death following an inhibition of mitochondrial electron transport, as a consequence most importantly of ischemia anoxia, over the last three years we have studied five models of apoptosis. The major conclusion that we reached is that the cell death in necrosis as well as in each model of apoptosis studied is a consequence of induction of the mitochondrial permeability transition (MPT). In the models of apoptosis considered, our data implicate the proteins Bax or Bid in induction of the MPT. Thus, the work proposed in the present application is based on the hypothesis that the MPT is a central event in the cell death from either necrosis or apoptosis. Furthermore, we propose that these two killing processes are distinguished in at least two ways. First, necrosis and apoptosis differ with respect to the mechanism of induction of the MPT. Second, apoptosis is characterized by the energy-dependent activation of caspases as a consequence of the MPT. Such a role for caspases cannot occur with necrosis where energy depletion is a necessary event in the induction of the MPT, a situation most clearly evidenced by ischemia/anoxia. The specific aims of the present proposal are to pursue the implications of this initial reconstruction of the mechanisms mediating both necrosis and apoptosis. Aim #1 - What is the mechanism of Bax activation in apoptosis, a process that results in induction of the MPT? In those cells that contain both Bax and Bid (L929 fibroblasts and HeLa cells), we propose to
Studies
21
distinguish between two hypotheses. Bax and Bid are redundant proteins and act independently. Bax activation (and that of Bid) is the result of a conformational change induced by alterations in cytosolic pH and/or ion composition. Alternatively, Bax translocation to the mitochondria is secondary to a primary activation of Bid. The mechanism action is also considered of other pro- and antiapoptotic proteins, including ERK (antiapoptotic) and JNK (proapoptotic) classes of MAP kinases, as well as NF(antiapoptotic). Aim #2- What is the energy-independent mechanism coupling the MPT to the loss of cell viability? With both necrosis and apoptosis, lethal cell injury depends on the MPT. We propose to test the hypothesis that in both necrosis and apoptosis direct physical connections through the cytoskeleton between the outer mitochondrial membrane (porin in particular) and the plasma membrane mediate the energyindependent coupling of the MPT to the loss of viability represented by lethal plasma membrane injury. Aim #3- How in apoptosis does the energy-dependent activation of caspases by cytochrome c as a consequence of the MPT alter (replace or modify) the mechanism of cell killing? It is our hypothesis that the phenotypic features distinguishing apoptosis from necrosis occur in this phase and are largely mediated by caspases. It is our aim to detail the specific biochemical mediators of the major phenotypic manifestations of both necrotic and apoptotic cell death. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PKC AND ISCHEMIC PRECONDITIONING OF MUSCLE Principal Investigator & Institution: Maldonado, Claudio; Surgery; University of Louisville Jouett Hall, Belknap Campus Louisville, Ky 40292 Timing: Fiscal Year 2002; Project Start 10-SEP-1998; Project End 29-FEB-2004 Summary: (Adapted from applicant's abstract) The overall objective of this plan will be to facilitate the development of the candidate into a highly trained scientist in the area of ischemic preconditioning (PC) of skeletal muscle to improve dynamic cardiomyoplasty. Ischemic PC is the phenomenon whereby brief ischemic episodes render skeletal muscle resistant to subsequent ischemia. Two windows of protection have been described: an early phase which occurs immediately after PC, and a delayed phase which manifests itself 24 hours after PC. The applicants hypothesize that the delayed phase of ischemic PC in skeletal muscle is mediated by activation of one or few individual PKC isoform(s). The specific aims are: 1) optimize the PC protocol for the delayed phase of protection; 2) determine the duration of the delayed phase of protection; 3) to fully characterize the activation of individual PKC isoforms during ischemic and pharmacological PC; 4) to determine the effect of PKC inhibitors on individual PKC isoform translocation; 5) to define in isolated myocytes the role of PKC isoform(s) responsible for the delayed phase of protection; and 6) to construct a transgenic mouse that overexpresses PKC isoforms responsible for PC. Rat latissimus dorsi muscle (LDM) flaps will be used in 4 studies. 1) LDMs will be preconditioned with ischemia and with monophosphoryl lipid A (MLA). Twenty-four hours after PC, muscles will be subjected to 4 h of ischemia, and 72 h later infarct size will be quantified. 2) LDMs will be PC with ischemia and MLA 4) Chelerythrine will be given prior to PC and biopsies taken after ischemic PC and MLA. In in vitro studies, using a model of anoxia-reoxygenation to mimic PC, myocytes will be preconditioned and 24 h later submitted to anoxia, and cell death will be the endpoint. The last study will involve the construct of Transgenic mice overexpressing PKC isoforms responsible for PC. The findings of this project will provide new information regarding the mechanisms of ischemic PC and important knowledge regarding the pathogenesis of ischemia in skeletal muscle. (End of Abstract) Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
22
•
Anoxia
Project Title: POSTTRANSLATIONAL REGULATION OF HSF ACTIVITY Principal Investigator & Institution: Bonner, James J.; Associate Professor; Biology; Indiana University Bloomington P.O. Box 1847 Bloomington, in 47402 Timing: Fiscal Year 2002; Project Start 01-MAY-1996; Project End 31-MAR-2004 Summary: (provided by applicant): In eukaryotes, the regulation of stress-induced genes is dependent upon the Heat Shock Transcription Factor, HSF. Recent reports show that HSF is activated by superoxide anion, O2-. O2- is produced nonenzymatically during heat shock, and by mitochondrial activity during hypoxia or recovery from anoxia. The response to O2- shows that HSF is an immediate cellular defense against reperfusion injury, incurred subsequent to ischemic stresses such as stroke. This proposal seeks to understand the mechanism of the HSF conformational change and regulation of transcriptional activation. How does HSF recognize 02-? Are specific amino acid residues modified by superoxide-and if so, which ones? How is the change in cooperativity, which involves the DNA binding domain, transmitted to the trimerization domain, and to the transcriptional activation domains to change the biological function of the protein?. These problems will be addressed through genetic manipulations and biochemical analyses. Specific mutations will be induced in the yeast HSF protein, and their effects will be determined on the superoxide-induced conformational change, and on the biological activity of HSF in vivo. Two regions within the DNA binding domain will be targeted to examine the role of these regions in the conformational change. The trimerization domain will be targeted to examine its role in the regulation of transcriptional activity, and to determine how it collaborates with the DNA binding domain to activate HSF. To move the genetic analysis onto a stronger biochemical foundation, unique cysteine residues will be put into HSF, and used to introduce probes for fluorescence resonance energy transfer. To expand the understanding of the heat shock system beyond the detailed mechanism of HSF regulation, synthetic lethal interactions will be exploited. These will identify those cellular systems that require HSF activity in the absence of stress, and thus reveal why HSF is an essential gene in yeast. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: PREVENTION ANTIOXIDANTS
OF
GRAFT
REJECTION
BY
CATALYTIC
Principal Investigator & Institution: Tocco, Georges; Eukarion, Inc. 6-F Alfred Circle Bedford, Ma 01730 Timing: Fiscal Year 2003; Project Start 15-JUN-2003; Project End 31-MAY-2004 Summary: (provided by the applicant): Transplantation represents the only therapy for end-stage organ failure caused by a variety of incurable diseases. However, rejection by the host represents a major obstacle to long-term survival of transplants. While acute rejection is currently controlled by immunosuppressive drugs, continuous treatment with these non-selective agents impairs the entire immune system thereby increasing the risk for infections and cancer in patients. In addition, many of these drugs exhibit longterm toxic effects. Most importantly, a large proportion of solid organ transplants succumb to chronic rejection, a phenomenon associated with fibrosis, and vasculopathy. At present time, there is no treatment for chronic rejection. These observations underscore the need for novel therapies in transplantation. Eukarion Inc. has developed a class of low molecular weight molecules that are catalytic reactive oxygen species scavengers, acting as mimics for the endogenous antioxidant enzymes, superoxide dismutase and catalase. These compounds have demonstrated efficacy in 3 of the main events associated with tranplant rejection" i) tissue damage due to anoxia, ii)
Studies
23
ischemia/reperfusion injury and iii) inflammation. Most importantly, we have shown that one of these compounds can delay the acute rejection of skin grafts in mice. Based on these observations we intend to develop a series a compounds with greater lipophilicity and in vivo half-life to be tested in the prevention of acute and/or chronic rejection of solid organ transplants for further development. To achieve this, we propose the following specific aims: 1) To synthesize and evaluate a series of analogs with greater potency or efficacy, i.e., a series with enhanced lipophilicity and improved in vivo half-life. 2) To test the effect of selected EUK compounds on anti-donor inflammatory immune response and on the rejection of heart allotransplants in mice. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF KIR CHANNELS IN RETINAL GLIAL CELLS Principal Investigator & Institution: Eaton, Misty J.; Assistant Professor; Universidad Central Del Caribe Bayamon, Pr 009606032 Timing: Fiscal Year 2002; Project Start 01-AUG-1994; Project End 31-DEC-2005 Summary: Potassium inwardly rectifying channels (Kir) stabilize the membrane potential and carry K+ ions. Kir are dominant in the astrocytic Muller (glial) cells responsible for maintaining extracellular homeostasis in the retina. Excitation of neurons increases levels of extracellular potassium ions (K+) at synapses, which if uncorrected would result in depolarization of neurons and a loss of synaptic transmission. Kir channels serve to equaliz4e intraretinal K+ gradients by a mechanism called spatial buffering or K" siphoning. Glial cells carry K+ currents inward in regions where the extracellular K+ concentration is increased and outward at more distant regions. In order to extrude K+ in distant regions, Muller cells need either one type of Kir with rectification that can be quickly regulated (to have outward current) or to have express additional Kir channels with weak or little rectification. The only Kir described in Muller cells to date is Kir 4.1. This channel is strongly rectifying and requires ATP to function and, thereby, could not function for K+ siphoning or when ATP is depleted (i.e., anoxia.). Our preliminary data demonstrate the existence of another Kir subunit, Kir 6.1 (KATP) expressed in Muller cells, which may complete the above- mentioned requirements. Our working hypothesis is that there are two possible ways of how these different subunits (Kir4.1 AND Kir6.1) may collaborate in Muller cell functioning, (i) by co-expression in functional heteromers, or (ii) by mutual switching between two distinct homomeric channels. Our long-term goal is to determine the identify and regulation of Kir channels from retinal glial cells. This will be accomplished using a multi-faceted approach. (1) By determining which Kir subunits are expressed in retinal Muller (glial) cells using immunocytochemistry. (2) By determining the electrophysiological properties and regulation by ATP, spermine and pH of homomeric and heteromeric channels expressed in HEK cells. (3) The electrophysiological properties and regulation of Kir channels and dissociated Muller cells will be compared with the expressed channels and will be examined under different metabolic conditions. The results of these studies will provide insight into normal Kir channel function as well as Kir channel regulation during anoxia and hypoglycemia. when ATP is depleted. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: RESEARCH CENTER FOR CEREBRAL VASCULAR DISEASE Principal Investigator & Institution: Ginsberg, Myron D.; Professor; Neurology; University of Miami-Medical Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2002; Project Start 01-AUG-1976; Project End 31-MAY-2005
24
Anoxia
Summary: The objective of the Cerebral Vascular Disease Research Center at the University of Miami is to carry out an integrated, multi-disciplinary program of experimental research into the mechanisms and therapies of ischemic brain injury. The overall goal of our research program is to identify and characterize those factors responsible for engendering ischemic injury that may be amenable to therapeutic or prophylactic intervention. The Program Project consists of three investigative proposals supported by General-Scientific and Image- Analysis/Computing Core facilities. Project areas include 1) focal cerebral ischemia: a study of the mechanisms of neuroprotection underlying human serum albumin therapy, and of exacerbation of injury due to hyperthermia (fever); 2) mitochondria and cerebral anoxia/ischemia: basic mechanistic studies of protection and dysfunction; and 3) the metabolic and structural consequences of evolving mitochondrial and ionic dysfunction in focal ischemia. The projects are closely integrated with one another, both conceptually and methodologically, and are strongly supported by close collaborative interactions among the investigators and research personnel. The core facilities contribute substantively to the implementation of each project and unify the overall program by common methodological approaches. The General Scientific Core compromises animal physiology; methods of focal and global cerebral ischemia; neurobehavioral strategies; morphological methods including quantitative light microscopy and stereology; immunohistochemistry, confocal microscopy; autoradiographic strategies for local cerebral blood flow and glucose utilization; enzymatic tissue sampling and metabolic analyses; and molecular biological methods, including in situ hybridization, Northern and Western blotting, and reverse transcription-polymerase chain reaction (RT-PCR). The Image-Analysis and Computing Core has pioneered in the development of three-dimensional autoradiographic imageaveraging and is a central resource supporting image-analysis of autoradiographic, molecular biological, and histopathological data; as well as acquisition, statistical analysis and archiving of laboratory data, instrumentation control, and data base management. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RESPIRATORY AND METABOLIC ADAPTATION TO CELLULAR HYPOXIA Principal Investigator & Institution: Schumacker, Paul T.; Professor; Medicine; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2002; Project Start 01-DEC-1985; Project End 30-JUN-2007 Summary: (provided by applicant): Mammalian cells respond to low 02 levels (hypoxia; P02=3-30 mm Hg) by activating adaptive responses that help to restore 02 supply and prevent hypoxic injury. Controversy exists regarding the identity of the cellular 02 sensor triggering these responses. Our studies have revealed that mitochondria act as 02 sensors by increasing their release of reactive oxygen species (ROS) during hypoxia. These ROS function as early signals in the pathway linking the 02 sensor to the downstream responses, which include the activation of the Hypoxia-Inducible Factor-1 (HIF-1). HIF-1 activation triggers the increased expression of glycolytic enzymes, glucose transporters, and other genes during hypoxia. This application proposes to test the hypothesis that mitochondria act as the 02 sensor responsible for activation of HIF-1 during hypoxia, by releasing ROS. Studies using pharmacological tools in the previous funding period implicated mitochondrial Complex Ill as the site of increased ROS production. To test this more definitively, in Aim 1 we will generate a targeted knockout of the Rieske iron-sulfur protein (RISP), a nuclear-encoded gene that is required for the generation of ROS at Complex III. In murine embryonic stem cells lacking this gene, we
Studies
25
predict that hypoxic stabilization of HIF-1 will be lost, while responses to anoxia, cobalt and exogenous H202 will be retained. Recent studies indicate that the small GTPase racl is required for HIF-1 alpha stabilization during hypoxia. Rac1 may act by amplifying the mitochondrial ROS signal generated during hypoxia by engaging additional oxidase systems, by amplifying mitochondrial ROS generation, or by triggering the relocation of mitochondria toward the nucleus. Aim 2 will determine whether mitochondrial ROS signals activate rac- 1 during hypoxia, and whether rac 1 then promotes the stabilization of HIF-1 alpha by amplifying the ROS signal. We hypothesize that the activity of prolyl hydroxylase, the enzyme that targets the HIF-l alpha subunit for proteasomal degradation during normoxia, is not intrinsically an 02 sensor but rather is regulated by signals initiated by the mitochondria. Aim 3 will clarify the role of increased mitochondrial ROS signaling in the stabilization of HIF-1 alpha during hypoxia by studying the regulation of prolyl hydroxylase activity by mitochondrial ROS signals. This will be tested in cultured cells and in an in vitro system where hydroxylation of a recombinant protein is assessed. Collectively, these studies will provide a more conclusive test of the hypothesis that mitochondrial ROS are the site of 02 sensing responsible for HIF-1 activation and gene expression during hypoxia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF T CELLS IN RENAL ISCHEMIC REPERFUSION INJURY Principal Investigator & Institution: Rabb, Hamid; Associate Professor; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 15-AUG-2000; Project End 31-AUG-2005 Summary: Ischemic acute renal failure is a major cause of native and transplant kidney damage. There is no specific therapy and the underlying mechanisms of ischemic reperfusion injury (IRI) are only partially understood. Our goal is to elucidate the mechanisms underlying renal IRI in order to develop new therapy. Experimental studies from a number of groups, including our own, have shown an important role for inflammation and white cells in renal IRI. Though most of the focus has been on neutrophils, new evidence points toward a role for lymphocytes. We have preliminary data in a mouse model that T cells migrate into postischemic kidney. Furthermore, mice deficient in T cells have significantly reduced renal injury and neutrophil infiltration. We therefore hypothesize that T lymphocytes play an important role in renal IRI. To test this hypothesis, we will use our established mouse model of renal IRI, which includes sensitive inulin clearances to measure glomerular filtration rate. We will evaluate the direct roles of different T cell populations by using mice genetically deficient in select T cells as well as depleting T cells in normal mice. New data demonstrates our ability to manipulate T cell populations using depletion and adoptive transfer techniques. Additional in vivo studies will be performed to compare the role of the neutrophil to that of the T cell in renal IRI. To elucidate the mechanisms of T cell interaction with renal tubular epithelial cells (RTEC) in IRI, we will examine T cell adhesion to RTEC in culture under conditions designed to mimic postischemic sequelae in vivo. We will measure T cell adhesion to RTEC exposed to hypoxia-reoxygenation, chemical anoxia and freeradical generating systems, and determine which adhesion molecules are responsible for T cell-RTEC interactions. Preliminary data demonstrate that these stimuli can significant up-regulate T cell-RTEC adhesion. We will also compare T cell adhesion with RTEC to neutrophils and macrophages. Our studies will potentially lead to important novel findings on the nature of IRI. In addition, due to focus on T cells and translational design of experiments, our data can lead to new therapeutic trials for renal IRI. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
26
•
Anoxia
Project Title: ROLE OF THE UNFOLDED PROTEIN RESPONSE IN TYPE 2 DIABETES Principal Investigator & Institution: Papa, Feroz R.; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 941222747 Timing: Fiscal Year 2004; Project Start 01-JUL-2004; Project End 30-JUN-2009 Summary: (provided by applicant): Dr. Feroz R. Papa is an endocrinologist, strongly committed to an academic career as an independent investigator in (-cell molecular biology. His specific interest is the role of endoplasmic reticulum (ER) stress in development of diabetes mellitus type 2 (DM2). Accordingly, he has initiated a postdoctoral fellowship in the lab of Dr. Peter Walter, in the Dept. of Biochemistry and Biophysics at UCSF, studying the Unfolded Protein Response (UPR), a homeostatic mechanism through which eukaryotic cells adjust to ER stress. ER stress occurs when there is an imbalance between the load of client proteins undergoing maturation in the ER lumen and the capacity of the ER to process this load. Pathophysiological conditions provoking ER stress include anoxia, nutrient deprivation, and polypeptide mutations, which result in protein misfolding. The UPR remodels the environment of the ER to respond to ER stress through two mechanisms: 1) a transcriptional upregulation of genes encoding ER chaperones, enzymatic activities, and structural ER components, and 2) a global translational halt, which reduces the load of ER client proteins. The ERtransmembrane kinase/endoribonuclease Ire1alpha is the sensor for the transcriptional arm of the UPR, and the ER-transmembrane elF-2alpha kinase Perk is the sensor for the translational arm. Dr. Papa is proposing a research program which will address the hypothesis that modulating the UPR, in real time using small molecule effectors, can influence the function of beta-cells, and ultimately their survival. He will address this hypothesis through three specific aims. First, using a chemical-genetic strategy, he will sensitize Ire1alpha by gene targeting of IRE1alpha to a cell-permeable ATP analog, 1NM PP1, which he has demonstrated is a permissive co-factor for signaling by sensitized Ire1 in yeast. Beta-cell-specific gene targeting would render this tissue unable to signal the transcriptional arm of the UPR in the absence of 1NM-PP1 Second, similar gene targeting of PERK will be conducted, conferring pharmacological conditionality on the translational arm of the UPR. Third, the biological consequences of these manipulations on beta-cells will be studied in these knock-in mutants, and in the genetic background of three other mouse mutants which develop DM2 as a consequence of unchecked ER stress: Akita, hlAPP, and perk-/-. Together this work promises to yield important insights into how professional secretory tissues (including, but not limited to beta-cells) adapt to physiological and pathophysiological stresses. Dr. Papa will conduct this work in the Dept. of Biochemistry and Biophysics at UCSF under the mentorship of Dr. Peter Walter, and in collaboration with Dr. Robert Farese, Jr. in the Gladstone Institute of Cardiovascular Disease, and Dr. Kevan Shokat in the Department of Cellular and Molecular Pharmacology. The UCSF Department of Medicine is fully committed to Dr. Papa's career development, and will make all necessary resources available to facilitate the success of the project. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: ROLE OF XANTHINE OXIDASE IN LUNG INJURY Principal Investigator & Institution: Hassoun, Paul M.; New England Medical Center Hospitals 750 Washington St Boston, Ma 021111533 Timing: Fiscal Year 2002; Project Start 01-JUL-1993; Project End 31-AUG-2002
Studies
27
Summary: Hypoxia produces significant cellular perturbations in the pulmonary vasculature in lung diseases, such as the adult respiratory distress syndrome and chronic obstructive lung disease, where hypoxia is prevalent. These changes include a marked proliferation of smooth muscle cells (SMC) in the medial layer of the distal vessels and possible alterations in endothelial functions as suggested by increased platelet adhesion to the endothelium. Using cell culture systems, we have found that hypoxia produces a significant release from endothelial cell (EC) of hypoxanthine, a metabolite of ATP. This finding led us to investigate the effect of O2 tension on the enzyme xanthine oxidase/xanthine dehydrogenase (XO/XD) which catalyzes the conversion of hypoxanthine and xanthine to uric acid. Our preliminary results indicate that O2 tension might regulate the intracellular XO/XD activity of EC. Indeed, we found that intracellular XO/XD activity is absent when EC are exposed to hyperoxia and maximal (an approximate 300% increase compared to activity of EC exposed to normoxia) when EC are exposed to hypoxia or anoxia. The latter finding, combined with our previous report of an increased release of hypoxanthine from hypoxic EC, bears great significance in light of the recognized-potential for the hypoxanthine/xanthine oxidase system to produce reactive O2 species. Production of O2-based free radicals have, indeed, been shown to cause several deleterious effects on EC including cell injury and inactivation of the endothelial-derived-relaxing-factor (EDRF). We postulate that changes in the EC hypoxanthine/xanthine oxidase system in response to hypoxia may be a very early phenomenon that might be responsible for subsequent cellular changes in the pulmonary vasculature. The Specific Aims of this project are to 1) further investigate changes in EC XO/XD in relation to O2 tension using a cDNA probe that we recently developed for the enzyme; 2) assess the potential for EC to produce reactive O2 species in response to changes in O2 tension; 3) examine possible cellular regulatory mechanisms of EC XO/XD in terms of transduction mechanisms, ion transport and second messengers; 4) examine the effects of selected cytokines and some known mediators of lung injury on XO/XD activity and mRNA expression; and 5) extend our cell culture work to in vivo studies by exposing rats to hypoxia and measuring XO/XD activity and mRNA expression of lung tissue. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SELECTIVE PRENATAL DOPAMINE DAMAGE IN NON HUMAN PRIMATES Principal Investigator & Institution: Elsworth, John D.; Senior Research Scientist; Psychiatry; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 01-AUG-2001; Project End 31-JUL-2004 Summary: Several brains disorders with onset before adulthood are thought to involve irregularities in the development of midbrain dopamine neurons. These include some dystonias, LeschNyhan disease, schizophrenia, and developmental hypoxicischemic injury. As relatively little is known about the ontogeny of primate dopamine neurons, the goal of this proposal is to advance understanding of the early development of these neurons, and the effects and compensations that occur in response to their selective damage. Initial studies will use normal African green monkey fetuses which will span in age from the time just after differentiation of dopamine neurons to the time just before birth. The assays performed will provide data regarding possible critical times in development in which damage to dopamine systems might have longlasting deleterious effects, including periods of natural cell death (apoptosis) in dopamine neurons and synaptogenesis of dopamine neurons with postsynaptic targets. Subsequently, the neurochemically specific protoxin, M11rP, will be given to pregnant monkeys at these
28
Anoxia
times. Fetuses that are exposed to MPTP during a peak of programmed cell death may mimic situation where exaggerated or abnormal natural cell death occurs in dopamine neurons. Other fetuses will be exposed to the effects of MPTP over a substantial proportion of the gestation period, incorporating an extended period of synaptogenesis, which may mimic situations where there are fewer than normal dopamine neurons, or where there are deficits in outgrowth or synapse formation. In humans such developmental abnormalities may occur as a result of genetics, drug abuse, environmental toxins, physical trauma, anoxia or infection. Postmortem measurements in monkey fetuses will include biochemical assays of dopamine neuron number, integrity and function, and will be made just prior to birth. Subsequently we plan to examine the brains of neonates which have been exposed to MPTP in utero, when have reached 6 months of age. In the latter group, behavioral observations and a challenge with Ldopa, will also be carried out to indicate whether the infants show deficits that compromise their survival, and identify potential abnormalities for more detailed behavioral and psychological studies which would need to follow later. We are hopeful that these studies will provide insight into both the normal development of primate dopamine neurons, and their response to injury at critical times in ontogeny. Thus, the proposed work may lead ultimately to an animal model for one or more pediatric brain disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SGP-2 (CLUSTERIN) AND REPRODUCTION Principal Investigator & Institution: Griswold, Michael D.; Professor & Dean of Science; School/Molecular Biosciences; Washington State University 423 Neill Hall Pullman, Wa 99164 Timing: Fiscal Year 2002; Project Start 01-JUL-1994; Project End 30-NOV-2003 Summary: Clusterin is the major protein secreted by cultured Sertoli cells. Clusterin is heavily glycosylated protein consisting of disulfide linked heteromonomers and is expressed by many cells but primarily by those of epithelial origin. It is secreted into fluid-tissue interfaces and the basal level of secretion is greatly increased under conditions of cellular stress such as heat shock or anoxia. In addition, it accumulates in apoptotic germ cells in the testis but it is synthesized primarily by the Sertoli cells in response to the impeding death of the nearby cells. The function of clusterin is unknown but we present a hypothesis supported by data from the literature and our own work that clusterin is necessary for solubilizing insoluble macromolecular complexes and presenting them for endocytosis by the surviving cells. This function would make clusterin important for keeping fluid-tissue interfaces free from cellular debris and would have implications for stressed or damaged or aged tissue. The evidence supports the notion that the biological function of clusterin is a result of its ability to bind tightly to hydrophobic macromolecules and molecular complexes. In this proposal we present experiments to directly test our proposed function for clusterin. In the first specific aim we will thoroughly analyze the impact of a knock-out of the clusterin gene on male reproductive function under normal and toxic conditions. We will examine the basis for the binding of clusterin to a variety of target proteins. In the second specific aim we will analyze a number of structural properties of clusterin and attempt to relate structure to function. We will make deletion and site-specific mutations and analyze the binding of modified clusterin to a defined substrate. We will analyze structure by limited proteolysis, by CD spectroscopy and by fluorescence and cross-linking. Since clusterin is clearly implicated as a marker for cellular damage and pathology, the elucidation of its function is very important.
Studies
29
Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SODIUM IONS AND CALCIUM SIGNALING IN CELL AND NEURONS Principal Investigator & Institution: Blaustein, Mordecai P.; Professor and Chair; Physiology; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2002; Project Start 01-AUG-1979; Project End 28-FEB-2005 Summary: (Applicant's Abstract) The goal of this program is to elucidate some critical aspects of Ca2+ signaling in astrocytes. The Na/Ca exchanger and high ouabain affinity isoforms (alpha2/alpha3) of the Na+ pump catalytic (alpha) subunit colocalize to plasma membrane (PM) microdomains that overlie "junctional" endoplasmic reticulum (jER) in astrocytes and neurons. This has fostered the hypothesis that the alpha2/alpha3 Na+ pumps help modulate Ca2+ signaling by regulating jER Ca2+ stores. To examine these ideas and test the hypothesis, the following specific aims are proposed: 1. To determine the functional organization of astrocyte ER Ca2+ stores: How are the inositol trisphosphate and ryanodine receptors (IP3R and RYR) and the ER Ca2+ pumps distributed in the ER? And, how does this distribution influence local and "global" cell Ca2+ signaling? High resolution Ca2+ imaging will be used to elucidate the sites of origin and mechanism(s) of propagation of agonist-evoked Ca2+ signals. PCR and immunoblotting will be used to identify the specific Ca2+ pumps, and IP3R and RYR isoforms expressed in primary cultured rat brain astrocytes. High spatial resolution immunocytochemistry will then be used to determine the specific locations of these pumps and receptors in the ER of cells in which Ca2+ signaling has been studied, to elucidate the relationship between transporter location and the sites of signal initiation and pathways of signal propagation. 2. To confirm that the different Na+ pump alpha subunits are differently distributed in astrocytes, and to determine how the isoforms are correctly sorted. Adenovirus transfection, a transgenic mouse model, and immunocytochemical methods, will be used to determine the specific distributions of these Na+ pump isoforms. Domain swapping with adenovirus transfection methods will be used to identify the region(s) of the Na+ pump alpha subunit isoforms that are responsible for targeting these isoforms to their specific locations on the PM. 3. To test the hypothesis that the high ouabain affinity Na+ pump isoforms and the Na/Ca exchanger, which colocalize to PM microdomains adjacent to the jER, play key roles in Ca2+ signaling. Digital imaging will be used to determine the effects of low-dose ouabain (which blocks only the alpha2/alpha3 Na+ pump isoforms) on the cytosolic Na+ concentration ([Na+]CYT; measured with SBFI) and on Ca2+ signaling (measured with Fura-2 and Furaptra). Astrocytes from normal animals, and from transgenic mice with null mutations for the Na+ pump alpha1 and alpha2 genes will be studied. The results will provide new insight into a fundamental mechanism of Ca2+ signal modulation that may also, during ischemia/anoxia, contribute to Ca2+ overload, excitotoxic injury and cell death. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: SONOTHROMBOLYSIS OF VASCULAR CLOTS WITH TARGETED BUBBLES Principal Investigator & Institution: Matsunaga, Terry O.; Senior Director of New Product Developme; Imarx Therapeutics, Inc. 1635 E 18Th St Tucson, Az 85719 Timing: Fiscal Year 2002; Project Start 15-AUG-2002; Project End 14-AUG-2004
30
Anoxia
Summary: (provided by applicant): Heart attacks and strokes account for 3.4 million deaths annually in the United States. Moreover, the morbidity from vascular disease accounts for billions of healthcare dollars as well. The basis for these vascular diseases generally involves the formation of occlusive clots in the vasculature, leading to loss of blood supply, anoxia and tissue death. Current treatments involve the use of procedures that 1) promote fibrinolysis (tissue plasminogen activator), 2) prevent blood coagulation (heparin), 3) retard platelet-induced clotting (aspirin, ticlopidine) or 4) require surgical intervention (angioplasty, bypass, transendarterectomy). These therapies are either invasive or involve significant adverse effects. We recently have developed a targeted microbubble that binds to intravascular clots with high avidity. Preliminary work suggests that these microbubbles in conjunction with ultrasound can aid in the dissolution of vascular clots, It is the objective of this proposal to determine the feasibility and practicality of using targeted microbubbles along with ultrasound as a potential therapeutic modality in the treatment of vascular occlusion. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: STRUCTURE AND FUNCTION OF PARALLEL CHANNELS IN THE FOVEA Principal Investigator & Institution: Sterling, Peter; Professor; Neuroscience; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2004; Project Start 01-APR-1989; Project End 31-MAR-2009 Summary: (provided by applicant): Our broad goal is to investigate key 'design' principles by which the primate retina transfers large amounts of information to the brain. Its 106 axons are strikingly heterogeneous. They comprise 15 channels, spanning a 50-fold range in axon diameter and a 10-fold range in spike rate. Noting that foveal circuits are strongly constrained for space and energy, we hypothesize that multiple channels exist in order to relay information at least cost in "wire volume' and metabolic energy. Preliminary studies suggest that channels transmitting at low information rates (few bits/second) are more efficient (more bits/spike) and physically smaller, thus using less space and probably less energy per bit. Thus central nuclei, which acquire information at different rates (e.g. geniculate M vs. K layers), can receive their messages at least cost. To test this, AIM 1 will measure for several ganglion cell types: (a) 'natural information rate' (bits/spike and bits/s in response to natural images); (b) total wire volume (soma + dendrites + axon + terminal arbor)(cell density); (c) relative energy costs, i.e., mitochondrial content. We predict that natural information rates differ strongly across channels and that 'low-rate' channels use less space and energy per bit. Noting that OFF channels are spatially finer and denser than ON channels and that 'blue/yellow' channels also occur on two spatial scales, we hypothesize that receptive field sizes and sampling rates are tuned to the distribution of information in natural scenes. To test this, AIM 2 will measure achromatic and chromatic information in natural images on scales corresponding to known receptive fields. We predict that in nature dark regions occupy higher spatial frequencies and contain more information per retinal area than bright regions and thus require finer channels with more synapses; there are analogous predictions for the blue/yellow channels. Noting that information transfer through the retina relies on 'ribbon' synapses, we hypothesize that they release and retrieve vesicles at very high rates. To test this, AIM 3 will measure release rates at the cone synapse (2-photon + electron microscopy of FM1-43 dye), and AIM 4 will measure the rates at the bipolar synapse (electrophysiology + EM of ferritin). Glaucoma, a major cause of blindness, has been attributed to both ganglion cell anoxia and reduced axonal transport. Our studies will relate ganglion cell signaling to both oxidative
Studies
31
capacity and axonal transport capacity, and thus should extend the basic foundation for future clinical studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE C-JUN PROTO-ONCOGENE AND TUMOR HYPOXIA Principal Investigator & Institution: Laderoute, Keith R.; Director, Cancer Biology Program; Sri International 333 Ravenswood Ave Menlo Park, Ca 940253493 Timing: Fiscal Year 2002; Project Start 15-JUL-1998; Project End 28-FEB-2006 Summary: Both basic and clinical studies demonstrate that low oxygen conditions in solid tumors (hypoxia/anoxia) are an important determinant of malignant progression. It is becoming clear that a network of transcription factors mediates the ability of normal and transformed cells to adapt to changes in tumor oxygenation. The studies described in this application are focused on understanding the role and biological importance of the master transcription factor c-Jun/AP-1 in this network. Our earlier research demonstrated that exposure of transformed cells to hypoxia/anoxia induces expression of the c-jun proto-oncogene and activates protein kinase and phosphatase activity that regulate the phosphorylation state of c-Jun/AP-1. Here we present the fundamental finding that the induction of c-jun expression and c-Jun phosphorylation by hypoxia has two components: a late component that is completely dependent on the transcription factor HIF-1, and an early component that is independent of HIF-1. HIF-1 is a ubiquitous mediator of hypoxia- responsive gene expression in mammalian cells. Based on this critical finding, we hypothesize that c-Jun/AP-1 and HIF-1 cooperate to regulate gene expression in hypoxic or anoxic tumor microenvironments. Moreover, because of the resemblance of the early component of hypoxia-inducible c-jun expression to the classic induction of immediate-early genes by serum growth factors, we hypothesize that the response of c-jun and c-Jun/AP-1 to physiological hypoxia overlaps with the general immediate- early response. To investigate these hypotheses, we propose two Specific Aims. In Aim 1, we will identify hypoxia-responsive phosphorylation sites in c-Jun and determine the role of c-Jun phosphorylation in promoting the growth of tumor xenografts. These studies will determine the relationship between hypoxia- responsive c-Jun phosphorylation and proliferation in the tumor microenvironment. In Aim 2, we will investigate specific serum- responsive pathways responsible for the immediateearly induction of c-jun expression by hypoxia. These studies will relate the serumdependent immediate-early response to cellular oxygen sensing mechanisms. They will also identify new mammalian transcriptional regulators responsive to a wide range of low oxygen conditions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
•
Project Title: WHITE MATTER EXCITOTOXICITY Principal Investigator & Institution: Stys, Peter K.; Ottawa Health Research Institute 725 Parkdale Ave Ottawa, On Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2003 Summary: (Verbatim from the Applicant's Abstract) Axonal connections within the white matter of the central nervous system play the crucial role of transmitting electrical signals. Common and devastating diseases such as stroke, spinal cord injury and multiple sclerosis almost always cause damage to white matter structures, yet far less is known about the pathophysiology of white matter injury. Despite the lack of synaptic machinery in this tissue, early reports indicate that glutamate-dependent excitotoxic mechanisms play an important role in mediating white matter injury. This application
32
Anoxia
aims to examine in greater detail how endogenous excitotoxins damage myelinated axons. Using the in vitro rat optic nerve and spinal dorsal columns as well studied models of isolated white matter, electrophysiology and immunchistochemistry for injury markers in myelin, axoplasm and glial cytoplasm will be used to examine the effects of exogenously applied excitotoxins such as glutamate, kainite, and ANIPA. Selective inhibitors will be applied to dissect out which subclass of ionotropic glutamate receptor(s) are responsible for injury. Abnormal fluxes of Na and Ca ions will be examined using ion-sensitive dyes and confocal microscopy to see which compartments (myelin, axon cylinder, glia) suffer excess accumulations as a result of glutamate receptor activation. Total (free + bound) elemental analysis of Na and Ca will be performed with electron probe x-ray microanalysis as the ionized fraction may underestimate the total amount of Na or Ca entry and may be a more reliable determinant of subsequent functional injury. The role of endogenous glutamate, released non-synaptically by in vitro anoxia or ischemia, will be studied using a simlar approach, with the goal of determining which sub cellular compartments suffer ionic overload and structural injury that is dependent on activation of glutamate receptors. Immunchistochemistry and high-resolution confocal microscopy, coupled with digital image processing techniques for resolution enhancement and 3-dimensional reconstruction, will be applied to examine the distribution of glutamate receptors in white matter using specific antisera. By elucidating glutamate-dependent injury mechanisms in CNS white matter, it is hoped that an important new avenue wil1 become available for pharmacological protection of this key tissue. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “anoxia” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for anoxia in the PubMed Central database: •
Differential Regulation of Sugar-Sensitive Sucrose Synthases by Hypoxia and Anoxia Indicate Complementary Transcriptional and Posttranscriptional Responses. by Zeng Y, Wu Y, Avigne WT, Koch KE.; 1998 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=35066
•
Influence of anoxia on radiation-induced breaks in the Escherichia coli chromosome. by Achey PM, Whitfield VG.; 1968 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=252150
3 4
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
Studies
33
•
N-Acylphosphatidylethanolamine Accumulation in Potato Cells upon Energy Shortage Caused by Anoxia or Respiratory Inhibitors. by Rawyler AJ, Braendle RA.; 2001 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=117980
•
Patterns of Protein Synthesis and Tolerance of Anoxia in Root Tips of Maize Seedlings Acclimated to a Low-Oxygen Environment, and Identification of Proteins by Mass Spectrometry. by Chang WW, Huang L, Shen M, Webster C, Burlingame AL, Roberts JK.; 2000 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=58868
•
Re-Aeration following Hypoxia or Anoxia Leads to Activation of the Antioxidative Defense System in Roots of Wheat Seedlings. by Biemelt S, Keetman U, Albrecht G.; 1998 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=35123
•
The Effects of Anoxia on the Morphology and Composite Metabolism of the Intact Aortic Intima-Media Preparation. by Morrison AD, Orci L, Berwick L, Perrelet A, Winegrad AI.; 1977 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=372314
•
The Pyruvate decarboxylase1 Gene of Arabidopsis Is Required during Anoxia But Not Other Environmental Stresses. by Kursteiner O, Dupuis I, Kuhlemeier C.; 2003 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=167035
•
The Role of Sugars, Hexokinase, and Sucrose Synthase in the Determination of Hypoxically Induced Tolerance to Anoxia in Tomato Roots. by Germain V, Ricard B, Raymond P, Saglio PH.; 1997 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=158291
•
Transgenic AEQUORIN reveals organ-specific cytosolic Ca2+ responses to anoxia and Arabidopsis thaliana seedlings. by Sedbrook JC, Kronebusch PJ, Borisy GG, Trewavas AJ, Masson PH.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=157832
•
Vacuolar H(+)-translocating pyrophosphatase is induced by anoxia or chilling in seedlings of rice. by Carystinos GD, MacDonald HR, Monroy AF, Dhindsa RS, Poole RJ.; 1995 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=157384
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 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.
34
Anoxia
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 anoxia, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “anoxia” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for anoxia (hyperlinks lead to article summaries): •
A new device for continuous monitoring of cerebral activity: its use following cerebral anoxia. Author(s): Prior PF, Maynard D, Scott DF. Source: Electroencephalography and Clinical Neurophysiology. 1970 April; 28(4): 423-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4191216
•
A note on the mechanism of resistance to anoxia and ischaemia in pathophysiological mammalian myelinated nerve. Author(s): Ritchie JM. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1985 March; 48(3): 274-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2984336
•
A pathological model for cerebral changes incident to paranatal anoxia. Report of a case of cerebral atrophy secondary to cardiorespiratory failure in infancy. Author(s): Courville CB. Source: Am J Dis Child. 1967 May; 113(5): 603-10. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6067241
•
Action myoclonus after cerebral anoxia. Author(s): Rizvi AH, Karetzky MS. Source: N J Med. 1993 December; 90(12): 918-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8309643
•
Action myoclonus following acute cerebral anoxia. Author(s): DeLisa JA, Stolov WC, Troupin AS. Source: Archives of Physical Medicine and Rehabilitation. 1979 January; 60(1): 32-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=420569
•
Acute cerebral anoxia in childhood followed by delayed EEG-reaction in spite of clinical improvement. Author(s): Lagergren J, Stensman R. Source: Neuropadiatrie. 1970 December; 2(2): 226-34. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5538065
Studies
35
•
Acute myocardial anoxia. Anatomical changes and their possible relation to immunological processes. Author(s): Laufer A. Source: Cardiology. 1971; 56(1): 65-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5152761
•
Adaptations to neonatal anoxia and control of ventilation. Author(s): Waddell AE, Fisher JT. Source: Pediatric Pulmonology. 1999 November; 28(5): 309-12. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10536060
•
Age-related changes in brain metabolism and vulnerability to anoxia. Author(s): Roberts EL Jr, Chih CP, Rosenthal M. Source: Advances in Experimental Medicine and Biology. 1997; 411: 83-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9269414
•
'alpha pattern coma' following cerebral anoxia. Author(s): Alving J, Moller M, Sindrup E, Nielsen BL. Source: Electroencephalography and Clinical Neurophysiology. 1979 July; 47(1): 95-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=88365
•
An anoxia inducible endonuclease and enhanced DNA breakage as contributors to genomic instability in cancer. Author(s): Russo CA, Weber TK, Volpe CM, Stoler DL, Petrelli NJ, Rodriguez-Bigas M, Burhans WC, Anderson GR. Source: Cancer Research. 1995 March 1; 55(5): 1122-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7866998
•
Anoxia and reoxygenation of human endothelial cells decrease ceramide glucosyltransferase expression and activates caspases. Author(s): Zhao H, Miller M, Pfeiffer K, Buras JA, Stahl GL. Source: The Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology. 2003 April; 17(6): 723-4. Epub 2003 February 05. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12586734
•
Anoxia at birth induced hyperresponsiveness to amphetamine and stress in postpubertal rats. Author(s): Juarez I, Silva-Gomez AB, Peralta F, Flores G. Source: Brain Research. 2003 December 5; 992(2): 281-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14625067
36
Anoxia
•
Anoxia induces human immunodeficiency virus expression in infected T cell lines. Author(s): Polonis VR, Anderson GR, Vahey MT, Morrow PJ, Stoler D, Redfield RR. Source: The Journal of Biological Chemistry. 1991 June 25; 266(18): 11421-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1904863
•
Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1. Author(s): Albertoni M, Shaw PH, Nozaki M, Godard S, Tenan M, Hamou MF, Fairlie DW, Breit SN, Paralkar VM, de Tribolet N, Van Meir EG, Hegi ME. Source: Oncogene. 2002 June 20; 21(27): 4212-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12082608
•
Anoxia pretreatment protects soybean cells against H(2)O(2)-induced cell death: possible involvement of peroxidases and of alternative oxidase. Author(s): Amora Y, Chevionb M, Levinea A. Source: Febs Letters. 2000 July 21; 477(3): 175-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10908716
•
Anoxia tolerant animals from a neurobiological perspective. Author(s): Lutz PL, Nilsson GE, Perez-Pinzon MA. Source: Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology. 1996 January; 113(1): 3-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8936038
•
Anoxia, wound healing, VL30 elements, and the molecular basis of malignant conversion. Author(s): Anderson GR, Stoler DL. Source: Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology. 1993 April; 15(4): 265-72. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8390832
•
Anoxia/induced membrane changes in human red blood cells. Author(s): Nicak A, Mojzis J, Jandosekova M, Mirossay L. Source: Physiological Research / Academia Scientiarum Bohemoslovaca. 1999; 48(3): 215-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10523058
•
Anoxia/reoxygenation-induced leukocyte-endothelial cell interactions. Author(s): Kokura S, Yoshida N, Yoshikawa T. Source: Free Radical Biology & Medicine. 2002 August 15; 33(4): 427-32. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12160924
Studies
37
•
Anoxia/reoxygenation-induced neutrophil adherence to cultured endothelial cells. Author(s): Yoshida N, Granger DN, Anderson DC, Rothlein R, Lane C, Kvietys PR. Source: The American Journal of Physiology. 1992 June; 262(6 Pt 2): H1891-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1352432
•
Anoxia/reoxygenation-induced tolerance with respect to polymorphonuclear leukocyte adhesion to cultured endothelial cells. A nuclear factor-kappaB-mediated phenomenon. Author(s): Cepinskas G, Lush CW, Kvietys PR. Source: Circulation Research. 1999 January 8-22; 84(1): 103-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9915779
•
Anoxia? Don't get excited! Author(s): Neubauer JA. Source: The Journal of Clinical Investigation. 1993 February; 91(2): 377. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8432844
•
Anoxia-hyperoxia induces monocyte-derived interleukin-8. Author(s): Metinko AP, Kunkel SL, Standiford TJ, Strieter RM. Source: The Journal of Clinical Investigation. 1992 September; 90(3): 791-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1522234
•
Anoxia-induced apoptosis occurs through a mitochondria-dependent pathway in lung epithelial cells. Author(s): Santore MT, McClintock DS, Lee VY, Budinger GR, Chandel NS. Source: American Journal of Physiology. Lung Cellular and Molecular Physiology. 2002 April; 282(4): L727-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11880298
•
Anoxia-induced changes in purine nucleoside metabolism of in vitro aged human fibroblasts. Author(s): Reisert PS, Dobson JG Jr, Fenton RA. Source: Life Sciences. 2002 February 8; 70(12): 1369-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11883713
•
Anoxia-induced up-regulation of interleukin-8 in human malignant melanoma. A potential mechanism for high tumor aggressiveness. Author(s): Kunz M, Hartmann A, Flory E, Toksoy A, Koczan D, Thiesen HJ, Mukaida N, Neumann M, Rapp UR, Brocker EB, Gillitzer R. Source: American Journal of Pathology. 1999 September; 155(3): 753-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10487833
38
Anoxia
•
Antenatal and perinatal anoxia as the probable cause of damage to the brain during birth. Author(s): Beamer PR, Courville CB. Source: Chic Med Sch Q. 1972; 31(1-4): 77-80. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4620950
•
Aphemia associated with bilateral striato-capsular lesions subsequent to cerebral anoxia. Author(s): Murdoch BE, Chenery HJ, Kennedy M. Source: Brain Injury : [bi]. 1989 January-March; 3(1): 41-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2924038
•
Astrocytic basic fibroblast growth factor expression in dopaminergic regions after perinatal anoxia. Author(s): Flores C, Stewart J, Salmaso N, Zhang Y, Boksa P. Source: Biological Psychiatry. 2002 August 15; 52(4): 362-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12208644
•
Attenuation of anoxia-induced retrograde amnesia in rats by a pretraining placebo injection. Author(s): David-Remacle M. Source: Physiology & Behavior. 1973 April; 10(4): 693-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4738984
•
Biochemistry of cerebral anoxia, hypoxia and ischemia. Author(s): Cohen MM. Source: Monogr Neural Sci. 1973; 1: 1-49. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4589448
•
Blood fibrinolytic activity in neonates: effect of period of gestation, birth weight, anoxia and sepsis. Author(s): Kolindewala JK, Das BK, Dube RK, Dube B, Bhargava V. Source: Indian Pediatrics. 1987 November; 24(11): 1029-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3450641
•
Brain antioxidant regulation in mammals and anoxia-tolerant reptiles: balanced for neuroprotection and neuromodulation. Author(s): Rice ME, Forman RE, Chen BT, Avshalumov MV, Cragg SJ, Drew KL. Source: Comparative Biochemistry and Physiology. Toxicology & Pharmacology : Cbp. 2002 December; 133(4): 515-25. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12458180
Studies
39
•
Brain injury by ischemic anoxia: hypothesis extension--a tale of two ions? Author(s): White BC, Aust SD, Arfors KE, Aronson LD. Source: Annals of Emergency Medicine. 1984 September; 13(9 Pt 2): 862-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6476556
•
Brain interstitial volume fraction and tortuosity in anoxia. Evaluation of the ionselective micro-electrode method. Author(s): Lundbaek JA, Hansen AJ. Source: Acta Physiologica Scandinavica. 1992 December; 146(4): 473-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1492565
•
Brain ischemic anoxia. Mechanisms of injury. Author(s): White BC, Wiegenstein JG, Winegar CD. Source: Jama : the Journal of the American Medical Association. 1984 March 23-30; 251(12): 1586-90. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6366268
•
Calculation of concentration profiles of excess acid in human brain tissue during conditions of partial anoxia. Author(s): Reneau DD, Lafitte LL. Source: Advances in Experimental Medicine and Biology. 1973; 37: 849-57. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4766508
•
Cardio-respiratory arrest associated with cerebral anoxia and vigilant akinetic mutism. Dynamic clinical and polygraphic study of a case with electroclinical recovery. Author(s): Pascu I, Popa IP, Corfariu O, Popoviciu L, Sipos C. Source: Neurol Psychiatr (Bucur). 1975; 13(2): 87-94. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1188271
•
Cerebral anoxia: cause of long "sit-in". Author(s): Scott RM. Source: The New England Journal of Medicine. 1969 October 2; 281(14): 797. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5807931
•
Cerebral, renal and splenic lesions due to fetal anoxia and their relationship to malformations. Author(s): Gosseye S, Golaire MC, Larroche JC. Source: Developmental Medicine and Child Neurology. 1982 August; 24(4): 510-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7117710
40
Anoxia
•
Cerebrospinal-fluid acid base and electrolyte changes resulting from cerebral anoxia in man. Author(s): Kalin EM, Tweed WA, Lee J, MacKeen WL. Source: The New England Journal of Medicine. 1975 November 13; 293(20): 1013-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=241018
•
Chemical anoxia delays germ cell apoptosis in the human testis. Author(s): Erkkila K, Suomalainen L, Wikstrom M, Parvinen M, Dunkel L. Source: Biology of Reproduction. 2003 August; 69(2): 617-26. Epub 2003 April 16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12700196
•
Cochlear microphonics and SDH activity in the hair cells under anoxia. Author(s): Ayani N, Yamashita T, Iwai H. Source: Arch Otorhinolaryngol. 1976 July 20; 212(3): 179-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=989731
•
Cortisol metabolism in human placenta and decidua is resistant to anoxia. Author(s): Lopez Bernal A, Turnbull AC. Source: Hormone and Metabolic Research. Hormon- Und Stoffwechselforschung. Hormones Et Metabolisme. 1985 March; 17(3): 167. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3997063
•
Death from anoxia in an abandoned cesspool. Author(s): Berlin CM. Source: Annals of Internal Medicine. 1981 September; 95(3): 387. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7271103
•
Determination of the mechanism of free radical generation in human aortic endothelial cells exposed to anoxia and reoxygenation. Author(s): Zweier JL, Broderick R, Kuppusamy P, Thompson-Gorman S, Lutty GA. Source: The Journal of Biological Chemistry. 1994 September 30; 269(39): 24156-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7929072
•
Development of GABA and calcium binding proteins immunoreactivity in the rat hippocampus following neonatal anoxia. Author(s): Dell'Anna E, Geloso MC, Magarelli M, Molinari M. Source: Neuroscience Letters. 1996 June 21; 211(2): 93-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8830852
Studies
41
•
Differential presynaptic modulation of noradrenaline release in human atrial tissue in normoxia and anoxia. Author(s): Munch G, Kurz T, Urlbauer T, Seyfarth M, Richardt G. Source: British Journal of Pharmacology. 1996 August; 118(7): 1855-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8842454
•
Diffusion anoxia at birth. Author(s): Reid DH. Source: Lancet. 1968 October 5; 2(7571): 757-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4175554
•
Diffusion anoxia: a critical reappraisal. Author(s): Frumin MJ, Edelist G. Source: Anesthesiology. 1969 September; 31(3): 243-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5801265
•
Diffusion-weighted MR imaging of global cerebral anoxia. Author(s): Arbelaez A, Castillo M, Mukherji SK. Source: Ajnr. American Journal of Neuroradiology. 1999 June-July; 20(6): 999-1007. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10445435
•
DNA damage in human endothelial cells after irradiation in anoxia. Author(s): Rosander K, Zackrisson B. Source: Acta Oncologica (Stockholm, Sweden). 1995; 34(1): 111-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7865225
•
Does laminated intraluminal thrombus within abdominal aortic aneurysm cause anoxia of the aortic wall? Author(s): Vorp DA, Federspiel WJ, Webster MW. Source: Journal of Vascular Surgery : Official Publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter. 1996 March; 23(3): 540-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8601904
•
Dynamics of brain resuscitation after ischemic anoxia. Author(s): Safar P. Source: Hosp Pract (Hosp Ed). 1981 February; 16(2): 67-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7193178
42
Anoxia
•
Early and late CT manifestations in the persistent vegetative state due to cerebral anoxia-ischemia. Author(s): Chu NS. Source: J Formos Med Assoc. 1993 August; 92(8): 697-701. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7904843
•
Early effects of nimodipine on intracranial and cerebral perfusion pressures in cerebral anoxia after out-of-hospital cardiac arrest. Author(s): Gueugniaud PY, Gaussorgues P, Garcia-Darennes F, Bancalari G, Roux H, Robert D, Petit P. Source: Resuscitation. 1990 December; 20(3): 203-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1965344
•
EEG and "brain death" following anoxia and ischemia. Author(s): Muller HR. Source: Electroencephalography and Clinical Neurophysiology. 1970 August; 29(2): 209. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4194614
•
EEG and rheoencephalographic investigations in a variety of vegetative conditions with respiratory anoxia. Author(s): Lorenzoni E, Geyer N, Lechner H. Source: Electroencephalography and Clinical Neurophysiology. 1967 August; 23(2): 185. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4166714
•
EEG features of the apallic syndrome resulting from cerebral anoxia. Author(s): Matsuo F. Source: Electroencephalography and Clinical Neurophysiology. 1985 August; 61(2): 11322. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2410220
•
EEG in acute vasomotor anoxia (syncope). Author(s): Espinosa LJ. Source: Electroencephalography and Clinical Neurophysiology. 1970 July; 29(1): 99. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4194080
•
Effect of anoxia on expression of endothelial leukocyte adhesion molecule 1 in cultured human endothelial cells. Author(s): Doughman T, Butterworth P, Mistry N, Horsburgh T, Nicholson M. Source: Transplantation Proceedings. 1999 February-March; 31(1-2): 990-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10083440
Studies
43
•
Effect of anoxia on ion distribution in the brain. Author(s): Hansen AJ. Source: Physiological Reviews. 1985 January; 65(1): 101-48. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3880896
•
Effect of anoxia on mitotic cycle of HeLa cells. Author(s): Tu LS. Source: Sov J Dev Biol. 1974 September; 4(5): 486-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4428227
•
Effect of cold anoxia and cryopreservation on metabolic and contractile functions of human mammary artery. Author(s): Nataf P, Hadjiisky P, Lechat P, Mougenot N, Peuchmaurd M, Gouezo R, Gerota J, Cabrol C, Gandjbakhch I. Source: Cryobiology. 1995 August; 32(4): 327-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7656567
•
Effect of glutathione on endothelial prostacyclin synthesis after anoxia. Author(s): Hempel SL, Wessels DA, Spector AA. Source: The American Journal of Physiology. 1993 June; 264(6 Pt 1): C1448-57. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8333500
•
Effect of initial myocardial anoxia on coronary flow during aortic valve replacement. Author(s): Larmi TK, Saarela E, Tuononen S, Pokela R, Karkola P, Nuutinen L, Kairaluoma MI. Source: Scand J Thorac Cardiovasc Surg. 1978; 12(3): 229-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=725563
•
Effect of NADPH oxidase inhibition on E-selectin expression induced by concomitant anoxia/reoxygenation and TNF-alpha. Author(s): Paysant JR, Rupin A, Verbeuren TJ. Source: Endothelium : Journal of Endothelial Cell Research. 2002; 9(4): 263-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12572857
•
Effects of anoxia on cerebral metabolism and electrolytes in man. Author(s): Meyer JS, Gotoh F, Ebihara S, Tomita M. Source: Neurology. 1965 October; 15(10): 892-901. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5890882
44
Anoxia
•
Effects of anoxia on megakaryocyte progenitors derived from cord blood CD34pos cells. Author(s): Saxonhouse MA, Rimsza LM, Christensen RD, Hutson AD, Stegner J, Koenig JM, Sola MC. Source: European Journal of Haematology. 2003 November; 71(5): 359-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14667199
•
Effects of early postnatal anoxia on adult learning and emotion in rats. Author(s): Buwalda B, Nyakas C, Vosselman HJ, Luiten PG. Source: Behavioural Brain Research. 1995 February; 67(1): 85-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7748505
•
Effects of glucose metabolism on the transmembrane action potential and contraction of human papillary muscle during surgical anoxia. Author(s): Prasad K, Callaghan JC. Source: The Annals of Thoracic Surgery. 1969 June; 7(6): 571-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5787209
•
Effects of hypothermic and pharmacological protection on myocardial metabolism in temporary heart anoxia. Author(s): Dementeva II, Babalyan GV, Solovova LE. Source: Cor Vasa. 1982; 24(1): 16-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6802570
•
Effects of paranatal anoxia on the corpus striatum. Significance of residual extrapyramidal symptoms in cerebral palsy. Author(s): Courville CB, Spears R. Source: Bull Los Angeles Neurol Soc. 1967 April; 32(2): 113-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6033816
•
Endogenous opioid-like substances in perinatal asphyxia and cerebral injury due to anoxia. Author(s): Cao L, Qian PD, Jing LJ, Liang QJ, Zhao ZZ. Source: Chinese Medical Journal. 1993 October; 106(10): 783-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7913434
•
Endothelial cells exposed to anoxia/reoxygenation are hyperadhesive to Tlymphocytes: kinetics and molecular mechanisms. Author(s): Kokura S, Wolf RE, Yoshikawa T, Ichikawa H, Granger DN, Aw TY. Source: Microcirculation (New York, N.Y. : 1994). 2000 February; 7(1): 13-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10708334
Studies
45
•
Enzyme release during myocardial anoxia: a study of metabolic protection. Author(s): Hearse DJ, Humphrey SM. Source: Journal of Molecular and Cellular Cardiology. 1975 July; 7(7): 463-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1152074
•
Epileptic seizures during and after acute cerebral anoxia. Author(s): Madison D, Niedermeyer E. Source: Electroencephalography and Clinical Neurophysiology. 1970 April; 28(4): 420. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4191205
•
Epileptic seizures resulting from acute cerebral anoxia. Author(s): Madison D, Niedermeyer E. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1970 June; 33(3): 381-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5431726
•
Experimental studies on continuous or intermittent selective brain cooling by means of carotico-carotid shunt in dogs, especially on the application of polarographic measurement in the prevention of cerebral anoxia. Author(s): Aoyagi M. Source: Nippon Geka Hokan. 1967 November 1; 36(6): 691-736. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4296529
•
Flattening of the EEG and periodic discharges during acute illnesses in the child involving the brain. Discussion of the role of cerebral anoxia. Author(s): Soulas B, Sternberg B. Source: Electroencephalography and Clinical Neurophysiology. 1967 October; 23(4): 382. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4167781
•
Free radical generation in human endothelial cells exposed to anoxia and reoxygenation. Author(s): Zweier JL. Source: Transplantation Proceedings. 1998 December; 30(8): 4228-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9865351
•
Galanin protects hippocampal neurons from the functional effects of anoxia. Author(s): Ari YB, Lazdunski M. Source: European Journal of Pharmacology. 1989 June 20; 165(2-3): 331-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2476325
46
Anoxia
•
Global cerebral anoxia. Author(s): Chan JW, Bell KE. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 2002 February; 29(1): 88-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11858543
•
Glutamate receptor requirement for neuronal death from anoxia-reoxygenation: an in Vitro model for assessment of the neuroprotective effects of estrogens. Author(s): Zaulyanov LL, Green PS, Simpkins JW. Source: Cellular and Molecular Neurobiology. 1999 December; 19(6): 705-18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10456232
•
Granulocyte function in patients with brain damage and anoxia. Author(s): Dodsworth H, Harris R. Source: Acta Haematologica. 1971; 45(6): 350-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5000684
•
Hemorrhagic infarction: A reperfusion injury following prolonged myocardial ischemic anoxia. Author(s): Cerra FB, Lajos TZ, Montes M, Siegel JH. Source: Surgery. 1975 July; 78(1): 95-104. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1138403
•
Hemostatic change in neonates with anoxia and sepsis. Author(s): Kulkarni KB. Source: Indian Pediatrics. 1990 April; 27(4): 405-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2210833
•
Hemostatic changes in neonates with anoxia and sepsis. Author(s): Dube B, Das BK, Kolindewala JK, Dube RK, Bhargava V. Source: Indian Pediatrics. 1989 January; 26(1): 26-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2759692
•
High levels of ascorbic acid, not glutathione, in the CNS of anoxia-tolerant reptiles contrasted with levels in anoxia-intolerant species. Author(s): Rice ME, Lee EJ, Choy Y. Source: Journal of Neurochemistry. 1995 April; 64(4): 1790-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7891107
Studies
47
•
Hippocampal potassium ATP channels and anoxia: presynaptic, postsynaptic or both? Author(s): Ben-Ari Y. Source: Trends in Neurosciences. 1990 October; 13(10): 409-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1700513
•
Histochemical evaluation of myocardial preservation by local cooling during anoxia. Author(s): Viskos DJ, Karatzas NB. Source: American Heart Journal. 1976 November; 92(5): 669-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=185896
•
Histological diagnosis of myocardial injury. Comparison of hematoxylin-basic fuchsin-picric acid (HBFP)-stained sections obtained during autopsy with isolated viable rat cardiac myocytes exposed to anoxia. Author(s): Rajs J. Source: Acta Pathol Microbiol Scand [a]. 1979 July; 87A(4): 289-97. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=89781
•
Hormonal regulation of dipeptide transporter (PepT1) in Caco-2 cells with normal and anoxia/reoxygenation management. Author(s): Sun BW, Zhao XC, Wang GJ, Li N, Li JS. Source: World Journal of Gastroenterology : Wjg. 2003 April; 9(4): 808-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12679938
•
Human hepatocytes are more resistant than rat hepatocytes to anoxia-reoxygenation injury. Author(s): Caraceni P, Gasbarrini A, Nussler A, Di Silvio M, Bartoli F, Borle AB, Van Thiel DH. Source: Hepatology (Baltimore, Md.). 1994 November; 20(5): 1247-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7927259
•
Human hepatocytes differ from rat hepatocytes in their sensitivity to anoxiareoxygenation injury. Author(s): Caraceni P, Gasbarrini A, Ryu HS, Nussler A, Bartoli F, Fagiuoli S, Borle AB, Van Thiel DH. Source: Transplantation Proceedings. 1994 December; 26(6): 3307-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7998147
•
Human neocortical excitability is decreased during anoxia via sodium channel modulation. Author(s): Cummins TR, Jiang C, Haddad GG. Source: The Journal of Clinical Investigation. 1993 February; 91(2): 608-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8381823
48
Anoxia
•
Hyperactivity in rats following postnatal anoxia. Author(s): Speiser Z, Korczyn AD, Teplitzky I, Gitter S. Source: Behavioural Brain Research. 1983 March; 7(3): 379-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6682332
•
Hypoxia, anoxia, and O2 sensing: the search continues. Author(s): Schumacker PT. Source: American Journal of Physiology. Lung Cellular and Molecular Physiology. 2002 November; 283(5): L918-21. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12376344
•
Impairment of platelet function in birth anoxia. Author(s): Bhargava M, Bhargava SK, Kumari S. Source: The Indian Journal of Medical Research. 1978 December; 68: 976-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=750448
•
Increased safety of aorto-coronary artery bypass surgery with induced ventricular fibrillation to avoid anoxia. Author(s): Wilson HE, Dalton ML, Kiphart RJ, Allison WM. Source: The Journal of Thoracic and Cardiovascular Surgery. 1972 August; 64(2): 193202. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5048373
•
Induced hypothermia following cerebral anoxia. Author(s): Strong MJ, Keats AS. Source: Anesthesiology. 1967 September-October; 28(5): 920-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5340647
•
Intellectual consequences of perinatal anoxia. Author(s): Gottfried AW. Source: Psychological Bulletin. 1973 September; 80(3): 231-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4731732
•
Interactive effects of anoxia and general anesthesia during birth on the degree of CNS and systemic hypoxia produced in neonatal rats. Author(s): Berger N, Vaillancourt C, Boksa P. Source: Experimental Brain Research. Experimentelle Hirnforschung. Experimentation Cerebrale. 2000 April; 131(4): 524-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10803420
Studies
49
•
Intersubject variability in corneal swelling response to anoxia. Author(s): Efron N. Source: Acta Ophthalmol (Copenh). 1986 June; 64(3): 302-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3529801
•
Introductory remarks (anoxia). Author(s): von Muralt A. Source: Schweiz Z Sportmed. 1966; 14(1): 1-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5958158
•
Ion and membrane changes in the brain during anoxia. Author(s): Hansen AJ. Source: Behavioural Brain Research. 1984 November; 14(2): 93-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6151843
•
L-arginine protects human heart cells from low-volume anoxia and reoxygenation. Author(s): Shiono N, Rao V, Weisel RD, Kawasaki M, Li RK, Mickle DA, Fedak PW, Tumiati LC, Ko L, Verma S. Source: American Journal of Physiology. Heart and Circulatory Physiology. 2002 March; 282(3): H805-15. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11834473
•
Latent severe anoxia associated with the fat embolism syndrome. A case report. Author(s): Ross AP, O'Higgins J. Source: British Journal of Anaesthesia. 1968 May; 40(5): 389-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4871888
•
Life, metabolism and anoxia. 3. Metabolism--the source of energy. Author(s): Zuck D. Source: Nurs Times. 1968 December 27; 64(52): 1746-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5727277
•
Lingual tonsillar hypertrophy causing failed intubation and cerebral anoxia. Author(s): Cohle SD, Jones DH, Puri S. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 1993 June; 14(2): 158-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8328439
50
Anoxia
•
Magnesium attenuates a striatal dopamine increase induced by anoxia in the neonatal rat brain: an in vivo microdialysis study. Author(s): Nakajima W, Ishida A, Takada G. Source: Pediatric Research. 1997 June; 41(6): 809-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9167193
•
Mechanisms of cell injury in low-flow, normal-flow and no-flow anoxia. Author(s): Kessler M, Hoper J. Source: Prog Clin Biol Res. 1988; 264: 7-16. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3289036
•
Mechanisms of hypothermic protection against anoxia. Author(s): Miller JA Jr, Miller FS. Source: Advances in Experimental Medicine and Biology. 1972; 33(0): 571-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4671938
•
Methods of assessing neonatal anoxia with EEG studies. Author(s): Monod N, Pajot N. Source: Electroencephalography and Clinical Neurophysiology. 1967 October; 23(4): 383. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4167784
•
Mitochondrial dysfunction during anoxia and acute cell injury. Author(s): Jones DP. Source: Biochimica Et Biophysica Acta. 1995 May 24; 1271(1): 29-33. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7599222
•
Mitochondrial hyperoxidation after cerebral anoxia/ischemia. Epiphenomenon or precursor to residual damage? Author(s): Rosenthal M, Mumford PL, Sick TJ, Perez-Pinzon MA. Source: Advances in Experimental Medicine and Biology. 1997; 428: 189-95. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9500047
•
Modulation of constitutive nitric oxide synthase, bcl-2 and Fas expression in cultured human coronary endothelial cells exposed to anoxia-reoxygenation and angiotensin II: role of AT1 receptor activation. Author(s): Li D, Tomson K, Yang B, Mehta P, Croker BP, Mehta JL. Source: Cardiovascular Research. 1999 January; 41(1): 109-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10325958
Studies
51
•
Molecular mechanisms of anoxia/reoxygenation-induced neutrophil adherence to cultured endothelial cells. Author(s): Ichikawa H, Flores S, Kvietys PR, Wolf RE, Yoshikawa T, Granger DN, Aw TY. Source: Circulation Research. 1997 December; 81(6): 922-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9400372
•
More about diffusion anoxia. Author(s): Hornbein TF. Source: Anesthesiology. 1970 March; 32(3): 284-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5412894
•
Morphology and evolution of the EEG in acute cerebral anoxia (42 cases). Author(s): Cloche R, Desmonts JM, Hennetier G, Robert F. Source: Electroencephalography and Clinical Neurophysiology. 1968 July; 25(1): 89. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4174817
•
MR appearance of cerebral cortex in children with and without a history of perinatal anoxia: preliminary observations. Author(s): Castillo M, Smith JK, Mukherji SK. Source: Ajr. American Journal of Roentgenology. 1995 June; 164(6): 1481-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7754897
•
Myocardial reactive hyperemia caused by initial myocardial anoxia during aortic valve replacement. Author(s): Kairaluoma MI, Saarela E, Tuononen S, Pokela R, Karkola P, Nuutinen L, Larmi TK. Source: The Journal of Thoracic and Cardiovascular Surgery. 1978 May; 75(5): 716-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=642566
•
Myoclonic syndrome after damage to the cerebellum and brain-stem due to anoxia. Author(s): Erbsloh F, Prull G. Source: Electroencephalography and Clinical Neurophysiology. 1969 April; 26(4): 449. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4183620
•
Na+/Ca2+ exchanger in Na+ efflux-Ca2+ influx mode of operation exerts a neuroprotective role in cellular models of in vitro anoxia and in vivo cerebral ischemia. Author(s): Tortiglione A, Pignataro G, Minale M, Secondo A, Scorziello A, Di Renzo GF, Amoroso S, Caliendo G, Santagada V, Annunziato L. Source: Annals of the New York Academy of Sciences. 2002 November; 976: 408-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12502588
52
Anoxia
•
Netilmicin effect on urinary retinol binding protein (RBP) and N-acetyl-beta-Dglucosaminidase (NAG) in preterm newborns with and without anoxia. Author(s): Cataldi L, Mussap M, Verlato G, Plebani M, Fanos V; Neonatal Nephrology Study Group of the Italian Society of Neonatology. Source: J Chemother. 2002 February; 14(1): 76-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11892904
•
Neuropathological problems posed by carbon monoxide poisoning and anoxia. Author(s): Brucher JM. Source: Prog Brain Res. 1967; 24: 75-100. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6075036
•
Neuropsychological and neuropathological sequelae of cerebral anoxia: a critical review. Author(s): Caine D, Watson JD. Source: Journal of the International Neuropsychological Society : Jins. 2000 January; 6(1): 86-99. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10761372
•
New physiological observations on the effect of anoxia. Author(s): Severinghouse JW. Source: Nord Med. 1971 June 17; 85(24): 754-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5091340
•
Nitric oxide prevents anoxia-induced apoptosis in colonic HT29 cells. Author(s): Madesh M, Ramachandran A, Balasubramanian KA. Source: Archives of Biochemistry and Biophysics. 1999 June 15; 366(2): 240-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10356289
•
Nonexocytotic noradrenaline release induced by pharmacological agents or anoxia in human cardiac tissue. Author(s): Kurz T, Richardt G, Seyfarth M, Schomig A. Source: Naunyn-Schmiedeberg's Archives of Pharmacology. 1996 June; 354(1): 7-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8832582
•
Novel cardioprotective effects of tetrahydrobiopterin after anoxia and reoxygenation: Identifying cellular targets for pharmacologic manipulation. Author(s): Verma S, Maitland A, Weisel RD, Fedak PW, Pomroy NC, Li SH, Mickle DA, Li RK, Rao V. Source: The Journal of Thoracic and Cardiovascular Surgery. 2002 June; 123(6): 1074-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12063453
Studies
53
•
Old warp, new weft: weaving a new life fabric after anoxia. Author(s): Kelleher JA. Source: Brain Injury : [bi]. 1998 April; 12(4): 299-306. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9562912
•
Oxygen consumption and electron spin resonance studies of free radical production by alveolar cells exposed to anoxia: inhibiting effects of the antibiotic ceftazidime. Author(s): Mouithys-Mickalad A, Mathy-Hartert M, Du G, Sluse F, Deby C, Lamy M, Deby-Dupont G. Source: Redox Report : Communications in Free Radical Research. 2002; 7(2): 85-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12189054
•
Oxygen radicals generated during anoxia followed by reoxygenation reduce the synthesis of tissue-type plasminogen activator and plasminogen activator inhibitor-1 in human endothelial cell culture. Author(s): Shatos MA, Doherty JM, Stump DC, Thompson EA, Collen D. Source: The Journal of Biological Chemistry. 1990 November 25; 265(33): 20443-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2122975
•
Pancreatitis complicated by pericardial effusion and cardiac tamponade. Recovery after prolonged cerebral anoxia. Author(s): Lipson JD, Stephenson HE Jr. Source: Archives of Surgery (Chicago, Ill. : 1960). 1971 September; 103(3): 414-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4998838
•
Perinatal anoxia and mental retardation. Author(s): Krynski S, Diament AJ, Levisky DL, Domingues WM. Source: Acta Paedopsychiatr. 1973; 39(12): 347-55. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4602542
•
Perinatal death due to anoxia. Author(s): Gibbs CE. Source: Hospital Topics. 1966 February; 44(2): 113-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5948141
•
Perivascular anoxia-ischemia lesions in the human brain. Author(s): Hart MN, Galloway GM, Dunn MJ. Source: Neurology. 1975 May; 25(5): 477-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1169706
54
Anoxia
•
Periventricular leukomalacia related to neonatal anoxia: recognition by computed tomography. Author(s): Di Chiro G, Arimitsu T, Pellock JM, Landes RD. Source: Journal of Computer Assisted Tomography. 1978 July; 2(3): 352-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=318108
•
Pituitary adenylate cyclase activating polypeptide is highly abundant in the nervous system of anoxia-tolerant turtle, Pseudemys scripta elegans. Author(s): Reglodi D, Somogyvari-Vigh A, Vigh J, Li M, Lengvari I, Arimura A. Source: Peptides. 2001 June; 22(6): 873-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11390016
•
Placebo-controlled study of pramiracetam in young males with memory and cognitive problems resulting from head injury and anoxia. Author(s): McLean A Jr, Cardenas DD, Burgess D, Gamzu E. Source: Brain Injury : [bi]. 1991 October-December; 5(4): 375-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1786500
•
Plasma amino acid clearance predicts hepatic recovery after normothermic anoxia and cold preservation. Author(s): Becker WK, Stock P, Fath JJ, Konstantinides FN, Ascher NL, Cerra FB. Source: Transplantation Proceedings. 1987 February; 19(1 Pt 2): 1331. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3274327
•
Platelet activation by superoxide anion and hydroxyl radicals intrinsically generated by platelets that had undergone anoxia and then reoxygenated. Author(s): Leo R, Pratico D, Iuliano L, Pulcinelli FM, Ghiselli A, Pignatelli P, Colavita AR, FitzGerald GA, Violi F. Source: Circulation. 1997 February 18; 95(4): 885-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9054746
•
Ponto-subicular lesions in perinatal anoxia. Author(s): Friede RL. Source: Arch Pathol. 1972 October; 94(4): 343-54. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5056927
•
Postoperative pulmonary insufficiency: anoxia, the shunted lung and mechanical assistance. Author(s): Moore FD. Source: Cardiovasc Clin. 1971; 3(3): 121-34. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4946018
Studies
55
•
Production of superoxide anion and hydrogen peroxide by KB cells in an anoxiareoxygenation model, and role of allopurinol. Author(s): Serhrouchni M. Source: Arch Int Physiol Biochim. 1990 December; 98(6): 455-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1705785
•
Progressive choreo-athetosis related to birth anoxia. Author(s): Montagna P, Cirignotta F, Gallassi R, Sacquegna T. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1981 October; 44(10): 957. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7198140
•
Progressive multifocal leukoencephalopathy following cerebral anoxia due to asphyxia. Report of a case. Author(s): Crompton MR, Hunter R, Jones M. Source: Journal of the Neurological Sciences. 1968 November-December; 7(3): 545-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5709862
•
Prolongation of anoxia-induced hyperemia in healthy middle-aged men treated with cinnarizine and flunarizine. Author(s): Jageneau A, Loots W, Brugmans J. Source: Arzneimittel-Forschung. 1974 November; 24(11): 1839-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4155635
•
Rapid development of basal ganglia calcification caused by anoxia. Author(s): Iwaski Y, Kinoshita M, Takamiya K. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1988 March; 51(3): 449-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3361340
•
Rapid development of basal ganglia hyperdensity caused by anoxia. Author(s): Bamford J, Bodansky H, Bradey N, Currie S, Barnett D. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1988 October; 51(10): 13645. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3147315
•
Rapidly evolving anoxia after inhalation of polluted water. Author(s): Servadio G, Guarino A, Frova G. Source: Lancet. 1980 April 5; 1(8171): 763. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6103173
56
Anoxia
•
Recovery from near death following cerebral anoxia: a case report demonstrating superiority of median somatosensory evoked potentials over EEG in predicting a favorable outcome after cardiopulmonary resuscitation. Author(s): Rothstein TL. Source: Advances in Experimental Medicine and Biology. 2004; 550: 189-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15053437
•
Re-evaluation of the oxygen diffusion model for predicting minimum contact lens Dk/t values needed to avoid corneal anoxia. Author(s): Harvitt DM, Bonanno JA. Source: Optometry and Vision Science : Official Publication of the American Academy of Optometry. 1999 October; 76(10): 712-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10524787
•
Regulation of a rat VL30 element in human breast cancer cells in hypoxia and anoxia: role of HIF-1. Author(s): Ameri K, Burke B, Lewis CE, Harris AL. Source: British Journal of Cancer. 2002 November 4; 87(10): 1173-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12402159
•
Renal failure following perinatal anoxia. Author(s): Dauber IM, Krauss AN, Symchych PS, Auld PA. Source: The Journal of Pediatrics. 1976 May; 88(5): 851-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1271150
•
Renal mouse proximal tubular cells are more susceptible than MDCK cells to chemical anoxia. Author(s): Sheridan AM, Schwartz JH, Kroshian VM, Tercyak AM, Laraia J, Masino S, Lieberthal W. Source: The American Journal of Physiology. 1993 September; 265(3 Pt 2): F342-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8214092
•
Residents' corner. Answer to case of the month #7. Appearance of "reversal sign" in computed tomography scans as an indicator of changes in the brain caused by anoxia and ischemia. Author(s): Assaf A, O'Gorman AM. Source: Canadian Association of Radiologists Journal = Journal L'association Canadienne Des Radiologistes. 1991 June; 42(3): 223-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2054685
Studies
57
•
Response of human hepatocyte lysosomes to postmortem anoxia. Author(s): Yu QC, Lipsky M, Trump BF, Marzella L. Source: Human Pathology. 1988 October; 19(10): 1174-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3169726
•
Results from tourniquet anoxia and hyperbaric oxygen techniques combined with megavoltage treatment of sarcomas of bone and soft tissues. Author(s): van den Brenk HA, Kerr RC, Madigan JP, Cass NM, Richter W. Source: Am J Roentgenol Radium Ther Nucl Med. 1966 March; 96(3): 760-76. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4955532
•
Resuscitation after global brain ischemia-anoxia. Author(s): Safar P, Bleyaert A, Nemoto EM, Moossy J, Snyder JV. Source: Critical Care Medicine. 1978 July-August; 6(4): 215-27. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=354869
•
Retrolental fibroplasia--associated with intrauterine anoxia? Author(s): Bruckner HL. Source: Archives of Ophthalmology. 1968 October; 80(4): 504-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5695472
•
Reversible anoxia of the brain and spinal cord: electrographic data. Author(s): Stern JE. Source: Electromyography. 1971 January-April; 11(1): 5-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5094622
•
Selective sparing of human nucleus accumbens in aging and anoxia. Author(s): Huang KW, Zhao Y. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 1995 November; 22(4): 290-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8599772
•
Selective stimulus-sensitive myoclonus in acute cerebral anoxia. A case report. Author(s): Niedermeyer E, Bauer G, Burnite R, Reichenbach D. Source: Archives of Neurology. 1977 June; 34(6): 365-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=860937
58
Anoxia
•
Serial changes in cerebral blood flow and metabolism following cerebral anoxia in man. Author(s): Tweed WA, Lee J, Beckstead JE, McKeen WJ. Source: Acta Neurologica Scandinavica. Supplementum. 1977; 64: 132-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=268759
•
Severe anoxia with and without concomitant brain atrophy and neuropsychological impairments. Author(s): Hopkins RO, Gale SD, Johnson SC, Anderson CV, Bigler ED, Blatter DD, Weaver LK. Source: Journal of the International Neuropsychological Society : Jins. 1995 September; 1(5): 501-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9375235
•
Specificity of neonatal anoxia in the EEG pattern of the child of school age who presents with praxic or language difficulties. Author(s): Harrison A. Source: Electroencephalography and Clinical Neurophysiology. 1967 October; 23(4): 383. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4167785
•
Sudden death and cerebral anoxia in a young woman with congenital ostial stenosis of the left main coronary artery. Author(s): Knobel B, Rosman P, Kriwisky M, Tamari I. Source: Catheterization and Cardiovascular Interventions : Official Journal of the Society for Cardiac Angiography & Interventions. 1999 September; 48(1): 67-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10467074
•
Superoxide production by human umbilical vein endothelial cells in an anoxiareoxygenation model. Author(s): Schinetti ML, Sbarbati R, Scarlattini M. Source: Cardiovascular Research. 1989 January; 23(1): 76-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2550129
•
Survival after severe cerebral anoxia with destruction of the cerebral cortex: the apallic syndrome. Author(s): Ingvar DH, Brun A, Johansson L, Samuelsson SM. Source: Annals of the New York Academy of Sciences. 1978 November 17; 315: 184-214. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=284735
•
Temporal epilepsy and hippocampal discharges induced by oxyprivic anoxia. Author(s): Passouant P, Cadilhac J, Pternitis C, Baldy-Moulinier M. Source: Electroencephalography and Clinical Neurophysiology. 1967 October; 23(4): 379. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4167772
Studies
59
•
The auditory pathology of anoxia. Author(s): Dublin WB. Source: Otolaryngology. 1978 January-February; 86(1): Orl-27-39. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=114918
•
The chemical basis for the intolerance of the brain to anoxia. Author(s): Reichelt KL. Source: Acta Anaesthesiologica Scandinavica. Supplementum. 1968; 29: 35-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4233924
•
The clinical problem: how much anoxia-ischemia damages the brain? Author(s): Plum F. Source: Archives of Neurology. 1973 December; 29(6): 359-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4759412
•
The effect of age, species and adrenaline on the recovery of isolated atria from anoxia. Author(s): Penn RG. Source: British Journal of Pharmacology. 1970 June; 39(2): 309-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5425275
•
The effect of anoxia on anthracycline-induced DNA damage in the RPMI-6410 human lymphoblastoid cell line. Author(s): Brox L, Gowans B, To R, Belch A. Source: Can J Biochem. 1982 September; 60(9): 873-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6959691
•
The effect of anoxia on the human corneal epithelium. Author(s): O'Leary DJ, Wilson G, Henson DB. Source: Am J Optom Physiol Opt. 1981 June; 58(6): 472-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7270656
•
The effect of hypothermia and anoxia upon oxygen consumption and contractility of human and rat heart muscle. Author(s): Tsifutis A, Burton RM, Goldring D. Source: American Heart Journal. 1970 January; 79(1): 88-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5410286
•
The effect of magnesium sulfate on anoxia and resuscitation in the neonate. Author(s): Dunne JT, Miliigan JE, Thomas BW. Source: American Journal of Obstetrics and Gynecology. 1971 February 1; 109(3): 369-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4323509
60
Anoxia
•
The effect of perinatal anoxia on amino acid metabolism in the developing brain. Part II: The effect of perinatal anoxia on the free amino acid patterns in CSF of infants and children. Author(s): Kaneko K. Source: Brain & Development. 1985; 7(4): 400-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4061776
•
The effects of anoxia on isozyme patterns and ultrastructure of cultured human fibroblasts. Author(s): Henderson NS. Source: The Journal of Experimental Zoology. 1973 August; 185(2): 247-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4146770
•
The electroretinogram during terminal anoxia in humans. Author(s): Wilkus RJ, Chatrian GE, Lettich E. Source: Electroencephalography and Clinical Neurophysiology. 1971 December; 31(6): 537-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4111477
•
The induction of chromosome aberrations in human lymphocytes by negative phimesons under conditions of anoxia and oxygenation. Author(s): Prosser JS, Priseman SJ. Source: Experientia. 1980 July 15; 36(7): 869-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7398854
•
The influence of anoxia or oxygenation on the induction of chromosome aberrations in human lymphocytes by 15-MeV neutrons. Author(s): Prosser JS, Stimpson LD. Source: Mutation Research. 1981 December; 84(2): 365-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7199617
•
The medicolegal aspects of rapid deaths initiated by hypoxia and anoxia. Author(s): Gordon I. Source: Leg Med Annu. 1975; : 29-47. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=768671
•
The neuropathological effects of anoxia and hypoglycemia in the newborn. Author(s): Banker BQ. Source: Developmental Medicine and Child Neurology. 1967 October; 9(5): 544-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6066019
Studies
61
•
The pathological changes produced by focal cerebral anoxia. Author(s): Feigin I. Source: Res Publ Assoc Res Nerv Ment Dis. 1966; 41: 23-39. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5957650
•
The pathophysiology of cerebral anoxia. Author(s): Ingvar DH. Source: Acta Anaesthesiologica Scandinavica. Supplementum. 1968; 29: 47-59. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5674578
•
The prognostic significance of coma-rating, duration of anoxia and cardiopulmonary resuscitation in out-of-hospital cardiac arrest. Author(s): Berek K, Schinnerl A, Traweger C, Lechleitner P, Baubin M, Aichner F. Source: Journal of Neurology. 1997 September; 244(9): 556-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9352452
•
The relation between EEG, cerebral metabolism and cerebral circulation as well as their disorders caused by anoxia. Author(s): Ingvar DH. Source: Electroencephalography and Clinical Neurophysiology. 1970 August; 29(2): 207. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4194607
•
The renal medulla: life at the edge of anoxia. Author(s): Heyman SN, Rosen S, Brezis M. Source: Blood Purification. 1997; 15(4-6): 232-42. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9435951
•
The role of neonatal anoxia and its prevention. Author(s): Jakab I. Source: Acta Paedopsychiatr. 1965 November; 32(11): 329-38. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5327719
•
The use in pediatric transplantation of livers from donors who died from anoxia. Author(s): Yandza T, Goulao J, Gauthier F, De Victor D, De Dreuzy O, Huault G, Dubousset AM, Valayer J. Source: Transplantation Proceedings. 1991 October; 23(5): 2617. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1926504
62
Anoxia
•
Theophylline treatment may adversely affect the anoxia-induced erythropoietic response without suppressing erythropoietin production. Author(s): Tsantes AE, Tassiopoulos ST, Papadhimitriou SI, Bonovas S, Poulakis N, Vlachou A, Filioussi K, Loukopoulos D. Source: European Journal of Clinical Pharmacology. 2003 September; 59(5-6): 379-83. Epub 2003 August 05. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12904930
•
Thrombospondin-1 is downregulated by anoxia and suppresses tumorigenicity of human glioblastoma cells. Author(s): Tenan M, Fulci G, Albertoni M, Diserens AC, Hamou MF, El Atifi-Borel M, Feige JJ, Pepper MS, Van Meir EG. Source: The Journal of Experimental Medicine. 2000 May 15; 191(10): 1789-98. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10811871
•
Tissue anoxia prevents inflammation and pigmentation caused by UVA but not by UVB or PUVA. Author(s): Tegner E. Source: Photodermatol. 1984 December; 1(6): 311-2. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6533624
•
T-lymphocyte-derived tumor necrosis factor exacerbates anoxia-reoxygenationinduced neutrophil-endothelial cell adhesion. Author(s): Kokura S, Wolf RE, Yoshikawa T, Granger DN, Aw TY. Source: Circulation Research. 2000 February 4; 86(2): 205-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10666417
•
Tolerance and resistance of myocardium to anoxia: experimental studies. Author(s): Dureau G, Schilt W, Loire R. Source: The Journal of Cardiovascular Surgery. 1975 May-June; 16(3): 261-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1097452
•
Total blood-flow, pulsatile blood-flow, and tissue anoxia in apparently ischaemic feet. Author(s): McEwan AJ, Ledingham IM. Source: The British Journal of Surgery. 1970 November; 57(11): 850. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5476307
•
Tourette's syndrome and neonatal anoxia: further evidence of an organic etiology. Author(s): Burnstein MH. Source: Journal of Psychiatry & Neuroscience : Jpn. 1992 September; 17(3): 89-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1390622
Studies
63
•
Transforming growth factor-beta(1) restores antiplatelet function of endothelial cells exposed to anoxia-reoxygenation injury. Author(s): Tatsumi M, Kishi Y, Miyata T, Numano F. Source: Thrombosis Research. 2000 June 1; 98(5): 451-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10828485
•
Transient choreo-athetosis following severe anoxia. Author(s): Cree JE. Source: Proc R Soc Med. 1969 April; 62(4): 323-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5811930
•
Transition from alpha to theta pattern coma in fatal cerebral anoxia. Author(s): Synek VM, Synek BJ. Source: Clin Exp Neurol. 1988; 25: 109-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3267481
•
Transitory ischemia/anoxia in young children and the prediction of quality of survival. Author(s): Pampiglione G, Chaloner J, Harden A, O'Brien J. Source: Annals of the New York Academy of Sciences. 1978 November 17; 315: 281-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=284740
•
Tumour anoxia and the response to radiation. Author(s): Thomlinson RH. Source: Sci Basis Med Annu Rev. 1965; : 74-90. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5321384
•
Umbilical cord blood histamine levels in newborn infants with and without perinatal anoxia. Author(s): Porter JF, Young JA, Rasheed S. Source: Biology of the Neonate. 1970; 15(56): 300-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5464006
•
Value of a revised EEG coma scale for prognosis after cerebral anoxia and diffuse head injury. Author(s): Synek VM. Source: Clin Electroencephalogr. 1990 January; 21(1): 25-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2297945
64
•
Anoxia
Varicocele: relation between anoxia and hypospermatogenesis. Author(s): Netto NR Jr, Lemos GC, De Goes GM. Source: Int J Fertil. 1977; 22(3): 174-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=24012
65
CHAPTER 2. ALTERNATIVE MEDICINE AND ANOXIA Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to anoxia. 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 anoxia 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 “anoxia” (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 anoxia: •
Acquired heterotopic ossification in the settings of cerebral anoxia and alternative therapy: two cases. Author(s): Chua KS, Kong KH. Source: Brain Injury : [bi]. 2003 June; 17(6): 535-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12745708
•
Ca2+-dependent and Ca2+-independent glutamate release, energy status and cytosolic free Ca2+ concentration in isolated nerve terminals following metabolic inhibition: possible relevance to hypoglycaemia and anoxia. Author(s): Kauppinen RA, McMahon HT, Nicholls DG. Source: Neuroscience. 1988 October; 27(1): 175-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2904664
66
Anoxia
•
Dynamics of Acetaldehyde Production during Anoxia and Post-Anoxia in Red Bell Pepper Studied by Photoacoustic Techniques. Author(s): Zuckermann H, Harren F, Reuss J, Parker DH. Source: Plant Physiology. 1997 March; 113(3): 925-932. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12223654
•
Effects of tetrandrine on changes of NMDA receptor channel in cortical neurons of rat induced by anoxia. Author(s): Wang ZF, Xue CS, Zhou QX, Wan ZB, Luo QS. Source: Zhongguo Yao Li Xue Bao. 1999 August; 20(8): 729-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10678107
•
EGb 761 protects liver mitochondria against injury induced by in vitro anoxia/reoxygenation. Author(s): Du G, Willet K, Mouithys-Mickalad A, Sluse-Goffart CM, Droy-Lefaix MT, Sluse FE. Source: Free Radical Biology & Medicine. 1999 September; 27(5-6): 596-604. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10490280
•
Generation of superoxide anion by mitochondria and impairment of their functions during anoxia and reoxygenation in vitro. Author(s): Du G, Mouithys-Mickalad A, Sluse FE. Source: Free Radical Biology & Medicine. 1998 December; 25(9): 1066-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9870560
•
Is genetics the unrecognized confounding factor in bioelectromagnetics? Flockdependence of field-induced anoxia protection in chick embryos. Author(s): Di Carlo AL, Litovitz TA. Source: Bioelectrochemistry and Bioenergetics (Lausanne, Switzerland). 1999 February; 48(1): 209-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10228589
•
Monosialoganglioside GM1 protects against anoxia-induced neuronal death in vitro. Author(s): Skaper SD, Facci L, Milani D, Leon A. Source: Experimental Neurology. 1989 December; 106(3): 297-305. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2687018
•
Protective effect of hachimi-jio-gan, an oriental herbal medicinal mixture, against cerebral anoxia. Author(s): Hirokawa S, Nose M, Amagaya S, Oyama T, Ogihara Y. Source: Journal of Ethnopharmacology. 1993 December; 40(3): 201-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8145576
Alternative Medicine 67
•
Protective effects of kamikihi-to, a traditional Chinese medicine, against cerebral ischemia, hypoxia and anoxia in mice and gerbils. Author(s): Nishizawa K, Inoue O, Saito Y, Suzuki A. Source: Japanese Journal of Pharmacology. 1994 March; 64(3): 171-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8022119
•
Role of cytosolic Ca in renal tubule damage induced by anoxia. Author(s): Jacobs WR, Sgambati M, Gomez G, Vilaro P, Higdon M, Bell PD, Mandel LJ. Source: The American Journal of Physiology. 1991 March; 260(3 Pt 1): C545-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2003577
•
Role of lipoxygenase, cyclooxygenase and cytochrome P-450 metabolites in contractions of isolated guinea pig pulmonary venules induced by hypoxia and anoxia. Author(s): Tracey WR, Bend JR, Hamilton JT, Paterson NA. Source: The Journal of Pharmacology and Experimental Therapeutics. 1989 September; 250(3): 1097-104. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2506335
•
Role of protein-phosphorylation events in the anoxia signal-transduction pathway leading to the inhibition of total protein synthesis in isolated hepatocytes. Author(s): Tinton S, Tran-Nguyen QN, Buc-Calderon P. Source: European Journal of Biochemistry / Febs. 1997 October 1; 249(1): 121-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9363762
•
Study on pharmacological effect of bile salts, sodium scymnol sulfate, from Rhizoprionodon acutus. I. Effect of scymnol, chimaerol and sodium scymnol sulfate on cerebral anoxia. Author(s): Ishida H, Kinoshita S, Yamamoto N, Nukaya H, Tsuji K, Kosuge T. Source: Chemical & Pharmaceutical Bulletin. 1994 December; 42(12): 2532-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7697769
•
Tone burst-evoked otoacoustic emissions in cats with acoustic overstimulation and anoxia. Author(s): Iwasaki S, Mizuta K, Hoshino T. Source: Hearing Research. 1998 April; 118(1-2): 83-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9606063
•
Translocation of two glucose transporters in heart: effects of rotenone, uncouplers, workload, palmitate, insulin and anoxia. Author(s): Wheeler TJ, Fell RD, Hauck MA.
68
Anoxia
Source: Biochimica Et Biophysica Acta. 1994 December 30; 1196(2): 191-200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7841183
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/
•
AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
•
Chinese Medicine: http://www.newcenturynutrition.com/
•
drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
•
Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
•
Google: http://directory.google.com/Top/Health/Alternative/
•
Healthnotes: http://www.healthnotes.com/
•
MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
•
Open Directory Project: http://dmoz.org/Health/Alternative/
•
HealthGate: http://www.tnp.com/
•
WebMDHealth: http://my.webmd.com/drugs_and_herbs
•
WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
•
Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to anoxia; 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: •
Herbs and Supplements Acorus Alternative names: Sweet Flag; Acorus calamus L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Piper Alternative names: Kava; Piper methysticum Forst.f Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Piper Nigrum Alternative names: Black Pepper Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
Alternative Medicine 69
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.
71
CHAPTER 3. DISSERTATIONS ON ANOXIA Overview In this chapter, we will give you a bibliography on recent dissertations relating to anoxia. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “anoxia” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on anoxia, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Anoxia ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to anoxia. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
Cerebral metabolism in anoxia and the effects of some neurotropic drugs by Shankar, Raj; PhD from The University of British Columbia (Canada), 1971 http://wwwlib.umi.com/dissertations/fullcit/NK10266
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
73
CHAPTER 4. PATENTS ON ANOXIA Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.7 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “anoxia” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on anoxia, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Anoxia By performing a patent search focusing on anoxia, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We
7Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
74
Anoxia
will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on anoxia: •
Amino acid derivatives of substituted quinoxaline 2,3-dione derivatives as glutamate receptor antagonists Inventor(s): Nikam; Sham (Ann Arbor, MI) Assignee(s): Warner-Lambert Company (Morris Plains, NJ) Patent Number: 5,614,508 Date filed: June 7, 1995 Abstract: A novel series of substituted quinoxaline 2,3-diones useful as neuroprotective agents are taught. Novel intermediates, processes of preparation, and pharmaceutical compositions containing the compounds are also taught. The compounds are glutamate antagonists and are useful in the treatment of stroke, cerebral ischemia, or cerebral infarction resulting from thromboembolic or hemorrhagic stroke, cerebral vasospasms, hypoglycemia, cardiac arrest, status epilepticus, perinatal asphyxia, anoxia, Alzheimer's, Parkinson's, and Huntington's diseases. Excerpt(s): This invention is for novel glutamate receptor antagonists which are new compounds of the 5,6,7,8-substituted quinoxaline 2,3-dione type. The fused ring system is substituted at the a- or b-position by amino acid derivatives. The compounds are active as excitatory amino acid receptor antagonists acting at glutamate receptors, including either or both N-methyl-D-aspartate (NMDA) receptors and non-NMDA receptors such as the.alpha.-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor and the kainate receptor. The invention also relates to the use of those quinoxaline-2,3-diones as neuroprotective agents for treating conditions such as cerebral ischemia or cerebral infarction resulting from a range of phenomena, such as thromboembolic or hemorrhagic stroke, cerebral vasospasms, hypoglycemia, cardiac arrest, status epilepticus, perinatal asphyxia, anoxia such as from drowning, pulmonary surgery, and cerebral trauma, as well as to treat chronic neurodegenerative disorders such as Alzheimer's Disease, Parkinsonism and Huntington's Disease, and as anticonvulsants. The compounds of the present invention may also be useful in the treatment of schizophrenia, epilepsy, anxiety, pain and drug addiction. Excessive excitation by neurotransmitters can cause the degeneration and death of neurons. It is believed that this degeneration is in part mediated by the excitotoxic actions of the excitatory amino acids (EAA) glutamate and aspartate at the N-methyl-D-aspartate (NMDA) receptor, the.alpha.-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor, and the kainate receptor. AMPA/kainate receptors may be referred to jointly as non-NMDA receptors. This excitotoxic action is considered responsible for the loss of neurons in cerebrovascular disorders such as cerebral ischemia or cerebral infarction resulting from a range of conditions, such as thromboembolic or hemorrhagic stroke, cerebral vasospasm, hypoglycemia, cardiac arrest, status epilepticus, perinatal asphyxia, anoxia such as from drowning, pulmonary surgery, and cerebral trauma, as well as lathyrism, Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease. Several classes of quinoxalinedione derivatives have been disclosed as glutamate (EAA) receptor antagonists. For example, among excitatory amino acid receptor antagonists recognized for usefulness in the treatment of disorders are those that block AMPA receptors (Bigge C. F. and Malone T. C., Curr. Opin. Ther. Pat., 1993:951; Rogawski M. A., TiPS, 1993;14:325). AMPA receptor antagonists have prevented neuronal injury in several models of global cerebral ischemia (Li H. and Buchan A. M., J. Cerebr. Blood Flow Metab., 1993;13:933; Nellg ard B. and Wieloch T., J. Cerebr. Blood Flow Metab.,
Patents 75
1992;12:2) and focal cerebral ischemia (Bullock R., Graham D. I., Swanson S., McCulloch J., J. Cerebr, Blood Flow Metab., 1994;14:466; Xue D., Huang Z.-G., Barnes K., Lesiuk H. J., Smith K. E., Buchan A. M., J. Cerebr. Blood Flow Metab., 1994;14:251). AMPA antagonists have also shown efficacy in models for analgesia (Xu X.-J., Hao J.-X, Seiger A., Wiesenfeld-Hallin Z., J. Pharmacol. Exp. Ther., 1993;267:140), and epilepsy (Namba T., Morimoto K., Sato K., Yamada N., Kuroda S., Brain Res., 1994;638:36; Brown S. E., McCulloch J., Brain Res., 1994;641:10; Yamaguchi S. I., Donevan S. D., Rogawski M. A., Epilepsy Res., 1993;15:179; Smith S. E., Durmuller N., Meldrum B. S., Eur, J, Pharmacol., 1991;201:179). AMPA receptor antagonists have also demonstrated promise in chronic neurodegenerative disorders such as Parkinsonism (Klockgether T., Turski L., Honor e T., Zhang Z., Gash D. M., Kurlan R., Greenamyre J. T., Ann. Neurol., 1993;34(4):585-593). Excitatory amino acid receptor antagonists that block NMDA receptors are also recognized for usefulness in the treatment of disorders. NMDA receptors are intimately involved in the phenomenon of excitotoxicity, which may be a critical determinant of outcome of several neurological disorders. Disorders known to be responsive to blockade of the NMDA receptor include acute cerebral ischemia (stroke or cerebral trauma, for example), muscular spasm, convulsive disorders, neuropathic pain, and anxiety, and may be a significant causal factor in chronic neurodegenerative disorders such as Parkinson's disease (Klockgether T., Turski L., Ann. Neurol., 1993;34:585-593), human immunodeficiency virus (HIV) related neuronal injury, amyotrophic lateral sclerosis (ALS), Alzheimer's disease (Francis P. T., Sims N. R., Procter A. W., Bowen D. M., J. Neurochem., 1993;60(5):1589-1604), and Huntington's disease. (See Lipton S., TINS, 1993;16(12):527-532; Lipton S. A., Rosenberg P. A., New Eng. J. Med., 1994;330(9):613-622; and Bigge C. F., Biochem. Pharmacol., 1993;45:1547-1561 and references cited therein.) NMDA receptor antagonists may also be used to prevent tolerance to opiate analgesia or to help control withdrawal symptoms from addictive drugs (Eur. Pat. Appl. 488,959A). Web site: http://www.delphion.com/details?pn=US05614508__ •
Inhibition of anoxia or hypoxia-induced, endothelium-mediated vasospasm with avermectins Inventor(s): Amer; Samir (P.O. Box 1439, Santa Barbara, CA 93102) Assignee(s): none reported Patent Number: 5,248,669 Date filed: December 17, 1991 Abstract: This invention relates to a method for inhibiting or suppressing in an animal the contraction of vessels lined with endothelial tissue, which contractions are caused by anoxia or hypoxia. The method comprises administering to such an animal an effective therapeutic (contraction-inhibiting) amount of an avermectin class antibiotic such as ivermectin or a derivative thereof for a time period sufficient to inhibit or suppress said contractions. Excerpt(s): This invention relates to a method for inhibiting or suppressing the release or contracting effect of Endothelium-Derived Contracting Factor (EDCF) caused by anoxia or hypoxia in an animal having an EDCF-releasing endothelium system, which comprises administering to such an animal an effective therapeutic (contractioninhibiting) amount of an avermectin class antibiotic such as ivermectin or a derivative thereof. Diseases of the circulatory system are a major cause of illness in animals, especially humans, and are responsible for many deaths. In such diseases, decreased
76
Anoxia
tissue oxygenation or ischemia is present. Such decreased tissue oxygenation may be due to a variety of causes. For example, decreased cardiac output can result in decreased perfusion, as can vasoconstriction, partial or complete blockage of blood vessels, leaking or burst blood vessels, decreased oxygenation of the perfusate (as a result of anemia or abnormal hemoglobin), and decreased ability of tissue to extract oxygen. One such disease is atherosclerosis, which is characterized by fatty deposits on the inner surfaces of arteries, which inner surfaces are lined with endothelial cells. These deposits narrow the arteries, resulting in reduced blood flow in such areas of constriction and cause the heart to work harder to drive blood through the circulatory system. In turn, this may lead to a rise in blood pressure. As the blood pressure rises, so does the risk that a blood vessel having a weakness in the wall may rupture, resulting in an aneurism. Other risks relate to the roughness of the artery walls, which may cause blood to clot, thereby causing a blockage where such a clot blocks an arteriole. Or, a piece of the roughened and irregular artery wall may break off and be carried by the blood flow until it reaches an arteriole so narrow that it cannot pass through and thus totally occludes it. If a blockage occurs in the heart, a myocardial infarction or heart attack results. If it occurs in the brain, a stroke results. In another serious condition, narrowing of coronary arteries due to atherosclerosis may lead to angina or chest pain upon exertion. When the coronary arteries narrow, less blood reaches the heart, and it cannot continue to pump because it needs more oxygen than the narrowed coronary arteries provide. It is this disparity between oxygen supply and demand that results in chest pain (angina) and, possibly, heart attack. Coronary arteries also contract and restrict blood flow in response to a variety of stimuli, one such stimulus being adrenaline or epinephrine, which is released in response to stress. As is well known, when a person faces a stressful situation, adrenaline is released from the adrenal glands and flows into the blood stream and then to the heart. The coronary arteries contract and even less oxygen becomes available to the heart. This may account for those situations which have been reported anecdotally in which people suffer heart attacks when faced with shock or tragic news. Web site: http://www.delphion.com/details?pn=US05248669__ •
Mammalian anoxia-responsive regulatory element Inventor(s): Anderson; Garth R. (Elma, NY), Estes; Scott D. (Somerville, MA), Stoler; Daniel L. (Getzville, NY) Assignee(s): Health Research Inc. (Buffalo, NY) Patent Number: 5,681,706 Date filed: March 1, 1996 Abstract: Genetic regulatory elements which effect anoxic induction of a DNA molecule in mammalian cells exposed to anoxia are identified. The genetic regulatory elements, designated mammalian anoxia-responsive elements, when operably linked to a DNA molecule and basal promoter regulate the transcription of the DNA molecule in response to anoxia. The invention relates to recombinant vectors useful for introduction into mammalian cells, and the selective expression in mammalian cells exposed to anoxic conditions. Also provided are methods of using such vectors. Excerpt(s): The present invention relates to mammalian gene expression under conditions of reduced oxygen tension. More particularly, the invention relates to a genetic element which regulates gene expression in response to anoxia. Nucleic acid constructs containing nucleic acid sequences, encoding a desired gene product and operably linked to this anoxia-responsive regulatory element will enable the selective
Patents 77
expression to the desired gene product under anoxic conditions in mammalian cells. Under most natural physiological conditions encountered by a mammalian cell, there are few instances where a cell is exposed for a prolonged period of time to anoxic conditions or anaerobiosis. However, there are some normal physiological conditions, and some pathological conditions, in which cells are exposed to anoxia. The cell response to anoxia is characterized by the ability to alter gene expression in coping with such conditions of reduced oxygen tension. A cell response to anoxia is physiologically expressed in wound healing. Wound healing is a multistep, multicellular process that involves shifting oxygen levels in the wound environment. The initial step of wound healing is characterized by clotting, fibrin formation, and neutrophil infiltration. Neutrophil infiltration provides phagocytic and lysosomal activity. A second step involves macrophage and fibroblast infiltration into the wound thereby facilitating debridement and inflammation. Web site: http://www.delphion.com/details?pn=US05681706__ •
Method of Regulating Aeration in a basin for bilogical treatment of wastewater Inventor(s): Audic; Jean-Marc (Conflans Sainte Honorine, FR), Lefevre; Fanny (Poissy, FR) Assignee(s): Lyonnaise Des Eaux (Nanterre, FR) Patent Number: 5,624,565 Date filed: September 13, 1995 Abstract: A method of regulating aeration in biological treatment of wastewater by implementing a step of eliminating carbon in aerobiosis, a step of nitrification in aerobiosis, and a step of denitrification in an anoxia, in which method the oxidationreduction potential is continuously measured in a treatment system, a curve is established of variation in oxidation-reduction potential as a function of time, and the derivative thereof is calculated, wherein, when the derivative tends towards zero, the derivative and the value of the oxidation-reduction potential are correlated to determine whether aeration should be started, continued, or stopped. Excerpt(s): The invention relates to a method of regulating aeration in a basin for biological treatment of wastewater by implementing a step of eliminating carbon, a step of nitrification, and a step of denitrification. Application of the European Directive on sewage disposal seeks to limit the amount of non-treated wastewater that is discharged into the natural environment. In particular, treatment stations should fully purify all collected water, with the exception of water due to exceptional rain events. In addition, greater reliability of works is to be required. Effluent discharged into the natural environment should be of constant quality even when the wastewater to be treated varies very considerably both with respect to pollution load and with respect to flow rate. It is therefore necessary to keep the purification station in the best possible operating state, and to adapt operating criteria on a permanent basis in order to respond to any event that modifies the operating conditions of the biological treatment. A large number of purification stations making use of activated sludge have only one treatment basin in which carbon pollution is eliminated and in which nitrification is performed, at least in part. Satisfying the European Directive makes it necessary, in certain cases, to achieve total nitrification and denitrification. All three treatment operations may be performed in a single basin, which then operates alternately in an aeration stage for eliminating carbon and for nitrification, and in an anoxia stage for denitrification.
78
Anoxia
Web site: http://www.delphion.com/details?pn=US05624565__ •
Oxamic acid compounds and pharmaceutical composition for use in improvement of damaged cerebral functions of brain Inventor(s): Atsumi; Kunio (Yokohama, JP), Hachisu; Mitsugu (Yokohama, JP), Katoh; Shinsuke (Yokohama, JP), Sato; Yasuo (Yokohama, JP), Shibahara; Seiji (Yokohama, JP) Assignee(s): Meiji Seika Kaisha, Ltd. (JP) Patent Number: 5,232,947 Date filed: September 4, 1991 Abstract: New N,N-di-alkyl- or alkenyl-substituted derivatives of oxamic acid of which the two alkyl or alkenyl groups are different from each other are now produced and found to exhibit the cerebral protective effect against cerebral anoxia in the brain of a mammalian animal, including human, and to be useful as an agent for improving or ameliorating the damaged or disturbed functions of the brain. Some known N,N-dialkyl-substituted derivatives of oxamic acid or which the two alkyl groups are identical to each other are now also found to have similar, cerebral protective effect against cerebral anoxia and to be useful as an agent for improving the damaged functions of the brain. Excerpt(s): This invention relates to new and useful oxamic acid compounds, particularly new N,N-di-substituted derivatives of oxamic acid which exhibit cerebral protective effect against cerebral anoxia (a reduced oxygen-supply from the blood) as induced in the brain of a mammalian animal, including human, by subjecting it to hypoxic conditions, and which owing to their cerebral protective effect, have medicinal effects of improving or ameliorating different symptoms of cerebral disorders or diseases caused by damaged or disturbed intracerebral energy metabolism. This invention also relates to a pharmaceutical composition comprising as the active ingredient said new oxamic acid compound or known analogous oxamic acid compound having similar medicinal effects. This pharmaceutical composition is of particular utility as a drug for improving or ameliorating the damaged or disturbed cerebral functions of the brain of a mammalian animal, including human. This invention also includes new medicinal use of the N,N-di-substituted oxamic acid compound. Furthermore, this invention relates to a process for the preparation of the new and useful oxamic acid compounds. Reflecting the advent of the so-called "high-age" society, it has become a serious public concern to develop medical measures for treatment of senile dementia as caused by damages or disturbances of the cerebral functions which are, in turn, attributable to cerebrovascular diseases or damages or disturbances of intracerebral energy metabolism. A variety of drugs has heretofore been developed as anti-dementia drugs. At the present time, senile dementia, amnesia as caused by cerebrovascular diseases and the biological mechanisms of occurrence of these disorders or diseases have not yet been elucidated fully. In these circumstances, no sufficient clue has yet been established to discover and screen effective cerebral drugs. As experimental methods for inducing amnesia in normal mammalian animals, it is known to administer such an agent which inhibits the in vivo synthesis of nucleic acids or proteins, or an anticholinergic agent. Amnesia is also known to be inducible by cerebral anoxia, ischemic load or the like. With using such model animals which have amnesia induced by these causative agents, it has been attempted to detect and develop cerebral drugs which are capable of amelioractively treating or preventing the amnesia. In addition, when using such model animals which have cerebral anoxia induced either by giving a
Patents 79
lethal dose of potassium cyanide or by subjecting to hypobaric or normabaric hypoxic conditions, namely, the reduced oxygen-supply conditions, attempts have also been made to develop cerebral drugs which are effective for the improvement or amelioration of cerebral circulation metabolism or intracerebral energy metabolism. These matters are related to e.g. in "Folia Pharmacol. Japan", 85, 323-328 (1985); ibid., 86, 445-456 (1986): and Japanese Patent Application first publication "Kokai" No. 117468/79 or its corresponding U.S. Pat. No. 4,369,139. It is well accepted that oxygen deprivation is one of the most damaging conditions affecting the animal or human brain, and that when oxygen supply tot he brain becomes deficient, cerebral functions cease after brief periods of cerebral anoxia and tissue destruction ensues. Consequently, any suitable agents which enable the brain to withstand even mild degrees of cerebral anoxia would be expected to be useful as a cerebral protective agent or a drug for improving or ameliorating the damaged or disturbed cerebral functions of the brain (the drug of this utility is hereinafter sometimes merely called "a cerebral drug"). Many compounds have been investigated for their cerebral protective effect on cerebral anoxia which is experimentally induced by subjecting the animal to hypoxic conditions, whereby there is obtained a suggestion or indication that the tested compounds are effective for treatment of cerebral anoxic or ischemic diseases or disorders (see, e.g. "Arch. int. Pharmacodyn."233, 136-144 (1978) and "Life Science" 13, 467-474 (1973)). Web site: http://www.delphion.com/details?pn=US05232947__ •
Process and installation for the treatment of effluents loaded with organic materials Inventor(s): Bonnet; Jean (Angers, FR), Cronier; Jean Noel (Saint Briac Sur Mer, FR), Juhere; Yannick (Cancale, FR) Assignee(s): Vaslin Buscher (Chalonnes Sur Loire, FR) Patent Number: 6,024,877 Date filed: June 15, 1998 Abstract: A process for treating effluents loaded with organic material, particularly wine-making effluents essential in the form of wash water, comprises pouring the effluents to be treated into a storage basin (1) and actuating a recirculation circuit (2) between this latter and an oxygenation reactor (3) for the effluents, actuating a superoxygenation device (4) when the volume of effluents stored is too great to avoid passing into anaerobic phase, then stopping the superoxygenation and maintaining the recirculation at a minimum level avoiding the passage into anoxia of the effluents, when these latter fulfill certain minimum pollution conditions. The effluents are poured over at least one purification body (5) and the purified effluents are withdrawn, until there is substantially nothing left but residual decantation sludges more or less mineralized, in the storage basin (1). These latter are treated to delay the organic components present and to lead to a substantially inert mineralized sludge. Excerpt(s): This application corresponds to French application 97 07547 of Jun. 13, 1997, the disclosure of which is incorporated herein by reference. The present invention relates to the field of treatment of effluents from processes producing liquid effluents loaded with organic materials and has for its object a process and an installation for the treatment of effluents of the type mentioned, particularly wine-making effluents essentially in the form of wash water. In the case of these latter effluents, the pollution generated is limited to relatively short time periods, during which the effluents are discharged in very great quantity and can constitute, because of this, a risk for the environment and the receiving medium.
80
Anoxia
Web site: http://www.delphion.com/details?pn=US06024877__ •
Protection of living systems from the adverse effects of stress Inventor(s): Litovitz; Theodore A. (Annapolis, MD) Assignee(s): Catholic University of America, The (Washington, DC) Patent Number: 5,968,527 Date filed: December 4, 1997 Abstract: Methods and apparatus are described to inhibit the adverse health effects of ischemia, hypoxia, anoxia or other stress by the application of a time-varying field to the region of the affected organ(s) for a short period of time (of the order of 20 minutes). A "field" means a time varying electric field, a time varying magnetic field and/or a radiating electromagnetic field. The exposure can be started up to two or more hours in advance of the ischemic event or other stress causing event. Inhibition occurs even if the field is applied after the onset of ischemic or anoxic stress. Excerpt(s): The inventions described herein relate in general to arrangements (apparatus and methods) for protecting living systems from the adverse effects upon them of ischemia, anoxia, hypoxia (a lack of sufficient oxygen), reperfusion and other environmental stresses. More specifically, the inventions are directed to methods and electrical, electronic, and electromagnetic devices, systems and installations and their effect on humans, animals, and other living systems comprising cells. The inventions limit the damage to living cells caused by any condition which stresses the cells, such as limits on the availability of oxygen to these cells. The methods may be employed in the combating of damage due to toxic chemicals such as used in chemotherapy, ionizing radiation (such as ultraviolet light, gamma rays or beta rays), atherosclerosis, restenosis after angioplasty, and nerve damage in human or animal subjects in need of such treatment. The inventions involve applying certain electric, magnetic or radiating electromagnetic fields for the purpose of activating endogenous protective mechanisms used by the cells to limit the deleterious effects such as those caused by ischemia, reperfusion, athersclerosis, ionizing radiation, toxic chemicals or other stress. When myocardial infarcts occur, loss of functional myocardium still persists despite numerous interventions available to achieve myocardial reperfusion. This loss of functional myocardium can lead to subsequent severe cardiac failure and represents a significant medical problem.sup.1. (Citations of numbered footnotes appear at the end of this specification.) Even when severe cardiac failure does not occur the salvage of additional myocardium is highly desirable to allow for a fuller more active life following a myocardial infarction. Similarly following ischemia to the brain (e.g. stroke) rapid reversal or limitation of extent of injury will lead to superior neurological outcomes. A number of changes within cells are produced by ischemia, hypoxia, or anoxia.sup.2. These changes in cellular function represent a form of metabolic or hypoxic stress which is known to produce protein denaturation. A similar increase in protein denaturation within the cell has been reported to result in the onset of the heat shock response which increases the synthesis of the so-called heat shock proteins.sup.3, now often called stress proteins. The heat shock response has been shown to occur in all organisms examined to date following an elevation in temperature. The response to this stress is an increase in the synthesis of the family of proteins collectively known as heat shock proteins (HSPs) of varying molecular weights. For example HSP70 is one member of the family whose molecular weight is 70 kilodaltons. Its inducible form is sometimes called HSP70i or HSP72. Below in this document when I refer to HSP70 I mean the inducible form.
Patents 81
Although first discovered following an elevation in temperature it is now recognized that the heat shock response is typical of the response to many stresses on the cell. These include but are not limited to the stress caused by ischemia, anoxia, hypoxia, reperfusion, hypoglycemia, hypotonicity, glucose deprivation and exposure to toxins or ionizing radiation and infections. Web site: http://www.delphion.com/details?pn=US05968527__ •
Use of conantokins Inventor(s): Layer; Richard T. (Salt Lake City, UT), McCabe; R. Tyler (Salt Lake City, UT), McIntosh; J. Michael (Salt Lake City, UT), Olivera; Baldomero M. (Salt Lake City, UT), Zhou; Li-Ming (Salt Lake City, UT) Assignee(s): Cognetix, Inc. (Salt Lake City, UT), University of Utah Research Foundation (Salt Lake City, UT) Patent Number: 6,172,041 Date filed: February 10, 1999 Abstract: The present invention is directed to the use of conantokin peptides, conantokin peptide derivatives and conantokin peptide chimeras, referred to collectively as conantokins, having 10-30 amino acids, including preferably two or more.gamma.carboxyglutamic acid residues, for the treatment of neurologic and psychiatric disorders, such as anticonvulsant agents, neuroprotective agents or analgesic agents. Neurologic disorders and psychiatric disorders include epilepsy, convulsions, neurotoxic injury (associated with conditions of hypoxia, anoxia or ischemia which typically follows stroke, cerebrovascular accident, brain or spinal cord trauma, myocardial infarct, physical trauma, drowning, suffocation, perinatal asphyxia, or hypoglycemic events), neurodegeneration (associated with Alzheimer's disease, senile dementia, Amyotrophic Lateral Sclerosis, Multiple Sclerosis, Parkinson's disease, Huntington's disease, Down's Syndrome, Korsakoff's disease, schizophrenia, AIDS dementia, multi-infarct dementia, Binswanger dementia and neuronal damage associated with uncontrolled seizures), chemical toxicity (such as addiction, morphine tolerance, opiate tolerance, opioid tolerance and barbiturate tolerance), pain (acute, chronic, migraine), anxiety, major depression, manic-depressive illness, obsessivecompulsive disorder, schizophrenia and mood disorders (such as bipolar disorder, unipolar depression, dysthymia and seasonal effective disorder) and dystonia (movement disorder), sleep disorder, muscle relaxation and urinary incontinence. In addition, the conantokins are useful for treating HIV infection, ophthalmic indications and memory, learning or cognitive deficits. Excerpt(s): The invention relates to the use of relatively short peptides, about 10-30 residues in length, which are naturally available in minute amounts in the venom of the cone snails or analogous to the naturaly available peptides, and which include preferably one to two or more.gamma.-carboxyglutamic acid residues for the treatment of neurologic and psychiatric disorders, such as anticonvulsant agents, as neuroprotective agents or for the management of pain. The publications and other materials used herein to illuminate the background of the invention, and in particular, cases to provide additional details respecting the practice, are incorporated by reference, and for convenience are referenced in the following text by author and date and are listed alphabetically by author in the appended bibliography. The predatory cone snails (Conus) have developed a unique biological strategy. Their venom contains relatively small peptides that are targeted to various neuromuscular receptors and may be
82
Anoxia
equivalent in their pharmacological diversity to the alkaloids of plants or secondary metabolites of microorganisms. Many of these peptides are among the smallest nucleic acid-encoded translation products having defined conformations, and as such, they are somewhat unusual. Peptides in this size range normally equilibrate among many conformations. Proteins having a fixed conformation are generally much larger. Web site: http://www.delphion.com/details?pn=US06172041__
Patent Applications on Anoxia As of December 2000, U.S. patent applications are open to public viewing.8 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to anoxia: •
APPLICATION OF LIGHT AT PLURAL TREATMENT SITES WITHIN A TUMOR TO INCREASE THE EFFICACY OF LIGHT THERAPY Inventor(s): CHEN, JAMES C.; (BELLEVUE, WA) Correspondence: Law Offices OF Ronald M Anderson; 600 108th Ave, NE; Suite 507; Bellevue; WA; 98004; US Patent Application Number: 20020010500 Date filed: June 24, 1998 Abstract: Light is administered during photodynamic therapy (PDT) for an extended period of time at a plurality of sites distributed within the abnormal tissue of a tumor. A clinical study has shown that a substantially greater volume of abnormal tissue in a tumor is destroyed by the extended administration of light therapy from a plurality of probes than would have been expected based upon the teaching of the prior art. In this process, a plurality of light emitting optical fibers or probes are deployed in a spacedapart array. After a photoreactive agent is absorbed by the abnormal tissue, the light therapy is administered for at least three hours. The greater volume of necrosis in the tumor is achieved due to one or more concomitant effects, including: the inflammation of damaged abnormal tissue and resultant immunological response of the patient's body; the diffusion and circulation of activated photoreactive agent outside the expected fluence zone, which is believed to destroy the abnormal tissue; a retrograde thrombosis or vascular occlusion outside of the expected fluence zone; and, the collapse of the vascular system that provides oxygenated blood to portions of the tumor outside the expected fluence zone. In addition, is possible that molecular oxygen diffusing and circulating into the expected fluence zone is converted to singlet oxygen during the extended light therapy, causing a gradient of hypoxia and anoxia that destroys the abnormal tissue outside the expected fluence zone. Excerpt(s): The present invention generally relates to the use of light therapy to destroy abnormal tissue in a tumor, and more specifically, to the use of multiple light sources disposed at spaced-apart treatment sites within a tumor to render the therapy. Abnormal tissue in the body is known to selectively absorb certain dyes that have been perfused into a treatment site to a much greater extent than surrounding tissue. For example, tumors of the pancreas and colon may absorb two to three times the volume of
8
This has been a common practice outside the United States prior to December 2000.
Patents 83
these dyes, compared to normal tissue. Once pre-sensitized by dye tagging in this manner, the cancerous or abnormal tissue can be destroyed by irradiation with light of an appropriate wavelength or waveband corresponding to an absorbing wavelength or waveband of the dye, with minimal damage to normal tissue. This procedure, which is known as photodynamic therapy (PDT), has been clinically used to treat metastatic breast cancer, bladder cancer, lung carcinomas, esophageal cancer, basal cell carcinoma, malignant melanoma, ocular tumors, head and neck cancers, and other types of malignant tumors. Because PDT may selectively destroy abnormal tissue that has absorbed more of the dye than normal tissue, it can successfully be used to kill the malignant tissue of a tumor with less effect on surrounding benign tissue than alternative treatment procedures. The effectiveness of PDT for treating tumors has become increasingly more evident to the medical community. Each year, numerous papers are published disclosing research that has been carried out to explore how PDT can more effectively be used and to better understand the processes by which PDT destroys abnormal cells. Much of the prior art discloses the use of relatively high powered lasers as an external light source employed to administer the light to a treatment site. Typically, the light from an external laser source is conveyed through an optical fiber to a treatment site on the skin of a patient or to an internal site within the patient's body. Penetration of a tumor by the optical fiber is achieved either through a small incision in the overlying dermal layer, or directly, if the tumor is surgically exposed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Therapeutic agent composition and method of use Inventor(s): Tran, Loi H.; (Elk Grove, CA) Correspondence: David R Preston & Associates; 12625 High Bluff Drive; Suite 205; San Diego; CA; 92130; US Patent Application Number: 20030109531 Date filed: November 12, 2002 Abstract: The invention relates to the use of cyclic Prolyl Glycine ("cyclic PG" or "cPG") and analogs and mimetics thereof, as neuroprotective agents for the treatment and or prevention of neurological disorders including but not limited to cerebral ischemia or cerebral infarction resulting from a range of phenomena, such as thromboembolic or hemorrhagic stroke, cerebral basospasms, hypoglycemia, cardiac arrest, status epilepticus, perinatal asphyxia, anoxia such as from drowning, pulmonary surgery, and cerebral trauma, as well as to the treatment and prevention of chronic neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, and as anticonvulsants. Excerpt(s): This application claims benefit of priority to New Zealand provisional patent No. 515432 filed Nov. 13, 2001, and U.S. provisional patent application Serial No. 60/405,909 filed Aug. 26, 2002, and both incorporated by reference herein. Excessive excitation by neurotransmitters can cause the degeneration and death of neurons. It is believed that this degeneration is in part mediated by the excitotoxic actions of the excitotoxic amino acids (EAA) glutamate and aspartate at the N-methyl-D-aspartate (NMDA) receptor, the alpha-amino-3-hydroxy-5-methyl 4-isoxazole proprionic acid (AMPA) receptor, and the kainate receptor. AMPA/Kainate receptors may be referred to jointly as non-NMDA receptors. This excitotoxic action is considered responsible for the loss of neurons in cerebrovascular disorders such as cerebral ischemia or cerebral
84
Anoxia
infarction resulting from a range of conditions, such as thromboembol or hemorrhagic stroke, cerebral vascospasm, hypoglycemia, cardiac drowning, pulmonary surgery, and cerebral trauma, as well as Alzheimer's disease, Parkinson's disease, and Huntington's disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Transgenic plants incorporating traits of zostera marina Inventor(s): Alberte, Randall S.; (Falmouth, ME), Smith, Robert; (Falmouth, ME) Correspondence: Foley, Hoag & Eliot, Llp; Patent Group; One Post Office Square; Boston; MA; 02109; US Patent Application Number: 20020016980 Date filed: May 10, 2001 Abstract: The invention provides methods and compositions related to transgenic plants which incorporate genetic traits of the marine eelgrass Zostera marina. These traits include pathogen resistance, which may be conferred by stimulating zosteric acid biosynthesis, and root anoxia resistance, which may be conferred by introducing one or more anoxia-induced or anoxia-resistance genes. Excerpt(s): Selective plant breeding has been used to genetically improve crop plants throughout human history. Early hunter-gatherers selectively propagated plants with preferred properties, while early agriculturists deliberately saved seeds from preferred plant types and thereby gradually domesticated a majority of the crop plants known today. Over the past 50 years the combined efforts of plant breeders to successfully develop new crop cultivars have provided the basis for the consistent supply of food in a changing global environment and ever-changing pest and disease populations. This has been a major contributing factor toward the alleviation of world hunger and suffering, and, in some instances, the consequent maintenance of political stability. The development of plant molecular genetics has facilitated plant breeding methods through such techniques as marker-assisted selection, in which genetic maps of polymorphic markers are used to monitor the selection of plant lines containing desirable alleles of closely-linked genes. Nevertheless, such breeding techniques are ultimately limited by the diversity of the existing genetic material in crop plants. This limitation to the development of crop plants with desirable new genetic traits is substantial in view of the limitations inherent in the genetic diversity of any individual plant species adapted to a select environment in general and the history of inbreeding of crop plants in particular. Recently developed method of plant genetic engineering offer a means to overcome this limitation by the introduction of new genes into single plant cells from which complete plants can be regenerated via cell and tissue culture methodologies. Genetic engineering of plants has been utilized to improve the quality of crop plant products, such as in the development of an improved tomato with superior ripening characteristics by the expression of an antisense polygalacturonase gene (see Kramer et al. (1994) Euphytica 79: 293-7). Indeed, entire biosynthetic pathways have been altered by plant genetic engineering techniques. For example, starch biosynthesis has been successfully manipulated in tomato (for paste production) and potato (for processing quality and reduced oil uptake) be expression of a bacterial ADP glucose pyrophosphorylase that is insensitive to feedback regulation (see Stark et al. (1996) Ann NY Acad Sci 792: 26-36). There is also great economic potential in the use of transgenic plants engineered for the production of biopharmaceutical compounds. Among the products that are likely to be produced in transgenic plants are cytokines, hormones, monoclonal antibodies,
Patents 85
enzymes, and vaccines. Some of these products may be expressed either from stably transformed plants, or from transient expression systems in the form of recombinant plant viral vectors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with anoxia, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “anoxia” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on anoxia. You can also use this procedure to view pending patent applications concerning anoxia. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
87
CHAPTER 5. BOOKS ON ANOXIA Overview This chapter provides bibliographic book references relating to anoxia. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on anoxia include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “anoxia” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on anoxia: •
Pediatric Brain Injury: A Practical Resource Source: San Antonio, TX: Communication Skill Builders, Inc. 1993. 192 p. Contact: Available from Communication Skill Builders. Psychological Corporation, Order Service Center, P.O. Box 839954, San Antonio, TX 78283-3954. Voice (800) 2118378; TTY (800) 723-1318; Fax (800) 232-1223. PRICE: $52.00 plus shipping and handling. ISBN: 0884506436. Summary: This book, intended for speech-language pathologists, parents, teachers, and students, presents information on treatment of children who experience brain injury after a history of normal development. The authors discuss the nature and incidence of brain injury in children, the philosophy of therapy, suggestions for working with parents and family members, and current research on brain injury in children. Factors in the prevention of injury to children are also discussed. Specific topics include closed head injury, open head injury, anoxia, infection, the structure of the brain, diagnostic
88
Anoxia
tests used to confirm or classify brain injuries, the neuropathology of brain injury in children, the implications of normal development stages in recovery, coma, the multidisciplinary care team involved in treating patients with brain injury, the family's role, philosophies of therapy, the functionally comatose child, the structure-dependent child, the concrete processor, issues of feeding, the continuum of care, and caring for the caregivers. For each of classification of brain injury, the authors discuss symptoms and specific therapeutic recommendations. The book concludes with a bibliography and appendices on levels of consciousness, suggested tests and assessment tools, and suggested language and cognitive activities. 73 references. (AA-M).
Chapters on Anoxia In order to find chapters that specifically relate to anoxia, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and anoxia using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “anoxia” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on anoxia: •
Types, Degrees, and Causes of Hearing Loss Source: in Flexer, C. Facilitating Hearing and Listening in Young Children. 2nd ed. San Diego, CA: Singular Publishing Group, Inc. 1999. p. 35-72. Contact: Available from Singular Publishing Group, Inc. 401 West 'A' Street, Suite 325, San Diego, CA 92101-7904. (800) 521-8545 or (619) 238-6777. Fax (800) 774-8398 or (619) 238-6789. E-mail:
[email protected]. Website: www.singpub.com. PRICE: $45.00 plus shipping and handling. ISBN: 1565939891. Summary: This chapter on the types, degrees, and causes of hearing loss is from a textbook that emphasizes the need to create an auditory world for children, in which their auditory brain centers continue to develop the neurological and experiential foundations for literacy and learning. This chapter presents an overview of the general classifications of hearing impairment and then details specific pathologies that can cause hearing impairment in children. Topics include congenital and acquired hearing impairments, distinguishing audiometric and functional definitions for hard of hearing and deaf persons, classification of hearing loss, genetic syndromes and the incidence of hearing loss associated with some syndromes (Treacher Collins, Crouzon, Waardenburg, Alport, Usher, Pendred, Jervell, Lange Nielsen), auditory pathologies, conductive hearing impairments (otitis media, collapsed ear canals, abnormalities of the middle ear ossicles, atresia, stenosis, cerumen impaction, otitis externa, perforated tympanic membrane, objects in the ear canal, cholesteatoma, and mastoiditis), sensorineural hearing impairments (tinnitus, noise induced hearing loss, viral and bacterial infections, anoxia, ototoxicity, large vestibular aqueduct, perilymph fistula, acoustic neuroma, Rh incompatibility), dysplasias (malformations or incomplete development of the inner ear), auditory neuropathy, mixed hearing impairments, progressive hearing impairments, and central and functional hearing impairments. A list of factors that place an infant or child at risk for hearing impairment is included at the end of the chapter. 2 figures. 3 tables.
89
CHAPTER 6. PERIODICALS AND NEWS ON ANOXIA Overview In this chapter, we suggest a number of news sources and present various periodicals that cover anoxia.
News Services and Press Releases One of the simplest ways of tracking press releases on anoxia 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 “anoxia” (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 anoxia. 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 “anoxia” (or synonyms). 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
90
Anoxia
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 “anoxia” (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 “anoxia” (or synonyms). If you know the name of a company that is relevant to anoxia, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “anoxia” (or synonyms).
Academic Periodicals covering Anoxia Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to anoxia. In addition to these sources, you can search for articles covering anoxia 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.”
Periodicals and News
91
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.”
93
APPENDICES
95
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 Institute9: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
•
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
•
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
•
National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
•
National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
•
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
9
These publications are typically written by one or more of the various NIH Institutes.
96
Anoxia
•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
•
National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
•
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
•
National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
•
National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
•
National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
•
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
•
National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
•
National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
•
National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
•
National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
•
National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
•
National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
•
Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
•
National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
•
National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
•
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
•
Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
Physician Resources
97
NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.10 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:11 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
•
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
•
Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
•
Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
•
Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
•
Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
10
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). 11 See http://www.nlm.nih.gov/databases/databases.html.
98
Anoxia
•
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 Gateway12 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.13 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “anoxia” (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 45319 454 336 3 191 46303
HSTAT14 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.15 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.16 Simply search by “anoxia” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
12
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
13
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). 14 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 15 16
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.
Physician Resources
99
Coffee Break: Tutorials for Biologists17 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.18 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.19 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/.
17 Adapted 18
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. 19 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.
101
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 anoxia 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 anoxia. 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 anoxia. 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 “anoxia”:
102
Anoxia
Ear Infections http://www.nlm.nih.gov/medlineplus/earinfections.html Head and Brain Injuries http://www.nlm.nih.gov/medlineplus/headandbraininjuries.html Hearing Problems in Children http://www.nlm.nih.gov/medlineplus/hearingproblemsinchildren.html Stroke http://www.nlm.nih.gov/medlineplus/stroke.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 anoxia. 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: •
Warren Grant Magnuson Clinical Center: 1992 Clinical Studies Source: Bethesda, MD: National Institutes of Health. July 1991. 93 p. Contact: Available from Clinical Center Communications, Warren Grant Magnuson Clinical Center, National Institutes of Health. Bethesda, MD 20892. (301) 496-2563. PRICE: Free; available to physicians only. NIH Publication Number 90-217. Summary: This booklet describes studies to which patients are currently admitted at the Warren Grant Magnuson Clinical Center of the National Institutes of Health (NIH) in Bethesda, Maryland. The Clinical Center is a hospital and laboratory facility shared by the 13 institutes that conducts combined laboratory and clinical study programs. Clinical studies associated with Alzheimer's disease and dementia include a study of brain function comparing healthy aging persons with patients who have Alzheimer's disease, multi-infarct dementia, geriatric depression, and hypertension (Laboratory of Neurosciences, National Institute on Aging); a study of separate patients and twins with early or moderate Alzheimer's dementia that includes diagnostic and neuropsychologic assessment and drug treatment that affects brain neurotransmitter systems (National Institute of Mental Health); diagnostic studies and experimental therapeutic interventions in patients with Alzheimer's disease and related presenile or senile dementias (Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke); and brain behavior studies that evaluate human cognition and mood states in patients with Alzheimer's disease, Parkinson's disease, head injury, anoxia, stroke, and other neurological disorders (Cognitive Neuroscience Branch,
Patient Resources
103
National Institute of Neurological Disorders and Stroke). A descriptive outline of each clinical program activity and the names, affiliations, and phone numbers of key scientists are included. 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 anoxia. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
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 anoxia. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with anoxia. 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 anoxia. 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.
104
Anoxia
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 “anoxia” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “anoxia”. 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 “anoxia” (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 “anoxia” (or a synonym) into the search box, and click “Submit Query.”
105
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.20
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
20
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
106
Anoxia
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)21: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
•
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
•
Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
•
California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
•
California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
•
California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
•
California: Gateway Health Library (Sutter Gould Medical Foundation)
•
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
•
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
•
California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
•
California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
•
California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
•
California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
•
California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
•
California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
•
Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
•
Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
•
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
21
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
Finding Medical Libraries
107
•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
•
Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
•
Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
•
Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
•
Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
•
Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
•
Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
•
Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
•
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
•
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
•
Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
•
Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
•
Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
•
Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
•
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
•
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
•
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
•
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
108
Anoxia
•
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/
Finding Medical Libraries
109
•
Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
•
New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
•
New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
•
New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
•
New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
•
New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
•
New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
•
New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
•
Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
•
Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
•
Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
•
Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
•
Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
•
Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
•
Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
•
Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
•
Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
•
Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
•
Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
110
Anoxia
•
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
111
ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
•
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
•
Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).
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
113
ANOXIA DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 3-dimensional: 3-D. A graphic display of depth, width, and height. Three-dimensional radiation therapy uses computers to create a 3-dimensional picture of the tumor. This allows doctors to give the highest possible dose of radiation to the tumor, while sparing the normal tissue as much as possible. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abducens: A striated, extrinsic muscle of the eyeball that originates from the annulus of Zinn. [NIH] Abducens Nerve: The 6th cranial nerve. The abducens nerve originates in the abducens nucleus of the pons and sends motor fibers to the lateral rectus muscles of the eye. Damage to the nerve or its nucleus disrupts horizontal eye movement control. [NIH] Acatalasia: A rare autosomal recessive disorder resulting from the absence of catalase activity. Though usually asymptomatic, a syndrome of oral ulcerations and gangrene may be present. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acoustic: Having to do with sound or hearing. [NIH] Actin: Essential component of the cell skeleton. [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] Acyl: Chemical signal used by bacteria to communicate. [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] 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
114
Anoxia
and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adenylate Cyclase: An enzyme of the lyase class that catalyzes the formation of cyclic AMP and pyrophosphate from ATP. EC 4.6.1.1. [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] Adoptive Transfer: Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (immunotherapy, adoptive). [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenaline: A hormone. Also called epinephrine. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerobiosis: Life or metabolic reactions occurring in an environment containing oxygen. [NIH]
Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Aggressiveness: The quality of being aggressive (= characterized by aggression; militant; enterprising; spreading with vigour; chemically active; variable and adaptable). [EU] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring
Dictionary 115
substances. [EU] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Akathisia: 1. A condition of motor restlessness in which there is a feeling of muscular quivering, an urge to move about constantly, and an inability to sit still, a common extrapyramidal side effect of neuroleptic drugs. 2. An inability to sit down because of intense anxiety at the thought of doing so. [EU] Akinetic Mutism: Lack of the faculty of speech. [NIH] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allopurinol: A xanthine oxidase inhibitor that decreases uric acid production. [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] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [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 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] Aminopropionitrile: 3-Aminopropanenitrile. Reagent used as an intermediate in the manufacture of beta-alanine and pantothenic acid. [NIH] Amnesia: Lack or loss of memory; inability to remember past experiences. [EU] Amnestic: Nominal aphasia; a difficulty in finding the right name for an object. [NIH]
116
Anoxia
Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is dextroamphetamine. [NIH] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] 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] Anesthetics: Agents that are capable of inducing a total or partial loss of sensation, especially tactile sensation and pain. They may act to induce general anesthesia, in which an unconscious state is achieved, or may act locally to induce numbness or lack of sensation at a targeted site. [NIH] Aneurism: A localized abnormal dilatation of a blood vessel filled with fluid or clotted blood, forming a pulsating tumor, and resulting from disease of the vessel wall. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angioplasty: Endovascular reconstruction of an artery, which may include the removal of atheromatous plaque and/or the endothelial lining as well as simple dilatation. These are procedures performed by catheterization. When reconstruction of an artery is performed surgically, it is called endarterectomy. [NIH] 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
Dictionary 117
or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Anterior Cerebral Artery: Artery formed by the bifurcation of the internal carotid artery. Branches of the anterior cerebral artery supply the caudate nucleus, internal capsule, putamen, septal nuclei, gyrus cinguli, and surfaces of the frontal lobe and parietal lobe. [NIH] Anterograde: Moving or extending forward; called also antegrade. [EU] Anthracycline: A member of a family of anticancer drugs that are also antibiotics. [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] Anticholinergic: An agent that blocks the parasympathetic nerves. Called also parasympatholytic. [EU] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]
Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are
118
Anoxia
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] Antithrombotic: Preventing or interfering with the formation of thrombi; an agent that so acts. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Aortic Aneurysm: Aneurysm of the aorta. [NIH] Aortic Valve: The valve between the left ventricle and the ascending aorta which prevents backflow into the left ventricle. [NIH] Apnea: A transient absence of spontaneous respiration. [NIH] Aponeurosis: Tendinous expansion consisting of a fibrous or membranous sheath which serves as a fascia to enclose or bind a group of muscles. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Approximate: Approximal [EU] Aqueous: Having to do with water. [NIH] 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]
Dictionary 119
Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Arteriosus: Circle composed of anastomosing arteries derived from two long posterior ciliary and seven anterior ciliary arteries, located in the ciliary body about the root of the iris. [NIH]
Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Arteriovenous Fistula: An abnormal communication between an artery and a vein. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aspartate: A synthetic amino acid. [NIH] Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. [NIH] Asphyxia: A pathological condition caused by lack of oxygen, manifested in impending or actual cessation of life. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Astrocytoma: A tumor that begins in the brain or spinal cord in small, star-shaped cells called astrocytes. [NIH] Athetosis: A derangement marked by ceaseless occurrence of slow, sinuous, writhing movements, especially severe in the hands, and performed involuntarily; it may occur after hemiplegia, and is then known as posthemiplegic chorea. Called also mobile spasm. [EU] Atmospheric Pressure: The pressure at any point in an atmosphere due solely to the weight of the atmospheric gases above the point concerned. [NIH] Atresia: Lack of a normal opening from the esophagus, intestines, or anus. [NIH]
120
Anoxia
Atrial: Pertaining to an atrium. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] 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] Auditory: Pertaining to the sense of hearing. [EU] 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] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [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] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as sedatives and anesthetics, and they have been used to treat the convulsions associated with epilepsy. [NIH] Basal cell carcinoma: A type of skin cancer that arises from the basal cells, small round cells found in the lower part (or base) of the epidermis, the outer layer of the skin. [NIH] Basal cells: Small, round cells found in the lower part (or base) of the epidermis, the outer layer of the skin. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Beta Rays: A stream of positive or negative electrons ejected with high energy from a disintegrating atomic nucleus; most biomedically used isotopes emit negative particles (electrons or negatrons, rather than positrons). Cathode rays are low-energy negative electrons produced in cathode ray tubes, also called television tubes or oscilloscopes. [NIH] Beta-pleated: Particular three-dimensional pattern of amyloidoses. [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.
Dictionary 121
Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biological Transport: The movement of materials (including biochemical substances and drugs) across cell membranes and epithelial layers, usually by passive diffusion. [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] Biphasic: Having two phases; having both a sporophytic and a gametophytic phase in the life cycle. [EU] Bipolar Disorder: A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence. [NIH] Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Coagulation Factors: Endogenous substances, usually proteins, that are involved in the blood coagulation process. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example,
122
Anoxia
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] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blotting and transferred to strips of nitrocellulose paper. The blots are then detected by radiolabeled antibody probes. [NIH] Body Fluids: Liquid components of living organisms. [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 scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [NIH] 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] Brain Hypoxia: Lack of oxygen leading to unconsciousness. [NIH] Brain Infarction: The formation of an area of necrosis in the brain, including the cerebral hemispheres (cerebral infarction), thalami, basal ganglia, brain stem (brain stem infarctions), or cerebellum secondary to an insufficiency of arterial or venous blood flow. [NIH] Brain Injuries: Acute and chronic injuries to the brain, including the cerebral hemispheres, cerebellum, and brain stem. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with diffuse axonal injury or coma, posttraumatic. Localized injuries may be associated with neurobehavioral manifestations; hemiparesis, or other focal neurologic deficits. [NIH] Brain Ischemia: Localized reduction of blood flow to brain tissue due to arterial obtruction or systemic hypoperfusion. This frequently occurs in conjuction with brain hypoxia. Prolonged ischemia is associated with brain infarction. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU]
Dictionary 123
Bronchitis: Inflammation (swelling and reddening) of the bronchi. [NIH] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels. [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] Carbohydrates: The largest class of organic compounds, including starches, glycogens, cellulose, gums, and simple sugars. Carbohydrates are composed of carbon, hydrogen, and oxygen in a ratio of Cn(H2O)n. [NIH] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carbon Monoxide Poisoning: Toxic asphyxiation due to the displacement of oxygen from oxyhemoglobin by carbon monoxide. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiac arrest: A sudden stop of heart function. [NIH] 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] Cardiomyoplasty: A surgical procedure that involves detaching one end of a back muscle and attaching it to the heart. An electric stimulator causes the muscle to contract to pump blood from the heart. [NIH] Cardiopulmonary: Having to do with the heart and lungs. [NIH]
124
Anoxia
Cardiopulmonary Resuscitation: The artificial substitution of heart and lung action as indicated for heart arrest resulting from electric shock, drowning, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation and closed-chest cardiac massage. [NIH] Cardiopulmonary Resuscitation: The artificial substitution of heart and lung action as indicated for heart arrest resulting from electric shock, drowning, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation and closed-chest cardiac massage. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carotid Body: A small cluster of chemoreceptive and supporting cells located near the bifurcation of the internal carotid artery. The carotid body, which is richly supplied with fenestrated capillaries, senses the pH, carbon dioxide, and oxygen concentrations in the blood and plays a crucial role in their homeostatic control. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Caspases: A family of intracellular cysteine endopeptidases. They play a key role in inflammation and mammalian apoptosis. They are specific for aspartic acid at the P1 position. They are divided into two classes based on the lengths of their N-terminal prodomains. Caspases-1,-2,-4,-5,-8, and -10 have long prodomains and -3,-6,-7,-9 have short prodomains. EC 3.4.22.-. [NIH] Catalase: An oxidoreductase that catalyzes the conversion of hydrogen peroxide to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in acatalasia. EC 1.11.1.6. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU]
Dictionary 125
Caudate Nucleus: Elongated gray mass of the neostriatum located adjacent to the lateral ventricle of the brain. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Ceftazidime: Semisynthetic, broad-spectrum antibacterial derived from cephaloridine and used especially for Pseudomonas and other gram-negative infections in debilitated patients. [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 Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Cephaloridine: A cephalosporin antibiotic. [NIH] Ceramide: A type of fat produced in the body. It may cause some types of cells to die, and is being studied in cancer treatment. [NIH] Cerebellum: Part of the metencephalon that lies in the posterior cranial fossa behind the brain stem. It is concerned with the coordination of movement. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [NIH] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebral Infarction: The formation of an area of necrosis in the cerebrum caused by an
126
Anoxia
insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., infarction, anterior cerebral artery), and etiology (e.g., embolic infarction). [NIH]
Cerebral Palsy: Refers to a motor disability caused by a brain dysfunction. [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] Cerebrovascular Disorders: A broad category of disorders characterized by impairment of blood flow in the arteries and veins which supply the brain. These include cerebral infarction; brain ischemia; hypoxia, brain; intracranial embolism and thrombosis; intracranial arteriovenous malformations; and vasculitis, central nervous system. In common usage, the term cerebrovascular disorders is not limited to conditions that affect the cerebrum, but refers to vascular disorders of the entire brain including the diencephalon; brain stem; and cerebellum. [NIH] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cerumen: The yellow or brown waxy secretions produced by vestigial apocrine sweat glands in the external ear canal. [NIH] 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] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotaxis: The movement of cells or organisms toward or away from a substance in response to its concentration gradient. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chest Pain: Pressure, burning, or numbness in the chest. [NIH] Chimera: An individual that contains cell populations derived from different zygotes. [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] Cholesteatoma: A non-neoplastic keratinizing mass with stratified squamous epithelium, frequently occurring in the meninges, central nervous system, bones of the skull, and most commonly in the middle ear and mastoid region. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially
Dictionary 127
the brain and spinal cord, and in animal fats and oils. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chondrocytes: Polymorphic cells that form cartilage. [NIH] Chorea: Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as choreatic disorders. Chorea is also a frequent manifestation of basal ganglia diseases. [NIH] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chromosome Aberrations: Deviations from the normal number or structure of chromosomes, not necessarily associated with disease. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Obstructive Pulmonary Disease: Collective term for chronic bronchitis and emphysema. [NIH] Cinnarizine: A piperazine derivative with histamine H1-receptor and calcium-channel blocking activity and considerable antiemetic properties. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] 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
128
Anoxia
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] Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis. [NIH] Cochlea: The part of the internal ear that is concerned with hearing. It forms the anterior part of the labyrinth, is conical, and is placed almost horizontally anterior to the vestibule. [NIH]
Cochlear: Of or pertaining to the cochlea. [EU] Cochlear Diseases: Diseases of the cochlea, the part of the inner ear that is concerned with hearing. [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] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Comatose: Pertaining to or affected with coma. [EU] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1
Dictionary 129
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] Compress: A plug used to occludate an orifice in the control of bleeding, or to mop up secretions; an absorbent pad. [NIH] Compulsions: In psychology, an irresistible urge, sometimes amounting to obsession to perform a particular act which usually is carried out against the performer's will or better judgment. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH]
130
Anoxia
Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Conjugated: Acting or operating as if joined; simultaneous. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constriction: The act of constricting. [NIH] Constriction, Pathologic: The condition of an anatomical structure's being constricted beyond normal dimensions. [NIH] Continuum: An area over which the vegetation or animal population is of constantly changing composition so that homogeneous, separate communities cannot be distinguished. [NIH]
Contractility: Capacity for becoming short in response to a suitable stimulus. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]
Conus: A large, circular, white patch around the optic disk due to the exposing of the sclera as a result of degenerative change or congenital abnormality in the choroid and retina. [NIH] Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] Convulsive: Relating or referring to spasm; affected with spasm; characterized by a spasm or spasms. [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 Artery Bypass: Surgical therapy of ischemic coronary artery disease achieved by grafting a section of saphenous vein, internal mammary artery, or other substitute between the aorta and the obstructed coronary artery distal to the obstructive lesion. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that
Dictionary 131
has ruptured and discharged its ovum. [NIH] Corpus Striatum: Striped gray and white matter consisting of the neostriatum and paleostriatum (globus pallidus). It is located in front of and lateral to the thalamus in each cerebral hemisphere. The gray substance is made up of the caudate nucleus and the lentiform nucleus (the latter consisting of the globus pallidus and putamen). The white matter is the internal capsule. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Cosmic Radiation: High-energy radiation or particles from extraterrestrial space that strike the earth, its atmosphere, or spacecraft and may create secondary radiation as a result of collisions with the atmosphere or spacecraft. [NIH] Courtship: The mutual attraction between individuals of the opposite sex. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Cryofixation: Fixation of a tissue by localized cooling at very low temperature. [NIH] Cryopreservation: Preservation of cells, tissues, organs, or embryos by freezing. In histological preparations, cryopreservation or cryofixation is used to maintain the existing form, structure, and chemical composition of all the constituent elements of the specimens. [NIH]
Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cyanide: An extremely toxic class of compounds that can be lethal on inhaling of ingesting in minute quantities. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cysteine Endopeptidases: Endopeptidases which have a cysteine involved in the catalytic process. This group of enzymes is inactivated by sulfhydryl reagents. EC 3.4.22. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU]
132
Anoxia
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] Cytoprotection: The process by which chemical compounds provide protection to cells against harmful agents. [NIH] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delirium: (DSM III-R) an acute, reversible organic mental disorder characterized by reduced ability to maintain attention to external stimuli and disorganized thinking as manifested by rambling, irrelevant, or incoherent speech; there are also a reduced level of consciousness, sensory misperceptions, disturbance of the sleep-wakefulness cycle and level of psychomotor activity, disorientation to time, place, or person, and memory impairment. Delirium may be caused by a large number of conditions resulting in derangement of cerebral metabolism, including systemic infection, poisoning, drug intoxication or withdrawal, seizures or head trauma, and metabolic disturbances such as hypoxia, hypoglycaemia, fluid, electrolyte, or acid-base imbalances, or hepatic or renal failure. Called also acute confusional state and acute brain syndrome. [EU] Delusions: A false belief regarding the self or persons or objects outside the self that persists despite the facts, and is not considered tenable by one's associates. [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] Dentate Gyrus: Gray matter situated above the gyrus hippocampi. It is composed of three layers. The molecular layer is continuous with the hippocampus in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called granule cells, whose axons pass through the polymorphic layer ending on the dendrites of pyramidal cells in the hippocampus. [NIH]
Dictionary 133
Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Dextroamphetamine: The d-form of amphetamine. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diffuse Axonal Injury: A relatively common sequela of blunt head injury, characterized by a global disruption of axons throughout the brain. Associated clinical features may include neurobehavioral manifestations; persistent vegetative state; dementia; and other disorders. [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] Digitalis: A genus of toxic herbaceous Eurasian plants of the Scrophulaceae which yield cardiotonic glycosides. The most useful are Digitalis lanata and D. purpurea. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] 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] Domesticated: Species in which the evolutionary process has been influenced by humans to meet their needs. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate
134
Anoxia
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] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dorsum: A plate of bone which forms the posterior boundary of the sella turcica. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dystonia: Disordered tonicity of muscle. [EU] Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electric shock: A dangerous patho-physiological effect resulting from an electric current passing through the body of a human or animal. [NIH] Electrode: Component of the pacing system which is at the distal end of the lead. It is the interface with living cardiac tissue across which the stimulus is transmitted. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU]
Dictionary 135
Electromagnetic Fields: Fields representing the joint interplay of electric and magnetic forces. [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] Electroretinogram: The electrical effect recorded from the surface of the eyeball and originated by a pulse of light. [NIH] Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e., radiation. [NIH] 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] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] Endarterectomy: Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called atherectomy. [NIH] Endocrine Glands: Ductless glands that secrete substances which are released directly into the circulation and which influence metabolism and other body functions. [NIH] Endocrinologist: A doctor that specializes in diagnosing and treating hormone disorders. [NIH]
Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. Endosomes play a central role in endocytosis. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endolymphatic Duct: Duct connecting the endolymphatic sac with the membranous labyrinth. [NIH] Endometrium: The layer of tissue that lines the uterus. [NIH] Endorphins: One of the three major groups of endogenous opioid peptides. They are large peptides derived from the pro-opiomelanocortin precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; opioid peptides is used for the broader group. [NIH] 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,
136
Anoxia
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] Enkephalins: One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla. [NIH] Entorhinal Cortex: Cortex where the signals are combined with those from other sensory systems. [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] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epilepticus: Repeated and prolonged epileptic seizures without recovery of consciousness between attacks. [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] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH]
Dictionary 137
Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Estrogens: A class of sex hormones associated with the development and maintenance of secondary female sex characteristics and control of the cyclical changes in the reproductive cycle. They are also required for pregnancy maintenance and have an anabolic effect on protein metabolism and water retention. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Excitability: Property of a cardiac cell whereby, when the cell is depolarized to a critical level (called threshold), the membrane becomes permeable and a regenerative inward current causes an action potential. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Excitatory Amino Acids: Endogenous amino acids released by neurons as excitatory neurotransmitters. Glutamic acid is the most common excitatory neurotransmitter in the brain. Aspartic acid has been regarded as an excitatory transmitter for many years, but the extent of its role as a transmitter is unclear. [NIH] Excitotoxicity: Excessive exposure to glutamate or related compounds can kill brain neurons, presumably by overstimulating them. [NIH] Excrete: To get rid of waste from the body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Expiration: The act of breathing out, or expelling air from the lungs. [EU] External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extrapyramidal: Outside of the pyramidal tracts. [EU] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Family Planning: Programs or services designed to assist the family in controlling
138
Anoxia
reproduction by either improving or diminishing fertility. [NIH] Fast Neutrons: Neutrons, the energy of which exceeds some arbitrary level, usually around one million electron volts. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Ferritin: An iron-containing protein complex that is formed by a combination of ferric iron with the protein apoferritin. [NIH] Fetal Anoxia: Fetal oxygen deficiency. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrillation: A small, local, involuntary contraction of muscle, invisible under the skin, resulting from spontaneous activation of single muscle cells or muscle fibres. [EU] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibrinolysis: The natural enzymatic dissolution of fibrin. [NIH] Fibrinolytic: Pertaining to, characterized by, or causing the dissolution of fibrin by enzymatic action [EU] Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Filarioidea: A superfamily of nematodes of the suborder Spirurina. Its organisms possess a filiform body and a mouth surrounded by papillae. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flatus: Gas passed through the rectum. [NIH] Flunarizine: Flunarizine is a selective calcium entry blocker with calmodulin binding properties and histamine H1 blocking activity. It is effective in the prophylaxis of migraine, occlusive peripheral vascular disease, vertigo of central and peripheral origin, and as an adjuvant in the therapy of epilepsy. [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] Fold: A plication or doubling of various parts of the body. [NIH] Forearm: The part between the elbow and the wrist. [NIH]
Dictionary 139
Fossa: A cavity, depression, or pit. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Frontal Lobe: The anterior part of the cerebral hemisphere. [NIH] Fructose: A type of sugar found in many fruits and vegetables and in honey. Fructose is used to sweeten some diet foods. It is considered a nutritive sweetener because it has calories. [NIH] 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] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastric: Having to do with the stomach. [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Targeting: The integration of exogenous DNA into the genome of an organism at sites where its expression can be suitably controlled. This integration occurs as a result of homologous recombination. [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
140
Anoxia
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 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] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Geriatric: Pertaining to the treatment of the aged. [EU] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestation period: The period of development of the young from the time of conception until birth. [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] Glioblastoma: A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures. [NIH] Globus Pallidus: The representation of the phylogenetically oldest part of the corpus striatum called the paleostriatum. It forms the smaller, more medial part of the lentiform nucleus. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomerular Filtration Rate: The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to inulin clearance. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH]
Dictionary 141
Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycols: A generic grouping for dihydric alcohols with the hydroxy groups (-OH) located on different carbon atoms. They are viscous liquids with high boiling points for their molecular weights. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanine: One of the four DNA bases. [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] Hair Cells: Mechanoreceptors located in the organ of Corti that are sensitive to auditory stimuli and in the vestibular apparatus that are sensitive to movement of the head. In each
142
Anoxia
case the accessory sensory structures are arranged so that appropriate stimuli cause movement of the hair-like projections (stereocilia and kinocilia) which relay the information centrally in the nervous system. [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] Hammer: The largest of the three ossicles of the ear. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [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] Heart Arrest: Sudden and usually momentary cessation of the heart beat. This sudden cessation may, but not usually, lead to death, sudden, cardiac. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heartbeat: One complete contraction of the heart. [NIH] Hematoma: An extravasation of blood localized in an organ, space, or tissue. [NIH] Hematoxylin: A dye obtained from the heartwood of logwood (Haematoxylon campechianum Linn., Leguminosae) used as a stain in microscopy and in the manufacture of ink. [NIH] Hemiparesis: The weakness or paralysis affecting one side of the body. [NIH] Hemiplegia: Severe or complete loss of motor function on one side of the body. This condition is usually caused by BRAIN DISEASES that are localized to the cerebral hemisphere opposite to the side of weakness. Less frequently, BRAIN STEM lesions; cervical spinal cord diseases; peripheral nervous system diseases; and other conditions may manifest as hemiplegia. The term hemiparesis (see paresis) refers to mild to moderate weakness involving one side of the body. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemorrhagic stroke: A disorder involving bleeding within ischemic brain tissue. Hemorrhagic stroke occurs when blood vessels that are damaged or dead from lack of blood supply (infarcted), located within an area of infarcted brain tissue, rupture and transform an
Dictionary 143
"ischemic" stroke into a hemorrhagic stroke. Ischemia is inadequate tissue oxygenation caused by reduced blood flow; infarction is tissue death resulting from ischemia. Bleeding irritates the brain tissues, causing swelling (cerebral edema). Blood collects into a mass (hematoma). Both swelling and hematoma will compress and displace brain tissue. [NIH] Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts. [NIH] Hepatic: Refers to the liver. [NIH] Hepatocyte: A liver cell. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] 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 Simplex Encephalitis: An inflammatory disease of the skin or mucous membrane characterized by the formation of clusters of small vesicles. [NIH] 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]
Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [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] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH]
144
Anoxia
Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxides: Inorganic compounds that contain the OH- group. [NIH] Hydroxyl Radical: The univalent radical OH that is present in hydroxides, alcohols, phenols, glycols. [NIH] Hydroxylation: Hydroxylate, to introduce hydroxyl into (a compound or radical) usually by replacement of hydrogen. [EU] Hyperbaric: Characterized by greater than normal pressure or weight; applied to gases under greater than atmospheric pressure, as hyperbaric oxygen, or to a solution of greater specific gravity than another taken as a standard of reference. [EU] Hyperbaric oxygen: Oxygen that is at an atmospheric pressure higher than the pressure at sea level. Breathing hyperbaric oxygen to enhance the effectiveness of radiation therapy is being studied. [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hyperoxia: An abnormal increase in the amount of oxygen in the tissues and organs. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthermia: A type of treatment in which body tissue is exposed to high temperatures to damage and kill cancer cells or to make cancer cells more sensitive to the effects of radiation and certain anticancer drugs. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] Hypoglycaemia: An abnormally diminished concentration of glucose in the blood, which may lead to tremulousness, cold sweat, piloerection, hypothermia, and headache, accompanied by irritability, confusion, hallucinations, bizarre behaviour, and ultimately, convulsions and coma. [EU] Hypoglycemia: Abnormally low blood sugar [NIH] Hypoglycemic: An orally active drug that produces a fall in blood glucose concentration. [NIH]
Hypotension: Abnormally low blood pressure. [NIH] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals; in man usually accidental or unintentional. [NIH] Hypoxanthine: A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway. [NIH] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hypoxic: Having too little oxygen. [NIH] Immune response: The activity of the immune system against foreign substances (antigens).
Dictionary 145
[NIH]
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] 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] Immunoblotting: Immunologic methods for isolating and quantitatively measuring immunoreactive substances. When used with immune reagents such as monoclonal antibodies, the process is known generically as western blot analysis (blotting, western). [NIH]
Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Impaction: The trapping of an object in a body passage. Examples are stones in the bile duct or hardened stool in the colon. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [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] Inbreeding: The mating of plants or non-human animals which are closely related genetically. [NIH] Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] 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]
146
Anoxia
Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [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] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH] Inotropic: Affecting the force or energy of muscular contractions. [EU] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insomnia: Difficulty in going to sleep or getting enough sleep. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] 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]
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.
Dictionary 147
IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Capsule: White matter pathway, flanked by nuclear masses, consisting of both afferent and efferent fibers projecting between the cerebral cortex and the brainstem. It consists of three distinct parts: an anterior limb, posterior limb, and genu. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestines: The section of the alimentary canal from the stomach to the anus. It includes the large intestine and small intestine. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracranial Embolism: The sudden obstruction of a blood vessel by an embolus. [NIH] Intracranial Embolism and Thrombosis: Embolism or thrombosis involving blood vessels which supply intracranial structures. Emboli may originate from extracranial or intracranial sources. Thrombosis may occur in arterial or venous structures. [NIH] Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Intravascular: Within a vessel or vessels. [EU] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is usually performed for the introducing or withdrawing of fluids from the body. [NIH] Inulin: A starch found in the tubers and roots of many plants. Since it is hydrolyzable to fructose, it is classified as a fructosan. It has been used in physiologic investigation for determination of the rate of glomerular function. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ion Transport: The movement of ions across energy-transducing cell membranes. Transport can be active or passive. Passive ion transport (facilitated diffusion) derives its energy from the concentration gradient of the ion itself and allows the transport of a single solute in one direction (uniport). Active ion transport is usually coupled to an energy-yielding chemical or photochemical reaction such as ATP hydrolysis. This form of primary active transport is called an ion pump. Secondary active transport utilizes the voltage and ion gradients produced by the primary transport to drive the cotransport of other ions or molecules. These may be transported in the same (symport) or opposite (antiport) direction. [NIH] Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a
148
Anoxia
net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ivermectin: A mixture of ivermectin component B1a (RN 71827-03-7) and B1b (RN 70209-813), which is a semisynthetic product from Streptomyces avermitilis. A potent macrocyclic lactone disaccharide antiparasitic agent used to prevent and treat parasite infestations in animals. The compound has activity against internal and external parasites and has been found effective against arthropods, insects, nematodes, filarioidea, platyhelminths, and protozoa. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]
Kainate: Glutamate receptor. [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] Kidney stone: A stone that develops from crystals that form in urine and build up on the inner surfaces of the kidney, in the renal pelvis, or in the ureters. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Labyrinth: The internal ear; the essential part of the organ of hearing. It consists of an osseous and a membranous portion. [NIH] Lathyrism: A paralytic condition of the legs caused by ingestion of lathyrogens, especially beta-aminopropionitrile, found in the seeds of plants of the genus Lathyrus. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU]
Dictionary 149
Leukemia: Cancer of blood-forming tissue. [NIH] Leukoencephalopathy: A condition with spongy holes in the brain's white matter. [NIH] Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Ligaments: Shiny, flexible bands of fibrous tissue connecting together articular extremities of bones. They are pliant, tough, and inextensile. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver Mitochondria: Yellow discoloration of the liver due to fatty degeneration of liver parenchymal cells; the cause may be chemical poisoning. [NIH] Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Lung Transplantation: The transference of either one or both of the lungs from one human or animal to another. [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]
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.
150
Anoxia
These tubes branch, like blood vessels, into all the tissues of the body. [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] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Macroglia: A type of neuroglia composed of astrocytes. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammary: Pertaining to the mamma, or breast. [EU] Mammogram: An x-ray of the breast. [NIH] Mania: Excitement of psychotic proportions manifested by mental and physical hyperactivity, disorganization of behaviour, and elevation of mood. [EU] Manic: Affected with mania. [EU] Mastoiditis: Inflammation of the cavity and air cells in the mastoid part of the temporal bone. [NIH] Meatus: A canal running from the internal auditory foramen through the petrous portion of the temporal bone. It gives passage to the facial and auditory nerves together with the auditory branch of the basilar artery and the internal auditory veins. [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and
Dictionary 151
store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Memory Disorders: Disturbances in registering an impression, in the retention of an acquired impression, or in the recall of an impression. Memory impairments are associated with dementia; craniocerebraltrauma; encephalitis; alcoholism (see also alcohol amnestic disorder); schizophrenia; and other conditions. [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] Menstrual Cycle: The period of the regularly recurring physiologic changes in the endometrium occurring during the reproductive period in human females and some primates and culminating in partial sloughing of the endometrium (menstruation). [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH]
Mesolimbic: Inner brain region governing emotion and drives. [NIH] Mesons: Short-lived elementary particles found in cosmic radiation or produced from nuclear disintegration. Their mass is between that of protons and electrons and they can be negative, positive, or neutral. pi-Mesons (pions) are heavier than mu-mesons (muons) and are proposed for cancer radiotherapy because their capture and disintegration by matter produces powerful, but short-lived, secondary radiation. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcalcifications: Tiny deposits of calcium in the breast that cannot be felt but can be detected on a mammogram. A cluster of these very small specks of calcium may indicate that cancer is present. [NIH]
152
Anoxia
Microdialysis: A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane. [NIH] Microglia: The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling. [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] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitogen-Activated Protein Kinase Kinases: A serine-threonine protein kinase family whose members are components in protein kinase cascades activated by diverse stimuli. These MAPK kinases phosphorylate mitogen-activated protein kinases and are themselves phosphorylated by MAP kinase kinase kinases. JNK kinases (also known as SAPK kinases) are a subfamily. EC 2.7.10.- [NIH] Mitogen-Activated Protein Kinases: A superfamily of protein-serine-threonine kinases that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by mitogen-activated protein kinase kinases which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP kinase kinase kinases). Families of these mitogen-activated protein kinases (MAPKs) include extracellular signal-regulated kinases (ERKs), stress-activated protein kinases (SAPKs) (also known as c-jun terminal kinases (JNKs)), and p38-mitogen-activated protein kinases. EC 2,7,1.- [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] Mitotic: Cell resulting from mitosis. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]
Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH]
Dictionary 153
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] Monoamine: Enzyme that breaks down dopamine in the astrocytes and microglia. [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] Mood Disorders: Those disorders that have a disturbance in mood as their predominant feature. [NIH] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motor Activity: The physical activity of an organism as a behavioral phenomenon. [NIH] Movement Disorders: Syndromes which feature dyskinesias as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions. [NIH] Mucinous: Containing or resembling mucin, the main compound in mucus. [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 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] Muscle Relaxation: That phase of a muscle twitch during which a muscle returns to a resting position. [NIH] Myelin: The fatty substance that covers and protects nerves. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing myocardial reperfusion injury. [NIH]
154
Anoxia
Myocardial Reperfusion Injury: Functional, metabolic, or structural changes in ischemic heart muscle thought to result from reperfusion to the ischemic areas. Changes can be fatal to muscle cells and may include edema with explosive cell swelling and disintegration, sarcolemma disruption, fragmentation of mitochondria, contraction band necrosis, enzyme washout, and calcium overload. Other damage may include hemorrhage and ventricular arrhythmias. One possible mechanism of damage is thought to be oxygen free radicals. Treatment currently includes the introduction of scavengers of oxygen free radicals, and injury is thought to be prevented by warm blood cardioplegic infusion prior to reperfusion. [NIH]
Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myoclonus: Involuntary shock-like contractions, irregular in rhythm and amplitude, followed by relaxation, of a muscle or a group of muscles. This condition may be a feature of some central nervous systems diseases (e.g., epilepsy, myoclonic). Nocturnal myoclonus may represent a normal physiologic event or occur as the principal feature of the nocturnal myoclonus syndrome. (From Adams et al., Principles of Neurology, 6th ed, pp102-3). [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms. [NIH] Neostriatum: The phylogenetically newer part of the corpus striatum consisting of the caudate nucleus and putamen. It is often called simply the striatum. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neurobehavioral Manifestations: Signs and symptoms of higher cortical dysfunction caused by organic conditions. These include certain behavioral alterations and impairments of skills involved in the acquisition, processing, and utilization of knowledge or information. [NIH]
Neuroleptic: A term coined to refer to the effects on cognition and behaviour of antipsychotic drugs, which produce a state of apathy, lack of initiative, and limited range of
Dictionary 155
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] Neuroma: A tumor that arises in nerve cells. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropharmacology: The branch of pharmacology dealing especially with the action of drugs upon various parts of the nervous system. [NIH] Neurophysiology: The scientific discipline concerned with the physiology of the nervous system. [NIH] Neuroprotective Agents: Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutrophil: A type of white blood cell. [NIH] Neutrophil Infiltration: The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions. [NIH] Nimodipine: A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure. [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]
Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a
156
Anoxia
widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleus Accumbens: Collection of pleomorphic cells in the caudal part of the anterior horn of the lateral ventricle, in the region of the olfactory tubercle, lying between the head of the caudate nucleus and the anterior perforated substance. It is part of the so-called ventral striatum, a composite structure considered part of the basal ganglia. [NIH] Obsessive-Compulsive Disorder: An anxiety disorder characterized by recurrent, persistent obsessions or compulsions. Obsessions are the intrusive ideas, thoughts, or images that are experienced as senseless or repugnant. Compulsions are repetitive and seemingly purposeful behavior which the individual generally recognizes as senseless and from which the individual does not derive pleasure although it may provide a release from tension. [NIH] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Ophthalmic: Pertaining to the eye. [EU] Opiate: A remedy containing or derived from opium; also any drug that induces sleep. [EU] Opium: The air-dried exudate from the unripe seed capsule of the opium poppy, Papaver somniferum, or its variant, P. album. It contains a number of alkaloids, but only a few morphine, codeine, and papaverine - have clinical significance. Opium has been used as an analgesic, antitussive, antidiarrheal, and antispasmodic. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]
Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH]
Dictionary 157
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] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Orthostatic: Pertaining to or caused by standing erect. [EU] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Ossicles: The hammer, anvil and stirrup, the small bones of the middle ear, which transmit the vibrations from the tympanic membrane to the oval window. [NIH] Ossification: The formation of bone or of a bony substance; the conversion of fibrous tissue or of cartilage into bone or a bony substance. [EU] Otitis: Inflammation of the ear, which may be marked by pain, fever, abnormalities of hearing, hearing loss, tinnitus, and vertigo. [EU] Otitis Media: Inflammation of the middle ear. [NIH] Ouabain: A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like digitalis. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-exchanging atpase. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxamic Acid: Amino-substituted glyoxylic acid derivative. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 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
158
Anoxia
nerve. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Papilla: A small nipple-shaped elevation. [NIH] Papillary: Pertaining to or resembling papilla, or nipple. [EU] 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] 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] Parietal Lobe: Upper central part of the cerebral hemisphere. [NIH] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] 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] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [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] Pericardial Effusion: Presence of fluid within the pericardium. [NIH] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Perilymph: The fluid contained within the space separating the membranous from the osseous labyrinth of the ear. [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] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral
Dictionary 159
sensory receptors. [NIH] Peripheral Vascular Disease: Disease in the large blood vessels of the arms, legs, and feet. People who have had diabetes for a long time may get this because major blood vessels in their arms, legs, and feet are blocked and these limbs do not receive enough blood. The signs of PVD are aching pains in the arms, legs, and feet (especially when walking) and foot sores that heal slowly. Although people with diabetes cannot always avoid PVD, doctors say they have a better chance of avoiding it if they take good care of their feet, do not smoke, and keep both their blood pressure and diabetes under good control. [NIH] Perivascular: Situated around a vessel. [EU] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photodynamic therapy: Treatment with drugs that become active when exposed to light. These drugs kill cancer cells. [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] Phytochrome: A blue-green biliprotein widely distributed in the plant kingdom. [NIH] Picric: Dermatitis from picric acid. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Piloerection: Involuntary erection or bristling of hairs. [NIH]
160
Anoxia
Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasmalogens: Any glycerophospholipid in which one of the two acyl chains is attached to glycerol with an ether alkenyl linkage instead of an ester as with the other glycerophospholipids. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Platelet 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] Platyhelminths: A phylum of acoelomate, bilaterally symmetrical flatworms, without a definite anus. It includes three classes: Cestoda, Turbellaria, and Trematoda. [NIH]
Dictionary 161
Pleomorphic: Occurring in various distinct forms. In terms of cells, having variation in the size and shape of cells or their nuclei. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polygalacturonase: A cell wall-degrading enzyme found in microorganisms and higher plants. It catalyzes the random hydrolysis of 1,4-alpha-D-galactosiduronic linkages in pectate and other galacturonans. EC 3.2.1.15. [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 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] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Pons: The part of the central nervous system lying between the medulla oblongata and the mesencephalon, ventral to the cerebellum, and consisting of a pars dorsalis and a pars ventralis. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-traumatic: Occurring as a result of or after injury. [EU] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potassium Channels: Cell membrane glycoproteins selective for potassium ions. [NIH] Potassium Cyanide: Potassium cyanide (K(CN)). A highly poisonous compound that is an inhibitor of many metabolic processes, but has been shown to be an especially potent inhibitor of heme enzymes and hemeproteins. It is used in many industrial processes. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of
162
Anoxia
health care and delivery. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Pregnancy Maintenance: Physiological mechanisms that sustain the state of pregnancy. [NIH]
Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] 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] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Kinase C: An enzyme that phosphorylates proteins on serine or threonine residues in the presence of physiological concentrations of calcium and membrane phospholipids. The additional presence of diacylglycerols markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by phorbol esters and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters. EC 2.7.1.-. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Protein-Serine-Threonine Kinases: A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate
Dictionary 163
donors. EC 2.7.10. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] 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] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Psychotomimetic: Psychosis miming. [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 Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulmonary Embolism: Embolism in the pulmonary artery or one of its branches. [NIH] Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of
164
Anoxia
pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Putamen: The largest and most lateral of the basal ganglia lying between the lateral medullary lamina of the globus pallidus and the external capsule. It is part of the neostriatum and forms part of the lentiform nucleus along with the globus pallidus. [NIH] Pyramidal Tracts: Fibers that arise from cells within the cerebral cortex, pass through the medullary pyramid, and descend in the spinal cord. Many authorities say the pyramidal tracts include both the corticospinal and corticobulbar tracts. [NIH] Quinoxaline: AMPA/Kainate antagonist. [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] 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] 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] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH]
Dictionary 165
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] Reflex: An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [NIH]
Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renal tubular: A defect in the kidneys that hinders their normal excretion of acids. Failure to excrete acids can lead to weak bones, kidney stones, and poor growth in children. [NIH] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH] Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Reproductive cells: Egg and sperm cells. Each mature reproductive cell carries a single set of 23 chromosomes. [NIH] Research Personnel: Those individuals engaged in research. [NIH] Resection: Removal of tissue or part or all of an organ by surgery. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] 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 Physiology: Functions and activities of the respiratory tract as a whole or of any of its parts. [NIH] Respiratory System: The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought
166
Anoxia
about. [NIH] Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Ganglion Cells: Cells of the innermost nuclear layer of the retina, the ganglion cell layer, which project axons through the optic nerve to the brain. They are quite variable in size and in the shapes of their dendritic arbors, which are generally confined to the inner plexiform layer. [NIH] Retinoids: Derivatives of vitamin A. Used clinically in the treatment of severe cystic acne, psoriasis, and other disorders of keratinization. Their possible use in the prophylaxis and treatment of cancer is being actively explored. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU] Retrograde Amnesia: Amnesia extending backward, to include material antedating the onset of amnesia proper. [NIH] Retroperitoneal: Having to do with the area outside or behind the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Rhamnose: A methylpentose whose L- isomer is found naturally in many plant glycosides and some gram-negative bacterial lipopolysaccharides. [NIH] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickettsiae: One of a group of obligate intracellular parasitic microorganisms, once regarded as intermediate in their properties between bacteria and viruses but now classified as bacteria in the order Rickettsiales, which includes 17 genera and 3 families: Rickettsiace. [NIH]
Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of
Dictionary 167
developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rotenone: A botanical insecticide that is an inhibitor of mitochondrial electron transport. [NIH]
Rubella: An acute, usually benign, infectious disease caused by a togavirus and most often affecting children and nonimmune young adults, in which the virus enters the respiratory tract via droplet nuclei and spreads to the lymphatic system. It is characterized by a slight cold, sore throat, and fever, followed by enlargement of the postauricular, suboccipital, and cervical lymph nodes, and the appearances of a fine pink rash that begins on the head and spreads to become generalized. Called also German measles, roetln, röteln, and three-day measles, and rubeola in French and Spanish. [EU] Ryanodine: Insecticidal alkaloid isolated from Ryania speciosa; proposed as a myocardial depressant. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saphenous: Applied to certain structures in the leg, e. g. nerve vein. [NIH] Saphenous Vein: The vein which drains the foot and leg. [NIH] Sarcolemma: The plasma membrane of a smooth, striated, or cardiac muscle fiber. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed pictures of organs inside the body. MRI scans use a large magnet connected to a computer to create pictures of areas inside the body. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] 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] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to
168
Anoxia
as epilepsy or "seizure disorder." [NIH] Semicircular canal: Three long canals of the bony labyrinth of the ear, forming loops and opening into the vestibule by five openings. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] 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] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] 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]
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 receptor-
Dictionary 169
mediated 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] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skin graft: Skin that is moved from one part of the body to another. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Sludge: A clump of agglutinated red blood cells. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Snails: Marine, freshwater, or terrestrial mollusks of the class Gastropoda. Most have an enclosing spiral shell, and several genera harbor parasites pathogenic to man. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] 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
170
Anoxia
bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Spermidine: A polyamine formed from putrescine. It is found in almost all tissues in association with nucleic acids. It is found as a cation at all pH values, and is thought to help stabilize some membranes and nucleic acid structures. It is a precursor of spermine. [NIH] Spermine: A biogenic polyamine formed from spermidine. It is found in a wide variety of organisms and tissues and is an essential growth factor in some bacteria. It is found as a polycation at all pH values. Spermine is associated with nucleic acids, particularly in viruses, and is thought to stabilize the helical structure. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] 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] Squamous: Scaly, or platelike. [EU] Squamous Epithelium: Tissue in an organ such as the esophagus. Consists of layers of flat, scaly cells. [NIH] Stabilization: The creation of a stable state. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Status Epilepticus: Repeated and prolonged epileptic seizures without recovery of consciousness between attacks. [NIH] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Stenosis: Narrowing or stricture of a duct or canal. [EU] 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] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Striatum: A higher brain's domain thus called because of its stripes. [NIH]
Dictionary 171
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] Stroke Volume: The amount of blood pumped out of the heart per beat not to be confused with cardiac output (volume/time). [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] Subiculum: A region of the hippocampus that projects to other areas of the brain. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Sweat Glands: Sweat-producing structures that are embedded in the dermis. Each gland consists of a single tube, a coiled body, and a superficial duct. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU]
172
Anoxia
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] Syncope: A temporary suspension of consciousness due to generalized cerebral schemia, a faint or swoon. [EU] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]
Systemic: Affecting the entire body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tamponade: The inserting of a tampon; a dressing is inserted firmly into a wound or body cavity, as the nose, uterus or vagina, principally for stopping hemorrhage. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late in appearing. [EU] Telencephalon: Paired anteriolateral evaginations of the prosencephalon plus the lamina terminalis. The cerebral hemispheres are derived from it. Many authors consider cerebrum a synonymous term to telencephalon, though a minority include diencephalon as part of the cerebrum (Anthoney, 1994). [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Tendon: A discrete band of connective tissue mainly composed of parallel bundles of collagenous fibers by which muscles are attached, or two muscles bellies joined. [NIH] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Thalamus: Paired bodies containing mostly gray substance and forming part of the lateral wall of the third ventricle of the brain. The thalamus represents the major portion of the diencephalon and is commonly divided into cellular aggregates known as nuclear groups. [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] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] 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.
Dictionary 173
[NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Ticlopidine: Ticlopidine is an effective inhibitor of platelet aggregation. The drug has been found to significantly reduce infarction size in acute myocardial infarcts and is an effective antithrombotic agent in arteriovenous fistulas, aorto-coronary bypass grafts, ischemic heart disease, venous thrombosis, and arteriosclerosis. [NIH] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts plasminogen to plasmin. It has fibrin-binding activity and is immunologically different from urinary plasminogen activator. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases. EC 3.4.21.68. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] 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] Tonicity: The normal state of muscular tension. [NIH] Tonus: A state of slight tension usually present in muscles even when they are not undergoing active contraction. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Tourniquet: A device, band or elastic tube applied temporarily to press upon an artery to stop bleeding; a device to compress a blood vessel in order to stop bleeding. [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
174
Anoxia
pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Toxoplasmosis: The acquired form of infection by Toxoplasma gondii in animals and man. [NIH]
Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Traction: The act of pulling. [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] Transient Ischemic Attacks: Focal neurologic abnormalities of sudden onset and brief duration that reflect dysfunction in the distribution of the internal carotid-middle cerebral or the vertebrobasilar arterial system. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [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] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Trigger zone: Dolorogenic zone (= producing or causing pain). [EU] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Tubercle: A rounded elevation on a bone or other structure. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A
Dictionary 175
new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Tympanic membrane: A thin, tense membrane forming the greater part of the outer wall of the tympanic cavity and separating it from the external auditory meatus; it constitutes the boundary between the external and middle ear. [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] Univalent: Pertaining to an unpaired chromosome during the zygotene stage of prophase to first metaphase in meiosis. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vasomotor: 1. Affecting the calibre of a vessel, especially of a blood vessel. 2. Any element or agent that effects the calibre of a blood vessel. [EU] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vegetative: 1. Concerned with growth and with nutrition. 2. Functioning involuntarily or unconsciously, as the vegetative nervous system. 3. Resting; denoting the portion of a cell cycle during which the cell is not involved in replication. 4. Of, pertaining to, or characteristic of plants. [EU] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venom: That produced by the poison glands of the mouth and injected by the fangs of poisonous snakes. [NIH] Venous: Of or pertaining to the veins. [EU]
176
Anoxia
Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Venous Thrombosis: The formation or presence of a thrombus within a vein. [NIH] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventral: 1. Pertaining to the belly or to any venter. 2. Denoting a position more toward the belly surface than some other object of reference; same as anterior in human anatomy. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Ventricular fibrillation: Rapid, irregular quivering of the heart's ventricles, with no effective heartbeat. [NIH] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertigo: An illusion of movement; a sensation as if the external world were revolving around the patient (objective vertigo) or as if he himself were revolving in space (subjective vertigo). The term is sometimes erroneously used to mean any form of dizziness. [EU] Vestibular: Pertaining to or toward a vestibule. In dental anatomy, used to refer to the tooth surface directed toward the vestibule of the mouth. [EU] Vestibular Aqueduct: A small bony canal linking the vestibule of the inner ear to the posterior part of the internal surface of the petrous temporal bone. It surrounds the endolymphatic duct. [NIH] Vestibule: A small, oval, bony chamber of the labyrinth. The vestibule contains the utricle and saccule, organs which are part of the balancing apparatus of the ear. [NIH] Vestibulocochlear Nerve: The 8th cranial nerve. The vestibulocochlear nerve has a cochlear part (cochlear nerve) which is concerned with hearing and a vestibular part (vestibular nerve) which mediates the sense of balance and head position. The fibers of the cochlear nerve originate from neurons of the spiral ganglion and project to the cochlear nuclei (cochlear nucleus). The fibers of the vestibular nerve arise from neurons of Scarpa's ganglion and project to the vestibular nuclei. [NIH] Vestibulocochlear Nerve Diseases: Diseases of the vestibular and/or cochlear (acoustic) nerves, which join to form the vestibulocochlear nerve. Vestibular neuritis, cochlear neuritis, and acoustic neuromas are relatively common conditions that affect these nerves. Clinical manifestations vary with which nerve is primarily affected, and include hearing loss, vertigo, and tinnitus. [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 vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor
Dictionary 177
cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the crystalline lens of the eye and in front of the retina. It is contained in a thin hyoid membrane and forms about four fifths of the optic globe. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] 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] Xanthine: An urinary calculus. [NIH] Xanthine Dehydrogenase: An enzyme that catalyzes the oxidation of xanthine in the presence of NAD+ to form urate and NADH. It acts also on a variety of other purines and aldehydes. EC 1.1.1.204. [NIH] Xanthine Oxidase: An iron-molybdenum flavoprotein containing FAD that oxidizes hypoxanthine, some other purines and pterins, and aldehydes. Deficiency of the enzyme, an autosomal recessive trait, causes xanthinuria. EC 1.1.3.22. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a
178
Anoxia
radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] 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]
179
INDEX 3 3-dimensional, 32, 113 A Abdomen, 113, 136, 149, 166, 170, 177 Abdominal, 41, 113, 158, 166 Abducens, 18, 113 Abducens Nerve, 18, 113 Acatalasia, 113, 124 Acceptor, 113, 149, 157 Acetylcholine, 113, 127, 155 Acoustic, 67, 88, 113, 176 Actin, 7, 113 Acute renal, 7, 13, 25, 113 Acyl, 113, 160 Adaptability, 113, 125 Adaptation, 8, 15, 113, 160 Adenosine, 113, 144, 159 Adenovirus, 29, 114 Adenylate Cyclase, 54, 114 Adjustment, 113, 114 Adjuvant, 114, 138 Adoptive Transfer, 25, 114 Adrenal Cortex, 114, 162 Adrenal Glands, 76, 114 Adrenal Medulla, 114, 124, 136, 155 Adrenaline, 59, 76, 114 Adrenergic, 114, 118, 134, 136, 171 Adverse Effect, 30, 80, 114, 128, 168 Aerobic, 17, 114, 152 Aerobiosis, 77, 114 Afferent, 18, 114, 147 Affinity, 29, 114, 119, 128, 169 Aggressiveness, 37, 114 Agonist, 16, 29, 114, 134 Airway, 115, 169 Akathisia, 115, 118 Akinetic Mutism, 39, 115 Aldehydes, 115, 177 Algorithms, 115, 121 Alkaline, 115, 123 Alkaloid, 115, 153, 167 Alleles, 84, 115 Allopurinol, 55, 115 Alpha Particles, 115, 164 Alternative medicine, 90, 115 Alveoli, 115, 176 Ameliorating, 78, 115 Amine, 115, 143
Amino Acids, 81, 83, 115, 119, 137, 140, 158, 161, 162, 166, 168, 171, 173, 174 Aminopropionitrile, 115, 148 Amnesia, 18, 78, 115, 166 Amnestic, 115, 151 Amphetamine, 35, 116, 133 Amyloid, 7, 116 Anabolic, 116, 137 Anaerobic, 79, 116 Anaesthesia, 49, 116, 145 Analgesic, 81, 116, 153, 156 Analog, 26, 116 Analogous, 17, 30, 78, 81, 116, 174 Anaphylatoxins, 116, 129 Anatomical, 35, 116, 120, 126, 130, 145, 152, 167 Anemia, 76, 116, 128 Anesthesia, 4, 6, 48, 115, 116, 135 Anesthetics, 116, 120, 136 Aneurism, 76, 116 Angina, 76, 116 Angioplasty, 30, 80, 116, 153 Animal model, 10, 13, 28, 116 Anions, 117, 148, 168, 171 Annealing, 117, 161 Antagonism, 117, 128 Anterior Cerebral Artery, 117, 126 Anterograde, 18, 117 Anthracycline, 59, 117 Antibacterial, 117, 125, 170 Antibiotic, 53, 75, 117, 122, 125, 170, 172 Antibodies, 117, 118, 142, 145, 153 Antibody, 114, 117, 122, 128, 142, 143, 145, 146, 148, 150, 153, 164, 169, 178 Anticholinergic, 78, 117 Anticoagulant, 117, 162 Anticonvulsant, 81, 117 Antiemetic, 117, 118, 127 Antigen, 114, 117, 118, 120, 129, 143, 145, 146, 150, 152 Antigen-Antibody Complex, 117, 129 Anti-infective, 117, 144 Anti-inflammatory, 117, 119 Anti-Inflammatory Agents, 117, 119 Antioxidant, 22, 38, 117, 119, 157 Antipsychotic, 20, 118, 127, 154 Antiserum, 118, 120 Antithrombotic, 118, 173
180
Anoxia
Anus, 118, 119, 128, 147, 160 Anxiety, 74, 81, 115, 118, 156 Aorta, 118, 130, 176 Aortic Aneurysm, 41, 118 Aortic Valve, 43, 51, 118 Apnea, 12, 118 Aponeurosis, 118, 139 Apoptosis, 7, 11, 15, 20, 27, 37, 40, 52, 118, 124 Approximate, 27, 118 Aqueous, 118, 120, 132, 144, 148 Arginine, 49, 116, 118, 155 Arterial, 118, 119, 122, 126, 144, 147, 162, 172, 174 Arteries, 5, 76, 118, 119, 121, 122, 126, 130, 153 Arterioles, 119, 122, 123 Arteriosclerosis, 119, 173 Arteriosus, 119, 163 Arteriovenous, 119, 126, 173 Arteriovenous Fistula, 119, 173 Artery, 5, 9, 43, 58, 76, 116, 117, 118, 119, 124, 130, 135, 150, 153, 163, 165, 173 Ascorbic Acid, 46, 119 Aspartate, 74, 83, 119 Aspartic Acid, 119, 124 Asphyxia, 44, 55, 74, 81, 83, 119 Aspirin, 30, 119 Assay, 15, 119 Astrocytes, 18, 29, 119, 150, 152, 153 Astrocytoma, 119, 140 Athetosis, 55, 63, 119 Atmospheric Pressure, 119, 144 Atresia, 88, 119 Atrial, 41, 120 Atrium, 120, 176 Atrophy, 34, 58, 120 Attenuated, 13, 120 Atypical, 120, 127 Auditory, 59, 88, 120, 141, 150, 175 Autoimmune disease, 120, 153 Autopsy, 47, 120 Avidity, 30, 120 Axons, 19, 30, 32, 120, 132, 133, 156, 166 B Bacteria, 16, 113, 117, 120, 121, 135, 136, 137, 141, 151, 152, 164, 166, 168, 170, 174, 175 Bacterial Infections, 88, 120 Bacterial Physiology, 113, 120 Barbiturate, 81, 120 Basal cell carcinoma, 83, 120
Basal cells, 120 Basal Ganglia, 55, 118, 120, 122, 127, 139, 140, 156, 164 Base, 24, 40, 120, 132, 140, 148, 172 Benign, 83, 120, 139, 142, 154, 164, 167 Beta Rays, 80, 120, 135 Beta-pleated, 116, 120 Beta-Thromboglobulin, 120, 147 Bilateral, 38, 121 Bile, 67, 121, 139, 145, 148, 149 Bile Acids, 121 Bile Acids and Salts, 121 Bile duct, 121, 145 Bilirubin, 121, 144 Biochemical, 9, 17, 20, 22, 28, 115, 121, 168 Biological therapy, 121, 141 Biological Transport, 121, 133 Biosynthesis, 5, 84, 121, 168 Biotechnology, 32, 33, 90, 97, 121 Biphasic, 12, 121 Bipolar Disorder, 81, 121 Bladder, 83, 121, 145, 153, 175 Blastocyst, 121, 129, 160 Blood Coagulation, 30, 121, 123, 172 Blood Coagulation Factors, 121 Blood Glucose, 121, 142, 144, 146 Blood pressure, 76, 121, 126, 144, 153, 155, 159, 169 Blood vessel, 5, 10, 76, 116, 121, 122, 124, 126, 127, 135, 140, 142, 147, 148, 149, 150, 158, 159, 169, 171, 173, 175 Blot, 122, 145 Blotting, Western, 122, 145 Body Fluids, 122, 123, 134, 169 Bone Marrow, 122, 136, 139, 145, 149, 169 Bone scan, 122, 167 Brachytherapy, 122, 147, 148, 164, 177 Bradykinin, 122, 155, 160 Brain Hypoxia, 122 Brain Infarction, 122 Brain Injuries, 88, 102, 122 Brain Ischemia, 57, 122, 126 Brain Stem, 122, 125, 126 Breeding, 10, 84, 122 Broad-spectrum, 122, 125 Bronchi, 122, 123, 136 Bronchial, 122, 143 Bronchitis, 123, 127 Bypass, 30, 123, 153, 173 C Calcification, 55, 119, 123
181
Calcium, 6, 12, 40, 123, 127, 128, 138, 151, 154, 155, 162, 168 Calmodulin, 123, 138 Capillary, 8, 122, 123, 140, 176 Capsules, 123, 140 Carbohydrates, 123, 125 Carbon Dioxide, 123, 124, 132, 139, 160, 165, 176 Carbon Monoxide Poisoning, 52, 123 Carcinogenic, 123, 146, 162 Carcinogens, 123, 156 Carcinoma, 123 Cardiac arrest, 42, 61, 74, 83, 123 Cardiac Output, 76, 123, 171 Cardiomyoplasty, 21, 123 Cardiopulmonary, 56, 61, 123, 124 Cardiopulmonary Resuscitation, 56, 61, 124 Cardiorespiratory, 34, 124 Cardiovascular, 26, 41, 48, 50, 51, 52, 58, 62, 116, 124, 168 Carotene, 124, 166 Carotid Body, 124, 126 Case report, 49, 56, 57, 124, 127 Case series, 124, 127 Caspases, 20, 35, 124 Catalase, 22, 113, 124 Catecholamine, 124, 133 Catheter, 124, 135, 147 Catheterization, 58, 116, 124, 147, 153 Cathode, 120, 124, 135 Cations, 124, 148 Caudal, 124, 156, 161 Caudate Nucleus, 117, 125, 131, 154, 156 Causal, 75, 125 Ceftazidime, 53, 125 Cell, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 20, 21, 23, 25, 26, 27, 29, 30, 36, 40, 43, 50, 53, 59, 62, 77, 80, 84, 113, 114, 116, 118, 119, 120, 121, 125, 126, 127, 129, 132, 133, 135, 136, 137, 139, 140, 141, 143, 145, 146, 147, 148, 150, 152, 153, 154, 155, 156, 157, 159, 160, 161, 162, 164, 165, 166, 168, 171, 172, 173, 174, 175, 177 Cell Adhesion, 25, 62, 125 Cell Cycle, 125, 175 Cell Death, 11, 20, 21, 27, 29, 36, 118, 125, 154 Cell Differentiation, 125, 168 Cell Division, 120, 125, 141, 150, 152, 160, 162
Cell membrane, 8, 121, 125, 133, 139, 147, 159, 161 Cell proliferation, 119, 125, 168 Cell Respiration, 125, 152, 165 Cell Survival, 11, 125, 141 Cephaloridine, 125 Ceramide, 35, 125 Cerebellum, 18, 51, 122, 125, 126, 161 Cerebral Cortex, 51, 58, 125, 137, 147, 164 Cerebral hemispheres, 120, 122, 125, 126, 140, 172 Cerebral Infarction, 74, 83, 84, 122, 125, 126 Cerebral Palsy, 44, 126 Cerebrospinal, 40, 126, 168 Cerebrospinal fluid, 126, 168 Cerebrovascular, 10, 74, 78, 81, 83, 126, 155 Cerebrovascular Disorders, 74, 83, 126 Cerebrum, 125, 126, 172 Cerumen, 88, 126 Cervical, 126, 142, 167 Chemoreceptor, 6, 118, 126 Chemotactic Factors, 126, 129 Chemotaxis, 13, 126 Chemotherapy, 80, 126 Chest Pain, 76, 126 Chimera, 8, 126 Chin, 126, 151 Cholesteatoma, 88, 126 Cholesterol, 121, 126, 130 Cholinergic, 118, 127 Chondrocytes, 127, 138 Chorea, 118, 119, 127 Choroid, 127, 130, 166 Chromatin, 118, 127, 150 Chromosome, 32, 60, 127, 142, 149, 174, 175 Chromosome Aberrations, 60, 127 Chronic, 4, 14, 17, 22, 27, 74, 81, 83, 122, 127, 146, 171 Chronic Obstructive Pulmonary Disease, 4, 127 Cinnarizine, 55, 127 Circulatory system, 75, 127 CIS, 11, 127, 166 Clamp, 12, 14, 127 Clinical Medicine, 127, 162 Clinical study, 20, 82, 102, 127 Clinical trial, 4, 20, 97, 127, 130, 163, 164 Cloning, 121, 127 Clozapine, 19, 127
182
Anoxia
Cobalt, 25, 128 Cochlea, 128, 146 Cochlear, 40, 128, 173, 176 Cochlear Diseases, 128, 173 Coenzyme, 119, 128 Cofactor, 128, 162, 172 Cognition, 102, 128, 154 Collagen, 128, 138, 160 Collapse, 82, 128, 169 Colloidal, 128, 168 Colon, 82, 128, 145 Comatose, 88, 128 Complement, 18, 116, 128, 129, 140, 160 Complementary and alternative medicine, 65, 69, 129 Complementary medicine, 65, 129 Compress, 129, 143, 173 Compulsions, 129, 156 Computational Biology, 97, 129 Computed tomography, 54, 56, 129, 167 Computerized axial tomography, 129, 167 Computerized tomography, 129 Conception, 129, 138, 140 Concomitant, 43, 58, 82, 129 Cones, 129, 166 Confounding, 66, 129 Confusion, 130, 144, 155, 175 Congestion, 118, 130 Conjugated, 121, 130, 131 Connective Tissue, 119, 122, 128, 130, 138, 139, 149, 172 Consciousness, 88, 116, 130, 132, 133, 136, 163, 166, 170, 172 Constipation, 118, 130 Constriction, 76, 130, 148, 175 Constriction, Pathologic, 130, 175 Continuum, 88, 130 Contractility, 59, 130 Contraindications, ii, 130 Controlled study, 54, 130 Conus, 81, 130, 163 Convulsions, 81, 117, 120, 130, 144, 155 Convulsive, 75, 130 Coordination, 125, 130, 153 Coronary, 5, 9, 43, 48, 50, 58, 76, 130, 153, 173 Coronary Artery Bypass, 48, 130 Coronary heart disease, 5, 130 Coronary Thrombosis, 130, 153 Corpus, 44, 130, 131, 140, 154, 162, 177 Corpus Luteum, 130, 162 Corpus Striatum, 44, 131, 140, 154
Cortex, 20, 131, 136 Cortical, 7, 19, 66, 131, 137, 154, 167 Cosmic Radiation, 131, 151 Courtship, 17, 131 Cranial, 113, 125, 131, 142, 147, 156, 158, 176 Craniocerebral Trauma, 131, 142, 173 Cryofixation, 131 Cryopreservation, 43, 131 Cultured cells, 25, 131 Curative, 131, 172 Cyanide, 131, 161 Cyclic, 83, 114, 123, 131, 141, 155 Cysteine, 22, 124, 131, 171 Cysteine Endopeptidases, 124, 131 Cystine, 131 Cytochrome, 16, 21, 67, 131 Cytokine, 36, 132, 146 Cytomegalovirus, 4, 132 Cytoplasm, 32, 118, 125, 132, 141, 150, 166 Cytoprotection, 11, 132 Cytoskeleton, 8, 11, 21, 132 Cytotoxic, 132, 164, 169 D Decarboxylation, 132, 143 Decidua, 40, 132, 160 Deletion, 28, 118, 132 Delirium, 118, 132 Delusions, 4, 132, 163 Dementia, 4, 78, 81, 102, 118, 132, 133, 151 Denaturation, 80, 132, 161 Dendrites, 30, 132, 155 Dentate Gyrus, 132, 143 Depolarization, 8, 16, 23, 133, 168 Deprivation, 14, 15, 19, 26, 79, 81, 133 Deuterium, 133, 143 Dextroamphetamine, 116, 133 Diabetes Mellitus, 26, 133, 140, 142 Diagnostic procedure, 73, 90, 133 Diastolic, 133, 144 Diffuse Axonal Injury, 122, 133 Diffusion, 41, 51, 56, 82, 121, 133, 146, 147, 155 Digestion, 15, 121, 133, 149, 170, 175 Digitalis, 133, 157 Diploid, 133, 160 Direct, iii, 12, 21, 25, 127, 133, 134, 165, 171 Disparity, 76, 133 Dissociation, 114, 133, 148 Distal, 27, 130, 133, 134, 163 Domesticated, 84, 133
183
Dopamine, 27, 50, 116, 118, 128, 133, 153, 155 Dorsal, 32, 134, 161 Dorsum, 134, 139 Drive, ii, vi, 7, 10, 13, 76, 134, 147 Drug Tolerance, 134, 173 Duct, 124, 134, 135, 137, 167, 170, 171 Duodenum, 121, 134, 170 Dura mater, 134, 151, 157 Dyes, 32, 82, 116, 134 Dyskinesia, 118, 134 Dystonia, 81, 118, 134 E Echocardiography, 5, 134 Edema, 134, 143, 147, 154 Effector, 113, 128, 134 Efficacy, 7, 20, 22, 75, 134 Elastic, 134, 173 Elective, 57, 134 Electric shock, 124, 134 Electrode, 39, 124, 134 Electrolyte, 40, 132, 134, 161, 169 Electromagnetic Fields, 80, 135 Electrons, 118, 120, 124, 135, 147, 148, 151, 157, 164 Electroretinogram, 60, 135 Elementary Particles, 135, 151, 155, 163 Embolism, 49, 135, 147, 163 Embolus, 135, 146, 147 Embryo, 121, 125, 135, 145 Emphysema, 127, 135 Encephalitis, 135, 151 Endarterectomy, 116, 135 Endocrine Glands, 135 Endocrinologist, 26, 135 Endocytosis, 28, 135 Endogenous, 5, 7, 10, 22, 32, 44, 80, 121, 133, 135, 136, 137, 155, 174 Endolymphatic Duct, 135, 176 Endometrium, 132, 135, 151 Endorphins, 135, 155 Endothelium, 8, 27, 43, 75, 135, 136, 155 Endothelium, Lymphatic, 136 Endothelium, Vascular, 136 Endothelium-derived, 136, 155 Endotoxin, 136, 174 Enkephalins, 136, 155 Entorhinal Cortex, 136, 143 Environmental Exposure, 136, 156 Environmental Health, 96, 98, 136 Enzymatic, 24, 26, 123, 124, 129, 136, 138, 143, 161, 166
Enzyme, 5, 25, 27, 45, 114, 124, 128, 134, 136, 140, 141, 153, 154, 157, 160, 161, 162, 163, 168, 171, 172, 173, 177, 178 Epidermis, 120, 136, 148 Epigastric, 136, 158 Epilepticus, 74, 136 Epinephrine, 76, 114, 134, 136, 155, 175 Epithelial, 7, 15, 25, 28, 37, 121, 132, 136 Epithelial Cells, 15, 25, 37, 136 Epithelium, 59, 135, 136 Erythrocytes, 116, 122, 136, 165 Erythropoietin, 5, 62, 136 Esophageal, 83, 137 Esophagus, 119, 137, 170 Estrogens, 46, 137 Ether, 137, 160 Eukaryotic Cells, 26, 137, 145, 157 Evoke, 137, 170 Excitability, 14, 47, 137 Excitation, 23, 74, 83, 126, 137, 155 Excitatory, 9, 74, 137, 141, 155 Excitatory Amino Acids, 9, 74, 137, 155 Excitotoxicity, 7, 75, 137 Excrete, 137, 165 Exocrine, 137, 158 Exogenous, 10, 25, 135, 137, 139 Expiration, 137, 165 External-beam radiation, 137, 148, 164, 177 Extracellular, 23, 116, 119, 130, 135, 137, 138, 152, 169 Extracellular Matrix, 130, 137, 138 Extracellular Space, 137, 152 Extrapyramidal, 44, 115, 118, 134, 137 Eye Infections, 114, 137 F Family Planning, 97, 137 Fast Neutrons, 138, 155 Fat, 49, 121, 122, 124, 125, 130, 135, 138, 149, 153, 169, 174 Fatty acids, 16, 138, 141 Ferritin, 30, 138 Fetal Anoxia, 39, 138 Fetus, 14, 136, 138, 160, 175 Fibrillation, 138 Fibrin, 77, 121, 138, 160, 172, 173 Fibrinogen, 138, 160, 172 Fibrinolysis, 30, 138 Fibrinolytic, 38, 138 Fibroblast Growth Factor, 5, 9, 38, 138 Fibroblasts, 20, 37, 60, 138, 146 Fibrosis, 22, 138, 167
184
Anoxia
Filarioidea, 138, 148 Fistula, 4, 88, 138 Flatus, 138, 139 Flunarizine, 55, 138 Fluorescence, 8, 22, 28, 138 Fold, 30, 138 Forearm, 122, 138 Fossa, 125, 139 Free Radicals, 9, 27, 117, 133, 139, 154 Frontal Lobe, 117, 126, 139 Fructose, 139, 141, 147 G Gallbladder, 113, 139 Gamma Rays, 80, 139, 164 Ganglia, 113, 139, 154, 158 Ganglion, 30, 139, 166, 176 Gap Junctions, 139, 172 Gas, 10, 20, 123, 133, 138, 139, 143, 155, 163, 165, 176 Gas exchange, 139, 165, 176 Gastric, 139, 143 Gastrointestinal, 122, 136, 139, 168, 171 Gene, 5, 6, 8, 10, 13, 16, 17, 22, 24, 26, 28, 31, 33, 76, 84, 114, 115, 121, 139, 140, 156, 160 Gene Expression, 25, 31, 76, 139 Gene Targeting, 26, 139 Gene Therapy, 8, 13, 114, 139 Genetic Code, 140, 156 Genetic Engineering, 84, 121, 127, 140 Genetic testing, 140, 161 Genetics, 4, 10, 17, 28, 66, 84, 140 Genotype, 140, 159 Geriatric, 4, 102, 140 Germ Cells, 28, 140, 150, 169, 172 Gestation, 28, 38, 140, 158, 160 Gestation period, 28, 140 Gland, 114, 140, 149, 158, 160, 167, 170, 171 Glioblastoma, 36, 62, 140 Globus Pallidus, 131, 140, 164 Glomerular, 25, 140, 147, 165 Glomerular Filtration Rate, 25, 140 Glomerulus, 140 Glucose, 19, 24, 44, 67, 81, 84, 119, 121, 133, 140, 141, 142, 144, 146 Glucose Intolerance, 133, 140 Glucuronic Acid, 141, 143 Glutamate, 18, 31, 46, 65, 74, 83, 137, 141, 148 Glutamic Acid, 141, 155 Glycerol, 141, 159, 160
Glycerophospholipids, 141, 159, 160 Glycine, 83, 121, 141, 155, 168 Glycogen, 18, 141 Glycols, 141, 144 Glycoprotein, 136, 138, 141, 172, 174 Glycoside, 141, 157 Governing Board, 141, 161 Graft, 141, 145, 153 Grafting, 130, 141 Gram-negative, 125, 141, 166 Granulocytes, 141, 153, 169, 177 Growth factors, 10, 31, 141, 152 Guanine, 10, 141, 164 Guanylate Cyclase, 141, 155 H Hair Cells, 40, 141 Half-Life, 23, 142 Hammer, 142, 157 Haploid, 142, 160 Haptens, 114, 142 Headache, 142, 144 Heart Arrest, 124, 142 Heart attack, 5, 30, 76, 142 Heartbeat, 142, 176 Hematoma, 142, 143 Hematoxylin, 47, 142 Hemiparesis, 122, 142 Hemiplegia, 119, 142 Hemoglobin, 76, 116, 136, 142 Hemoglobinopathies, 140, 142 Hemorrhage, 131, 142, 154, 171, 172 Hemorrhagic stroke, 74, 83, 84, 142 Heparin, 30, 143, 160 Hepatic, 13, 54, 132, 143 Hepatocyte, 14, 57, 143 Heredity, 139, 140, 143 Herpes, 4, 143 Herpes Simplex Encephalitis, 4, 143 Herpes Zoster, 143 Heterogeneity, 114, 143 Hippocampus, 40, 132, 143, 171 Histamine, 63, 116, 118, 127, 138, 143 Histidine, 143 Homeostasis, 23, 143 Homogeneous, 130, 143 Homologous, 115, 139, 143, 153, 171, 174 Hormonal, 47, 120, 143 Hormone, 40, 114, 135, 136, 143, 146, 162, 168 Hydrogen, 55, 113, 115, 120, 123, 124, 132, 133, 143, 144, 149, 152, 155, 157, 159, 163, 171
185
Hydrogen Peroxide, 55, 124, 144, 149, 171 Hydrolysis, 144, 147, 159, 161, 163 Hydrophobic, 28, 141, 144 Hydroxides, 144 Hydroxyl Radical, 54, 144 Hydroxylation, 25, 144 Hyperbaric, 57, 144 Hyperbaric oxygen, 57, 144 Hyperbilirubinemia, 4, 144, 148 Hyperoxia, 27, 37, 144 Hypertension, 4, 102, 144, 147 Hyperthermia, 24, 144 Hypertrophy, 49, 144 Hypnotic, 120, 144 Hypoglycaemia, 65, 132, 144 Hypoglycemia, 9, 19, 23, 60, 74, 81, 83, 84, 144 Hypoglycemic, 81, 144 Hypotension, 118, 130, 144 Hypothermia, 48, 59, 144 Hypoxanthine, 27, 144, 177 Hypoxic, 6, 12, 24, 27, 31, 78, 80, 144 I Immune response, 23, 114, 117, 120, 142, 144, 145, 171, 177 Immune system, 7, 22, 121, 144, 145, 150, 153, 159, 175, 177 Immunization, 114, 145 Immunoblotting, 9, 29, 145 Immunodeficiency, 36, 75, 145 Immunohistochemistry, 24, 145 Immunologic, 7, 114, 126, 145, 164 Immunology, 114, 145 Immunosuppressive, 22, 145 Immunotherapy, 114, 121, 145 Impaction, 88, 145 Impairment, 48, 66, 88, 126, 132, 134, 137, 145, 151, 163 Implant radiation, 145, 147, 148, 164, 177 In situ, 8, 16, 24, 145 In Situ Hybridization, 24, 145 In vitro, 8, 9, 10, 11, 13, 18, 19, 21, 25, 32, 37, 51, 66, 139, 145, 161, 173 In vivo, 8, 10, 11, 13, 22, 23, 25, 27, 50, 51, 78, 139, 143, 145, 152 Inbreeding, 84, 145 Incision, 83, 145, 147 Incontinence, 81, 145 Induction, 12, 20, 31, 60, 76, 118, 145 Infancy, 34, 146 Infarction, 46, 74, 126, 143, 146, 165, 173
Infection, 4, 28, 81, 87, 121, 126, 132, 135, 137, 145, 146, 149, 155, 171, 174, 177 Infiltration, 77, 146 Ingestion, 146, 148, 161 Inhalation, 55, 146, 161 Initiation, 7, 8, 9, 29, 146, 174 Inner ear, 88, 128, 146, 176 Inositol, 29, 146 Inotropic, 134, 146 Insight, 17, 23, 28, 29, 146 Insomnia, 4, 146 Insulator, 146, 153 Insulin, 67, 146 Insulin-dependent diabetes mellitus, 146 Intensive Care, 4, 146 Interleukin-8, 37, 146 Intermittent, 45, 147 Internal Capsule, 117, 131, 147 Internal radiation, 147, 148, 164, 177 Interstitial, 39, 122, 137, 147, 148, 165, 177 Intestines, 113, 119, 139, 147 Intoxication, 132, 147, 177 Intracellular, 6, 8, 9, 12, 15, 18, 27, 124, 146, 147, 155, 161, 166, 168 Intracranial Embolism, 126, 147 Intracranial Embolism and Thrombosis, 126, 147 Intracranial Hypertension, 142, 147, 173 Intravascular, 30, 147 Intrinsic, 16, 114, 147 Intubation, 49, 124, 147 Inulin, 25, 140, 147 Invasive, 30, 147, 150 Involuntary, 127, 138, 147, 154, 159, 165, 169 Ion Channels, 119, 147, 172 Ion Transport, 27, 147 Ionization, 147, 148 Ionizing, 80, 115, 136, 148, 164 Ions, 23, 32, 39, 120, 123, 133, 134, 143, 147, 148, 161 Irradiation, 41, 83, 148, 178 Ivermectin, 75, 148 J Jaundice, 144, 148 K Kainate, 74, 83, 148, 164 Kb, 96, 148 Keratinocytes, 146, 148 Kidney stone, 148, 165, 175 Kinetic, 148
186
Anoxia
L Labile, 128, 148 Labyrinth, 128, 135, 146, 148, 158, 168, 176 Lathyrism, 74, 148 Lens, 56, 148, 177 Lesion, 12, 130, 148, 149, 172 Lethal, 9, 21, 22, 79, 131, 148 Leukemia, 140, 149 Leukoencephalopathy, 55, 149 Life cycle, 121, 149 Ligaments, 130, 149 Ligation, 5, 149 Linkage, 149, 160 Lipid, 21, 119, 141, 146, 149, 153, 157, 174 Lipid Peroxidation, 149, 157 Lithium, 118, 149 Liver, 13, 20, 66, 113, 121, 132, 136, 139, 141, 143, 149, 167 Liver Mitochondria, 66, 149 Liver scan, 149, 167 Liver Transplantation, 13, 149 Lobe, 126, 149 Localization, 10, 15, 17, 145, 149 Localized, 116, 122, 131, 142, 146, 149, 160 Locomotion, 149, 160 Lung Transplantation, 11, 149 Lymph, 126, 127, 135, 136, 149, 167 Lymph node, 126, 149, 167 Lymphatic, 136, 146, 149, 167, 169, 170 Lymphatic system, 149, 167, 169, 170 Lymphocytes, 25, 44, 60, 117, 145, 146, 149, 150, 170, 177 Lymphoid, 117, 150 M Macroglia, 150, 152 Macrophage, 36, 77, 150 Magnetic Resonance Imaging, 150, 167 Malignant, 31, 36, 37, 83, 140, 150, 154, 164 Malignant tumor, 83, 150 Malnutrition, 120, 150 Mammary, 43, 130, 150 Mammogram, 123, 150, 151 Mania, 150 Manic, 81, 118, 121, 149, 150, 163 Mastoiditis, 88, 150 Meatus, 150, 175 Medial, 27, 119, 140, 150, 156 Mediate, 8, 11, 21, 134, 150 Mediator, 31, 150, 160, 168 MEDLINE, 97, 150 Medullary, 7, 150, 164 Meiosis, 150, 153, 171, 175
Melanocytes, 150, 151 Melanoma, 37, 83, 151 Membrane Glycoproteins, 151 Memory, 17, 18, 19, 54, 81, 115, 132, 151 Memory Disorders, 18, 151 Meninges, 125, 126, 131, 134, 151 Meningitis, 4, 151 Menstrual Cycle, 151, 162 Menstruation, 132, 151 Mental, iv, 4, 53, 96, 98, 102, 125, 126, 128, 130, 132, 133, 150, 151, 163, 167, 175 Mental Retardation, 53, 151 Mesolimbic, 118, 151 Mesons, 60, 151 Metabolite, 9, 27, 151 Metastasis, 151, 154 Metastatic, 83, 151 Microbe, 151, 173 Microbiology, 113, 120, 151 Microcalcifications, 123, 151 Microdialysis, 50, 152 Microglia, 7, 119, 152, 153 Microorganism, 128, 152, 158, 177 Microscopy, 14, 16, 24, 30, 32, 142, 152 Mitochondria, 9, 15, 21, 24, 37, 66, 152, 154, 157 Mitochondrial Swelling, 152, 154 Mitogen-Activated Protein Kinase Kinases, 152 Mitogen-Activated Protein Kinases, 11, 152 Mitosis, 118, 152 Mitotic, 43, 152 Modification, 140, 152 Modulator, 11, 152 Monitor, 7, 19, 84, 153, 156 Monoamine, 116, 133, 153 Monoclonal, 84, 145, 148, 153, 164, 178 Monoclonal antibodies, 84, 145, 153 Monocyte, 37, 153 Mononuclear, 153, 174 Mood Disorders, 81, 153 Morphine, 81, 153, 154, 156 Morphological, 17, 18, 24, 135, 150, 153 Morphology, 11, 33, 51, 153 Motor Activity, 130, 153 Movement Disorders, 118, 153 Mucinous, 139, 153 Multiple sclerosis, 31, 153 Multivalent, 120, 153 Muscle Relaxation, 81, 153 Myelin, 7, 32, 153
187
Myeloid Cells, 13, 153 Myocardial infarction, 76, 80, 120, 130, 153 Myocardial Reperfusion, 80, 153, 154, 165 Myocardial Reperfusion Injury, 153, 154, 165 Myocardium, 5, 62, 80, 153, 154 Myoclonus, 34, 57, 154 N Narcotic, 153, 154 Nausea, 117, 118, 154, 175 NCI, 1, 95, 127, 154 Necrosis, 7, 15, 20, 82, 118, 122, 125, 140, 146, 153, 154, 165 Neonatal, 4, 6, 10, 35, 40, 48, 50, 52, 54, 58, 61, 62, 154 Neoplasms, 114, 123, 154, 164 Neostriatum, 125, 131, 154, 164 Nervous System, 10, 19, 31, 54, 113, 114, 116, 125, 126, 127, 133, 139, 140, 141, 142, 150, 152, 153, 154, 155, 156, 158, 161, 168, 171, 172, 175 Networks, 7, 12, 154 Neural, 9, 12, 18, 19, 38, 114, 116, 152, 154 Neurobehavioral Manifestations, 122, 133, 154 Neuroleptic, 115, 118, 128, 154 Neurologic, 81, 122, 140, 155, 174 Neuroma, 88, 155 Neuromuscular, 81, 113, 155 Neuronal, 7, 9, 12, 14, 17, 19, 46, 66, 74, 81, 155 Neurons, 9, 14, 17, 18, 19, 23, 27, 29, 45, 66, 74, 83, 132, 137, 139, 155, 171, 176 Neuropathy, 88, 155 Neuropharmacology, 20, 155 Neurophysiology, 34, 35, 42, 45, 50, 51, 58, 60, 61, 133, 155 Neuroprotective Agents, 74, 81, 83, 155 Neurotoxic, 81, 155 Neurotransmitter, 6, 102, 113, 114, 119, 122, 133, 137, 141, 143, 147, 155, 156, 168, 171, 172 Neutrons, 60, 115, 138, 148, 155, 164 Neutrophil, 13, 14, 25, 37, 51, 62, 77, 155 Neutrophil Infiltration, 25, 77, 155 Nimodipine, 42, 155 Nitric Oxide, 9, 14, 50, 155 Norepinephrine, 114, 134, 155 Nuclear, 24, 37, 120, 128, 135, 137, 139, 140, 147, 151, 154, 156, 166, 172 Nuclei, 30, 115, 117, 135, 139, 140, 150, 152, 155, 156, 161, 163, 167, 176
Nucleic acid, 76, 78, 82, 140, 144, 145, 156, 164, 170 Nucleus Accumbens, 57, 156 O Obsessive-Compulsive Disorder, 81, 156 Ocular, 83, 156 Oncogene, 31, 36, 156 Ophthalmic, 81, 156 Opiate, 75, 81, 153, 156 Opium, 153, 156 Opsin, 156, 166 Optic Chiasm, 156 Optic Nerve, 19, 32, 156, 158, 166 Organ Culture, 157, 173 Organelles, 132, 151, 157 Orthostatic, 118, 157 Osmotic, 152, 157, 168 Ossicles, 88, 142, 157 Ossification, 65, 157 Otitis, 4, 88, 157 Otitis Media, 4, 88, 157 Ouabain, 29, 157 Ovum, 131, 132, 140, 149, 157, 162 Oxamic Acid, 78, 157 Oxidation, 77, 113, 118, 131, 149, 157, 177 Oxidation-Reduction, 77, 157 Oxidative Stress, 17, 157 Oxygen Consumption, 59, 157, 165 Oxygenase, 11, 157 Oxygenation, 8, 31, 60, 76, 79, 143, 157 P Pachymeningitis, 151, 157 Palliative, 158, 172 Pancreas, 82, 113, 146, 158 Papilla, 158 Papillary, 44, 158 Parasite, 148, 158 Parietal, 20, 117, 158 Parietal Lobe, 117, 158 Parkinsonism, 74, 118, 158 Particle, 158, 174 Patch, 9, 12, 14, 130, 158 Pathogen, 84, 158 Pathologic, 13, 118, 130, 144, 158 Pathologic Processes, 118, 158 Pathologies, 88, 158 Pathophysiology, 10, 19, 31, 61, 158 Patient Education, 102, 106, 108, 111, 158 Peptide, 81, 138, 158, 161, 162, 163 Perfusion, 7, 13, 42, 76, 144, 158 Pericardial Effusion, 53, 158 Pericardium, 158
188
Anoxia
Perilymph, 4, 88, 158 Perinatal, 38, 44, 48, 51, 53, 54, 56, 60, 63, 74, 81, 83, 158 Peripheral Nervous System, 136, 142, 155, 158, 171 Peripheral Vascular Disease, 138, 159 Perivascular, 53, 152, 159 PH, 30, 33, 36, 159 Phagocyte, 13, 159 Phagocytosis, 152, 159 Pharmacologic, 52, 116, 142, 159, 174 Phenotype, 10, 159 Phospholipases, 159, 168 Phospholipids, 138, 146, 159, 162 Phosphorus, 123, 159 Phosphorylation, 14, 31, 67, 152, 159, 162 Photodynamic therapy, 82, 83, 159 Physiologic, 10, 18, 114, 121, 142, 147, 151, 154, 159, 164 Physiology, 9, 19, 24, 29, 36, 37, 38, 43, 48, 49, 56, 66, 67, 155, 159 Phytochrome, 16, 159 Picric, 47, 159 Pigment, 121, 150, 151, 159 Pigmentation, 62, 159 Piloerection, 144, 159 Pituitary Gland, 138, 160 Placenta, 40, 160, 162 Plaque, 116, 160 Plasma, 21, 29, 54, 117, 120, 125, 136, 138, 140, 142, 160, 167, 168 Plasma protein, 136, 160, 168 Plasmalogens, 5, 160 Plasmin, 160, 173 Plasticity, 10, 17, 160 Platelet Activation, 160, 169 Platelet Aggregation, 116, 155, 160, 173 Platelet Factor 4, 147, 160 Platelets, 54, 120, 155, 160, 168, 172 Platyhelminths, 148, 160 Pleomorphic, 156, 161 Pneumonia, 130, 161 Poisoning, 132, 147, 149, 154, 161 Polygalacturonase, 84, 161 Polymerase, 24, 161 Polymerase Chain Reaction, 24, 161 Polymorphic, 84, 127, 132, 161 Polypeptide, 9, 26, 54, 128, 138, 160, 161, 178 Pons, 113, 122, 161 Posterior, 20, 119, 125, 127, 134, 147, 158, 161, 176
Postnatal, 6, 44, 48, 161, 170 Postsynaptic, 27, 47, 161, 168, 172 Post-traumatic, 122, 153, 161 Potassium, 12, 23, 47, 79, 161 Potassium Channels, 12, 161 Potassium Cyanide, 79, 161 Potentiation, 161, 169 Practice Guidelines, 98, 161 Preclinical, 20, 162 Precursor, 50, 134, 135, 136, 155, 162, 170, 175 Pregnancy Maintenance, 137, 162 Presynaptic, 41, 47, 155, 162, 172 Prevalence, 4, 162 Probe, 27, 32, 152, 162 Progesterone, 5, 162 Progression, 31, 116, 162 Progressive, 16, 55, 88, 125, 132, 134, 154, 160, 162, 165, 175 Projection, 156, 162 Promoter, 76, 162 Prophase, 153, 162, 171, 175 Prophylaxis, 138, 162, 166 Protease, 162, 173 Protein C, 16, 28, 138, 162 Protein Kinase C, 152, 162 Protein S, 17, 28, 33, 67, 121, 140, 162, 166, 172 Protein-Serine-Threonine Kinases, 152, 162 Proteolytic, 128, 138, 160, 163, 173 Protocol, 3, 9, 21, 163 Protons, 115, 143, 148, 151, 163, 164 Protozoa, 148, 152, 163 Proximal, 56, 133, 162, 163 Psychiatric, 81, 163 Psychiatry, 4, 19, 27, 34, 38, 45, 55, 62, 163, 176 Psychic, 151, 163, 167 Psychoactive, 163, 177 Psychosis, 118, 163 Psychotomimetic, 116, 133, 163 Public Policy, 97, 163 Publishing, 32, 88, 163 Pulmonary, 6, 8, 11, 27, 54, 67, 74, 83, 84, 121, 163, 165, 176 Pulmonary Artery, 8, 121, 163, 176 Pulmonary Edema, 11, 163 Pulmonary Embolism, 11, 163 Pulmonary Ventilation, 163, 165 Pulse, 135, 153, 163 Purines, 164, 168, 177
189
Putamen, 117, 131, 154, 164 Pyramidal Tracts, 137, 164 Q Quinoxaline, 74, 164 R Radiation, 32, 63, 80, 113, 131, 135, 136, 137, 138, 139, 144, 147, 148, 151, 164, 167, 177 Radiation therapy, 113, 137, 144, 147, 148, 164, 177 Radioactive, 122, 142, 143, 145, 147, 148, 149, 153, 156, 164, 167, 177 Radiolabeled, 122, 148, 164, 178 Radiotherapy, 122, 148, 151, 164, 178 Randomized, 134, 164 Reactive Oxygen Species, 13, 16, 22, 24, 164 Receptor, 5, 18, 32, 46, 50, 66, 74, 83, 113, 117, 126, 127, 134, 148, 162, 164, 168 Recombinant, 25, 76, 85, 164, 175 Recombination, 139, 164 Rectum, 118, 128, 138, 139, 145, 164 Recurrence, 121, 164 Red blood cells, 36, 136, 157, 165, 169 Refer, 1, 80, 128, 135, 143, 149, 154, 155, 163, 165, 174, 176 Reflex, 18, 165 Refraction, 165, 169 Regeneration, 138, 165 Regimen, 134, 165 Reliability, 77, 165 Remission, 121, 164, 165 Renal failure, 10, 56, 132, 165 Renal tubular, 25, 165 Reperfusion, 5, 7, 8, 9, 11, 13, 15, 22, 23, 25, 46, 80, 153, 154, 165 Reperfusion Injury, 7, 9, 13, 22, 23, 25, 46, 165 Reproductive cells, 140, 165 Research Personnel, 24, 165 Resection, 13, 165 Respiration, 12, 15, 118, 123, 126, 153, 165, 166 Respiratory distress syndrome, 27, 165 Respiratory Physiology, 165, 176 Respiratory System, 12, 165 Resuscitation, 41, 42, 57, 59, 124, 166 Retina, 23, 30, 127, 129, 130, 148, 156, 166, 167, 177 Retinal, 23, 30, 133, 156, 166 Retinal Ganglion Cells, 156, 166 Retinoids, 166, 177
Retinol, 52, 166 Retrograde, 18, 38, 82, 166 Retrograde Amnesia, 38, 166 Retroperitoneal, 114, 166 Retroviral vector, 139, 166 Rhamnose, 157, 166 Rhodopsin, 156, 166 Ribosome, 166, 174 Rickettsiae, 166 Rigidity, 158, 160, 166 Risk factor, 4, 166 Rod, 127, 167 Rotenone, 67, 167 Rubella, 4, 167 Ryanodine, 29, 167 S Salivary, 132, 167 Salivary glands, 132, 167 Saphenous, 130, 167 Saphenous Vein, 130, 167 Sarcolemma, 9, 154, 167 Scans, 56, 167 Schizoid, 167, 177 Schizophrenia, 19, 27, 74, 81, 151, 167, 177 Schizotypal Personality Disorder, 167, 177 Sclerosis, 75, 81, 119, 153, 167 Screening, 3, 127, 167 Secretion, 28, 143, 146, 152, 167, 175 Secretory, 5, 26, 167, 172 Sedative, 120, 167 Seizures, 45, 81, 132, 136, 140, 167, 170 Semicircular canal, 146, 168 Semisynthetic, 125, 148, 168 Senile, 78, 81, 102, 168 Sensor, 24, 26, 168 Sepsis, 38, 46, 168 Sequencing, 161, 168 Serine, 152, 162, 168, 173 Serotonin, 118, 127, 155, 168 Serous, 136, 168 Serum, 20, 24, 31, 114, 116, 118, 128, 168, 174 Serum Albumin, 24, 168 Sex Characteristics, 137, 168 Shock, 15, 22, 28, 76, 80, 154, 168, 174 Shunt, 45, 168 Side effect, 114, 115, 118, 121, 168, 173 Signal Transduction, 16, 146, 168 Skeletal, 21, 127, 169 Skeleton, 113, 169 Skin graft, 23, 169 Skull, 126, 131, 169, 172
190
Anoxia
Sleep apnea, 12, 169 Sludge, 77, 79, 169 Smooth muscle, 27, 116, 143, 153, 169, 171 Snails, 81, 169 Sodium, 47, 67, 169, 171 Soft tissue, 57, 122, 169 Solid tumor, 31, 169 Soma, 30, 169 Somatic, 5, 150, 152, 158, 169 Spasm, 75, 119, 130, 169 Specialist, 103, 169 Species, 8, 13, 17, 18, 27, 46, 59, 84, 133, 136, 150, 152, 153, 158, 164, 169, 171, 174, 177 Specificity, 58, 114, 169 Spectrum, 14, 152, 169 Sperm, 127, 165, 170 Spermidine, 170 Spermine, 23, 170 Spirochete, 170, 172 Spleen, 132, 149, 170 Squamous, 126, 170 Squamous Epithelium, 126, 170 Stabilization, 25, 170 Staging, 167, 170 Status Epilepticus, 74, 83, 170 Steel, 127, 170 Stem Cells, 24, 136, 170 Stenosis, 58, 88, 170, 171 Stimulant, 116, 133, 143, 170 Stimulus, 57, 76, 130, 134, 137, 146, 147, 165, 170, 172 Stomach, 113, 137, 139, 143, 147, 154, 170 Stool, 128, 145, 170 Strand, 161, 170 Stress, 6, 8, 9, 22, 26, 28, 35, 76, 80, 124, 152, 154, 157, 170 Striatum, 154, 156, 170 Stricture, 170, 171 Stroke, 4, 5, 7, 19, 22, 31, 74, 76, 80, 81, 96, 102, 123, 142, 155, 171 Stroke Volume, 123, 171 Subacute, 146, 171 Subclinical, 146, 167, 171 Subiculum, 143, 171 Subspecies, 169, 171 Substance P, 151, 167, 171 Substrate, 19, 28, 171 Sulfur, 24, 171 Superoxide, 22, 54, 55, 58, 66, 171 Superoxide Dismutase, 22, 171 Suppression, 12, 171
Sweat, 126, 144, 171 Sweat Glands, 126, 171 Sympathomimetic, 116, 133, 134, 136, 156, 171 Synapse, 28, 30, 114, 162, 171, 172, 174 Synapsis, 171 Synaptic, 7, 10, 12, 17, 18, 23, 31, 155, 169, 171, 172 Synaptic Transmission, 12, 17, 23, 172 Syncope, 42, 172 Syphilis, 4, 172 Systemic, 48, 118, 121, 122, 132, 136, 146, 147, 148, 164, 172, 177 Systolic, 144, 172 T Tamponade, 53, 172 Tardive, 118, 172 Telencephalon, 120, 125, 172 Temporal, 4, 8, 17, 58, 143, 150, 172, 176 Tendon, 139, 172 Testis, 28, 40, 172 Tetracycline, 5, 172 Thalamus, 131, 172 Therapeutics, 19, 29, 67, 102, 172 Thermal, 133, 155, 161, 172 Threshold, 16, 137, 144, 172 Thrombin, 138, 160, 162, 172 Thrombocytes, 160, 172 Thrombomodulin, 162, 172 Thrombosis, 63, 82, 120, 147, 162, 171, 173 Ticlopidine, 30, 173 Tinnitus, 88, 157, 173, 176 Tissue Culture, 84, 173 Tissue Plasminogen Activator, 30, 173 Tolerance, 15, 33, 37, 62, 75, 81, 113, 140, 173 Tomography, 54, 173 Tone, 10, 18, 67, 173 Tonicity, 134, 173 Tonus, 173 Tooth Preparation, 113, 173 Topical, 144, 173 Torsion, 146, 173 Tourniquet, 57, 173 Toxic, iv, 4, 9, 22, 28, 80, 123, 131, 133, 136, 155, 173, 174 Toxicity, 81, 173 Toxicology, 38, 98, 173 Toxin, 136, 173, 174 Toxoplasmosis, 4, 174 Trace element, 128, 174 Traction, 127, 174
191
Transcription Factors, 12, 31, 174 Transduction, 27, 67, 168, 174 Transfection, 29, 121, 139, 174 Transient Ischemic Attacks, 4, 174 Translation, 20, 82, 174 Translational, 25, 26, 174 Translocating, 33, 174 Translocation, 21, 67, 174 Transmitter, 113, 119, 134, 137, 147, 150, 156, 174 Transplantation, 22, 42, 45, 47, 54, 61, 145, 174 Trauma, 4, 19, 28, 74, 81, 83, 84, 122, 132, 154, 155, 174 Trigger zone, 118, 174 Triglyceride, 5, 174 Tubercle, 156, 174 Tumor Necrosis Factor, 62, 174 Tumour, 63, 139, 174 Tympanic membrane, 88, 157, 175 Tyrosine, 133, 175 U Univalent, 144, 157, 175 Uremia, 165, 175 Uric, 27, 115, 164, 175 Urinary, 52, 81, 145, 173, 175, 177 Urine, 121, 145, 148, 175 Uterus, 126, 130, 132, 135, 151, 162, 172, 175 V Vaccine, 114, 163, 175 Vacuoles, 135, 157, 175 Vagina, 151, 172, 175 Vascular, 4, 7, 10, 13, 17, 24, 30, 41, 82, 126, 127, 136, 146, 155, 160, 175 Vasculitis, 126, 175 Vasoconstriction, 76, 136, 175 Vasodilator, 122, 134, 143, 153, 175 Vasomotor, 42, 175 Vector, 5, 174, 175 Vegetative, 42, 133, 175 Vein, 58, 119, 156, 167, 175, 176 Venereal, 172, 175 Venom, 81, 175 Venous, 119, 120, 122, 126, 147, 162, 173, 175, 176
Venous blood, 122, 126, 176 Venous Thrombosis, 120, 173, 176 Ventilation, 35, 124, 176 Ventral, 156, 161, 176 Ventricle, 118, 125, 143, 156, 163, 164, 172, 176 Ventricular, 9, 48, 154, 176 Ventricular fibrillation, 48, 176 Venules, 67, 122, 123, 136, 176 Vertebrae, 170, 176 Vertigo, 138, 157, 176 Vestibular, 88, 141, 176 Vestibular Aqueduct, 88, 176 Vestibule, 128, 146, 168, 176 Vestibulocochlear Nerve, 173, 176 Vestibulocochlear Nerve Diseases, 173, 176 Veterinary Medicine, 97, 176 Viral, 85, 88, 135, 174, 176 Viral vector, 85, 176 Virulence, 120, 173, 177 Virus, 36, 75, 140, 160, 166, 167, 174, 176, 177 Viscera, 169, 177 Vitamin A, 146, 166, 177 Vitreous, 148, 166, 177 Vitreous Body, 166, 177 Vitro, 12, 14, 18, 32, 46, 143, 177 Vivo, 12, 13, 23, 25, 177 W White blood cell, 117, 149, 150, 153, 155, 177 Withdrawal, 6, 75, 132, 177 Wound Healing, 36, 77, 138, 177 X Xanthine, 27, 115, 177 Xanthine Dehydrogenase, 27, 177 Xanthine Oxidase, 27, 115, 177 Xenograft, 117, 177 X-ray, 32, 124, 129, 138, 139, 148, 150, 156, 164, 167, 177 X-ray therapy, 148, 177 Y Yeasts, 159, 178 Z Zymogen, 162, 178
192
Anoxia
