Cerebral Edema - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

CEREBRAL EDEMA A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES

J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS

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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1

Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Cerebral Edema: 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: 0-497-00211-6 1. Cerebral Edema-Popular works. I. Title.

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

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

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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on cerebral edema. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.

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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.

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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health

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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON CEREBRAL EDEMA .................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Cerebral Edema ............................................................................. 9 E-Journals: PubMed Central ....................................................................................................... 22 The National Library of Medicine: PubMed ................................................................................ 22 CHAPTER 2. NUTRITION AND CEREBRAL EDEMA .......................................................................... 57 Overview...................................................................................................................................... 57 Finding Nutrition Studies on Cerebral Edema ............................................................................ 57 Federal Resources on Nutrition ................................................................................................... 58 Additional Web Resources ........................................................................................................... 59 CHAPTER 3. ALTERNATIVE MEDICINE AND CEREBRAL EDEMA .................................................... 61 Overview...................................................................................................................................... 61 National Center for Complementary and Alternative Medicine.................................................. 61 Additional Web Resources ........................................................................................................... 63 General References ....................................................................................................................... 63 CHAPTER 4. PATENTS ON CEREBRAL EDEMA ................................................................................. 65 Overview...................................................................................................................................... 65 Patents on Cerebral Edema .......................................................................................................... 65 Patent Applications on Cerebral Edema ...................................................................................... 73 Keeping Current .......................................................................................................................... 78 CHAPTER 5. BOOKS ON CEREBRAL EDEMA .................................................................................... 81 Overview...................................................................................................................................... 81 Chapters on Cerebral Edema........................................................................................................ 81 APPENDIX A. PHYSICIAN RESOURCES ............................................................................................ 85 Overview...................................................................................................................................... 85 NIH Guidelines............................................................................................................................ 85 NIH Databases............................................................................................................................. 87 Other Commercial Databases....................................................................................................... 89 APPENDIX B. PATIENT RESOURCES ................................................................................................. 91 Overview...................................................................................................................................... 91 Patient Guideline Sources............................................................................................................ 91 Finding Associations.................................................................................................................... 93 APPENDIX C. FINDING MEDICAL LIBRARIES .................................................................................. 95 Overview...................................................................................................................................... 95 Preparation................................................................................................................................... 95 Finding a Local Medical Library.................................................................................................. 95 Medical Libraries in the U.S. and Canada ................................................................................... 95 ONLINE GLOSSARIES................................................................................................................ 101 Online Dictionary Directories ................................................................................................... 101 CEREBRAL EDEMA DICTIONARY.......................................................................................... 103 INDEX .............................................................................................................................................. 159

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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with cerebral edema is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about cerebral edema, 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 cerebral edema, 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 cerebral edema. 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 cerebral edema, 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 cerebral edema. The Editors

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

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CHAPTER 1. STUDIES ON CEREBRAL EDEMA Overview In this chapter, we will show you how to locate peer-reviewed references and studies on cerebral edema.

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

Review Article: The Management of Acute Liver Failure Source: Alimentary Pharmacology and Therapeutics. 12(5): 405-418. May 1998. Contact: Available from Blackwell Science Ltd. Journal Subscriptions, P.O. Box 88, Oxford, OX2 0NE, England. Phone 44 (0) 1865 206180 or 44 (0) 1865 206038. Fax 44 (0) 1865 206219. Summary: Acute liver failure (ALF) is a relatively uncommon but dramatic clinical syndrome with high mortality rates, in which a previously normal liver fails within days or weeks. This article reviews the management of ALF. A number of conditions can cause this sudden dysfunction, which triggers a multiorgan response. Paracetamol overdose remains the major cause of ALF in the United Kingdom, while viral hepatitis is the commonest cause worldwide. The severity of clinical signs and illness depends on

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the adverse metabolic consequences of loss of liver function, the systemic effect of toxins from the necrotic liver, and the rate and degree of regeneration. In addition, and as a result of toxic injury, the immune system is compromised; secondary bacterial infections and endotoxinemia give rise to symptoms similar to those of septic shock. Cerebral edema is the leading cause of death in patients with ALF. Despite advances in intensive care and the development of new treatment modalities, mortality remains high and ALF is best managed in specialist centers. Orthotopic liver transplantation is the only new treatment modality that has made a significant impact in improving outcome. Bioartificial liver support systems and hepatocyte transplantation are promising new options that may change the future management of ALF. 5 tables. 120 references. (AAM). •

Acute Liver Failure Source: Journal of Clinical Gastroenterology. 33(3): 191-198. 2001. Contact: Available from Lippincott Williams and Wilkins, Inc. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-3030 or (301) 714-2300. Summary: Acute liver failure is defined as hepatic encephalopathy (a brain manifestation of extensive liver damage) complicating acute liver injury. This article reviews the definitions, etiologies, prognostic factors, and issues in the management of patients with acute liver failure (ALF). The most common etiologies (causes) are acute viral hepatitis A and B, medication overdose (e.g., acetaminophen), idiosyncratic drugs reactions, ingestion of other toxins (e.g., amanita mushroom poisoning), and metabolic disorders (e.g., Reye's syndrome). Despite advances in intensive care management, mortality (death) continues to be high (40 to 80 percent) and is partly related to ALF's complications, such as cerebral edema (fluid accumulation), sepsis, hypoglycemia (low blood glucose), gastrointestinal bleeding, and acute renal (kidney) failure. Several prognostic models have been developed to determine which patients will spontaneously recover. Treatment is directed at early recognition of the complications and general supportive measures. The only proven therapy for those who are unlikely to recover is liver transplantation. Therefore, recognition of ALF is paramount, and urgent referral to a transplant center is critical to assess transplantation status. 2 figures. 5 tables. 62 references.

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'Diabetic' Emergencies: They Happen with or without Diabetes Source: Postgraduate Medicine. 88(3): 90, 96, 99. September 1, 1990. Summary: This article describes three of the most serious diabetic emergencies and suggests how to manage them. Ketoacidosis, severe hyperosmolality due to hyperglycemia, and severe hypoglycemia are all life-threatening emergencies that often occur in the absence of any history of diabetes. The author stresses that successful management of these emergencies depends on rapid recognition and institution of direct treatment measures. One sidebar addresses the issue of cerebral edema. 2 figures. 4 tables. 11 references. (AA-M).

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Dialysis Disequilibrium Syndrome Source: AJN. American Journal of Nursing. 100(2): 53-54. February 2000. Contact: Available from Lippincott Williams and Wilkins. AJN, P.O. Box 50480, Boulder, CO 80322-0480. (800) 627-0484 or (303) 604-1464.

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Summary: This article familiarizes nurses with dialysis disequilibrium syndrome, which is characterized by a change in mental status accompanied by hypotension. The syndrome is thought to result from the rapid removal of fluid and the decrease in BUN (blood urea nitrogen) during hemodialysis, which cause changes in blood osmolarity. The author offers a patient case report and describes how this patient is diagnosed with dialysis disequilibrium syndrome. Dialysis patients commonly present to the emergency department (ED) with nausea, vomiting, headache, restlessness, and a decreased level of consciousness. These symptoms may be caused by the uremic toxins that accumulate in the bloodstream as a result of the decreased glomerular filtration rate (GFR) in renal failure. In uremia, patients are often overloaded with fluid and become hypertensive. But patients can also be hypotensive (low blood pressure) as a result of the rapid removal of fluid. This fluid shift can cause cerebral edema (fluid in the brain), resulting in increased intracranial pressure and visible signs of decreasing level of consciousness. Symptoms may include sudden onset headaches, blurred vision, dizziness, nausea, vomiting, nervousness, muscle twitching, palpitations, disorientation, and seizures. If signs and symptoms are not recognized and treated immediately, coma and death can occur. The article concludes by stressing that prevention is the key to managing dialysis disequilibrium syndrome, especially in patients at higher risk (pediatric patients, older patients, patients new to hemodialysis, etc.). •

Bioartificial Liver (BAL) Source: Practical Gastroenterology. 25(3): 13-14, 17, 20-21. March 2001. Contact: Available from Shugar Publishing. 12 Moniebogue Lane, Westhampton Beach, NY 11978. (516) 288-4404. Fax (516) 288-4435. Summary: This article reports on the development of a bioartificial liver (BAL) system that has been used to treat patients with various forms of severe liver failure in uncontrolled clinical trials, primarily to examine the safety and feasibility of the system. The two main components of the BAL were a cartridge containing thawed cryopreserved porcine (pig) hepatocytes and a cellulose coated charcoal column. The former was used to provide both liver synthetic functions and detoxification and the latter for detoxification. The system appears to be safe. The author reports that they were able to bridge patients to either spontaneous recovery or transplantation. The most striking observation seen in patients with cerebral edema and fulminant hepatic (liver) failure was that they experienced significant reduction in intracranial pressure and clinical neurologic improvement. A prospective, randomized, controlled, phase II and III pivotal clinical trial is now in progress to definitively determine the efficacy of this system. The author concludes that liver support therapy will become a viable, effective therapeutic option for the treatment of patients with severe acute liver failure. 2 tables. 14 references.

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Treatment Strategies for Diabetic Ketoacidosis in Children and Adolescents With Insulin-Dependent Diabetes Mellitus Source: Clinical Diabetes. 11(5): 102-106. September-October 1993. Summary: This article reviews the current thinking on treatment strategies for diabetic ketoacidosis (DKA) in children and adolescents with insulin-dependent diabetes mellitus (IDDM). Topics include a brief review of DKA and how it happens; rehydrating patients; replenishing potassium; lowering the glucose level; correcting acidosis; treating other DKA symptoms; avoiding cerebral edema; continuing insulin therapy; and monitoring patients. 2 tables. 11 references.

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Managing Fluid Abnormalities in Uncontrolled Diabetes Mellitus Source: Journal of Critical Illness. 12(5): 278-282. May 1997. Summary: This article reviews the pathogenesis of uncontrolled diabetes mellitus, the fluid abnormalities that commonly occur, and recommended corrections. Despite advances in the understanding of the pathogenesis of uncontrolled diabetes, complications remain extremely common and deadly. The primary cause of fluid and electrolyte abnormalities in uncontrolled diabetes is persistent glucosuric diuresis, which occurs when the amount of glucose presented to the proximal tubule exceeds the normal kidney's reabsorptive threshold of 225 mg/min. Patients at greatest risk for uncontrolled diabetes include the elderly, those receiving hyperosmotic nasogastric feedings, those with preexisting kidney disease, and those with other disabilities that leave them unable to ingest or retain fluids in the presence of ongoing osmotic diuresis. The author discusses the process by which fluid loss develops and the selection of replacement fluids. Concerns have been voiced about the adverse effects of rapid fluid administration, the use of hypotonic fluids to treat hyperglycemic hyperosmolarity, and the dangers of rapid reduction of Eosm to 320 mOsm/L or of glucose levels to 250 to 300 mg/dL. However, many more patients die of undertreatment of uncontrolled diabetes than of overtreatment. Fatal cerebral edema is rare. 11 references. 4 tables. (AA-M).

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Concussion in Sports: Minimizing the Risk for Complications Source: American Family Physician. 64(6): 1007-1014. September 15, 2001. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237 or (913) 906-6000. E-mail: [email protected]. Website: www.aafp.org. Summary: This journal article provides health professionals with information on pathologic features, diagnosis, and management of concussion. Mild traumatic brain injury, or concussion, is a common consequence of collisions, falls, and other forms of contact in sports. Concussion may be defined as an acute trauma induced alteration of mental function lasting less than 24 hours, with or without preceding loss of consciousness. The hallmarks of concussion are confusion and amnesia, often without preceding loss of consciousness. Axonal shear injury is the primary pathologic feature of traumatic brain injury at all levels of severity. The physician's responsibilities in assessing an athlete with concussion include determining the need for emergency intervention and offering guidance about the athlete's ability to return to play. Concussion may be complicated by cerebral edema related to the second impact syndrome, cumulative neuropsychologic deficits, intracranial bleeding, or postconcussion syndrome. The risk of complications is increased in athletes who return to play prematurely and in those with prolonged loss of consciousness or posttraumatic amnesia. An athlete with prolonged loss of consciousness or signs and symptoms that worsen or persist after a concussion should be evaluated in the emergency department. An athlete should not be allowed to resume sports participation until all symptoms of a concussion have resolved. 1 figure, 5 tables, and 25 references. (AA-M).

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Hyperglycemic Crises in Patients with Diabetes Mellitus Source: Diabetes Care. 24(1): 154-161. January 2001. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org.

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Summary: This position paper presents information on the pathogenesis, diagnosis, treatment, and prevention of hyperglycemic crises in patients who have diabetes mellitus. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the two most serious acute metabolic complications of diabetes. They can occur in both type 1 and type 2 diabetes. The basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones. The most common precipitating factor in the development of these hyperglycemic crises is infection. Other factors include cerebrovascular accident, alcohol abuse, pancreatitis, myocardial infarction, trauma, and drugs. Diagnosis involves obtaining a medical history, performing a physical examination, and conducting laboratory tests. Successful treatment of DKA and HHS requires correcting dehydration, hyperglycemia, and electrolyte imbalances; identifying comorbid precipitating events; and monitoring the patient frequently. The article presents guidelines for fluid therapy for adults and children; insulin therapy; and potassium, bicarbonate, and phosphate therapy. In addition, the article identifies the most common complications of DKA and HHS, including hypoglycemia, hypokalemia, and hyperglycemia secondary to interruption of discontinuance of intravenous insulin therapy after recovery. Other complications include cerebral edema and hypoxemia. Measures to prevent DKA and HHS include better access to medical care, proper education, and effective communication with a health care provider during an intercurrent illness. 4 figures. 3 tables. 39 references. •

Management of Diabetic Ketoacidosis Source: American Family Physician. 60(2): 455-464. August 1999. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237. Website: www.aafp.org. Summary: This review article discusses the management of diabetic ketoacidosis. This emergency medical condition is a triad of hyperglycemia, ketonemia, and acidemia. Although diabetic ketoacidosis most often occurs in people who have type 1 diabetes, more recent studies suggest that it can sometimes be the presenting condition in obese African American patients with newly diagnosed type 2 diabetes. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has persisted since the 1970s. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The therapeutic goals for diabetic ketoacidosis consist of improving circulatory volume and tissue perfusion, reducing blood glucose and serum osmolality toward normal levels, clearing ketones from serum and urine at a steady rate, correcting electrolyte imbalances, and identifying precipitating factors. The initial priority in the treatment of this condition is rehydration with subsequent potassium replacement. Low dose insulin therapy should be initiated after the diagnosis of diabetic ketoacidosis has been confirmed by laboratory tests and fluid replacement has been begun. The use of bicarbonate is not recommended in most patients. Prospective studies have indicated no clinical benefit for phosphate replacement in the treatment of diabetic ketoacidosis. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than adults. Adult respiratory distress syndrome is a rare but potentially fatal complication of treatment of diabetic ketoacidosis. Continuous follow up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. 3 figures. 2 tables. 26 references. (AA-M).

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Management of Hyperglycemic Crises in Patients with Diabetes Source: Diabetes Care. 24(1): 131-153. January 2001. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This review article presents updated recommendations for management of patients with hyperglycemic crises based on the pathophysiological basis of these conditions. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most serious acute metabolic complications of diabetes. A common precipitating factor in the development of these hyperglycemic crises is infection. Other factors include omission of insulin or undertreatment with insulin, alcohol abuse, trauma, pulmonary embolism, and myocardial infarction. Various drugs that alter carbohydrate metabolism and excessive use of diuretics in the elderly may also precipitate the development of DKA and HHS. Psychological factors and poor compliance are important precipitating factors for recurring ketoacidosis. The basic underlying mechanism for DKA and HHS is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones. Diagnosis involves obtaining a medical history, performing a physical examination, and conducting laboratory tests. Successful treatment of DKA and HHS requires correcting dehydration, hyperglycemia, and electrolyte imbalances; identifying comorbid precipitating events; and monitoring the patient frequently. The article presents guidelines for fluid therapy; insulin therapy; and potassium, bicarbonate, and phosphate therapy. In addition, the article identifies the most common complications of DKA and HHS, including hypoglycemia, hypokalemia, cerebral edema, adult respiratory distress syndrome, and hyperchloremic metabolic acidosis. Measures to prevent DKA and HHS include better access to medical care, proper education, and effective communication with a health care provider during an intercurrent illness. 7 figures. 7 tables. 220 references.

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Acute Diabetic Emergencies and Their Management Source: Care of the Critically Ill. 15(4): 132-135. August 1999. Contact: Available from Stockton Press. Houndmills, Basingstoke, Hampshire RG21 6XS, UK. 44(0) 1256 329242. Fax: 44(0) 1256 810526. Website: http://www.stocktonpress.co.uk/cci/. Summary: This review article provides information on the presentation, management, and complications of acute diabetic emergencies. Diabetic ketoacidosis (DKA) and hyperosmolar nonketotic coma are two life threatening emergencies of diabetes. DKA is precipitated either by absolute or relative insulin deficiency. Patients who have DKA present with a history of increased thirst, polyuria, and weakness. Most patients exhibit clouding of consciousness, and the majority are tachycardic. Treatment of DKA depends on correcting the glucose, fluid, and electrolyte disturbances that occur, as well as identifying and treating the precipitating factor. Withdrawal of insulin, surgery, and trauma can be identified as precipitating factors from the clinical history. Of the various precipitating factors, identification of infection is very important because it is the precipitating factor in up to 60 percent of cases. Infected diabetic ulcers, carbuncles, and furuncles must be excluded by a careful clinical examination. Two head and neck infections characteristically occurring in diabetes are malignant external otitis and rhino cerebral mucormycosis. Central nervous system, pulmonary, and urinary tract infections must also be considered. DKA predisposes to thrombosis due to dehydration increased blood viscosity and increase coagulability. Cerebral edema is a rare

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complication that usually occurs in children. Pulmonary edema and development of acute respiratory distress syndrome may also complicate DKA. Upper gastrointestinal hemorrhage may occur in up to 10 percent of DKA cases. Hyperosmolar nonketotic coma is characterized by hyperglycemia, hyperosmolarity, and severe dehydration. Precipitating factors include infection, trauma, surgery, and thromboembolic events. Symptoms and signs are similar to those of DKA. Treatment involves replacing fluids, infusing insulin at a low rate, and administering prophylactic heparin. DKA and hyperosmolar nonketotic coma are important causes of morbidity and mortality among people who have diabetes, so early recognition and treatment are essential. 40 references. (AA-M).

Federally Funded Research on Cerebral Edema The U.S. Government supports a variety of research studies relating to cerebral edema. 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 cerebral edema. 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 cerebral edema. The following is typical of the type of information found when searching the CRISP database for cerebral edema: •

Project Title: BLOOD-BRAIN BARRIER IN CEREBRAL ISCHEMIA Principal Investigator & Institution: O'donnell, Martha E.; Human Physiology; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 956165200 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2006 Summary: (provided by applicant): The long term goal of this project is to identify blood-brain barrier (BBB) ion transporters that mediate ischemia induced brain edema, a major cause of brain damage in stroke. During the early hours of cerebral ischemia, brain edema formation occurs in the presence of an intact BBB. In this process, BBB endothelial cells transport Na and Cl from blood into brain interstitium, with osmotically obliged water following. The specific ion transporters responsible are unknown, however BBB luminal Na and Cl transporters appear to play a key role. Much evidence indicates that hypoxia, which rapidly develops during ischemia, aglycemia occurring as glucose is depleted, and also centrally-released vasopressin are mediators of ischemia-induced brain edema formation. A novel aspect of this proposed project is the preliminary finding that a Na-K-Cl cotransporter appears to be localized in the luminal membrane of brain microvessel endothelial cells and that vasopressin, hypoxia

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

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and aglycemia stimulate activity of the cotransporter. This has led to the central hypothesis that a Na-K-Cl cotransporter, located at the luminal membrane of the BBB, is stimulated during ischemia to increase transport of Na and Cl with osmotically obliged water from blood to brain, causing edema formation. The present project has three specific aims. The first aim is to test the hypothesis that Na-K-Cl cotransport is present in luminal membranes of cerebral microvascular endothelial cells (CMEC). These studies will evaluate bovine brain microvessel luminal and abluminal membrane preparations for cotransport activity by radioisotopic flux analyses. Also, the in situ distribution of the cotransporter will be examined by immunoelectron microscopy of brain sections. The second aim is to test the hypothesis that Na-K-CI cotransport of BBB endothelial cells is stimulated by agents that mediate ischemia-induced cerebral edema. Here, the effects of hypoxia, aglycemia and vasopressin on cotransport activity will be examined in cultured human and bovine CMEC and freshly isolated bovine cerebral microvessels. The third aim is to test the hypothesis that inhibition of Na-K-Cl cotransport activity attenuates ischemia-induced brain edema. To do this, the effect of inhibiting the cotransporter on ischemia-induced changes in rat brain Na and water will be examined by nuclear magnetic resonance methods, which allow in vivo changes in brain Na and water to be followed in real time. The proposed studies should reveal whether therapeutic approaches aimed at blocking BBB Na-K-Cl cotransporter activity may be of value for attenuating ischemia-induced brain edema. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BRAIN VASCULAR AND METABOLIC ADAPTATION TO HYPOXIA Principal Investigator & Institution: Lamanna, Joseph Charles.; Professor; Anatomy; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 15-MAR-2000; Project End 28-FEB-2005 Summary: Hypoxia is one of the more common and serious stresses challenging metabolic homeostasis. Yet, both shorter and longer term adaptations allow metabolic, vascular and ventilatory adjustments to hypoxia that maintain normal brain function. The mechanisms that regulate the adaptive response are not well known or understood. It is the overall long term goal of this proposed research project to elucidate these mechanisms which fall into 2 categories. First, there are brainstem integrated control systems that adjust ventilation rates, blood pressure and cerebral blood flow to provide acute responses to hypoxic exposure. Second, persistent hypoxic exposure leads to genecontrolled reversible adaptive responses that include systemic (increased red cell volume through erythropoietin activation) and central (increased capillary density through angiogenesis and hypometabolism) components. This indicates a principle of structural and functional plasticity in the postdevelopmental, adult mammalian brain at a level not previously appreciated. This is significant because the gene mechanisms responsible for these responses appear to be activated in the pathophysiological responses to many other sources of metabolic stress such as tumors, ischemia, reperfusion injury, stroke, and aging. This application proposes to use the wellestablished model of inducing brain metabolic and vascular adaptation to hypobaric hypoxia in rats to focus on several questions concerning the control mechanisms of hypoxic adaptation and de-adaptation: 1) the hypothesis that unsuccessful adaptation to hypoxia as occurs for example in high altitude cerebral edema, results from vasogenic brain edema as a consequence of the early stages of a too vigorous cytokine stimulated angiogenesis, 2) the control mechanisms and signals that control the adaptive brain blood flow response to continued hypoxia, 3) the role that programmed cell death might play in the microvascular regression that accompanies de-adaptation after return to a

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normoxic environment. A combination of techniques will be used to measure brain metabolites (quantitative microhistochemistry), intracellular pH (imaging histophotometry), blood flow (iodoantipyrene autoradiography), ultrastructural indicators of cell division and cell death (electron microscopy), brainstem function (noninvasive plethysmography), cytokines and growth factors (such as vascular endothelial growth factor, hypoxia inducible factor, angiopoietin-1 and -2) by molecular techniques (Western and Northern blot analyses, in situ hybridization and PCR). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ENERGY METABOLISM Principal Investigator & Institution: Smith, Michael B.; Chief, Center for Nmr Research; Pennsylvania State Univ Hershey Med Ctr 500 University Drive Hershey, Pa 170332390 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2003 Summary: The overall objective of this research component is to investigate the highenergy biochemical mechanisms whereby the perinatal brain is damaged by hypoxiaischemia and how brain injury can be prevented or reduced through specific modalities of therapy. Specific Aims include: 1) to characterize the earliest alterations in highenergy phosphate reserves which occur during perinatal cerebral hypoxia-ischemia and to correlate these changes with perturbations in cerebral energy utilization, cerebral glucose utilization, glutamate and nitric oxide neurotoxicity, and intracellular calcium accumulation; 2) to correlate the concentrations in cerebral high-energy phosphate reserves and the changes which occur during hypoxia-ischemia using 31P magnetic resonance (MR) spectroscopic methods and enzymatic, fluorometric techniques; 3) to characterize the secondary (delayed) energy failure which occurs during recovery from perinatal cerebral hypoxia-ischemia and to correlate the alterations with the presence and severity of hypoxia-ischemic brain damage; 4) to ascertain underlying biochemical mechanisms whereby the glucocorticosteroid, dexamethasone, protects the perinatal brain from hypoxic-ischemic damage; 5) to determine the protective influence of magnesium sulfate on perinatal hypoxic-ischemic brain damage and, if so, to ascertain its mechanism of action; and 6) to investigate further the presence and extend of alterations in diffusion-weighted and T2-weighted imaging during recovery from perinatal cerebral hypoxia-ischemia and to correlate any changes with the nature and extent of cerebral edema and associated neuropathologic alterations. Seven-days postnatal rats will undergo unilateral cerebral hypoxia-ischemia, during and following which the animals will undergo those procedures necessary to obtain sequential 31P and 1H NMR spectra which will allow for measurements of the alterations in high-energy phosphate reserves and other metabolites which result from the insult. Other animals will undergo MR imaging at specific intervals following cerebral hypoxia-ischemia. Other experiments will elucidate the neuroprotective effect of dexamethasone, magnesium sulfate, and L-NAME on hypoxic-ischemic brain damage in the developing rat. Analytic procedures will include sequential measures with NMR spectroscopy as well as brain tissue analysis of high-energy phosphate reserves and other metabolites using enzymatic, fluorometric techniques. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: EXCERCISE INDUCED RISE IN SEVERITY OF ALTITUDE ILLNESS Principal Investigator & Institution: Roach, Robert C.; New Mexico Resonance 2301 Yale Blvd Se, Ste C1 Albuquerque, Nm 87106 Timing: Fiscal Year 2002; Project Start 10-SEP-2001; Project End 31-JUL-2005

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Cerebral Edema

Summary: (Applicant's abstract): Many hundreds of studies of acute mountain sickness (AMS) over the past two centuries have examined the role of ventilation, pulmonary gas exchange and fluid balance, yet the pathophysiology of AMS remains largely unsolved. AMS incurs significant medical risks and costs since as many as 5 percent of cases can develop life-threatening high altitude cerebral edema (HACE). AMS itself is a substantial public health problem with a prevalence of 15-65 percent in visitors to high altitude. This proposal focuses on the role of brain swelling, which can include elevated brain water and blood volume, in the pathophysiology of AMS. This proposal uses exercise as a tool to develop more severe symptoms of AMS sooner than would be the case in resting subjects. Our approach departs from the traditional paradigm, followed by many of us in this field, of searching for clues to the pathophysiology of AMS in the observed peripheral responses (pulmonary, renal, vascular). Our rationale for focusing on brain swelling is that a) the symptoms of AMS are largely neurological; b) HACE, considered the end-stage of severe AMS, has recently been identified as a vasogenic edema, opening the door for a role for blood-brain barrier (BBB) permeability in AMS; c) new, noninvasive techniques make measurement of brain water and blood volume possible; and d) available experimental evidence and theoretical arguments support a significant role for brain swelling in the pathophysiology of AMS. We recently showed that exercise caused a more than 3 fold rise in AMS symptom severity, a drop in arterial oxygen saturation (SaO2) during exercise, and slight fluid retention. We also recently showed that subjects ill with AMS had a small drop in plasma volume and a large rise in extracellular water compared to those that remained free of AMS. In further studies, magnetic resonance imaging revealed that most brains swell when humans ascend to high altitude. Our overall hypothesis is that brain swelling causes the symptoms of AMS. Our approach is to apply several new and innovative technologies to solving the pathophysiology of AMS. These include noninvasive techniques to measure and manipulate cerebral blood volume, intracranial pressure, BBB opening, cerebrospinal volumes and selected cellular, molecular and genetic responses to hypoxia in people developing AMS. Our three specific aims are 1) to determine the role of elevated brain water in brain swelling and AMS; 2) to determine the role of BBB permeability in AMS; and 3) to determine the role of select cellular, molecular and genetic factors in AMS. The results from the proposed studies will increase our understanding of the role of the brain, brain water and brain swelling in other conditions, both those associated with oxygen depravation, and those where the primary insult is to the brain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EXTRAHYPOTHALAMIC AVP: SYNTHESIS AND SECRETION Principal Investigator & Institution: Chodobski, Adam; Associate Professor; Rhode Island Hospital (Providence, Ri) Providence, Ri 029034923 Timing: Fiscal Year 2002; Project Start 26-APR-2000; Project End 31-MAR-2004 Summary: Choroid plexus (CP), a major generator of cerebrospinal fluid (CSF), produces and secretes into the CSF various neuropeptides, growth factors, and cytokines. Our general working hypothesis is that the CP-derived polypeptides not only regulate the function of CP epithelium locally, by autocrine actions, but also exert distal paracrine effects on target cells in the brain. The distal brain regions may be reached through CSF pathways due to continual production and flow of CSF. The focus of this application is on arginine vasopressin (AVP). CSF-borne AVP plays an important role in promoting cerebral edema and vasospasm that accompany several CNS disorders, including trauma, subarachnoid hemorrhage (SAH), and ischemia. However, the sources of CSF AVP and the regulation of AVP release into the CSF are not well

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understood. Our previous studies have demonstrated that CP epihelium is a likely source of CSF AVP. Specific aims of the present proposal are to obtain an insight into 1) the regulation of choroidal AVP gene expression, 2) intracellular mediators and neurohormonal secretagogues promoting AVP release from CP epithelium, and 3) the nature of this secretory process (via either the regulated or constitutive pathway). We will approach the above questions by applying both in vivo rat model and in vitro CP epithelial cell cultures. The functional experiments on AVP release will be complemented with molecular and immuno-chemical analyses, such as reverse transcriptase- polymerase chain reaction, Western blotting, and immuno- cytochemistry. Radioimmunoassay will be used to quantify AVP content. The long-term objective is to obtain a comprehensive view of how the CP-CSF system regulates the internal milieu for neuronal and glial cells. These studies will form the basis for development of pathological models and, consequently, effective therapies for the treatment of CNS disorders, such as trauma, SAH, and stroke. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INFLAMMATORY MECHANISMS IN CEREBRAL ISCHEMIA Principal Investigator & Institution: Yenari, Midori A.; Assistant Professor; Neurology & Neurological Scis; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 15-AUG-2001; Project End 31-JUL-2004 Summary: At the experimental level, hypothermia has consistently been an effective means of reducing cerebral ischemic injury. Although the mechanisms underlying this neuroprotection have been attributed to the preservation of metabolic stores and reducing excitatory amino acid release, this cannot explain the equally robust protection seen with only small decreases in brain temperature, or when brain cooling is delayed by a few hours. Recent work in the area of stroke has also shown that inflammatory processes are activated and exacerbate injury by the release of reactive oxygen species (ROS), proteases, and lipases leading to increases in cerebral edema and local tissue destruction. Inflammatory stimuli upregulate inflammatory cytokines, which activate microglia and stimulate expression of adhesion molecules. These latter proteins are involved in attracting leukocytes to activated and damaged endothelium, which then enter damaged tissue. We, and a few other groups have found that inhibition of neutrophil migration reduces ischemic injury following experimental stroke, and that mild hyopthermia attenuates neutrophil infiltration into ischemic brain regions. We purpose to further explore the mechanisms known to mediate this inflammatory response, and determine whether mild hypothermia alters them. Using models of brain ischemia and inflammation, we will first test the hypothesis that mild hypothermia attenuates cerebral infiltration of leukocyte subpopulations, and suppresses microglial activation. We will then study whether mild hypothermia alters expression of inflammatory mediators such as the inflammatory cytokines IL- 1beta (interleukin1beta) and TNF-alpha (tumor necrosis factor- alpha), and adhesion molecules. We will then determine whether mild hypothermia attenuates inflammatory cell generation of potentially toxic substances such as ROS, inducible nitric oxide synthase (iNOS), and excitatory amino acids. To further confirm the temperature dependence of inflammation and its effects on brain injury, we will determine whether mice deficient in ICAM-1 are protected against hyperthermia. The results of this study should provide insight into the protective role of hypothermia, and may suggest anti-inflammatory targets for stroke treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ISCHEMIC BLOOD BRAIN BARRIER: GLIAL AND ENDOTHELIAL CELL INTERACTIONS Principal Investigator & Institution: Giffard, Rona G.; Associate Professor; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 27-SEP-2002; Project End 30-JUN-2007 Summary: The blood brain barrier (BBB) is necessary to regulate and limit the transport of solutes and proteins into the brain under normal conditions. Under pathological conditions, the BBB can be altered or damaged to permit transmigration of leukocytes and large molecules leading to edema and in the case of complete breakdown, hemorrhage. Such damage is often observed during cerebral ischemia and may result in significant cerebral hemorrhage, a feared complication of thrombolytic therapy. The BBB consists of endothelial cells surrounded by astrocytes and microglia. Following ischemia, reactive oxygen and nitrogen species are generated in the brain by a variety of cell types. These conditions lead to activation of microglia, the brain's resident immune cell. In response to activating stimuli, microglia are capable of expressing inflammatory cytokines, reactive species including superoxide and nitric oxide, and degradative enzymes including matrix metalloproteinases (MMPs). MMPs, once expressed, lead to direct disruption of the BBB resulting in cerebral edema and hemorrhage. We recently observed that microglia potentiate damage to endothelial cells and astrocytes subjected to simulated ischemia. We plan to characterize the mechanisms underlying this observation by examining the effects of simulated ischemia-induced BBB injury as it pertains to 1) the inflammatory cytokines IL-1 beta and TNF-alpha, 2) reactive oxygen and nitrogen species and 3) MMPs. This proposal plans to study these effects both in coculture models of the BBB and in a whole animal model of hemorrhagic embolic stroke. This work may help identify novel therapeutic targets to reduce brain damage and hemorrhage in the setting of impaired BBB. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MECHANISMS NEUROTOXICITY

AND

PREVENTION

OF

HEMOGLOBIN

Principal Investigator & Institution: Panter, S Scott.; Northern California Institute Res & Educ 4150 Clement Street (151-Nc) San Francisco, Ca 941211545 Timing: Fiscal Year 2002; Project Start 01-SEP-1994; Project End 31-JUL-2004 Summary: (Adapted from investigator's abstract) The central hypothesis of this proposal is that hemoglobin is cytotoxic and will significantly worsen cellular injury produced by the original ischemic episode. This contribution of hemoglobin to neurological injury can be reduced by pretreatment with antioxidants, chelators, the hemoglobin binding protein haptoglobin, or agents that will plug the barrier, blocking the entry of hemoglobin. This proposal will focus on a rat model of focal ischemia and reperfusion that has been demonstrated to disrupt the blood-brain barrier. To attempt to model the clinical situation, stroma-free or purified human hemoglobin will be infused into the vasculature of rats at the start of reperfusion following focal ischemia. This procedure results in the direct deposition of hemoglobin into the ischemic area of the brain through the disrupted BBB. Increasing doses of hemoglobin will be administered to assess behavioral impairment and survivability. At different time intervals following stroke, the brains will be evaluated for infarct size, cerebral edema, and the degree of disruption of the blood-brain barrier. Neuronal degeneration will be assessed by conventional histology and fluorescence microscopy using fluoro-jade. Finally, animals will be pretreated with an antioxidant (polynitroxyl-albumin), an iron chelator (a starch

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deferoxamine conjugate), the normal hemoglobin-binding protein haptoglobin, or a subfraction of pentastarch that has been shown to physically plug the holes of a disrupted blood-brain barrier. These studies will delineate a hemoglobin-dependent contribution to neural injury following opening of the blood-brain barrier and will test several therapeutic candidates that could be used in the clinical setting of CABG surgery. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISMS OF OXIDATIVE INJURY IN VASOGENIC EDEMA Principal Investigator & Institution: Chan, Pak H.; Professor; Neurosurgery; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 01-FEB-1988; Project End 31-JAN-2004 Summary: (Adapted from Investigator's abstract): Vasogenic edema is the most common form of brain edema observed in clinical practice. It is characterized by an increased permeability of brain capillary endothelial cells to macromolecules and by an increased extracellular space and brain water. Although the causes of vasogenic edema following brain ischemia and injury appear to be multifactorial, the basic mechanisms are dependent upon alteration sin the structural and functional integrity of brain endothelial cells. we have postulated that oxygen radicals, superoxide radicals in particular, are involved in the perturbation of the structural and functional integrity of the endothelial cells. We have demonstrated that cerebral edema and infarction induced by either cold injury or by focal cerebral ischemia and reperfusion are significantly reduced in transgenic (Tg) mice overexpressing human CuZn-superoxide dismutase (SOD-1) activity. We now propose to continue to investigate the role of oxidative stress in the pathogenesis of vasogenic edema using both in vivo mouse models of focal cerebral ischemia and reperfusion and in vitro cerebral capillary endothelial cell cultures. Our specific aims are: 1) to elucidate the role of CuZn-SOD in vasogenic edema and infarction following focal cerebral ischemia and reperfusion in SOD-1 transgenic mice and in sod-1 knockout mutants; 2) to investigate the temporal pattern of bcl-2 and hsp 70 gene expression in neurons and endothelial cells in mice that overexpress SOD-1 transgene, wild-type or in mutant mice with reduced sod-1 expression following focal cerebral ischemia and reperfusion; 3) to elucidate the superoxide-dependent oxidative pathways involving the pathogenesis of vasogenic edema after focal cerebral ischemia using genetically modified mice with altered levels of glutathione peroxidase and nitric oxide synthase activities; 4) to investigate the role of oxidative stress in vasogenic edema and infarction in a newly developed mitochondrial manganese superoxide dismutase (sod-2) knockout mutant mouse; and 5) to study the role of superoxide dismutase on hypoxia-induced injury and degeneration in primary culture of cerebral endothelial cells of Tg and knockout mutants. These studies have therapeutic implications and will further shed light on molecular and cellular mechanisms underlying the pathogenesis of vasogenic edema following ischemia and reperfusion. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MEDIATORS OF BLOOD-BRAIN BARRIER DISRUPTION Principal Investigator & Institution: Mayberg, Marc R.; Chairman; Cleveland Clinic Foundation 9500 Euclid Ave Cleveland, Oh 44195 Timing: Fiscal Year 2004; Project Start 01-MAY-2004; Project End 28-FEB-2008 Summary: (provided by applicant): Cerebral ischemia causes disruption of the bloodbrain barrier (BBB), which may be associated with cerebral edema, hemorrhage, and

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increased infarct volume. There is substantial evidence linking BBB disruption to inflammatory processes involving cytokines, chemokines, and leukocyte-endothelial cell interactions. In experimental stroke models, inhibition of the inflammatory cascade after stroke reduces BBB disruption and stroke volume. However, analysis of pathologic mechanisms related to BBB disruption in vivo is complicated by inherent variability in stroke models, co-dependence of multiple variables (e.g., arterial blood gases and blood flow), and multi-factorial effects of drugs upon different cell types and cellular processes. A dynamic in vitro BBB (DIV-BBB) model has been developed in our laboratory that recapitulates morphologic, biochemical, and physiologic properties of the blood-brain barrier. Preliminary studies using this model showed that flow cessation (reduction of shear stress) under normoxic normoglycemic conditions produced immediate leukocyte-independent cytokine expression, which was followed by delayed BBB disruption only when leukocytes (VVBC) were present in the perfusate. The unifying hypothesis of this proposal is that reduction of shear stress in ischemia (independent of hypoxia or hypoglycemia) triggers a cascade of inflammatory processes leading to BBB disruption. The DIV-BBB model will be used to test four Aims by assessing the response to flow cessation over time in intra-and extraluminal fluid compartments and cell types comprising the DIVBBB (endothelium, leukocytes, and astrocytes). The first Aim will determine that nitric oxide (NO)-modulated, WBCindependent cytokine production by astrocytes and WBC-dependent cytokine release by WBC endothelium and astrocytes are critical precedents to subsequent inflammation. In Aim 2, expression of EC surface antigens after flow cessation will be correlated to leukocyte adhesion and subsequent BBB disruption. In Aim 3, the nature of WBC-EC adhesion and activated WBC phenotype will be examined in terms of cytokinestimulated prostaglandin synthesis and release of reactive oxygen species. Finally, the role of matrix metalloproteinases (MMP-2, -3 and -9) in inflammation-mediated BBB disruption will be determined. These experiments should provide a better understanding of the relationship between microvascular blood flow reductions and blood-brain barrier, and may lead to effective therapies to prevent BBB disruption after stroke. In addition, basic understanding of the relationship of shear stress and BBB function may be applied to other neurodegenerative and neoplastic disorders characterized by abnormal BBB physiology (e.g. Alzheimer's, demyelinating diseases, brain tumors). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MMP-9 MEDIATES CEREBRAL EDEMA IN FULMINANT LIVER FAILURE Principal Investigator & Institution: Nguyen, Justin H.; Mayo Clinic Coll of Med, Jacksonville Mayo Clinic Jacksonville Jacksonville, Fl 322243899 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-APR-2005 Summary: (provided by applicant): Fulminant hepatic failure (FHF) is a life-threatening disease. The definitive treatment for FHF is a liver transplant. Unfortunately, 35% of all FHF patients and 62% of nonacetaminophen-induced FHF patients die within 48 hours after reaching stage 3 or 4 coma, while awaiting a transplant. Increasing this narrow therapeutic window would provide substantially more opportunities for these patients to be transplanted. One of the primary causes of death in these individuals is cerebral edema. The mechanisms responsible for cerebral edema in these FHF patients are poorly understood. Recent evidence from other laboratories has shown that matrix metalloproteinase-9 (MMP-9) may play a pivotal role in the development of cerebral edema in other disease states. For example, treatment with either MMP-9 synthetic

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inhibitors or anti-MMP-9 monoclonal antibodies has been shown to result in a significant reduction in the size of cerebral infarcts. Further, studies using MMP-9 knockout mice have shown a significant attenuation in cerebral edema following either cerebral ischemic or traumatic events. Based on these data we hypothesize that MMP-9 plays a critical role in the development of cerebral edema following FHF. Significant support for this hypothesis has come from two observations made in our laboratory. First, both proMMP-9 and MMP-9 are elevated in the sera of FHF patients and in rats with experimentally induced FHF. Second, in a pilot study, we have shown that treatment with an MMP-9 inhibitor (GM6001) results in an approximate 30% reduction in cerebral edema in rats with experimentally induced FHF. In this application, we specifically propose to: 1. To further determine if inhibition of MMP-9 by the MMP synthetic inhibitor GM6001 attenuates cerebral edema in rats with experimentally induced FHF. 2. To determine whether cerebral edema is attenuated in MMP-9 knockout mice following experimentally induced FHF. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NA-K-CI COTRANSPORTER IN CEREBRAL ISCHEMIA Principal Investigator & Institution: Sun, Dandan; Neurological Surgery; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2003; Project Start 01-FEB-2000; Project End 30-APR-2007 Summary: (provided by applicant): This proposal is a competing renewal application of our current project to study a role of Na+-K+-Cl- cotransporter isoform1 (NKCC1) in cerebral ischemic damage. The long-term goal of the research is to understand ischemiainduced cell death and develop a more effective approach to ischemia treatment. NKCC1 is important in regulation of intracellular Na+ and Cl-, cell volume, and K+ uptake in the central nervous system (CNS). In the initial funding period, we have investigated NKCC1 activity under several conditions that are associated with ischemic insults. We found the NKCC1 activity in cultured cortical astrocytes was significantly stimulated under high extracellular K+ ([K+]0). Pharmacological inhibition or genetic ablation of NKCC1 abolished high [K+]0-induced astrocyte swelling and decreased glutamate release. In cultured neurons, activation of both ionotropic and mGluR group l glutamate receptors stimulated NKCC1 activity in a Ca++-dependent manner. Infarct volume and cerebral edema were significantly reduced by bumetanide, a potent inhibitor for NKCC1. Lour preliminary study revealed a neuroprotection in NKCC1 knockout mice following focal ischemia. These data strongly suggest that NKCC1 has an important role in cerebral ischemic damage. However, the cellular mechanisms underlying the role of NKCC1 in ischemic cell damage have not been fully understood. We hypothesize that NKCC1 contributes to perturbation in ion homeostasis and necrotic ischemic cell death. We will test the hypothesis by following Specific Aims: Aim 1: Determine the role of NKCC1 in intracellular Na+ and Cl- overload, swelling, and the swelling-mediated glutamate release from cortical astrocytes in an in vitro oxygen and glucose deprivation (OGD) model of ischemia. Aim 2: Investigate the contribution of NKCC1 to OGD-mediated ischemic cell death in cortical neurons. Aim 3: Investigate whether genetic ablation of NKCC1 reduced brain damage (gray and white matter) in NKCC1-/- mice following transient focal ischemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: OSMOTHERAPY IN ACUTE ISCHEMIC STROKE Principal Investigator & Institution: Bhardwaj, Anish; Associate Professor; Neurology and Neurosurgery; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218

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Timing: Fiscal Year 2004; Project Start 01-JUL-2004; Project End 31-MAR-2009 Summary: (provided by applicant): Cerebral edema associated with large hemispheric infarctions is frequently encountered in clinical practice and is a major cause of morbidity and mortality. Clinically, osmotherapy is the mainstay of medical management of cerebral edema associated with ischemic stroke. While mannitol has been the conventional osmotic agent of choice, its therapeutic efficacy is limited by several untoward side effects. A few experimental studies and clinical case series suggest that hypertonic saline (HS) is efficacious in the treatment of cerebral edema in some brain injury paradigms, but its effects in ischemic stroke are not well studied. The overall goal of this research proposal is to test the hypotheses that institution and maintenance of a hyper-osmolar state with HS is an important treatment of cerebral edema following experimental ischemic stroke. We will further utilize HS as a tool to delineate the complex interactions of aquaporins and ariginine-vasopressin (A VP) in the pathogenesis of ischemia-evoked cerebral edema. In Aim 1, we will define the most efficacious treatment paradigm with HS for cerebral edema following transient as well as permanent middle cerebral artery occlusion (MCAO). We will discern the optimal serum osmolality necessary for ameliorating cerebral edema and test the hypothesis, utilizing magnetic resonance imaging in vivo, that treatment duration, timing of withdrawal from therapy and integrity of the blood brain barrier determine anti-edema efficacy of HS in focal cerebral ischemia. Aim 2 will test the hypothesis that amelioration in brain edema with HS occurs via modulation of AQP4 in injured and contralateral non-ischemic brain following MCAO. We will determine if systemic osmolar changes a) alter 3erivascular localization of AQP4 in the brain and b) alter the evolution (rate and degree) of cerebral edema following MCAO in mice lacking alpha-syntrophin (alphasyn -/-) (a component of the dystrophin protein complex required for perivascular localization of AQP4) as compared to wild type (WT) mice. Aim 3 will determine if AVP release plays a significant role in ischemia-induced cerebral edema and test the hypothesis that it serves as an important link in how HS attenuates brain edema via alterations in AQP4 following focal ischemia. Specifically, we will determine if plasma and brain AVP levels are a) modulated by changes in systemic osmolality with HS treatment, and b) are attenuated in alpha-syn -/-mice as compared to WT mice following focal cerebral ischemia. These studies 1) have important translational significance for treatment of cerebral edema in patients with large cerebral infarctions, 2) will enhance our understanding of the complex mechanisms of edema formation following ischemic stroke, and 3) provide insights into potential newer therapeutic targets and strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: RADIO FREQUENCY IMPEDANCE MAPPING FOR MEDICAL IMAGING Principal Investigator & Institution: Grant, Aaron K.; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2006 Summary: (provided by applicant): Radio frequency impedance mapping (RFIM) is a proposed new medical imaging modality. Image intensity in RFIM is based on the local electrical properties (namely conductivity and permittivity) of tissues inside the body. Since these properties vary widely between different tissues and notably, between normal and malignant tissues, images based on these properties should have significant diagnostic value. Potential clinical applications include cancer detection and imaging of conditions such as myocardial ischemia, cerebral edema, and spreading depression. In

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RFIM imaging, a large array of radio frequency coils (such as are used in magnetic resonance imaging) are placed on the patient. Measurements of the impedance matrix (or S parameters) of the array are used to derive a system of equations that constrain the local electrical properties of the patient's body. These equations are then solved to obtain an image. The patient is not exposed to ionizing radiation or high levels of radio frequency power. Preliminary work on RFIM has included both numerical simulations and experimental work. The simulations indicate that RFIM is capable of producing accurate, fully three-dimensional images of internal anatomy. Early experimental results have begun to confirm this. The proposed project will involve staged development of a prototype RFIM imaging system. The prototype will be tested to determine the overall feasibility of RFIM, including tests of the achievable resolution, reconstruction accuracy, and sensitivity to tumor-like variations in conductivity and permittivity. Results from the study will enable early assessment of the feasibility of RFIM, and the prototype will serve as a starting point for future designs. Successful implementation of RFIM will provide a new and potentially robust technique for measurement of tissue dielectric properties. Furthermore, RFIM is highly non-invasive and RFIM imaging systems are likely to be both inexpensive and easily portable. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REDUCTION OF CEREBRAL EDEMA USING VENTRICULAR THERAPIES Principal Investigator & Institution: Fowler, William V.; Director; Twin Star Medical 914 S 8Th St, Mc 860C Roseville, Mn 55415 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 30-JUN-2004 Summary: (provided by applicant): Cerebral edema after traumatic brain injury and severe stroke is a life-threatening condition that is refractory to conventional treatments in a significant population of patients. Current treatments (i.e. hyperventilation, osmotic diuretic(s) or hypothermia) are associated with serious side effects that increase with prolonged use. Intracranial hypertension is caused by elevated tissue water content, primarily due to hyperosmosis of ischemic tissue. Thus, removal of water may be an effective treatment. The research plan details feasibility tests of a novel, safe, and effective method of removing water that can be placed within a standard ventriculostomy catheter. Pilot studies have shown a 50% reduction in water uptake by brain tissue in an ex vivo model. In vitro studies will be completed to optimize catheter material and design. Further ex vivo tissue studies will be completed, as well as studies of human post-traumatic CSF. Tissue water removal in a scale model of the human cerebroventricular system will be tested. The goal is to reduce edema in tissue samples without an increase in CSF osmolarity. Successful development and marketing of this proprietary methodology could significantly reduce morbidity and mortality after human TBI, stroke, and other neurological disorders associated with cerebral edema. In Phase II, further efficacy testing of catheter systems is planned in experimental models of cerebral edema and human studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: REGULATION OF CEREBRAL BLOOD FLOW AFTER TRAUMATIC BRAIN INJURY Principal Investigator & Institution: Robertson, Claudia S.; Professor; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2003

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Cerebral Edema

Summary: The overall hypothesis of this proposal is that traumatic brain injury causes impairment of cerebral blood flow (CBF) regulation that produces a spectrum of injury in our head injured patients, ranging from frank ischemia to increased susceptibility to secondary insults. During the last grant period, we valuated a management strategy to prevent ischemia by providing the brain with a higher perfusion pressure that would compensate for the impaired ability of the injured brain to pressure autoregulate. This study demonstrated that we could significantly reduce the occurrence of secondary insults, but other consequences of the higher perfusion pressure (more adult respiratory distress syndrome, possibly worsened cerebral edema) offset the beneficial effects of reducing ischemic insults. The results of this study emphasize the importance of the proposed works. The overall goals of the proposed work are to develop methods for identifying those patients who are at greatest risk of secondary insults and to develop a way to prevent secondary cerebral ischemia by correcting the underlying vascular abnormalities that cause the injured brain to be sensitive to ischemic insults. The first overall goal will be achieved by studying CBF regulation in head injured patients and determining if abnormalities on these tests predict a greater risk of secondary insults (Specific Aims #1-2). At the end of the study, we plan to have identified simple tests that can be performed on admission to identify patients at greater risk from secondary insults and who therefore would benefit most from CBF-targeted therapy. The second goal will be achieved by studying the relationship of the myogenic response in isolated vessels to the impairment of autoregulation observed in vivo (Specific Aim #3), by studying the relationship of various vasoactive mediators to the impairment of CBF regulation observed in vivo (Specific Aim #3), and by studying the effect of L-arginine on CBF and on CBF regulation (Specific Aim #4). The specific aims include: 1. To develop practical methods for monitoring CBF regulation in the intensive care unit: 2. To study the incidence and severity of impairment of CBF regulation after TBI: 3. To study the cause of impairment of CBF regulation after TBI: 4. To study the effect of Larginine on cerebral hemodynamics in patients with regional or global ischemia (CBF<20 ml/100gm/min) after TBI: Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: THE EFFECTS OF PROGESTERONE AND ITS METABOLITES ON TBI Principal Investigator & Institution: Stein, Donald G.; Asa G. Candler Professor; Emergency Medicine; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2002; Project Start 15-DEC-2001; Project End 30-NOV-2004 Summary: At present, there are no clinically effective treatments for traumatic brain injury (TBI). The long-term objective of this research is to develop such a therapy that will enhance morphological and behavioral recovery of function. TBI triggers a cascade of dramatic, biochemical events leading to primary and secondary neuronal loss and dysfunction. Many of these events, such as disruption of the blood brain barrier, excitotoxicity, ischemia, oxidative stress, glial activation and the inflammatory immune response, contribute to an increase in cerebral edema, which is often severely disabling or fatal to patients. There is growing experimental evidence that, in laboratory animals, progesterone and its metabolites are safe and effective in providing neuroprotection and in reducing cerebral edema after TBI. How these neurosteroids act specifically in the central nervous system to enhance recovery of function is not yet completely understood, and this gap in our knowledge limits interest in proceeding to clinical trials. The focus of the proposed research is to extend our knowledge of how progesterone and its metabolites enhance neuronal repair and recovery of function in the damaged

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nervous system by controlling the events causing cerebral edema and neuronal death. We will use a model of brain injury that creates controlled contusions of the frontal cortex in rodents. We will then measure the effects of progesterone, allopregnanolone and epiallopregnanolone treatments on behavioral recovery, cytokine expression, and oxidative stress following TBI. Four projects are proposed: (1) determines whether the progesterone-related metabolites, allopregnanolone and epiallopregnanolone, have effects similar to progesterone in promoting neuroprotection and behavioral recovery after TBI; (2) examines whether the metabolites are as effective as progesterone in reducing post-injury inflammatory signals; (3) explores whether these progesteronerelated hormones modulate the temporal and spatial distribution of inflammatory cells; (4) investigates whether reducing these inflammatory signals results in the decrease of oxidative stress and neural cell death. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VEGF AND ANGIOPOIETIN 1 THERAPY FOR STROKE Principal Investigator & Institution: Zhang, Zheng G.; Senior Staff; Neurology; Case Western Reserve Univ-Henry Ford Hsc Research Administraion Cfp-046 Detroit, Mi 48202 Timing: Fiscal Year 2003; Project Start 15-DEC-2002; Project End 30-NOV-2006 Summary: (provided by applicant): In this application, we propose to investigate the roles of vascular endothelial growth factor (VEGF) and angiopoietin 1 (Ang 1) in cerebral angiogenesis and blood brain barrier (BBB) leakage after focal cerebral embolic ischemia. Our preliminary data demonstrate that administration of VEGF at the time when endogenous Ang 1 is upregulated enhances angiogenesis in ischemic brain and improves functional recovery after stroke. Furthermore, an increase in levels of Ang 1 reduces BBB leakage after acute stroke. Our hypotheses are: 1) Co-administration of recombinant human VEGF165 (rhVEGF165) and BowAng 1, a forced Ang1 homodimer containing an Fc fusion protein, enhances angiogenesis and consequently improves neurological recovery. Enhancement of angiogenesis in ischemic brain promotes axonal and dendritic sprouting and synapse formation which leads to improved functional recovery; 2) VEGF and Ang 1 cooperatively maintain the integrity of BBB. An increase in levels of Ang 1 counteracts the effects of VEGF on vascular permeability and consequently decreases BBB leakage after stroke. The proposed experiments have been designed to test these hypotheses. We will first determine the effect of administration of rhVEGF165 and BowAng1 on cerebral angiogenesis and functional recovery after stroke. We will also investigate potential molecular and cellular mechanisms by which rhVEGF165 and BowAng1 treatments enhance functional recovery by measuring axonal and dendritic sprouting and synapse formation. Second, we will determine the effect of administration of BowAng1 on BBB leakage after ischemia. These studies will provide insights into roles of VEGF and Ang 1 in maintaining BBB integrity. Changes of BBB permeability, angiogenesis and axonal and dendritic sprouting will be measured by means of Magnetic Resonance Imaging, quantitative autoradiography, Laser Scanning Confocal Microscopy, and a novel software program for three-dimensional image analysis. We believe that these are unique and fresh approaches that may yield promising insights into the fundamental basis for angiogenic growth factors in controlling BBB integrity and angiogenesis and may lead to development of an effective restorative therapy for the treatment of ischemic stroke and cerebral edema. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Cerebral Edema

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

Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS. by Arieff AI, Kleeman CR.; 1973 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=302295

The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with cerebral edema, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “cerebral edema” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for cerebral edema (hyperlinks lead to article summaries): •

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203Hg brain scan for the detection and localization of cerebral edema. Author(s): Nagai H, Kobayashi T, Hayakawa R. Source: Bull Los Angeles Neurol Soc. 1967 April; 32(2): 93-103. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6033818

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

With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print. 6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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A case of typhoid fever complicated by unexpected diffuse cerebral edema. Author(s): van de Wetering J, Visser LG, van Buchem MA, van der Hoeven JG. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1995 October; 21(4): 1057-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8645816

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A correlative study of computed tomography and histology in human and experimental vasogenic cerebral edema. Author(s): Clasen RA, Huckman MS, Von Roenn KA, Pandolfi S, Laing I, Lobick JJ. Source: Journal of Computer Assisted Tomography. 1981 June; 5(3): 313-27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7240505

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A history of the study of cerebral edema. Author(s): Bell BA. Source: Neurosurgery. 1983 December; 13(6): 724-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6361601

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A lethal complication of psychogenic polydipsia: cerebral edema and herniation. Author(s): Ligtenberg JJ, Wymenga AN, Tulleken JE, van der Werf TS, Zijlstra JG. Source: Intensive Care Medicine. 1998 June; 24(6): 644-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9681796

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Acute cerebral edema as part of the syndrome of hepatic encephalopathy in an individual with chronic liver disease: a case report. Author(s): Jabbour N, Karavias D, Van Thiel DH. Source: J Okla State Med Assoc. 1994 November; 87(11): 501-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7815183

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Acute glomerulonephritis and cerebral edema. Author(s): Nieto Rodriguez JA, Bilbao Garay J, Perez Maestu R, Martinez J, de Letona L. Source: Nephron. 1988; 48(4): 330. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3362284

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Addison's disease presenting with cerebral edema. Author(s): Geenen C, Tein I, Ehrlich RM. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 1996 May; 23(2): 141-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8738929

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Adenylate kinase, amino acids, and other substances in cerebrospinal fluid as markers either for recent cerebral infarction or for concomitant cerebral edema. Author(s): Ionescu DA, Hategan D, Balaita C, Jipescu I. Source: Neurol Psychiatr (Bucur). 1988 April-June; 26(2): 77-84. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2841750

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Adrenal corticosteroid therapy of cerebral edema. Author(s): Maha GE. Source: Pa Med. 1970 January; 73(1): 50-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5410001

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Agents for cerebral edema. Author(s): de los Reyes RA, Ausman JI, Diaz FG. Source: Clin Neurosurg. 1981; 28: 98-107. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6797771

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Arginase deficiency with lethal neonatal expression: evidence for the glutamine hypothesis of cerebral edema. Author(s): Picker JD, Puga AC, Levy HL, Marsden D, Shih VE, Degirolami U, Ligon KL, Cederbaum SD, Kern RM, Cox GF. Source: The Journal of Pediatrics. 2003 March; 142(3): 349-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12640389

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Arterial thrombosis causing cerebral edema in association with diabetic ketoacidosis. Author(s): Krane EJ. Source: Critical Care Medicine. 1988 January; 16(1): 100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3123137

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Arterial thrombosis causing cerebral edema in association with diabetic ketoacidosis. Author(s): Kanter RK, Oliphant M, Zimmerman JJ, Stuart MJ. Source: Critical Care Medicine. 1987 February; 15(2): 175-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3100139

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Autopsy diagnoses of pulmonary edema and cerebral edema. Author(s): Hinckley ME. Source: Aerosp Med. 1974 August; 45(8): 968-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4844260

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Beneficial effect of human albumin on neonatal cerebral edema. Author(s): Gurkan F, Haspolat K, Yaramis A, Ece A. Source: American Journal of Therapeutics. 2001 July-August; 8(4): 253-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11441325

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Bifrontal decompressive craniotomy for massive cerebral edema. Author(s): Kjellberg RN, Prieto A Jr. Source: Journal of Neurosurgery. 1971 April; 34(4): 488-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5554353

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Bilateral nephrectomy and chronic hemodialysis in renal failure due to diabetic nephropathy complicated by malignant hypertension and cerebral edema. Author(s): Nik-Akhtar B, Khonsari H. Source: Nephron. 1978; 21(4): 236. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=683408

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Bilateral putaminal hemorrhage with cerebral edema in hyperglycemic hyperosmolar syndrome. Author(s): Cho SJ, Won TK, Hwang SJ, Kwon JH. Source: Yonsei Medical Journal. 2002 August; 43(4): 533-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12205743

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Biochemical study of cerebral edema in cerebrovascular accidents. Author(s): Schwartz B, Meiu F, Epure V. Source: Rev Roum Neurol. 1972; 9(1): 3-13. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5019766

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Biological features of meningiomas that determine the production of cerebral edema. Author(s): Smith HP, Challa VR, Moody DM, Kelly DL Jr. Source: Neurosurgery. 1981 April; 8(4): 428-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7242894

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Brief repeated umbilical cord occlusions cause sustained cytotoxic cerebral edema and focal infarcts in near-term fetal lambs. Author(s): De Haan HH, Gunn AJ, Williams CE, Gluckman PD. Source: Pediatric Research. 1997 January; 41(1): 96-104. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8979296

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Can perinatal asphyxia cause cerebral edema and affect cerebral blood flow velocity? Author(s): van Bel F, Hirasing RA, Grimberg MT. Source: European Journal of Pediatrics. 1984 April; 142(1): 29-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6714256

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Case for diagnosis: subglottic hemangioma and cerebral edema. Author(s): Gordon LP. Source: Military Medicine. 1979 October; 144(10): 659, 664. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=119169

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Cases from the aerospace medicine residents' teaching file. Case #44. An aviator with high attitude pulmonary and cerebral edema presenting acute mountain sickness. Author(s): Stephens PJ. Source: Aviation, Space, and Environmental Medicine. 1991 June; 62(6): 593-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1859351

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Cerebral atrophy and convulsive seizures after recovery from cerebral edema and coma in a patient with fulminant hepatitis B. Author(s): Honda S, Taniguchi A, Murai K, Kuzuhara S. Source: Intern Med. 2001 March; 40(3): 255-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11310495

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Cerebral edema after hemodialysis: the "reverse urea effect" lives. Author(s): Silver SM. Source: Int J Artif Organs. 1998 May; 21(5): 247-50. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9684904

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Cerebral edema and brain swelling. Author(s): Rosomoff HL. Source: Acta Anaesthesiologica Scandinavica. Supplementum. 1968; 29: 75-97. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5674580

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Cerebral edema and depression of sensorium in nonketotic hyperosmolar coma. Author(s): Arieff AI, Carroll HJ. Source: Diabetes. 1974 June; 23(6): 525-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4834291

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Cerebral edema and galactosemia. Author(s): Welch RJ, Milligan DW. Source: Pediatrics. 1987 October; 80(4): 597-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3658581

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Cerebral edema and intracranial hypertension in acute liver failure: distinct aspects of the same problem. Author(s): Blei AT. Source: Hepatology (Baltimore, Md.). 1991 February; 13(2): 376-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1847353

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Cerebral edema and intracranial pressure monitoring. Author(s): Cordoba J, Blei AT. Source: Liver Transplantation and Surgery : Official Publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society. 1995 May; 1(3): 187-94. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9346564

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Cerebral edema and its medical management. Author(s): Nair KG. Source: J Assoc Physicians India. 1972 December; 20(12): 935. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4659156

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Cerebral edema and neurointensive care. Author(s): Hahn JF. Source: Pediatric Clinics of North America. 1980 August; 27(3): 587-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7413293

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Cerebral edema and neurological function in human beings. Author(s): Penn RD. Source: Neurosurgery. 1980 March; 6(3): 249-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7383287

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Cerebral edema and neurological function: CT, evoked responses, and clinical examination. Author(s): Penn RD. Source: Adv Neurol. 1980; 28: 383-94. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7457253

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Cerebral edema and ophthalmoplegia reversed by mannitol in a new case of insulindependent diabetes mellitus. Author(s): Franklin B, Liu J, Ginsberg-Fellner F. Source: Pediatrics. 1982 January; 69(1): 87-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6798545

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Cerebral edema and priapism in an adolescent with acute lymphoblastic leukemia. Author(s): Choo-Kang LR, Jones DM, Fehr JJ, Eskenazi AE, Toretsky JA. Source: Pediatric Emergency Care. 1999 April; 15(2): 110-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10220081

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Cerebral edema associated with acute hepatic failure. Author(s): Fujiwara M, Watanabe A, Yamauchi Y, Hashimoto M, Nakatsukasa H, Kobayashi M, Higashi T, Nagashima H. Source: Acta Medica Okayama. 1985 February; 39(1): 73-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3984783

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Cerebral edema associated with betaine treatment in classical homocystinuria. Author(s): Devlin AM, Hajipour L, Gholkar A, Fernandes H, Ramesh V, Morris AA. Source: The Journal of Pediatrics. 2004 April; 144(4): 545-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15069409

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Cerebral edema associated with intracranial tumors. Author(s): Challa VR. Source: Surgical Neurology. 1987 January; 27(1): 68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3787444

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Cerebral edema associated with meningioma. Author(s): Lee ST, Hsueh S. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 1989 May; 16(2): 211-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2731092

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Cerebral edema associated with meningiomas. Author(s): Maiuri F, Gangemi M, Cirillo S, Delehaye L, Gallicchio B, Carandente M, Giamundo A. Source: Surgical Neurology. 1987 January; 27(1): 64-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3787443

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Cerebral edema associated with meningiomas. Author(s): Gilbert JJ, Paulseth JE, Coates RK, Malott D. Source: Neurosurgery. 1983 June; 12(6): 599-605. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6877541

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Cerebral edema associated with meningiomas: possible role of a secretory-excretory phenomenon. Author(s): Philippon J, Foncin JF, Grob R, Srour A, Poisson M, Pertuiset BF. Source: Neurosurgery. 1984 March; 14(3): 295-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6709154

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Cerebral edema associated with meningiomas: the role of peritumoral brain tissue. Author(s): Vaz R, Borges N, Cruz C, Azevedo I. Source: Journal of Neuro-Oncology. 1998 February; 36(3): 285-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9524107

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Cerebral edema caused by perinatal asphyxia. Detection and follow-up. Author(s): van Bel F, van de Bor M. Source: Helv Paediatr Acta. 1985 December; 40(5): 361-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2935513

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Cerebral edema causing death in children with maple syrup urine disease. Author(s): Riviello JJ Jr, Rezvani I, DiGeorge AM, Foley CM. Source: The Journal of Pediatrics. 1991 July; 119(1 ( Pt 1)): 42-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2066857

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Cerebral edema complicating diabetic ketoacidosis in childhood. Author(s): Rosenbloom AL, Riley WJ, Weber FT, Malone JI, Donnelly WH. Source: The Journal of Pediatrics. 1980 March; 96(3 Pt 1): 357-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6767008

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Cerebral edema complicating eclampsia. Author(s): Cunningham FG, Twickler D. Source: American Journal of Obstetrics and Gynecology. 2000 January; 182(1 Pt 1): 94100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10649162

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Cerebral edema complicating nonketotic hyperosmolar coma. Author(s): Arieff AI. Source: Mineral and Electrolyte Metabolism. 1986; 12(5-6): 383-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3543638

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Cerebral edema complicating therapy for diabetic ketoacidosis. Author(s): Duck SC, Weldon VV, Pagliara AS, Haymond MW. Source: Diabetes. 1976 February; 25(2): 111-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=814023

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Cerebral edema due to hemodialysis in paracetamol-induced fulminant hepatic failure. Author(s): Schiodt FV, Clemmesen JO, Hansen BA, Larsen FS. Source: Scandinavian Journal of Gastroenterology. 1995 September; 30(9): 927-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8578195

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Cerebral edema during hepatic encephalopathy in fulminant hepatic failure. Author(s): Watanabe A, Shiota T, Tsuji T. Source: J Med. 1992; 23(1): 29-38. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1573340

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Cerebral edema following acute sodium valproate overdose. Author(s): Khoo SH, Leyland MJ. Source: Journal of Toxicology. Clinical Toxicology. 1992; 30(2): 209-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1588670

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Cerebral edema following iodine-131 therapy for thyroid carcinoma metastatic to the brain. Author(s): Datz FL. Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 1986 May; 27(5): 637-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3712081

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Cerebral edema from blood-brain glucose differences complicating peritoneal dialysis. Second membrane syndrome. Author(s): Fernandez JP, McGinn JT, Hoffman RS. Source: N Y State J Med. 1968 March 1; 68(5): 677-80. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5238731

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Cerebral edema from valproate? Author(s): Longmire AW, Seger DL. Source: Journal of Toxicology. Clinical Toxicology. 1992; 30(4): 685-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1433437

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Cerebral edema in acute hepatic failure: clinicopathologic correlation. Author(s): Liu GT, Urion DK, Volpe JJ. Source: Pediatric Neurology. 1993 May-June; 9(3): 224-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8352857

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Cerebral edema in children with diabetic ketoacidosis. Author(s): Glaser N. Source: Curr Diab Rep. 2001 August; 1(1): 41-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12762956

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Cerebral edema in developing brain. II. Asphyxia in the five-day-old rat. Author(s): De Souza SW, Dobbing J. Source: Experimental Neurology. 1973 June; 39(3): 414-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4712899

Studies

31

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Cerebral edema in diabetic ketoacidosis. Author(s): Steinhart CM, Hoffman WH. Source: The Journal of Pediatrics. 1989 May; 114(5): 905-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2497238

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Cerebral edema in diabetic ketoacidosis. Author(s): Winegrad AI, Kern EF, Simmons DA. Source: The New England Journal of Medicine. 1985 May 2; 312(18): 1184-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3920522

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Cerebral edema in diabetic ketoacidosis. Author(s): Duck SC, Kohler E. Source: The Journal of Pediatrics. 1981 April; 98(4): 674-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6782223

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Cerebral edema in intracranial meningiomas: evidence for local and diffuse patterns and factors associated with its occurrence. Author(s): Abe T, Black PM, Ojemann RG, Hedley-White ET. Source: Surgical Neurology. 1994 December; 42(6): 471-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7825100

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Cerebral edema in maple syrup urine disease. Author(s): Levin ML, Scheimann A, Lewis RA, Beaudet AL. Source: The Journal of Pediatrics. 1993 January; 122(1): 167-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8419609

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Cerebral edema in maple syrup urine disease. Author(s): Lungarotti MS, Calabro A, Signorini E, Garibaldi LR. Source: Am J Dis Child. 1982 July; 136(7): 648. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7091101

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Cerebral edema in severe pregnancy-induced hypertension. Author(s): Benedetti TJ, Quilligan EJ. Source: American Journal of Obstetrics and Gynecology. 1980 August 1; 137(7): 860-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7405980

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Cerebral edema in stroke: a common, often fatal complication. Author(s): Sherman DG, Easton JD. Source: Postgraduate Medicine. 1980 July; 68(1): 107-13, 116, 119-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6771748

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Cerebral edema in the Himalayas: too high, too fast! Author(s): Graham LE, Basnyat B. Source: Wilderness Environ Med. 2001 Spring; 12(1): 62. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11294557

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Cerebral edema leading to decompressive craniectomy: an assessment of the preceding clinical and neuromonitoring trends. Author(s): Strege RJ, Lang EW, Stark AM, Scheffner H, Fritsch MJ, Barth H, Mehdorn HM. Source: Neurological Research. 2003 July; 25(5): 510-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12866200

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Cerebral edema on high mountains. Author(s): Pines A. Source: Lancet. 1978 October 28; 2(8096): 938-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=81946

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Cerebral edema unresponsive to conventional therapy in neurosurgical patients with unsuspected nutritional failure. Author(s): Bryan-Brown CW, Savitz MH, Elwyn DH, Shoemaker WC. Source: Critical Care Medicine. 1973 May-June; 1(3): 125-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4201968

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Cerebral edema with herniation during acetaminophen-induced fulminant hepatic failure. Author(s): Nyberg SL, Pfeifer EA. Source: Liver Transplantation : Official Publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society. 2000 July; 6(4): 495-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10915174

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Cerebral edema with irreversible coma in severe diabetic ketoacidosis. Author(s): Young E, Bradley RF. Source: The New England Journal of Medicine. 1967 March 23; 276(12): 665-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4959859

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Cerebral edema, cell volume regulation, and the role of ion channels in organic osmolyte transport. Author(s): Jackson PS, Madsen JR. Source: Pediatric Neurosurgery. 1997 December; 27(6): 279-85. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9655141

Studies

33

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Cerebral edema, diabetes insipidus, and sudden death during the treatment of diabetic ketoacidosis. Author(s): Taubin H, Matz R. Source: Diabetes. 1968 February; 17(2): 108-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4965823

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Cerebral edema, mass effects, and regional blood volume in man. Author(s): Penn RD, Kurtz D. Source: Journal of Neurosurgery. 1977 March; 46(3): 282-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=839253

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Cerebral edema. Author(s): Kempski O. Source: Semin Nephrol. 2001 May; 21(3): 303-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11320499

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Cerebral edema. Author(s): Hariri RJ. Source: Neurosurg Clin N Am. 1994 October; 5(4): 687-706. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7827479

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Cerebral edema. Author(s): Weiss MH. Source: Acute Care. 1985; 11(3-4): 187-204. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3916397

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Cerebral edema. Author(s): Shields CB. Source: International Anesthesiology Clinics. 1977 Fall; 15(3): 111-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=914378

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Cerebral edema. Author(s): Bucy PC, Winston SR. Source: Mod Treat. 1972 February; 9(1): 90-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5029637

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Cerebral edema: a major complication of massive hepatic necrosis. Author(s): Ware AJ, D'Agostino AN, Combes B. Source: Gastroenterology. 1971 December; 61(6): 877-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5125688

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Cerebral edema: bringing the brain back down to size. Author(s): Specht DM. Source: Nursing. 1995 November; 25(11): 34-8; Quiz 46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7478323

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Cerebral edema: present perspectives. Author(s): Ignelzi RJ. Source: Neurosurgery. 1979 April; 4(4): 338-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=450234

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Cerebral edema: role of fatty acid metabolism of brain capillaries. Author(s): Goldstein GW. Source: The New England Journal of Medicine. 1977 March 17; 296(11): 632-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=840248

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Cerebrospinal fluid circulation, cerebral edema, and intracranial pressure. Author(s): Williams MA, Razumovsky AYe. Source: Current Opinion in Neurology. 1993 December; 6(6): 847-53. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8293158

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Changes of cerebral perfusion after osmotherapy in acute cerebral edema assessed with perfusion weighted MRI. Author(s): Stoll M, Hagen T, Bartylla K, Weber M, Jost V, Treib J. Source: Neurological Research. 1998 September; 20(6): 474-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9713836

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Clinical and radiologic features of cerebral edema in fulminant hepatic failure. Author(s): Wijdicks EF, Plevak DJ, Rakela J, Wiesner RH. Source: Mayo Clinic Proceedings. 1995 February; 70(2): 119-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7845036

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Clinical quiz. Diabetic ketoacidosis with severe dehydration, cerebral edema, and acute hypokalemia. Author(s): Segar WE. Source: Pediatric Nephrology (Berlin, Germany). 1991 January; 5(1): 99-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1902702

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Clinico-morphological considerations in cerebral edema. Author(s): Arseni C, Oprescu I, Nicolescu P, Nereantiu F, Carp N. Source: Rev Roum Neurol. 1973; 10(3): 175-82. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4726777

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Combined lung injury, meningitis and cerebral edema: how permissive can hypercapnia be? Author(s): Nichani S. Source: Intensive Care Medicine. 1999 January; 25(1): 125-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10051094

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Combined lung injury, meningitis and cerebral edema: how permissive can hypercapnia be? Author(s): Tasker RC, Peters MJ. Source: Intensive Care Medicine. 1998 June; 24(6): 616-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9681785

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Computed axial tomography scan demonstration of cerebral edema in eclampsia preceded by blindness. Author(s): Beeson JH, Duda EE. Source: Obstetrics and Gynecology. 1982 October; 60(4): 529-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7121942

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Computed tomographic demonstration of cerebral edema in a child with galactosemia. Author(s): Belman AL, Moshe SL, Zimmerman RD. Source: Pediatrics. 1986 October; 78(4): 606-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3763268

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Correlation of tumor plasminogen activator with peritumoral cerebral edema. A CT and biochemical study. Author(s): Quindlen EA, Bucher AP. Source: Journal of Neurosurgery. 1987 May; 66(5): 729-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3106592

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Correlation of vascular endothelial growth factor messenger RNA expression with peritumoral vasogenic cerebral edema in meningiomas. Author(s): Kalkanis SN, Carroll RS, Zhang J, Zamani AA, Black PM. Source: Journal of Neurosurgery. 1996 December; 85(6): 1095-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8929501

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Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema. Author(s): Polin RS, Shaffrey ME, Bogaev CA, Tisdale N, Germanson T, Bocchicchio B, Jane JA. Source: Neurosurgery. 1997 July; 41(1): 84-92; Discussion 92-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9218299

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Decompressive craniectomy for intractable cerebral edema: experience of a single center. Author(s): Ziai WC, Port JD, Cowan JA, Garonzik IM, Bhardwaj A, Rigamonti D. Source: Journal of Neurosurgical Anesthesiology. 2003 January; 15(1): 25-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12499979

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Delayed cerebral edema and fatal coma after minor head trauma: role of the CACNA1A calcium channel subunit gene and relationship with familial hemiplegic migraine. Author(s): Kors EE, Terwindt GM, Vermeulen FL, Fitzsimons RB, Jardine PE, Heywood P, Love S, van den Maagdenberg AM, Haan J, Frants RR, Ferrari MD. Source: Annals of Neurology. 2001 June; 49(6): 753-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11409427

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Delayed cerebral edema complicating cerebral arterial gas embolism: case histories. Author(s): Pearson RR, Goad RF. Source: Undersea Biomed Res. 1982 December; 9(4): 283-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7168093

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Devastating cerebral edema in diabetic ketoacidosis before therapy. Author(s): Glasgow AM. Source: Diabetes Care. 1991 January; 14(1): 77-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1899369

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Diabetic ketoacidosis and cerebral edema. Author(s): Bohn D, Daneman D. Source: Current Opinion in Pediatrics. 2002 June; 14(3): 287-91. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12011666

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Diabetic ketoacidosis with fatal cerebral edema. Author(s): Warren P, Villaluz ES, Rosenberg H. Source: Pediatrics. 1969 April; 43(4): 620-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4975838

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Diffuse cerebral edema following endoscopy. Author(s): Herman BE, Swenson J, Siebert W, Kelly B, Hamilton F. Source: The American Journal of Gastroenterology. 1993 April; 88(4): 616-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8470657

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Diffusion-weighted MRI in cyclosporin A neurotoxicity for the classification of cerebral edema. Author(s): Debaere C, Stadnik T, De Maeseneer M, Osteaux M. Source: European Radiology. 1999; 9(9): 1916-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10602976

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Disoriented and ataxic pilgrims: an epidemiological study of acute mountain sickness and high-altitude cerebral edema at a sacred lake at 4300 m in the Nepal Himalayas. Author(s): Basnyat B, Subedi D, Sleggs J, Lemaster J, Bhasyal G, Aryal B, Subedi N. Source: Wilderness Environ Med. 2000 Summer; 11(2): 89-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10921358

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Dose response curve of intravenous glycerol in the treatment of cerebral edema due to trauma. A case report. Author(s): Reinglass JL. Source: Neurology. 1974 August; 24(8): 743-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4858419

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Dyke award. Influence of fiber tracts on the CT appearance of cerebral edema: anatomic-pathologic correlation. Author(s): Cowley AR. Source: Ajnr. American Journal of Neuroradiology. 1983 July-August; 4(4): 915-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6410876

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Early onset fatal cerebral edema in diabetic ketoacidosis. Author(s): Couch RM, Acott PD, Wong GW. Source: Diabetes Care. 1991 January; 14(1): 78-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1899370

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Effect of glycerol on ischemic cerebral edema assessed by magnetic resonance imaging. Author(s): Sakamaki M, Igarashi H, Nishiyama Y, Hagiwara H, Ando J, Chishiki T, Curran BC, Katayama Y. Source: Journal of the Neurological Sciences. 2003 May 15; 209(1-2): 69-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12686405

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Electrolytes, fluids, and energy metabolism in human cerebral edema. Author(s): Reulen HJ, Medzihradsky F, Enzenbach R, Marguth F, Brendel W. Source: Archives of Neurology. 1969 November; 21(5): 517-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5344360

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Electron microscopic study of brain capillaries in cerebral edema from fulminant hepatic failure. Author(s): Kato M, Hughes RD, Keays RT, Williams R. Source: Hepatology (Baltimore, Md.). 1992 June; 15(6): 1060-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1592344

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Electron microscopic study of capillary wall in human cerebral edema. Author(s): Castejon OJ. Source: Journal of Neuropathology and Experimental Neurology. 1980 May; 39(3): 296328. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7365510

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Energy state and glycolysis in human cerebral edema. The application of a new freeze-stop technique. Author(s): Schmiedek P, Baethmann A, Sippel G, Oettinger W, Enzenbach R, Marguth F, Brendel W. Source: Journal of Neurosurgery. 1974 March; 40(3): 251-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4813710

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Evolution of cerebral edema and its relationship with power in the theta band. Author(s): Fernandez-Bouzas A, Harmony T, Marosi E, Fernandez T, Silva J, Rodriguez M, Bernal J, Reyes A, Casian G. Source: Electroencephalography and Clinical Neurophysiology. 1997 April; 102(4): 27985. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9146487

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Extrapontine myelinolysis in a pediatric case of diabetic ketoacidosis and cerebral edema. Author(s): Bonkowsky JL, Filloux FM. Source: Journal of Child Neurology. 2003 February; 18(2): 144-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12693785

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Factors associated with adverse outcomes in children with diabetic ketoacidosisrelated cerebral edema. Author(s): Marcin JP, Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J, Kaufman F, Quayle K, Roback M, Malley R, Kuppermann N; American Academy of Pediatrics. The Pediatric Emergency Medicine Collaborative Research Commitee. Source: The Journal of Pediatrics. 2002 December; 141(6): 793-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12461495

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Factors predicting cerebral edema in young children with diabetic ketoacidosis and new onset type I diabetes. Author(s): Hale PM, Rezvani I, Braunstein AW, Lipman TH, Martinez N, Garibaldi L. Source: Acta Paediatrica (Oslo, Norway : 1992). 1997 June; 86(6): 626-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9202799

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Fatal cerebral edema and intracranial hemorrhage associated with hypernatremic dehydration. Author(s): Mocharla R, Schexnayder SM, Glasier CM. Source: Pediatric Radiology. 1997 October; 27(10): 785-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9323240

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Fatal cerebral edema complicating toxic shock syndrome. Author(s): Smith DB, Gulinson J. Source: Neurosurgery. 1988 March; 22(3): 598-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3362331

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Fatal cerebral edema following angiocardiography: a case report. Author(s): Shrivastava S, Mohan JC, Chopra P. Source: International Journal of Cardiology. 1985 August; 8(4): 490-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4030150

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Formation and treatment of cerebral edema. Author(s): Baethmann A, Lanksch W, Schmiedek P. Source: Neurochirurgia (Stuttg). 1974 March; 17(2): 37-47. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4838721

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Giant intracranial aneurysms presenting with massive cerebral edema. Author(s): Heros RC, Kolluri S. Source: Neurosurgery. 1984 October; 15(4): 572-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6493468

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Global cerebral edema after subarachnoid hemorrhage. Author(s): Lagares A, Gomez PA, Alen JF, Lobato RD, Campollo J. Source: Stroke; a Journal of Cerebral Circulation. 2002 September; 33(9): 2153-4; Author Reply 2153-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12215578

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Global cerebral edema after subarachnoid hemorrhage: frequency, predictors, and impact on outcome. Author(s): Claassen J, Carhuapoma JR, Kreiter KT, Du EY, Connolly ES, Mayer SA. Source: Stroke; a Journal of Cerebral Circulation. 2002 May; 33(5): 1225-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11988595

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Global cerebral edema and subarachnoid hemorrhage in a patient with systemic lupus erythematosus. Author(s): Rozet I, Vavilala MS, Souter M, Lam AM. Source: Journal of Neurosurgical Anesthesiology. 2004 April; 16(2): 164-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15021288

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Guillain-Barre syndrome presenting as high-altitude cerebral edema. Author(s): Shlim DR, Cohen MT. Source: The New England Journal of Medicine. 1989 August 24; 321(8): 545. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2761595

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Hepatic encephalopathy and cerebral edema. Author(s): Ede RJ, Williams RW. Source: Seminars in Liver Disease. 1986 May; 6(2): 107-18. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3018935

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Hepatic encephalopathy in chronic liver disease: a clinical manifestation of astrocyte swelling and low-grade cerebral edema? Author(s): Haussinger D, Kircheis G, Fischer R, Schliess F, vom Dahl S. Source: Journal of Hepatology. 2000 June; 32(6): 1035-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10898326

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High altitude cerebral edema and acute mountain sickness. A pathophysiology update. Author(s): Hackett PH. Source: Advances in Experimental Medicine and Biology. 1999; 474: 23-45. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10634991

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High altitude cerebral edema. Author(s): Hamilton AJ, Cymmerman A, Black PM. Source: Neurosurgery. 1986 November; 19(5): 841-9. Erratum In: Neurosurgery 1987 May; 20(5): 822. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3537835

Studies

41

•

High altitude cerebral edema: a pathophysiological review. Author(s): Wohns RN. Source: Critical Care Medicine. 1981 December; 9(12): 880-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7318462

•

High-altitude cerebral edema (HACE): the Denver/Front Range experience. Author(s): Yarnell PR, Heit J, Hackett PH. Source: Seminars in Neurology. 2000; 20(2): 209-17. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10946741

•

High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. Author(s): Hackett PH, Yarnell PR, Hill R, Reynard K, Heit J, McCormick J. Source: Jama : the Journal of the American Medical Association. 1998 December 9; 280(22): 1920-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9851477

•

High-altitude cerebral edema. Author(s): Baumgartner RW. Source: Jama : the Journal of the American Medical Association. 1999 May 19; 281(19): 1794-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10340364

•

High-altitude cerebral edema. Author(s): Surks MI. Source: Jama : the Journal of the American Medical Association. 1999 May 19; 281(19): 1794; Author Reply 1795. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10340363

•

High-altitude cerebral edema. Author(s): Basnyat B. Source: Jama : the Journal of the American Medical Association. 1999 May 19; 281(19): 1794; Author Reply 1795. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10340362

•

Historical aspects of normal and abnormal brain fluids. III. Cerebral edema. Author(s): Torack RM. Source: Archives of Neurology. 1982 June; 39(6): 355-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7046704

42

Cerebral Edema

•

Hydrocephalus requiring urgent external ventricular drainage in a patient with diabetic ketoacidosis and cerebral edema: case report. Author(s): Eskandar EN, Weller SJ, Frim DM. Source: Neurosurgery. 1997 April; 40(4): 836-8; Discussion 838-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9092859

•

Hyperbaric oxygenation for the treatment of acute cerebral edema. Author(s): Sukoff MH, Ragatz RE. Source: Neurosurgery. 1982 January; 10(1): 29-38. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7057975

•

Hypertonic glycerol therapy of cerebral edema and its possible side-effects. Author(s): Tachibana H, Seki T, Nara M. Source: The Keio Journal of Medicine. 1979 June; 28(1): 19-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=544894

•

Hypertonic maintenance fluids for patients with cerebral edema: Does the evidence support a "phase II" trial? Author(s): Prough DS, Zornow MH. Source: Critical Care Medicine. 1998 March; 26(3): 421-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9504560

•

Hypertonic saline for cerebral edema and elevated intracranial pressure. Author(s): Suarez JI. Source: Cleve Clin J Med. 2004 January; 71 Suppl 1: S9-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14964472

•

Hypertonic saline for cerebral edema. Author(s): Georgiadis AL, Suarez JI. Source: Curr Neurol Neurosci Rep. 2003 November; 3(6): 524-30. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14565909

•

Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Author(s): Ayus JC, Varon J, Arieff AI. Source: Annals of Internal Medicine. 2000 May 2; 132(9): 711-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10787364

•

Hypothermia and hypotension in experimental cerebral edema. Author(s): Clasen RA, Pandolfi S, Russell J, Stuart D, Hass GM. Source: Archives of Neurology. 1968 November; 19(5): 472-86. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4971732

Studies

43

•

Hypothetical roles of angiogenesis, osmotic swelling, and ischemia in high-altitude cerebral edema. Author(s): Severinghaus JW. Source: Journal of Applied Physiology (Bethesda, Md. : 1985). 1995 August; 79(2): 375-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7592190

•

Idiopathic intracranial hypertension. Lack of histologic evidence for cerebral edema. Author(s): Wall M, Dollar JD, Sadun AA, Kardon R. Source: Archives of Neurology. 1995 February; 52(2): 141-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7848121

•

Intensive care management of patients with acute liver failure with emphasis on systemic hemodynamic instability and cerebral edema: a critical appraisal of pathophysiology. Author(s): Larsen FS, Hansen BA, Blei AT. Source: Canadian Journal of Gastroenterology = Journal Canadien De Gastroenterologie. 2000 November; 14 Suppl D: 105D-111D. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11110622

•

Intracranial meningiomas: factors that influence the development of cerebral edema after stereotactic radiosurgery and radiation therapy. Author(s): Kalapurakal JA, Silverman CL, Akhtar N, Laske DW, Braitman LE, Boyko OB, Thomas PR. Source: Radiology. 1997 August; 204(2): 461-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9240536

•

Ischemic cerebral edema. A review. Author(s): O'Brien MD. Source: Stroke; a Journal of Cerebral Circulation. 1979 November-December; 10(6): 6238. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=524402

•

Isolated growth hormone deficiency after cerebral edema complicating diabetic ketoacidosis. Author(s): Keller RJ, Wolfsdorf JI. Source: The New England Journal of Medicine. 1987 April 2; 316(14): 857-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3102962

44

Cerebral Edema

•

Isolation and characterization of adenovirus 5 from the brain of an infant with fatal cerebral edema. Author(s): Chatterjee NK, Samsonoff WA, Balasubramaniam N, Rush-Wilson K, Spargo W, Church TM. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2000 September; 31(3): 830-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11017844

•

Ketoacid levels may alter osmotonicity in diabetic ketoacidosis and precipitate cerebral edema. Author(s): Puliyel JM, Bhambhani V. Source: Archives of Disease in Childhood. 2003 April; 88(4): 366. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12651778

•

Letter: The pathology of cerebral edema. Author(s): Ransom BR, Blank WF. Source: Human Pathology. 1975 September; 6(5): 642-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1176116

•

Lipid metabolism in cerebral edema associated with brain tumor. Author(s): Yanagihara T, Cumings JN. Source: Trans Am Neurol Assoc. 1968; 93: 51-5. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5711052

•

Lipid metabolism in cerebral edema associated with human brain tumor. Author(s): Yanagihara T, Cumings JN. Source: Archives of Neurology. 1968 September; 19(3): 241-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5698039

•

Localized cerebral edema after high-dose chemotherapy and ABMT for germ cell tumor. Author(s): Wandt H, Birkmann J, Seifert M, Meisner M, Gallmeier WM, Ritter W, Zeitler E. Source: Bone Marrow Transplantation. 1993 May; 11(5): 419-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8389220

•

Magnetic resonance imaging of human cerebral edema. Author(s): Clasen RA. Source: Adv Neurol. 1990; 52: 491-509. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2396543

Studies

45

•

Malignant cerebral edema and intracranial hypertension. Author(s): Bingaman WE, Frank JI. Source: Neurologic Clinics. 1995 August; 13(3): 479-509. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7476816

•

Malignant cerebral edema in patients with hypertensive intracerebral hemorrhage associated with hypertonic saline infusion: a rebound phenomenon? Author(s): Qureshi AI, Suarez JI, Bhardwaj A. Source: Journal of Neurosurgical Anesthesiology. 1998 July; 10(3): 188-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9681408

•

Management of cerebral edema and intracranial hypertension. Author(s): Krishnamoorthy KS, Todres DI. Source: Indian J Pediatr. 1994 January-February; 61(1): 27-32. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7927595

•

Management of diabetic ketoacidosis and cerebral edema. Author(s): Bullock DG. Source: American Family Physician. 1994 November 15; 50(7): 1468. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7976982

•

Management of diabetic ketoacidosis and cerebral edema. Author(s): Bruzzo PJ. Source: American Family Physician. 1994 November 15; 50(7): 1468. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7976981

•

Management of severe cerebral edema in the metabolic encephalopathy of ReyeJohnson syndrome. Author(s): Venes JL, Shaywitz BA, Spencer DD. Source: Journal of Neurosurgery. 1978 June; 48(6): 903-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=275471

•

Massive cerebral edema after I.V. cyclosporin overdose. Author(s): de Perrot M, Spiliopoulos A, Cottini S, Nicod L, Ricou B. Source: Transplantation. 2000 October 27; 70(8): 1259-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11063353

46

Cerebral Edema

•

Massive cerebral edema after recanalization post-thrombolysis. Author(s): Cruz-Flores S, Thompson DW, Boiser JR. Source: Journal of Neuroimaging : Official Journal of the American Society of Neuroimaging. 2001 October; 11(4): 447-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11677890

•

Massive cerebral edema associated with fulminant hepatic failure in acetaminophen overdose: possible role of cranial decompression. Author(s): Sutherland LR, Muller P, Lewis DR Jr. Source: The American Journal of Gastroenterology. 1981 November; 76(5): 446-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7337133

•

Massive cerebral edema associated with meningioma. Author(s): Jagadha V, Deck JH. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 1987 February; 14(1): 55-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3815166

•

Massive ST-segment elevation without myocardial injury in a patient with fulminant hepatic failure and cerebral edema. Author(s): Rosenbloom AJ. Source: Chest. 1991 September; 100(3): 870-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1889293

•

Mediators of cerebral edema. Author(s): Schilling L, Wahl M. Source: Advances in Experimental Medicine and Biology. 1999; 474: 123-41. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10634998

•

Meningeal syndrome in diabetic ketoacidosis. Consider cerebral edema. Author(s): Chan NN, Darko D, O'Shea D. Source: Diabetes Care. 1999 February; 22(2): 370-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10333968

•

Migraine associated with focal cerebral edema, cerebrospinal fluid pleocytosis, and progressive cerebellar ataxia: MRI documentation. Author(s): Goldstein JM, Shaywitz BA, Sze G, Nallainathan S. Source: Neurology. 1990 August; 40(8): 1284-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2381540

Studies

47

•

Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS): adolescent onset with severe cerebral edema. Author(s): Danks RA, Dorevitch M, Cummins JT, Byrne E. Source: Aust N Z J Med. 1988 February; 18(1): 69-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3395302

•

Monitoring of increased intracranial pressure resulting from cerebral edema with transcranial Doppler sonography in patients with middle cerebral artery infarction. Author(s): Asil T, Uzunca I, Utku U, Berberoglu U. Source: Journal of Ultrasound in Medicine : Official Journal of the American Institute of Ultrasound in Medicine. 2003 October; 22(10): 1049-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14606560

•

Mononuclear leukocyte ADP-ribosylation as an indicator of immune function in malignant-glioma patients treated with betamethasone for cerebral edema. Author(s): Pero RW, Salford LG, Stromblad LG, Andersson C. Source: Journal of Neurosurgery. 1992 October; 77(4): 601-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1527620

•

Morbidity and mortality due to cerebral edema complicating the treatment of severe leptospiral infection. Author(s): Davenport A, Bramley PN, Wyatt JI. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1990 August; 16(2): 160-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2382655

•

Nonkitotoc hyperosmolar hyperglycemia during glycerol therapy for cerebral edema. Author(s): Sears ES. Source: Neurology. 1976 January; 26(1): 89-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=942774

•

Novel therapeutic strategy to treat brain ischemia: overexpression of hepatocyte growth factor gene reduced ischemic injury without cerebral edema in rat model. Author(s): Shimamura M, Sato N, Oshima K, Aoki M, Kurinami H, Waguri S, Uchiyama Y, Ogihara T, Kaneda Y, Morishita R. Source: Circulation. 2004 January 27; 109(3): 424-31. Epub 2004 Jan 05. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14707023

48

Cerebral Edema

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Nuclear magnetic resonance in the investigation of cerebral tumors and cerebral edema: a clue to the cellular alterations that may affect the distribution of water. Author(s): Megyesi JF, Del Maestro RF. Source: Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire. 1988 October; 66(10): 1100-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3063297

•

Osmotonicity of acetoacetate: possible implications for cerebral edema in diabetic ketoacidosis. Author(s): Puliyel JM. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2003 April; 9(4): Br130-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12709664

•

Outcome of children with cerebral edema caused by fulminant hepatic failure. Author(s): Alper G, Jarjour IT, Reyes JD, Towbin RB, Hirsch WL, Bergman I. Source: Pediatric Neurology. 1998 April; 18(4): 299-304. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9588523

•

Pathophysiology of cerebral edema in fulminant hepatic failure. Author(s): Blei AT, Larsen FS. Source: Journal of Hepatology. 1999 October; 31(4): 771-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10551405

•

Peritumoral cerebral edema in meningiomas: the role of the tumor-brain interface. Author(s): Ohno K, Matsushima Y, Aoyagi M, Ikeda J, Suzuki R, Ichimura K, Tamaki M, Hirakawa K. Source: Clinical Neurology and Neurosurgery. 1992; 94(4): 291-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1335855

•

Postoperative cerebral edema occurring in children with slit ventricles. Author(s): Eldredge EA, Rockoff MA, Medlock MD, Scott RM, Millis MB. Source: Pediatrics. 1997 April; 99(4): 625-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9093317

•

Postoperative nutritional failure and chronic cerebral edema in neurosurgical patients. Author(s): Savitz MH, Bryan-Brown CW, Elwyn DH, Malis LI. Source: The Mount Sinai Journal of Medicine, New York. 1978 May-June; 45(3): 394-401. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=97519

Studies

49

•

Predicting cerebral edema during diabetic ketoacidosis. Author(s): Dunger DB, Edge JA. Source: The New England Journal of Medicine. 2001 January 25; 344(4): 302-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11172161

•

Progressive cerebral edema associated with high methionine levels and betaine therapy in a patient with cystathionine beta-synthase (CBS) deficiency. Author(s): Yaghmai R, Kashani AH, Geraghty MT, Okoh J, Pomper M, Tangerman A, Wagner C, Stabler SP, Allen RH, Mudd SH, Braverman N. Source: American Journal of Medical Genetics. 2002 February 15; 108(1): 57-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11857551

•

Prolonged focal cerebral edema associated with partial status epilepticus. Author(s): Sammaritano M, Andermann F, Melanson D, Pappius HM, Camfield P, Aicardi J, Sherwin A. Source: Epilepsia. 1985 July-August; 26(4): 334-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4006892

•

Propylene glycol toxicity following continuous etomidate infusion for the control of refractory cerebral edema. Author(s): McConnel JR, Ong CS, McAllister JL, Gross TG. Source: Neurosurgery. 1996 January; 38(1): 232-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8747981

•

Propylene glycol toxicity following continuous etomidate infusion for the control of refractory cerebral edema. Author(s): Levy ML, Aranda M, Zelman V, Giannotta SL. Source: Neurosurgery. 1995 August; 37(2): 363-9; Discussion 369-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7477798

•

Pseudo-subarachnoid hemorrhage: a potential imaging pitfall associated with diffuse cerebral edema. Author(s): Given CA 2nd, Burdette JH, Elster AD, Williams DW 3rd. Source: Ajnr. American Journal of Neuroradiology. 2003 February; 24(2): 254-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12591643

•

Radical decompression and dural grafting in severe cerebral edema. Author(s): Kerr FW. Source: Mayo Clinic Proceedings. 1968 December; 43(12): 852-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5710720

50

Cerebral Edema

•

Rat brain VEGF expression in alveolar hypoxia: possible role in high-altitude cerebral edema. Author(s): Xu F, Severinghaus JW. Source: Journal of Applied Physiology (Bethesda, Md. : 1985). 1998 July; 85(1): 53-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9655755

•

Recurrent reversible cerebral edema after long term immunosuppression with tacrolimus. Author(s): Reinohs M, Straube T, Baum P, Berrouschot J, Wagner A. Source: Journal of Neurology. 2002 June; 249(6): 780-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12173578

•

Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema. Author(s): Alexander MJ, Martin NA, Khanna R, Caron M, Becker DP. Source: Acta Neurochir Suppl (Wien). 1994; 60: 479-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7976625

•

Relation of colloid osmotic pressure to arterial hypoxemia and cerebral edema during crystalloid volume loading of patients with diabetic ketoacidosis. Author(s): Fein IA, Rachow EC, Sprung CL, Grodman R. Source: Annals of Internal Medicine. 1982 May; 96(5): 570-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6803635

•

Reversible hypoxic cerebral edema in severe hemolytic crisis. Author(s): David WJ, Wadhera P, Narasimhan S, Narasimhan P. Source: N Y State J Med. 1990 October; 90(10): 518. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2234625

•

Review of cerebral edema. Author(s): Maier RJ, Ketel WB, Mathews T, Ouyang R. Source: Proc Wkly Semin Neurol. 1969 July; 19(1): 1-12. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4907939

•

Risk factors for cerebral edema in children with diabetic ketoacidosis. Author(s): Gebara BM. Source: The New England Journal of Medicine. 2001 May 17; 344(20): 1556. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11368049

Studies

51

•

Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. Author(s): Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J, Kaufman F, Quayle K, Roback M, Malley R, Kuppermann N; Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. Source: The New England Journal of Medicine. 2001 January 25; 344(4): 264-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11172153

•

Role of leukocytes and 5-lipoxygenase products in induction of cerebral edema. Author(s): Bednar MM. Source: Neurosurgery. 1990 February; 26(2): 360-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2106631

•

Severe cerebral edema in a patient with anasarca and hypernatremia. Author(s): Wacks I, Oster JR, Roth D, Norenberg M, Gardner LB, Perez GO, Burke G, Milgrom M. Source: Clinical Nephrology. 1992 January; 37(1): 19-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1541060

•

Severe high-altitude cerebral edema on the Inca Trail. Author(s): Hart O. Source: Journal of Travel Medicine : Official Publication of the International Society of Travel Medicine and the Asia Pacific Travel Health Association. 2004 January-February; 11(1): 64-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14769291

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Shunt malfunction presenting with cerebral edema. Author(s): Owen R, Pittman T. Source: Pediatric Neurosurgery. 2003 February; 38(2): 110-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12566847

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Steroid therapy of cerebral edema. Author(s): Smith RA, Smith WA. Source: J Med Assoc Ga. 1967 August; 56(8): 324-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6042095

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Systemic management of cerebral edema based on a new concept in severe head injury patients. Author(s): Hayashi N, Hirayama T, Udagawa A, Daimon W, Ohata M. Source: Acta Neurochir Suppl (Wien). 1994; 60: 541-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7976643

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The action of cardiac glycosides in cerebral edema. Author(s): Arseni C, Alexianu D, Bacalbasa N, Slavescu D. Source: Rev Roum Neurol. 1973; 10(1): 3-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4792845

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The association of hyperglycemia with cerebral edema in stroke. Author(s): Berger L, Hakim AM. Source: Stroke; a Journal of Cerebral Circulation. 1986 September-October; 17(5): 865-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3764956

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The cerebral etiology of high-altitude cerebral edema and acute mountain sickness. Author(s): Hackett PH. Source: Wilderness Environ Med. 1999 Summer; 10(2): 97-109. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10442158

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The development of low-grade cerebral edema in cirrhosis is supported by the evolution of (1)H-magnetic resonance abnormalities after liver transplantation. Author(s): Cordoba J, Alonso J, Rovira A, Jacas C, Sanpedro F, Castells L, Vargas V, Margarit C, Kulisewsky J, Esteban R, Guardia J. Source: Journal of Hepatology. 2001 November; 35(5): 598-604. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11690705

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The effect of human corticotrophin releasing factor on the formation of posttraumatic cerebral edema. Author(s): Beaumont A, Marmarou A. Source: Acta Neurochir Suppl (Wien). 1998; 71: 149-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9779170

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The effects of mannitol on cerebral edema after large hemispheric cerebral infarct. Author(s): Manno EM, Adams RE, Derdeyn CP, Powers WJ, Diringer MN. Source: Neurology. 1999 February; 52(3): 583-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10025792

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The management of cerebral edema in pediatric practice. Author(s): Batzdorf U. Source: Pediatrics. 1976 July; 58(1): 78-87. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=945541

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The management of renal failure in patients at risk of cerebral edema/hypoxia. Author(s): Davenport A. Source: New Horiz. 1995 November; 3(4): 717-24. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8574602

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The pathogeny and treatment of cerebral edema. Author(s): Arseni C, Alexianu D. Source: Neurol Psychiatr (Bucur). 1975; 13(3): 179-85. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1188276

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The pathology of cerebral edema associated with gliomas in man. Report based on ten biopsies. Author(s): Aleu F, Samuels S, Ransohoff J. Source: American Journal of Pathology. 1966 June; 48(6): 1043-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5944935

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The pathology of cerebral edema. Author(s): Manz HJ. Source: Human Pathology. 1974 May; 5(3): 291-313. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4597855

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The response of human cerebral edema to glucosteroid administration. An electron microscopic study. Author(s): Long DM, Hartmann JF, French LA. Source: Neurology. 1966 May; 16(5): 521-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5949272

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The reversible posterior cerebral edema syndrome. Author(s): Dillon WP, Rowley H. Source: Ajnr. American Journal of Neuroradiology. 1998 March; 19(3): 591. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9541327

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The ultrastructural characteristics of superacute cerebral edema. Author(s): Arseni C, Alexianu D, Alexianu M, Petrovici A. Source: Rev Roum Neurol Psychiatr. 1974; 11(3): 211-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4846956

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The ultrastructure of human cerebral edema. Author(s): Long DM, Hartmann JF, French LA. Source: Journal of Neuropathology and Experimental Neurology. 1966 July; 25(3): 37395. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5946174

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The use of corticotropin releasing factor (CRE) for the treatment of post-operative cerebral edema. A preliminary study. Author(s): Wen XL, Guo ZG, Datta N. Source: Chinese Medical Journal. 1991 July; 104(7): 557-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1879218

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The vascular component in meningiomas associated with severe cerebral edema. Author(s): Challa VR, Moody DM, Marshall RB, Kelly DL Jr. Source: Neurosurgery. 1980 October; 7(4): 363-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7442977

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Transient blindness in a preeclamptic patient secondary to cerebral edema. Author(s): Shieh T, Kosasa TS, Tomai E, Nakayama RT. Source: Hawaii Med J. 1996 July; 55(7): 116-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8771987

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Trauma, sport, and malignant cerebral edema. Author(s): McQuillen JB, McQuillen EN, Morrow P. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 1988 March; 9(1): 12-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3354517

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Traumatic cerebral edema relieved by stellate ganglion anesthesia. Author(s): Floyd JB Jr. Source: Southern Medical Journal. 1987 October; 80(10): 1328. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3660055

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Typhoid fever complicated by cerebral edema. Author(s): Lal V, Sawhney IM. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1996 July; 23(1): 210. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8816174

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Understanding cerebral edema: implications for oncology nurses. Author(s): Saba MT, Magolan JM. Source: Oncology Nursing Forum. 1991 April; 18(3): 499-505. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2057394

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Use of betamethasone in reduction of cerebral edema. Author(s): Johnson JA, Assam S. Source: Military Medicine. 1966 January; 131(1): 44-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4954871

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Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema: Effect on intracranial pressure and lateral displacement of the brain. Author(s): Qureshi AI, Suarez JI, Bhardwaj A, Mirski M, Schnitzer MS, Hanley DF, Ulatowski JA. Source: Critical Care Medicine. 1998 March; 26(3): 440-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9504569

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Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension. Author(s): Qureshi AI, Suarez JI. Source: Critical Care Medicine. 2000 September; 28(9): 3301-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11008996

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Use of hypertonic saline/acetate infusion in treatment of cerebral edema in patients with head trauma: experience at a single center. Author(s): Qureshi AI, Suarez JI, Castro A, Bhardwaj A. Source: The Journal of Trauma. 1999 October; 47(4): 659-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10528599

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Use of steroids in cerebral edema: therapeutic implications. Author(s): Harper J. Source: Heart & Lung : the Journal of Critical Care. 1988 January; 17(1): 70-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3276650

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Valproate-associated carnitine deficiency and malignant cerebral edema in the absence of hepatic failure. Author(s): Triggs WJ, Gilmore RL, Millington DS, Cibula J, Bunch TS, Harman E. Source: Int J Clin Pharmacol Ther. 1997 September; 35(9): 353-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9314085

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Vascular tunnel creation to improve the efficacy of decompressive craniotomy in post-traumatic cerebral edema and ischemic stroke. Author(s): Csokay A, Egyud L, Nagy L, Pataki G. Source: Surgical Neurology. 2002 February; 57(2): 126-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11904208

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CHAPTER 2. NUTRITION AND CEREBRAL EDEMA Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and cerebral edema.

Finding Nutrition Studies on Cerebral Edema The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail: [email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “cerebral edema” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.

7

Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.

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The following information is typical of that found when using the “Full IBIDS Database” to search for “cerebral edema” (or a synonym): •

Development of cytotoxic cerebral edema in rats following intracaudatum injection of tACPD, an agonist of metabotropic glutamate receptors. Author(s): Beijing Neurosurgical Institute, Beijing 100050, China. [email protected] Source: Yuan, F Wang, T Luo, L Sun, Y Zhang, L Qu, B Chin-Med-J-(Engl). 2000 August; 113(8): 728-32 0366-6999

•

Effect of melatonin on cerebral edema in rats. Author(s): Department of Neurosurgery, School of Medicine, University of Trakya, Edirne, Turkey. [email protected] Source: Gorgulu, A Palaoglu, S Ismailoglu O Tuncel, M Surucu, M T Erbil, M Kilinc, K Neurosurgery. 2001 December; 49(6): 1434-41; discussion 1441-2 0148-396X

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Effects of lipoxygenase inhibitor on cerebral edema induced by freezing lesion in rats. Author(s): Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan, R.O.C. Source: Yen, M H Lee, S H Chin-J-Physiol. 1990; 33(4): 385-97 0304-4920

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Enalapril prevents imminent and reduces manifest cerebral edema in stroke-prone hypertensive rats. Author(s): Department of Nephrology, University Hospital Utrecht, Netherlands. Source: Blezer, E L Nicolay, K Bar, D Goldschmeding, R Jansen, G H Koomans, H A Joles, J A Stroke. 1998 August; 29(8): 1671-7; discussion 1677-8 0039-2499

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Melatonin reduces cerebral edema formation caused by transient forebrain ischemia in rats. Author(s): Institute of Life Sciences, Ajinomoto Co., Inc., Suzuki-cho 1-1, Kawasaki-ku, 210-8681, Kawasaki, Japan. Source: Kondoh, T Uneyama, H Nishino, H Torii, K Life-Sci. 2002 December 20; 72(4-5): 583-90 0024-3205

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Proteinuria precedes cerebral edema in stroke-prone rats: a magnetic resonance imaging study. Author(s): Department of Nephrology, University Hospital Utrecht, The Netherlands. Source: Blezer, E L Schurink, M Nicolay, K Bar, P R Jansen, G H Koomans, H A Joles, J A Stroke. 1998 Jan; 29(1): 167-74 0039-2499

Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •

healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0

•

The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov

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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov

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•

The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/

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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/

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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/

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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/

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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/

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

AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats

•

Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html

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

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

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

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

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

•

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

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CHAPTER 3. ALTERNATIVE MEDICINE AND CEREBRAL EDEMA Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to cerebral edema. 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 cerebral edema 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 “cerebral edema” (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 cerebral edema: •

Cerebral air embolism and cerebral edema: one regimen of treatment. Author(s): Thiede WH, Manley J. Source: Aviation, Space, and Environmental Medicine. 1976 May; 47(5): 553-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1275847

•

Effect of an extract of Ginkgo biloba on triethyltin-induced cerebral edema. Author(s): Otani M, Chatterjee SS, Gabard B, Kreutzberg GW. Source: Acta Neuropathologica. 1986; 69(1-2): 54-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3962598

•

Experimental cerebral edema: enzyme-histochemical study. Author(s): Yanagihara T, Goldstein NP, Svien HJ, Bahn RC.

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Source: Neurology. 1967 July; 17(7): 669-79. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4165505 •

Experimental cerebral edema: vital staining with Evans blue during the developmental and regressive phases. Author(s): Bryar GE, Goldstein NP, Svien HJ, Sayre GP, Jones JD. Source: Journal of Neurosurgery. 1969 April; 30(4): 391-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4184403

•

Experimental cerebral edema: vital staining with Evans blue during the developmental and regressive phases. Author(s): Bryar GE, Goldstein NP, Svien HJ, Sayre GP, Jones JD. Source: Journal of Neuropathology and Experimental Neurology. 1968 January; 27(1): 128-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4172924

•

Hyperbaric oxygenation, carbon monoxide, and cerebral edema. Author(s): James PB. Source: British Medical Journal (Clinical Research Ed.). 1988 February 13; 296(6620): 5001. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3126880

•

Response of radiochemotherapy-associated cerebral edema to a phytotherapeutic agent, H15. Author(s): Streffer JR, Bitzer M, Schabet M, Dichgans J, Weller M. Source: Neurology. 2001 May 8; 56(9): 1219-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11342692

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The protective effect of hyperbaric oxygenation in experimental cerebral edema. Author(s): Sukoff MH, Hollin SA, Espinosa OE, Jacobson JH 2nd. Source: Journal of Neurosurgery. 1968 September; 29(3): 236-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5684405

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The protective effect of hyperbaric oxygenation in experimentally produced cerebral edema and compression. Author(s): Hollin SA, Sukoff MH, Jacobson JH 2nd. Source: Prog Brain Res. 1968; 30: 479-89. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5735480

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The response of focal ischemic cerebral edema to dexamethasone. Author(s): Fenske A, Fischer M, Regli F, Hase U.

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Source: Journal of Neurology. 1979 May 2; 220(3): 199-209. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=88511

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/

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

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

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

•

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

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

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

•

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

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

•

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

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

The following is a specific Web list relating to cerebral edema; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •

General Overview Meningitis Source: Integrative Medicine Communications; www.drkoop.com

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

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CHAPTER 4. PATENTS ON CEREBRAL EDEMA Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.8 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “cerebral edema” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on cerebral edema, we have not necessarily excluded nonmedical patents in this bibliography.

Patents on Cerebral Edema By performing a patent search focusing on cerebral edema, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an 8Adapted

from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.

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example of the type of information that you can expect to obtain from a patent search on cerebral edema: •

Cerebral edema solute catheter and method of draining cerebral edema Inventor(s): Andrews; David W. (Philadelphia, PA) Assignee(s): Thomas Jefferson University (Philadelphia, PA) Patent Number: 5,810,760 Date filed: August 8, 1996 Abstract: Catheters for removing interstitial fluid from a cerebral edema that comprises an edema drainage section terminating in a proximal tip linked to a fluid transport section terminating in a distal tip are disclosed. The edema drainage section comprises an outer wall, an inner drainage tube and an intermediate solute compartment that comprises a solute. Methods of removing fluid from a cerebral edema of an individual are disclosed, and comprise the steps of inserting the edema drainage section of the catheter into communication with the fluid of the cerebral edema and inserting the fluid transport section of the catheter into a fluid receptacle or the individual's peritoneal cavity. The fluid is drawn into the edema drainage section and emerges from the distal tip of the fluid transport section of the catheter. Excerpt(s): The present invention relates to solute drainage catheters and, in particular, to a catheter for draining interstitial fluid from a cerebral edema. Cerebral edema is a type of brain swelling most commonly associated with cerebral trauma or mass lesions, which results in an increase in volume of intracranial contents leading to serious, and sometimes fatal, intracranial pressure. Interstitial (extracellular) fluid, or free water, is abnormal in the brain and accumulates as a result of swelling from a nearby brain tumor, or other type of cerebral lesion. This fluid enters the white matter in the brain due to a compromise of the blood-brain barrier. The fluid can contain small proteins, as well as other small molecular weight molecules, which escape the circulatory system or are a result from the tissue damage itself. Currently, there is no known approach for removing or draining interstitial fluid from a cerebral edema. Methods exist only for improving the symptoms of swelling due to the accumulation of the fluid. These methods involve the use of oral or intravenous steroids, which have known systemic side effects. For example, the steroid DECADRON.TM. has only a modest effect on cerebral edema and has systemic side effects including water retention, osteoporosis, aseptic necrosis of the femoral head, capillary fragility with easy bruising, increased appetite, and insomnia. Web site: http://www.delphion.com/details?pn=US05810760__

•

Method for treating cerebral edema Inventor(s): Gainer, Jr.; James V. (Kingwood, WV) Assignee(s): University of Virginia Patents Foundation (Charlottesville, VA) Patent Number: 4,070,460 Date filed: November 10, 1975 Abstract: A method for the treatment of cerebral edema in mammals which comprises administering to said affected mammal an effective dose of a water soluble carotenoid.

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Excerpt(s): This invention relates to a novel technique for the treatment of cerebral edema in mammals. In U.S. Pat. Nos. 3,853,992 and 3,788,468, it is disclosed that certain water-soluble carotenoids had been observed to possess quite unique properties. In particular, these water-soluble carotenoids have been found to increase the diffusivity of oxygen through aqueous media. The effect was found further to be useful biologically in the treatment of atherosclerosis, which had been theorized as being a disease resulting from local hypoxia of the vascular walls. The study of the biological effects of this compound has continued with the present discovery that it has effectiveness in the treatment of cerebral edema. Web site: http://www.delphion.com/details?pn=US04070460__ •

Protecting and survival promoting agent for central nervous cell Inventor(s): Furuya; Shigeki (Saitama, JP), Hirabayashi; Yoshio (Saitama, JP), Mitoma; Jyunya (Saitama, JP) Assignee(s): Riken (Saitama, JP), Taisho Pharmaceutical Co., Ltd. (Tokyo, JP) Patent Number: 6,310,097 Date filed: April 17, 2000 Abstract: An agent for enhancing cell survival of central nerve cells, which comprises a substance selected from the group consisting of L-serine, glycine, and fatty acid compounds thereof as an active ingredient, and a medicament for preventive and/or therapeutic treatment of cerebral dysfunction which comprises said substance as an active ingredient. The substance has an action for protecting cerebral cells to suppress cell death and prolong cell life. For example, cerebral cell death caused by cerebral edema or the raise of intracerebral temperature due to cerebral hemorrhage, cerebral infarction head injury and the like can be suppressed. Excerpt(s): Hippocampal neurons have widely been used in the field of the neurophysiology as central nerve cells that can be cultured in laboratories. It has been known that a significant number of the neurons die in one week from the start of the culture when the cells are primarily cultured alone. As a method for long-term culture of hippocampal neurons, co-culture of the cells with glial cells (gliacytes that fill spaces between neurons and their neurites) is known. However, since the culture system is not a monoculture system, it is not suitable for researches on auxotrophy of hippocampal neurons alone, neuronal responses to polypeptide neurotrophic factors and the like. As a method for culturing hippocampal neurons in the absence of glial cells, a method is known wherein the neurons are cultured in the presence of all non-essential amino acids. However, survival time of the cells and number of survived cells are significantly lower than those attained by the co-culture with glial cells. In primary culture system of hippocampal neurons, it has also been known that long term survival of neurons can be achieved by the addition of culture supernatant of glial cells (astrocyte conditioned medium, ACM). A method for such culture has been established by Goslin et al. (Goslin, K. and Banker, G., "Culturing Nerve Cells", Ed. by Banker, G. et al., p.251-278, The MIP Press, England). However, it has not been revealed which substance in the culture supernatant enhances survival of the neurons. An object of the present invention is to provide a substance that enhances survival of neurons. Another object of the present invention is to provide an agent for improving cerebral functions. Web site: http://www.delphion.com/details?pn=US06310097__

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Pyridinecarboxamide derivatives Inventor(s): Hamada; Tamiko (Saitama-ken, JP), Itoh; Koichi (Saitama-ken, JP), Mimaki; Yoji (Saitama-ken, JP), Muraki; Yukiko (Saitama-ken, JP), Nishimura; Kazumi (Saitamaken, JP), Oshida; Norio (Saitama-ken, JP), Sakai; Hiroshi (Saitama-ken, JP), Sakurai; Einosuke (Saitama-ken, JP), Satoh; Hiroaki (Saitama-ken, JP), Sugai; Toshiji (Saitamaken, JP), Tonoike; Tomomi (Saitama-ken, JP), Yokoyama; Shinji (Komoro, JP) Assignee(s): Nisshin Flour Milling Co., Ltd. (Tokyo, JP) Patent Number: 6,046,201 Date filed: July 15, 1998 Abstract: N-(12-Nitroxydodecyl)-6-(4-ethyl or isopropyl-1-piperazinyl)pyridine-3carboxamide or physiologically acceptable salts thereof. The said compounds have excellent inhibiting activity of cerebral edema, especially ischemic cerebral edema, and inhibiting activity of delayed neuronal death (an inhibiting activity of Ca-influx in neuronal cells). Cerebral edema is a pathologic condition accompanying cerebrovascular disorders, especially the acute stage cerebrovascular disorders and then the compounds are useful as an inhibiting agent for cerebral edema or a therapeutic agent for cerebrovascular disorders. Moreover, because the compounds do hardly show a behavior suppressing action, which is considered to be side effect in treating cerebrovascular disorders at the acute stage, they are an excellent therapeutic agent for, in particular, the acute stage cerebrovascular disorders. Moreover, the compounds show a cerebral protective activity (an anti-anoxic activity), an activity of increasing cerebral blood flow, and an activity of inhibiting lipid peroxidation, and these activities may lead to the increased utility as a therapeutic agent for cerebrovascular disorders. Excerpt(s): This invention relates to a pyridinecarboxamide derivative. More particularly, this invention relates to an N-(12-nitroxydodecyl)-6-piperazinylpyridine-3carboxamide derivative, a process for the preparation thereof and a pharmaceutical preparation which comprises as an active ingredient said derivative. Moreover, this invention relates to a therapeutic agent for cerebrovascular disorders or cerebral edema which comprises as an active ingredient said pyridine carboxamide derivative. Moreover, this invention relates to a method for the treatment of cerebrovascular disorders or cerebral edema which comprises administering said pyridinecarboxamide derivative. Moreover, this invention relates to an intermediate for the synthesis of said pyridinecarboxamide derivative. Neuronal cells are weak to ischemia and may easily be damaged, but there is a recoverable area around the ischemic neuronal cells, which is referred to as the "Penumbra" (Astrup, J., Siesjo, B., Symon, L.; Stroke, 12:723-725 1981). In the therapy of cerebrovascular disorders at the acute stage, it is important to protect the neuronal cells in the penumbra area from cell damage and maintain cerebral functions. It has been known that cerebrovascular disorders caused by ischemia may accompany cerebral edema with an unusually increased moisture content in the brain in the ischemic center and penumbra area (Kenji Inamura and Akiro Terashi: Brain Nerv. 44(9): 779-785, 1992). Cerebral edema may be also caused by cerebral tumor, encephalitis, heat stroke, cerebral trauma by a traffic accident. The edema may increase the cerebral capacity, which results in the increase in cerebral pressure, because the brain is closed within the hard skull. A precipitous increase in cerebral pressure may cause cerebral hernia, which makes patients fall in the dangerous state of their life. Web site: http://www.delphion.com/details?pn=US06046201__

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Therapeutic use of acetazolamide for the treatment of brain edema Inventor(s): Rodriguez; Victorio C. (7791 Hoertz Rd., Parma, OH 44134) Assignee(s): none reported Patent Number: 5,755,237 Date filed: June 7, 1995 Abstract: A method for treating victims of cerebral edema is presented that includes the intravenous injection of acetazolamide (A.K.A., DIAMOX.RTM.), which is a readilyavailable and often-prescribed diuretic. Such edema, or brain swelling may be caused as a result of ischemic strokes especially, but also swelling due to tumors, surgeries, or cerebral trauma. It is preferred to combine the acetazolamide therapy with hyperventilation of the lungs, even including the use of supplemental oxygen, thereby to reduce the concentration of carbon dioxide in the blood and hence in the brain. Excerpt(s): This invention relates to the medical treatment of victims of cerebral edema, and especially to the relief of brain swelling as a result of ischemic strokes especially, but also swelling due to tumors, surgeries, or cerebral trauma, which swelling usually results in severe disability and often death of the patient. More particularly, this invention relates to the therapeutic use of acetazolamide as a medication to relieve such brain swelling or edema. Acetazolamide is a commonly-prescribed diuretic distributed under the trade names DIAMOX.RTM. acetazolamide SEQUELS.RTM. sustained release capsules, DIAMOX.RTM. acetazolamide tablets, and DIAMOX.RTM. sterile acetazolamide sodium parenteral (supplied as a sodium salt). DIAMOX.RTM. and SEQUELS.RTM. are registered trade marks of Lederle Laboratories Division of American Cyanamid Company. Ischemic strokes are the result of a sudden compromising of the blood supply to the brain, that often causes brain cell swelling, abnormal electric discharges from the brain, and brain death. Whereas the causative factor in the compromising of the blood supply to the brain may be transient, as small emboli that occlude a vessel and then pass on, allowing blood flow to be reestablished. How often such transient ischemic attacks result in completed stroke (i.e., with no immediate progression or regression of symptoms) is unknown. Some patients with such attacks develop strokes; in others, the symptoms disappear without sequelae. Even transient ischemic attacks can produce brain cell swelling, a symptom that carries its own potential death threat. a. Airway support and ventilatory assistance are given to patients with depressed levels of consciousness; supplemental oxygen is used for hypoxic patients. Web site: http://www.delphion.com/details?pn=US05755237__

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Treatment of cerebral disorders by inhibition of IL-8 binding to receptor Inventor(s): Ikeda; Kiyonobu (Kanazawa, JP), Matsumoto; Tetsuya (Kanazawa, JP), Matsushima; Kouji (Matsudo, JP), Yamashita; Junkoh (Kanazawa, JP) Assignee(s): Chugai Seiyaku Kabushiki Kaisha (Tokyo, JP) Patent Number: 6,497,878 Date filed: October 19, 1998 Abstract: Methods and compositions for treating or preventing cerebral stroke, cerebral infarction, cerebral edema, reperfusion injury and increased cerebral vascular

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permeability which employ an agent that prevents the binding of IL-8 to its receptor are disclosed. Excerpt(s): The present invention relates to a preventive or therapeutic agent for cerebral stroke comprising an interleukin-8 (IL-8)-binding-inhibition agent as an active ingredient. The present invention also relates to a preventive or therapeutic agent for cerebral edema comprising an IL-8-binding-inhibition agent as an active ingredient. The present invention also relates to a preventive or therapeutic agent for reperfusion injury of cerebral ischemia comprising an IL-8-binding-inhibition agent as an active ingredient. Furthermore, the present. invention relates to a preventive or therapeutic agent for increased cerebral vascular permeability comprising an IL-8-binding-inhibition agent as an active ingredient. In order for IL-8 to exhibit its biological activity, it is necessary that IL-8 binds to IL-8 receptor and thereby stimulates the cells that are expressing IL-8 receptors. IL-8 receptors that transmit signals into the cell by binding to IL-8 have already been cloned and the amino acid sequences thereof have been elucidated. Human IL-8 receptors include those referred to as IL-8 receptor A (.alpha. or 2) and those referred to as IL-8 receptor B (.beta. or 1) (Murphy, P. M. and Tiffany, H. L., Science (1991) 253, 1280-1283; Holmes, W. E. et al., Science (1991) 253, 1278-1280). Both receptors are thought to have a structure that penetrates the cell membrane seven times, and both are associated with GTP-binding proteins in the cytoplasmic domain (Horuk, R., Trends Pharmacol. Sci. (1994) 15, 159-165), and transmit IL-8 signals into the cell. Therefore, inhibition of binding,between IL-8 and IL-8 receptor enables the inhibition of biological activity of IL-8. The IL-8 binding-inhibition agents so far known include the following substances. As anti-IL-8 antibodies, there are known WS-4 antibody (Ko, Y. et al., J. Immunol. Methods (1992) 149, 227-235), 14E4, 46E5 (Sticherling, M. et al., J. Immunol. (1989) 143, 1628-1634), and human antibody (International Patent Application WO 96/33735), and besides, a polysaccharide (International Patent Application WO 94/18989), a chemical synthetic compound (Sola, F. et al., Invasion Metastasis (1995) 15, 222-231), a peptide fragment (Hayashi, S. et al., J. Immunol. (1995) 154, 814-824), and the like. Web site: http://www.delphion.com/details?pn=US06497878__ •

Treatment of cerebral edema with ANP pharmaceutical compositions Inventor(s): Hayashi; Hiroshi (Shizuoka, JP), Kiyota; Takao (Shizuoka, JP), Sugawara; Shuichi (Shizuoka, JP) Assignee(s): Ashi Kasei Kogyo Kabushiki Kaisha (JP) Patent Number: 5,204,327 Date filed: November 13, 1989 Abstract: A pharmaceutical composition and its use in the treatment of cerebral edema are provided wherein the composition comprises an atrial natriuretic peptide having an amino acid sequence of 28 amino acids and at least one pharmaceutically acceptable carrier, diluent or excipient. Excerpt(s): This invention relates to a pharmaceutical composition for use in the treatment of cerebral edema. More particularly, the present invention relates to a pharmaceutical composition containing a peptide having anti-cerebral edema activity. The pharmaceutical composition of the present invention can advantageously be used not only as a medicine for the treatment of cerebral edema, but also as a medicine for the prevention of cerebral edema. Cerebral edema is a symptom defined as an excessive

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accumulation of water in a brain tissue, which is caused by various brain injuries. Cerebral edema accompanies an increase in intracranial pressure. In more serious cases, cerebral edema itself functions to increase the intracranial pressure. The mechanism of the occurrence of cerebral edema varies according to the type of brain injury. Klatzo defined two types of cerebral edemas. One type is vasogenic edema which is caused by the transfer of water into a brain tissue, which water is leaked out of a blood-brain barrier, simultaneously with the leakage of a serum protein from the blood-brain barrier due to the damage thereof. The other type is cytotoxic edema which is caused by the water retained in a brain tissue due to the inhibition of the transfer of ions between the inside and the outside of the cell membrane of a brain tissue, which inhibition accompanies the metabolic inhibition of a brain tissue cell [Klatzo, I., "Neuropathological aspects of brain edema", J. Neuropath. Exp. Neurol., 26, 1-14(1967)]. According to clinical observation, most of the cerebral edemas are vasogenic edemas, while cytotoxic edema accompanies limited types of diseases, such as cerebral ischemia at a primary stage thereof, water poisoning and meningitis purulenta. Further, Fishman reported another type of cerebral edema, that is, interstitial edema which is caused by the reservation of cerebrospinal fluid in a cerebral medulla surrounding the cerebral venticles, ascribed to hydrocephalus [Fishman, R.A., "Brain edema", New Eng. J. Med., 293, 706 (1975)]. Heretofore, with respect to the treatment of cerebral edema, it has generally been attempted to remove water from a brain tissue on one hand and block intracranial pressure-increasing factors on the other. In this attempt, a surgical method and a pharmaceutical method are employed. In the surgical method, water is removed from a brain tissue so that the intracranial pressure can be reduced. As the pharmaceutical method, there can be mentioned, for example, a method in which a hypertonic solution, such as a glycerol solution, is administered. In this method, excess water in a brain tissue and other tissues is drawn out into a blood, followed by excretion as urine by the osmotic diuresis action of the hypertonic solution. Further, a steroid therapy and a barbital therapy can be mentioned as a therapeutic method for the treatment of cerebral edema. In the steroid therapy, a steroid is administered in a large amount in a short period so as to suppress the symptoms of cerebral edema. In the barbital method, barbital is administered for controlling the metabolism of a brain to thereby relieve the symptom. The administration of barbital is also effective to capture free radicals accumulated in the blood-brain barrier, which free radicals are likely to cause vasogenic edema, one type of cerebral edema, to thereby remove the cause of cerebral edema. Web site: http://www.delphion.com/details?pn=US05204327__ •

Treatment with lys-plasminogen of reperfusion injury and brain edema caused by ischemia Inventor(s): Eibl; Johann (Vienna, AT), Pichler; Ludwig (Vienna, AT), Schwarz; HansPeter (Vienna, AT) Assignee(s): Immuno Aktiengesellschaft (Vienna, AT) Patent Number: 5,597,800 Date filed: November 21, 1994 Abstract: A treatment of ischemia and the attendant reperfusion injury entails the administration plasmin and plasmin-forming proteins, including lys-plasminogen and similar substances. Lys-plasminogen, which can be obtained from the proteolytic cleavage of glu-plasminogen, has been found to have a protective effect on tissue that

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has been injured by ischemic conditions. The administration of lys-plasminogen alone, in a dosage of about 10-1000 caseinolytic units/kg, can be used to treat subjects during the time of reperfusion and after reperfusion has already occurred. Lys-plasminogen also can be administered in conjunction with clot lysis therapies, such as those that employ tissue plasminogen activator and the like. Lys-plasminogen can also lessen cerebral edema which results from cerebral ischemia. Excerpt(s): Stroke remains the third most common cause of death in the industrial world, ranking behind ischemic heart disease and cancer. Strokes are responsible for about 300,000 deaths annually in the United States and about 11,000 deaths annually in Austria. Strokes are also a leading cause of hospital admissions and long-term disabilities. Accordingly, the socioeconomic impact of stroke and its attendant burden on society is practically immeasurable. Strokes are typically caused by blockages or occlusions of the blood vessels to the brain or within the brain. With complete occlusion, arrest of cerebral circulation causes cessation of neuronal electrical activity within seconds. Within a few minutes after the deterioration of the energy state and ion homeostasis, depletion of high energy phosphates, membrane ion pump failure, efflux of cellular potassium, influx of sodium chloride and water, and membrane depolarization occur. If the occlusion persists for more than five to ten minutes, irreversible damage results. With incomplete ischemia, however, the outcome is difficult to evaluate and depends largely on residual perfusion and the availability of oxygen. After a thrombotic occlusion of a cerebral vessel, ischemia is rarely total. Some residual perfusion usually persists in the ischemic area, depending on collateral blood flow and local perfusion pressure. Cerebral blood flow can compensate for drops in mean arterial blood pressure from 90 to 60 mm Hg by autoregulation. This phenomenon involves dilatation of downstream resistant vessels. Below the lower level of autoregulation (about 60 mm Hg), vasodilatation is inadequate and the cerebral blood flow falls. The brain, however, has perfusion reserves that can compensate for the fall in cerebral blood fall. This reserve exists because under normal conditions only about 35% of the oxygen delivered by the blood is extracted. Therefore, increased oxygen extraction can take place, provided that normoxia and normocapnea exist. When distal blood pressure falls below approximately 30 mm Hg, the two compensatory mechanisms (autoregulation and perfusion reserve) are inadequate to prevent failure of oxygen delivery. Web site: http://www.delphion.com/details?pn=US05597800__ •

Tricyclic benzodiazepines as vasopressin receptor antagonists Inventor(s): Dyatkin; Alexey B. (Lansdale, PA), Hoekstra; William J. (Chapel Hill, NC), Maryanoff; Bruce E. (Forest Grove, PA), Matthews; Jay M. (Lansdale, PA) Assignee(s): Ortho-McNeil Pharmaceutical, Inc. (Raritan, NJ) Patent Number: 6,713,475 Date filed: July 24, 2001 Abstract: The invention is directed to tricyclic benzodiazepines useful as vasopressin receptor antagonists for treating conditions involving increased vascular resistance and cardiac insufficiency. Pharmaceutical compositions comprising tricyclic benzodiazepines of the present invention and methods of treating conditions such as hypertension, congestive heart failure, cardiac insufficiency, coronary vasospasm, cardiac ischemia, liver cirrhosis, renal vasospasm, renal failure, cerebral edema and ischemia, stroke, thrombosis, or water retention are also disclosed.

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Excerpt(s): This invention relates to novel tricyclic vasopressin receptor antagonists. More particularly, the compounds of the present invention interrupt the binding of the peptide hormone vasopressin to its receptors and are therefore useful for treating conditions involving increased vascular resistance and cardiac insufficiency. Vasopressin is a nonapeptide hormone that is secreted primarily from the posterior pituitary gland. The hormone effects its actions through membrane-bound V-1 and V-2 receptor subtypes. The functions of vasopressin include contraction of uterine, bladder, and smooth muscle; stimulation of glycogen breakdown in the liver; release of corticotropin from the anterior pituitary; induction of platelet aggregation; and central nervous system modulation of behaviors and stress responses. The V-1 receptor mediates the contraction of smooth muscle, and hepatic glycogenolytic and central nervous system effects of vasopressin. The V-2 receptor, presumably found only in the kidney, effects the antidiuretic actions of vasopressin via stimulation of adenylate cyclase. Elevated plasma vasopressin levels appear to play a role in the pathogenesis of congestive heart failure (P. A. Van Zwieten, Progr. Pharmacol. Clin. Pharmacol. 1990, 7, 49). As progress toward the treatment of congestive heart failure, nonapeptide vasopressin V-2 receptor antagonists have induced low osmolality aquaresis and decreased peripheral resistance in conscious dogs with congestive heart failure (H. Ogawa, J. Med. Chem. 1996, 39, 3547). In certain pathological states, plasma vasopressin levels may be inappropriately elevated for a given osmolality, thereby resulting in renal water retention and hyponatremia. Hyponatremia, associated with edematous conditions (cirrhosis, congestive heart failure, renal failure), can be accompanied by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Treatment of SIADH-compromised rats with a vasopressin V-2 antagonist has corrected their existing hyponatremia (G. Fujisawa, Kidney Int. 1993, 44(1), 19). Due in part to the contractile actions of vasopressin at the V-1 receptor in the vasculature, vasopressin V-1 antagonists have reduced blood pressure as a potential treatment for hypertension. Thus, vasopressin receptor antagonists could be useful as therapeutics in the conditions of hypertension, congestive heart failure/cardiac insufficiency, coronary vasospasm, cardiac ischemia, liver cirrhosis, renal vasospasm, renal failure, cerebral edema and ischemia, stroke, thrombosis, and water retention. Web site: http://www.delphion.com/details?pn=US06713475__

Patent Applications on Cerebral Edema As of December 2000, U.S. patent applications are open to public viewing.9 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to cerebral edema:

9

This has been a common practice outside the United States prior to December 2000.

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ADENOVIRAL VECTORS ANGIOGENIC INHIBITORS

INCLUDING

DNA

SEQUENCES

ENCODING

Inventor(s): CHEN, CHEAUYUN THERESA; (ELLICOTT CITY, MD), HALLENBECK, PAUL; (GAITHERSBURG, MD) Correspondence: Elliott M Olstein Esq; C/o Carella Byrne Bain Gilfillan Cecchi; Stewart & Olstein; 6 Becker Farm Road; Roseland; NJ; 07068 Patent Application Number: 20020115202 Date filed: August 13, 1999 Abstract: An adenoviral vector which includes at least one DNA sequence encoding an angiogenic inhibitor, such as endostatin. Such vectors may be employed in treating diseases or disorders associated with angiogenesis, such as cancer, vascular diseases of the eye, including diabetic retinopathy, psoriasis, arthritis, cardiovascular disease, cerebral edema and Kasabach-Merritt syndrome. Excerpt(s): This invention relates to adenoviral vectors which may be employed in treating tumors. More particularly, this invention relates to adenoviral vectors including at least one DNA sequence encoding an angiogenic inhibitor and, in particular, endostatin. Such vectors may inhibit, prevent, or destroy the growth of tumors by preventing the formation of blood vessels in such tumors. Angiogenesis, the process of new blood vessel formation from the existing vessels, is known to be important for tumor growth (Folkman, N. Engl. J. Med., Vol. 285, pgs. 1182-1186 (1971)). Thus, antiangiogenesis has been studied extensively in cancer therapy applications over the decade. Numerous anti-angiogenesis approaches have been reported and reviewed by Zetter, Ann. Res. Med., Vol. 49, pgs. 407-424 (1998). These include (1) naturally occurring angiogenic inhibitors, e.g., thrombospondin,.alpha.-Interferon, platelet factor VI, metalloproteinase inhibitors; (2) synthetic angiogenesis inhibitors, e.g., synthetic protease inhibitors, anti-adhesive peptides (cRGD peptide), anti-integrin antibody (directed against.alpha.v.beta.p3); (3) pharmacological inhibitor agents, e.g., TNP470, thalidomide, carboxyamidotrizaole (CAI); and (4) tumor-derived inhibitors, e.g., angiostatin, endostatin. Others are currently either in clinical trial or under development, e.g., anti-signaling agents, and ribozymes inhibiting VEGF receptor synthesis. Among them, endostatin has been one of the inhibitors demonstrating the most dramatic anti-tumor effect through systemic protein administration (O'Reilly, et al., Cell, Vol. 88, pgs. 277-285 (1997); Boehm, et al., Nature, Vol. 380, pgs. 404-407 (1997)). After several cycles of treatment, the tumors were at their dormancy ultimately resulting in complete tumor arrest. No drug resistance or side effects were reported (O'Reilly, et al., 1997; Boehm, et al., 1997). However, like most angiogenic inhibitors, it functions through cytostatic rather cytotoxic effect, relying on a prolonged maintenance of an antiangiogenesis state. Direct protein injection may not be sufficient for prolonging maintenance of an anti-angiogenesis state and also likely to be too costly and cumbersome. Thus, the gene therapy approach for anti-angiogenic protein delivery was thought to be more applicable and realistic. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Composition and treatment method for brain and spinal cord injuries Inventor(s): Wang, Yanming; (Malden, MA) Correspondence: Cesari And Mckenna, Llp; 88 Black Falcon Avenue; Boston; MA; 02210; US Patent Application Number: 20030059476 Date filed: September 24, 2001 Abstract: After interruption of blood supply to central nervous system tissue, cerebral edema sets in. It has been shown that restoring blood flow to injured areas of the central nervous system after the onset of edema does not result in blood reperfusing the tissue. A composition and method for treating injured central nervous tissue, or preventing injury to central nervous system tissue is provided. The composition is generally an amphipathic lipid in an oil solution. The method provides for withdrawing cerebrospinal fluid from the subarachnoid spaces around the tissue to be treated or protected, and replacing that fluid with an approximately equivalent volume of the amphipathic lipid in oil composition. The treatment can be augmented with agents that suppress production of cerebrospinal fluid, or with other known agents. Excerpt(s): This invention is related to medical formulations used to treat and protect the central nervous system and methods of using those formulations. In particular, the invention relates to neuroprotective compositions and methods using those compositions to protect the brain or minimize lasting damage. Most Central Nervous System (CNS) injuries, including stroke, trauma, hypoxia-ischemia, multiple sclerosis, seizure, infection, and poisoning directly or indirectly involve a disruption of blood supply to the CNS, and share the same common pathologic process, that is: rapid cerebral edema leading to irreversible brain damage, and eventually to brain cell death. One common injury to the CNS is stroke, the destruction of brain tissue as a result of intracerebral hemorrhage or infarction. Stroke is a leading cause of death in the developed world. It may be caused by reduced blood flow or ischemia that results in deficient blood supply and death of tissues in one area of the brain (infarction). Causes of ischemic strokes include blood clots that form in the blood vessels in the brain (thrombus) and blood clots or pieces of atherosclerotic plaque or other material that travel to the brain from another location (emboli). Bleeding (hemorrhage) within the brain may also cause symptoms that mimic stroke. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Methods for the treatment of a traumatic central nervous system injury Inventor(s): Hoffman, Stuart Wayne; (Atlanta, GA), Stein, Donald Gerald; (Atlanta, GA) Correspondence: Alston & Bird Llp; Bank OF America Plaza; 101 South Tryon Street, Suite 4000; Charlotte; NC; 28280-4000; US Patent Application Number: 20020072509 Date filed: October 9, 2001 Abstract: The present invention provides methods for conferring a neuroprotective effect on a population of cells in a subject following a traumatic injury to the central nervous system. Specifically, the methods of the invention provide for the administration of a progestin or progestin metabolite following a traumatic brain injury. The progestin or progestin metabolite is administered at therapeutically effective

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concentrations that produce a neuroprotective effect (i.e., a decrease in the loss of neuronal activity) and reduces and/or prevents the various physiological events leading to neurodegeneration, such as, cerebral edema and the immune/inflammatory response. Excerpt(s): This application claims the benefit of U.S. Provisional Application Nos. 60/245,798, filed Nov. 3, 2000, and 60/239,505, filed Oct. 11, 2000, both of which are herein incorporated by reference in their entirety. The invention relates to methods for treating a traumatic injury to the central nervous system. There is growing experimental evidence that progesterone, its metabolites and other gonadal steroids such as estrogen and possibly testosterone, are effective neuroprotective agents; although the specific, physiological mechanisms by which these hormones act in the central nervous system to enhance repair are not completely understood. In addition to being a gonadal steroid, progesterone also belongs to a family of autocrine/paracrine hormones called neurosteroids. Neurosteroids are steroids that accumulate in the brain independently of endocrine sources and which can be synthesized from sterol precursors in nervous cells. These neurosteroids can potentiate GABA transmission, modulate the effects of glutamate, enhance the production of myclin, and prevent release of free radicals from activated microglia. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Nonpeptide substituted spirobenzoazepines as vasopressin antagonists Inventor(s): Chen, Robert H.K.; (Belle Mead, NJ), Xiang, Min A.; (Bridgewater, NJ) Correspondence: Audley A. Ciamporcero JR.; Johnson & Johnson; One Johnson & Johnson Plaza; New Brunswick; NJ; 08933-7003; US Patent Application Number: 20030045517 Date filed: July 2, 2001 Abstract: The invention is directed to nonpeptide substituted benzodiazepines of Formula I, 1wherein A, X, n, R.sup.1, R.sup.2, R.sup.3, R.sup.4, R.sup.5, a and b are as described in the specification, which are useful as vasopressin receptor antagonists for treating conditions associated with vasopressin receptor activity such as those involving increased vascular resistance and cardiac insufficiency. Pharmaceutical compositions comprising a compound of Formula I and methods of treating conditions such as hypertension, congestive heart failure, cardiac insufficiency, coronary vasospasm, cardiac ischemia, liver cirrhosis, renal vasospasm, renal failure, cerebral edema and ischemia, stroke, thrombosis, or water retention are also disclosed. Excerpt(s): This application claims priority from U.S. Ser. No. 60/216,220, filed Jul. 5, 2000. This invention relates to novel nonpeptide substituted vasopressin receptor antagonists. More particularly, the compounds of the present invention interrupt the binding of the peptide hormone vasopressin to its receptors and are therefore useful for treating conditions involving increased vascular resistance and cardiac insufficiency. Vasopressin is a nonapeptide hormone that is secreted primarily from the posterior pituitary gland. The hormone effects its actions through the vascular V-1 and renal V-2 receptor subtypes. The functions of vasopressin include contraction of uterine, bladder, and smooth muscle; stimulation of glycogen breakdown in the liver; induction of platelet aggregation; release of corticotropin from the anterior pituitary and stimulation of renal water reabsorption. As a neurotransmitter within the central nervous system (CNS), vasopressin can affect aggressive behavior, sexual behavior, the stress response,

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social behavior and memory. The V-1a receptor mediates central nervous system effects, contraction of smooth muscle and hepatic glycogenolytic effects of vasopressin, while the V-1b receptor mediates anterior pituitary effects of vasopressin. The V-2 receptor, presumably found only in the kidney, effects the antidiuretic actions of vasopressin via stimulation of adenylate cyclase. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

System and method for site specific therapy Inventor(s): Odland, Rick Mathew; (Roseville, MN) Correspondence: Intellectual Property Group; Fredrikson & Byron, P.A.; 4000 Pillsbury Center; 200 South Sixth Street; Minneapolis; MN; 55402; US Patent Application Number: 20030167031 Date filed: March 24, 2003 Abstract: A system, including catheter apparatus, and related method for performing site specific therapy. The catheter apparatus can include one or more semipermeable microcatheters for use in performing site specific microdialysis. The system and method are particularly suited for use in addressing cerebral edema by affecting the osmolar relationship between fluids making up the brain tissue.Also disclosed is an apparatus having a delivery/recovery mechanism in the form of a pump reservoir and one or more catheters in the form of semipermeable microcatheters, for use in delivering and/or recovering fluid to and/or from a tissue site or for performing tissue engineering outside of the body. The apparatus can be used in a method to perform site specific microtherapy, including for the treatment of avascular necrosis, compartment syndrome, cerebral edema, and to improve skin flap survival in the course of reconstructive surgery. Excerpt(s): The present application is a continuation of US patent application filed May 17, 1999 and assigned Ser. No. 09/313,341, which is a continuation of an international patent application filed Aug. 7, 1998 and assigned Serial No. PCT/US98/16416 which is a continuation-in-part of U.S. patent application filed Aug. 8, 1997 and assigned Ser. No. 08/908,555, the entire disclosure of which is incorporated herein by reference. In one aspect, the present invention relates to methods and apparatuses for treating microcirculatory problems, including transient and reversible conditions that do no involve structural injury, as well as permanent or chronic conditions that do involve structural injury to the microcirculation. In another aspect, the invention relates to methods and apparatuses for augmenting normal microcirculation. In a related aspect, the invention relates to methods and apparatuses for treating conditions that involve osteonecrosis, compartment syndrome, edema, and skin flap survival. In yet another aspect, the present invention relates to methods and devices for addressing cerebral edema, and to materials, such as catheters (including vetnriculosotomy catheters) and semipermeable membranes, for use in site specific treatment of tissues and tissue disorders. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Use of n-acetyl-d-glucosamine in the manufacture of pharmaceutical useful for treating cardio-cerebrovascular anoxemia Inventor(s): Liu, Junkang; (Chongqing, CH), Xu, Qiwang; (Chongqing, CH), Yuan, Zetao; (Chongqing, CH) Correspondence: Ladas & Parry; 26 West 61st Street; New York; NY; 10023; US Patent Application Number: 20040106577 Date filed: January 12, 2004 Abstract: The present invention has disclosed a use of N-acetyl-D-glucosamine in the manufacture of a medicament for resisting cardiac and cerebral ischemia and oxygendeficiency. N-acetyl-D-glucosamine can obviously prolong the survival time of the experimental animal under the condition of cerebral ischemia and oxygen-deficiency at normal pressure, can decrease cerebral edema degree and other symptoms of the nerve behavior caused by cerebral ischemia and re-infusion. Excerpt(s): The present invention relates to the use of N-acetyl-D-glucosamine and pharmaceutical acceptable salts thereof in the manufacture of a medicament for resisting cardiac and cerebral ischemia as well as oxygen-deficiency. The cardiac and cerebral ischemia as well as oxygen-deficiency is clinically a common phenomenon, for instance, the heart disease caused by ischemia and oxygen-deficiency of the cardiac muscle due to heart coronary artery constriction or occlusion, and the cerebral disease caused by constriction or occlusion of the cerebral vessels, which is characterized by ischemia and oxygen-deficiency. Over a long period of time, people have worked all along for finding various medicaments which are able to effectively cure the diseases related to ischemia and oxygen-deficiency. In the research of "bio-waves" theory, the present inventor has set up a bacterial wave growth model. Through researching, it is known that this wave is of its intrinsic regulation mechanism: some chemical substances are able to participate the regulation in the bio-wave process, so as to transform an abnormal periodic slow wave into a normal physiological chaotic quick wave, and this kind of substances are known as promoting wave factors. Through separating, purifying and identifying, it is determined that one of the factors is N-acetyl-D-glucosamine, the promoting wave function of which is shown in lubricating and protecting the cell. Many biochemical and physiological process of human body need the participation of the promoting wave factors, and it would lead to an abnormal state, if this kind of promoting wave factors is lacked in the living body. 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 cerebral edema, 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 “cerebral edema” (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 cerebral edema.

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You can also use this procedure to view pending patent applications concerning cerebral edema. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

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CHAPTER 5. BOOKS ON CEREBRAL EDEMA Overview This chapter provides bibliographic book references relating to cerebral edema. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on cerebral edema include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.

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

Diabetic Ketoacidosis Source: in Bushore, M.; Fleisher, G.; Seidel, J.; and Wagner, D. Advanced Pediatric Life Support. Elk Grove Village, IL: American Academy of Pediatrics. 1991. p. 185-191. Contact: Available from American Academy of Pediatrics. 141 Northwest Point Boulevard, P.O. Box 927, Elk Grove Village, IL 60009-0927. PRICE: $55 (for members); $75 (non-members); $8.25 soft cover. ISBN: 091076123X. Summary: This chapter, from a book describing pediatric emergencies and their care, discusses diabetic ketoacidosis. The chapter addresses three areas: the disordered metabolic process that led to the ketoacidotic state in a child with diabetes and the mechanism of reversal of those processes; the appropriate sequence of therapeutic interventions during the first hour of management of a child with diabetic ketoacidosis; and the common pitfalls encountered in the management of diabetic ketoacidosis. Specific topics include classification; pathophysiology; assessment issues, including

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signs and symptoms, assessment of dehydration, laboratory evaluation, and erroneous interpretations of laboratory results; management factors, including electrolytes, continued reassessment, insulin, and bicarbonate; complications of acute therapy, notably cerebral edema; and disposition, focusing on whether or not hospital admission is required. The chapter concludes with a case example. 4 references. (AA-M).

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APPENDICES

85

APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.

NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute10: •

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

•

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/

10

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

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•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.11 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:12 •

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

•

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

11

Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 12 See http://www.nlm.nih.gov/databases/databases.html.

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•

Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html

•

Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html

The NLM Gateway13 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “cerebral edema” (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 10080 83 780 10 317 11270

HSTAT15 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.16 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.17 Simply search by “cerebral edema” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

13

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

14

The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17

The HSTAT URL is http://hstat.nlm.nih.gov/.

Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.

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Coffee Break: Tutorials for Biologists18 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.19 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.20 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.

Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •

CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.

•

Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.

18 Adapted 19

from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.

The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 20 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.

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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on cerebral edema 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 cerebral edema. 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 cerebral edema. 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 “cerebral edema”:

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Brain Cancer http://www.nlm.nih.gov/medlineplus/braincancer.html Cerebral Palsy http://www.nlm.nih.gov/medlineplus/cerebralpalsy.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 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 cerebral edema. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •

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

•

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

•

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

•

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

•

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

•

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

•

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

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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to cerebral edema. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with cerebral edema. 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 cerebral edema. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “cerebral edema” (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 “cerebral edema”. 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 “cerebral edema” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months.

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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 “cerebral edema” (or a synonym) into the search box, and click “Submit Query.”

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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.

Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.21

Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.

Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of

21

Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.

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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)22: •

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

•

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

•

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

•

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/

22

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

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•

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

•

Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm

•

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

•

Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm

•

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/

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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/

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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm

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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html

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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm

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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/

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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/

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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10

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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/

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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html

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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp

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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

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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/

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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html

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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm

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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/

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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html

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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm

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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330

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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)

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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html

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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/

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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/

Finding Medical Libraries

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

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

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

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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm

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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/

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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp

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

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

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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72

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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •

ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html

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

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

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Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html

•

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

•

Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp

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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm

Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).

Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •

Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical

•

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

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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

•

Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

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CEREBRAL EDEMA DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 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] Ablation: The removal of an organ by surgery. [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] Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak antiinflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [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] Acidemia: Increased acidity of blood. [NIH] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Actinin: A protein factor that regulates the length of R-actin. It is chemically similar, but immunochemically distinguishable from actin. [NIH] Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH] Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphoblastic leukemia. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenovirus: A group of viruses that cause respiratory tract and eye infections.

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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] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerospace Medicine: A specialty which is concerned with the health and medical problems of man in aviation (aviation medicine) and space (space medicine). [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] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]

Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Air Embolism: Occurs when the lungs over expand to the point that air bubbles are forced through the air sacs of the lungs into the circulatory system. [NIH] Air Sacs: Thin-walled sacs or spaces which function as a part of the respiratory system in birds, fishes, insects, and mammals. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU]

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Alkaline: Having the reactions of an alkali. [EU] 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] Amanita: A genus of fungi of the family Agaricaceae, order Agaricales; most species are poisonous. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amnesia: Lack or loss of memory; inability to remember past experiences. [EU] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Angiocardiography: Radiography of the heart and great vessels after injection of a contrast medium. [NIH]

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Angiogenesis inhibitor: A substance that may prevent the formation of blood vessels. In anticancer therapy, an angiogenesis inhibitor prevents the growth of blood vessels from surrounding tissue to a solid tumor. [NIH] Angiopathy: Disease of the blood vessels (arteries, veins, and capillaries) that occurs when someone has diabetes for a long time. There are two types of angiopathy: macroangiopathy and microangiopathy. In macroangiopathy, fat and blood clots build up in the large blood vessels, stick to the vessel walls, and block the flow of blood. In microangiopathy, the walls of the smaller blood vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood through the body. Then the cells, for example, the ones in the center of the eye, do not get enough blood and may be damaged. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]

Anoxemia: Clinical manifestation of respiratory distress consisting of relatively complete absence of oxygen in arterial blood. [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] Antiallergic: Counteracting allergy or allergic conditions. [EU] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]

Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidiuretic: Suppressing the rate of urine formation. [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] Anti-infective: An agent that so acts. [EU]

Dictionary 107

Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Approximate: Approximal [EU] Aquaporins: Membrane proteins which facilitate the passage of water. They are members of the family of membrane channel proteins which includes the lens major intrinsic protein and bacterial glycerol transporters. [NIH] Aqueous: Having to do with water. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Asphyxia: A pathological condition caused by lack of oxygen, manifested in impending or actual cessation of life. [NIH] 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] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atmospheric Pressure: The pressure at any point in an atmosphere due solely to the weight of the atmospheric gases above the point concerned. [NIH]

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Atrial: Pertaining to an atrium. [EU] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoradiography: A process in which radioactive material within an object produces an image when it is in close proximity to a radiation sensitive emulsion. [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] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Barbital: A long-acting barbiturate that depresses most metabolic processes at high doses. It is used as a hypnotic and sedative and may induce dependence. Barbital is also used in veterinary practice for central nervous system depression. [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 Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [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]

Benzodiazepines: A two-ring heterocyclic compound consisting of a benzene ring fused to a diazepine ring. Permitted is any degree of hydrogenation, any substituents and any Hisomer. [NIH]

Dictionary 109

Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bewilderment: Impairment or loss of will power. [NIH] 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] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [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] Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Flow Velocity: A value equal to the total volume flow divided by the cross-sectional area of the vascular bed. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood urea: A waste product in the blood that comes from the breakdown of food protein. The kidneys filter blood to remove urea. As kidney function decreases, the BUN level increases. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Viscosity: The internal resistance of the blood to shear forces. The in vitro measure of whole blood viscosity is of limited clinical utility because it bears little relationship to the actual viscosity within the circulation, but an increase in the viscosity of circulating blood

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can contribute to morbidity in patients suffering from disorders such as sickle cell anemia and polycythemia. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [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] 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 Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain. [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] Bumetanide: A sulfamyl diuretic. [NIH] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH]

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Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capillary Fragility: The lack of resistance, or susceptibility, of capillaries to damage or disruption under conditions of increased stress. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogenic: Producing carcinoma. [EU] 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 Glycosides: Substances obtained from species of Digitalis, Strophanthus, and other plants that contain specific steroid glycosides or their semisynthetic derivatives and used in congestive heart failure. They increase the force of cardiac contraction without significantly affecting other parameters, but are very toxic at larger doses. Their mechanism of action usually involves inhibition of the Na(+)-K(+)-exchanging ATPase and they are often used in cell biological studies for that purpose. [NIH] Cardiac Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume (volume per beat). [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [NIH] Carnitine: Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. [NIH] Carotenoids: Substance found in yellow and orange fruits and vegetables and in dark green, leafy vegetables. May reduce the risk of developing cancer. [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]

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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] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [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] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell motility: The ability of a cell to move. [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] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] 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 Arteries: The arteries supplying the cerebral cortex. [NIH] 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 Hemorrhage: Bleeding into a cerebral hemisphere of the brain, including lobar, subcortical white matter, and basal ganglia hemorrhages. Commonly associated conditions include hypertension; intracranial arteriosclerosis; intracranial aneurysm; craniocerebral

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trauma; intracranial arteriovenous malformations; cerebral amyloid angiopathy; and cerebral infarction. [NIH] Cerebral Infarction: The formation of an area of necrosis in the cerebrum caused by an 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]

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] 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] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] 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

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molecules. [NIH] Clot Retraction: Retraction of a clot resulting from contraction of platelet pseudopods attached to fibrin strands that is dependent on the contractile protein thrombosthenin. Used as a measure of platelet function. [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] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [NIH] Computational Biology: A field of biology concerned with the development of techniques

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for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Concomitant: Accompanying; accessory; joined with another. [EU] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constriction: The act of constricting. [NIH] 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] Contralateral: Having to do with the opposite side of the body. [NIH] Contrast medium: A substance that is introduced into or around a structure and, because of the difference in absorption of x-rays by the contrast medium and the surrounding tissues, allows radiographic visualization of the structure. [EU] Contusions: Injuries resulting in hemorrhage, usually manifested in the skin. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [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] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains

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oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [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 Arteriosclerosis: Thickening and loss of elasticity of the coronary arteries. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Coronary Vasospasm: Spasm of the large- or medium-sized coronary arteries. [NIH] Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that has ruptured and discharged its ovum. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH]

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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] Craniotomy: An operation in which an opening is made in the skull. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cystathionine beta-Synthase: A multifunctional pyridoxal phosphate enzyme. In the second stage of cysteine biosynthesis it catalyzes the reaction of homocysteine with serine to form cystathionine with the elimination of water. Deficiency of this enzyme leads to hyperhomocysteinemia and homocystinuria. EC 4.2.1.22. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeletal Proteins: Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible. [NIH]

Cytostatic: An agent that suppresses cell growth and multiplication. [EU] Cytotoxic: Cell-killing. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decompression: Decompression external to the body, most often the slow lessening of external pressure on the whole body (especially in caisson workers, deep sea divers, and persons who ascend to great heights) to prevent decompression sickness. It includes also sudden accidental decompression, but not surgical (local) decompression or decompression applied through body openings. [NIH] Decompression Sickness: A condition occurring as a result of exposure to a rapid fall in ambient pressure. Gases, nitrogen in particular, come out of solution and form bubbles in body fluid and blood. These gas bubbles accumulate in joint spaces and the peripheral circulation impairing tissue oxygenation causing disorientation, severe pain, and potentially death. [NIH] Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the form of its mesylate. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydration: The condition that results from excessive loss of body water. [NIH] 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

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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] Demyelinating Diseases: Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system. [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] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] 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] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [NIH] Diabetes Insipidus: A metabolic disorder due to disorders in the production or release of vasopressin. It is characterized by the chronic excretion of large amounts of low specific gravity urine and great thirst. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Ketoacidosis: Complication of diabetes resulting from severe insulin deficiency coupled with an absolute or relative increase in glucagon concentration. The metabolic acidosis is caused by the breakdown of adipose stores and resulting increased levels of free fatty acids. Glucagon accelerates the oxidation of the free fatty acids producing excess ketone bodies (ketosis). [NIH] Diabetic Retinopathy: Retinopathy associated with diabetes mellitus, which may be of the background type, progressively characterized by microaneurysms, interretinal punctuate macular edema, or of the proliferative type, characterized by neovascularization of the retina and optic disk, which may project into the vitreous, proliferation of fibrous tissue, vitreous hemorrhage, and retinal detachment. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diastolic: Of or pertaining to the diastole. [EU] 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

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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] Diffusivity: Of a reverberant sound field. The degree to which the directions of propagation of waves are random from point to point. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Dilution: A diluted or attenuated medicine; in homeopathy, the diffusion of a given quantity of a medicinal agent in ten or one hundred times the same quantity of water. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU] Disposition: A tendency either physical or mental toward certain diseases. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Diuretic: A drug that increases the production of urine. [NIH] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dormancy: The period when an organism (i. e., a virus or a bacterium) is in the body but not producing any ill effects. [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] 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 Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated

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dose and no-observed-adverse-effect level. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dystrophin: A muscle protein localized in surface membranes which is the product of the Duchenne/Becker muscular dystrophy gene. Individuals with Duchenne muscular dystrophy usually lack dystrophin completely while those with Becker muscular dystrophy have dystrophin of an altered size. It shares features with other cytoskeletal proteins such as spectrin and alpha-actinin but the precise function of dystrophin is not clear. One possible role might be to preserve the integrity and alignment of the plasma membrane to the myofibrils during muscle contraction and relaxation. MW 400 kDa. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eclampsia: Onset of convulsions or coma in a previously diagnosed pre-eclamptic patient. [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] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Emboli: 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] 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] Emollient: Softening or soothing; called also malactic. [EU] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] 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] Encephalitis, Viral: Inflammation of brain parenchymal tissue as a result of viral infection.

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Encephalitis may occur as primary or secondary manifestation of Togaviridae infections; Herpesviridae infections; Adenoviridae infections; Flaviviridae infections; Bunyaviridae infections; Picornaviridae infections; Paramyxoviridae infections; Orthomyxoviridae infections; Retroviridae infections; and Arenaviridae infections. [NIH] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endorphins: One of the three major groups of endogenous opioid peptides. They are large peptides derived from the pro-opiomelanocortin precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; opioid peptides is used for the broader group. [NIH] Endoscopy: Endoscopic examination, therapy or surgery performed on interior parts of the body. [NIH] Endostatin: A drug that is being studied for its ability to prevent the growth of new blood vessels into a solid tumor. Endostatin belongs to the family of drugs called angiogenesis inhibitors. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] Enkephalins: One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]

Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] 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

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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] Erection: The condition of being made rigid and elevated; as erectile tissue when filled with blood. [EU] Erythrocyte Volume: Volume of circulating erythrocytes. It is usually measured by radioisotope dilution technique. [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] Estrogen: One of the two female sex hormones. [NIH] Etomidate: Imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system. It has been proposed as an induction anesthetic. [NIH]

Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Excipient: Any more or less inert substance added to a prescription in order to confer a suitable consistency or form to the drug; a vehicle. [EU] 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] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]

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 Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an

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intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] 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 reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]

Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Femoral: Pertaining to the femur, or to the thigh. [EU] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinolytic: Pertaining to, characterized by, or causing the dissolution of fibrin by enzymatic action [EU] Fibrinolytic Agents: Fibrinolysin or agents that convert plasminogen to fibrinolysin (plasmin). [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Flatus: Gas passed through the rectum. [NIH] Fluid Therapy: Therapy whose basic objective is to restore the volume and composition of the body fluids to normal with respect to water-electrolyte balance. Fluids may be administered intravenously, orally, by intermittent gavage, or by hypodermoclysis. [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] Foramen: A natural hole of perforation, especially one in a bone. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or

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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] Fulminant Hepatic Failure: Liver failure that occurs suddenly in a previously healthy person. The most common causes of FHF are acute hepatitis, acetaminophen overdose, and liver damage from prescription drugs. [NIH] Galactosemia: Buildup of galactose in the blood. Caused by lack of one of the enzymes needed to break down galactose into glucose. [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] 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] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal Hemorrhage: Bleeding in the gastrointestinal tract. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gavage: Feeding by a tube passed into the stomach; called also tube feeding. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]

Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] Generator: Any system incorporating a fixed parent radionuclide from which is produced a daughter radionuclide which is to be removed by elution or by any other method and used

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in a radiopharmaceutical. [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] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glioma: A cancer of the brain that comes from glial, or supportive, cells. [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] Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] 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]

Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [NIH] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9.

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[NIH]

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

Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycolysis: The pathway by which glucose is catabolized into two molecules of pyruvic acid with the generation of ATP. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Gonad: A sex organ, such as an ovary or a testicle, which produces the gametes in most multicellular animals. [NIH] Gonadal: Pertaining to a gonad. [EU] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grafting: The operation of transfer of tissue from one site to another. [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] 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] 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] Headache Disorders: Common conditions characterized by persistent or recurrent headaches. Headache syndrome classification systems may be based on etiology (e.g., vascular headache, post-traumatic headaches, etc.), temporal pattern (e.g., cluster headache, paroxysmal hemicrania, etc.), and precipitating factors (e.g., cough headache). [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartbeat: One complete contraction of the heart. [NIH] Heat Stroke: A condition characterized by cessation of sweating, hot dry skin, delirium, collapse, and coma and resulting from prolonged exposure to high environmental temperature. [NIH] Hemiparesis: The weakness or paralysis affecting one side of the body. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH]

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Hemodynamics: The movements of the blood and the forces involved in systemic or regional blood circulation. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] 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] Hepatic Encephalopathy: A condition that may cause loss of consciousness and coma. It is usually the result of advanced liver disease. Also called hepatic coma. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocyte: A liver cell. [NIH] Hepatocyte Growth Factor: Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is proto-oncogene protein C-met. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Hernia: Protrusion of a loop or knuckle of an organ or tissue through an abnormal opening. [NIH]

Histology: The study of tissues and cells under a microscope. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homodimer: Protein-binding "activation domains" always combine with identical proteins. [NIH]

Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small

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intestine. [NIH] Hydrocephalus: Excessive accumulation of cerebrospinal fluid within the cranium which may be associated with dilation of cerebral ventricles, intracranial hypertension; headache; lethargy; urinary incontinence; and ataxia (and in infants macrocephaly). This condition may be caused by obstruction of cerebrospinal fluid pathways due to neurologic abnormalities, intracranial hemorrhages; central nervous system infections; brain neoplasms; craniocerebral trauma; and other conditions. Impaired resorption of cerebrospinal fluid from the arachnoid villi results in a communicating form of hydrocephalus. Hydrocephalus ex-vacuo refers to ventricular dilation that occurs as a result of brain substance loss from cerebral infarction and other conditions. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrogenation: Specific method of reduction in which hydrogen is added to a substance by the direct use of gaseous hydrogen. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] 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] Hypercapnia: A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperhomocysteinemia: An inborn error of methionone metabolism which produces an excess of homocysteine in the blood. It is often caused by a deficiency of cystathionine betasynthase and is a risk factor for coronary vascular disease. [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] Hyperventilation: A pulmonary ventilation rate faster than is metabolically necessary for the exchange of gases. It is the result of an increased frequency of breathing, an increased tidal volume, or a combination of both. It causes an excess intake of oxygen and the blowing off of carbon dioxide. [NIH] Hypnotic: A drug that acts to induce sleep. [EU]

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Hypoglycemia: Abnormally low blood sugar [NIH] Hypotension: Abnormally low blood pressure. [NIH] Hypotensive: Characterized by or causing diminished tension or pressure, as abnormally low blood pressure. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals; in man usually accidental or unintentional. [NIH] Hypoxemia: Deficient oxygenation of the blood; hypoxia. [EU] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hypoxic: Having too little oxygen. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]

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

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agents. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]

Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] 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] 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-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage

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requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus. IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] 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 Aneurysm: A saclike dilatation of the walls of a blood vessel, usually an artery. [NIH]

Intracranial Arteriosclerosis: Vascular diseases characterized by thickening, hardening, and remodeling of the walls of intracranial arteries. There are three subtypes: (1) atherosclerosis, marked by fatty depositions in the innermost layer of the arterial walls, (2) Monckeberg's sclerosis, which features calcium deposition in the media and (3) arteriolosclerosis, which refers to sclerosis of small caliber arteries. Clinically, this process may be associated with transient ischemic attack, brain infarction, intracranial embolism and thrombosis, or intracranial aneurysm. [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 Hemorrhages: Bleeding within the intracranial cavity, including hemorrhages in the brain and within the cranial epidural, subdural, and subarachnoid spaces. [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] Intracranial tumors: Tumors that occur in the brain. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] 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]

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Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH] Iodine-131: Radioactive isotope of iodine. [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 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] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic stroke: A condition in which the blood supply to part of the brain is cut off. Also called "plug-type" strokes. Blocked arteries starve areas of the brain controlling sight, speech, sensation, and movement so that these functions are partially or completely lost. Ischemic stroke is the most common type of stroke, accounting for 80 percent of all strokes. Most ischemic strokes are caused by a blood clot called a thrombus, which blocks blood flow in the arteries feeding the brain, usually the carotid artery in the neck, the major vessel bringing blood to the brain. When it becomes blocked, the risk of stroke is very high. [NIH] Isopropyl: A gene mutation inducer. [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] Ketoacidosis: Acidosis accompanied by the accumulation of ketone bodies (ketosis) in the body tissues and fluids, as in diabetic acidosis. [EU] Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can

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also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Ketosis: A condition of having ketone bodies build up in body tissues and fluids. The signs of ketosis are nausea, vomiting, and stomach pain. Ketosis can lead to ketoacidosis. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kinetic: Pertaining to or producing motion. [EU] 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] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leukemia: Cancer of blood-forming tissue. [NIH] Ligaments: Shiny, flexible bands of fibrous tissue connecting together articular extremities of bones. They are pliant, tough, and inextensile. [NIH] Linkages: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver Cirrhosis: Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. [NIH] Liver 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] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries

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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] Lymphoblastic: One of the most aggressive types of non-Hodgkin lymphoma. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [NIH] Lymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation. [NIH] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each); those with characteristics of neither major class are called null cells. [NIH] 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] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mannitol: A diuretic and renal diagnostic aid related to sorbitol. It has little significant energy value as it is largely eliminated from the body before any metabolism can take place. It can be used to treat oliguria associated with kidney failure or other manifestations of inadequate renal function and has been used for determination of glomerular filtration rate. Mannitol is also commonly used as a research tool in cell biological studies, usually to control osmolarity. [NIH] Maple Syrup Urine Disease: A genetic disorder involving deficiency of an enzyme necessary in the metabolism of branched-chain amino acids, and named for the characteristic odor of the urine. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH]

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Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningioma: A type of tumor that occurs in the meninges, the membranes that cover and protect the brain and spinal cord. Meningiomas usually grow slowly. [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] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Health: The state wherein the person is well adjusted. [NIH] Metabolic acidosis: (met-ah-BOL-ik as-id-O-sis): A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metabotropic: A glutamate receptor which triggers an increase in production of 2 intracellular messengers: diacylglycerol and inositol 1, 4, 5-triphosphate. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] 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] Microcirculation: The vascular network lying between the arterioles and venules; includes capillaries, metarterioles and arteriovenous anastomoses. Also, the flow of blood through this network. [NIH] 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,

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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] Middle Cerebral Artery: The largest and most complex of the cerebral arteries. Branches of the middle cerebral artery supply the insular region, motor and premotor areas, and large regions of the association cortex. [NIH] Middle Cerebral Artery Infarction: Terminal branch of the internal carotid artery which supplies the lateral portion of the cortex, the optic chiasm, the optic tract, and the optic radiations. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Mineralocorticoids: A group of corticosteroids primarily associated with the regulation of water and electrolyte balance. This is accomplished through the effect on ion transport in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by plasma volume, serum potassium, and angiotensin II. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular Structure: The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds. [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH] Mononuclear: A cell with one nucleus. [NIH]

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Morphological: Relating to the configuration or the structure of live organs. [NIH] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [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] Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments. [NIH] Mushroom Poisoning: Poisoning from ingestion of mushrooms, primarily from, but not restricted to, toxic varieties. [NIH] Myelin: The fatty substance that covers and protects nerves. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardial Reperfusion: Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing myocardial reperfusion injury. [NIH] Myocardial Reperfusion Injury: Functional, metabolic, or structural changes in ischemic heart muscle thought to result from reperfusion to the ischemic areas. Changes can be fatal to muscle cells and may include edema with explosive cell swelling and disintegration, sarcolemma disruption, fragmentation of mitochondria, contraction band necrosis, enzyme washout, and calcium overload. Other damage may include hemorrhage and ventricular arrhythmias. One possible mechanism of damage is thought to be oxygen free radicals. Treatment currently includes the introduction of scavengers of oxygen free radicals, and injury is thought to be prevented by warm blood cardioplegic infusion prior to reperfusion. [NIH]

Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myofibrils: Highly organized bundles of actin, myosin, and other proteins in the cytoplasm of skeletal and cardiac muscle cells that contract by a sliding filament mechanism. [NIH] Myopathy: Any disease of a muscle. [EU] N-acetyl: Analgesic agent. [NIH] Nasogastric: The process of passing a small, flexible plastic tube through the nose or mouth into the stomach or small intestine. [NIH]

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Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Nephrectomy: Surgery to remove a kidney. Radical nephrectomy removes the kidney, the adrenal gland, nearby lymph nodes, and other surrounding tissue. Simple nephrectomy removes only the kidney. Partial nephrectomy removes the tumor but not the entire kidney. [NIH]

Nephropathy: Disease of the kidneys. [EU] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Nervousness: Excessive excitability and irritability, with mental and physical unrest. [EU] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neurites: In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell. [NIH] 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]

Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropeptides: Peptides released by neurons as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells. [NIH] Neurophysiology: The scientific discipline concerned with the physiology of the nervous system. [NIH] 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] Neurotoxicity: The tendency of some treatments to cause damage to the nervous system. [NIH]

Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many

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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] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]

Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] 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] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncology: The study of cancer. [NIH] Oncology nurse: A nurse who specializes in treating and caring for people who have cancer. [NIH]

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Ophthalmoplegia: Paralysis of one or more of the ocular muscles due to disorders of the eye muscles, neuromuscular junction, supporting soft tissue, tendons, or innervation to the muscles. [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 Disk: The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve. [NIH]

Osmolality: The concentration of osmotically active particles in solution expressed in terms of osmoles of solute per kilogram of solvent. The osmolality is directly proportional to the colligative properties of solutions; osmotic pressure, boiling point elevation, freezing point depression, and vapour pressure lowering. [EU] Osmolarity: The concentration of osmotically active particles expressed in terms of osmoles of solute per litre of solution. [EU] Osmoles: The standard unit of osmotic pressure. [NIH] Osmosis: Tendency of fluids (e.g., water) to move from the less concentrated to the more concentrated side of a semipermeable membrane. [NIH] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Osteonecrosis: Death of a bone or part of a bone, either atraumatic or posttraumatic. [NIH] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Otitis: Inflammation of the ear, which may be marked by pain, fever, abnormalities of hearing, hearing loss, tinnitus, and vertigo. [EU] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]

Oxidative 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] 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

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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] Pancreatic: Having to do with the pancreas. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [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] 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]

Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [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] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [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 sensory receptors. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneal Dialysis: Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure. [NIH]

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Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Perivascular: Situated around a vessel. [EU] 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] Phosphates: Inorganic salts of phosphoric acid. [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] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]

Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasma Volume: Volume of plasma in the circulation. It is usually measured by indicator dilution techniques. [NIH]

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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] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] 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] Plethysmography: Recording of change in the size of a part as modified by the circulation in it. [NIH] Plexus: A network or tangle; a general term for a network of lymphatic vessels, nerves, or veins. [EU] 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] Polydipsia: Chronic excessive thirst, as in diabetes mellitus or diabetes insipidus. [EU] 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] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyuria: Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes. [NIH]

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Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] 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] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precipitating Factors: Factors associated with the definitive onset of a disease, illness, accident, behavioral response, or course of action. Usually one factor is more important or more obviously recognizable than others, if several are involved, and one may often be regarded as "necessary". Examples include exposure to specific disease; amount or level of an infectious organism, drug, or noxious agent, etc. [NIH] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Pre-eclamptic: A syndrome characterized by hypertension, albuminuria, and generalized oedema, occurring only in 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] Priapism: Persistent abnormal erection of the penis, usually without sexual desire, and accompanied by pain and tenderness. It is seen in diseases and injuries of the spinal cord, and may be caused by vesical calculus and certain injuries to the penis. [EU] 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] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH]

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Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Prone: Having the front portion of the body downwards. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (endopeptidases). [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH]

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Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Pseudotumor Cerebri: A condition marked by raised intracranial pressure and characterized clinically by headaches; nausea; papilledema, peripheral constriction of the visual fields, transient visual obscurations, and pulsatile tinnitus. Obesity is frequently associated with this condition, which primarily affects women between 20 and 44 years of age. Chronic papilledema may lead to optic nerve injury (optic nerve diseases) and visual loss (blindness). [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] 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] Psychogenic: Produced or caused by psychic or mental factors rather than organic factors. [EU]

Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]

Pulmonary: Relating to the lungs. [NIH] Pulmonary 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 Gas Exchange: The exchange of oxygen and carbon dioxide between alveolar air and pulmonary capillary blood. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [NIH] Purifying: Respiratory equipment whose function is to remove contaminants from otherwise wholesome air. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Putamen: The largest and most lateral of the basal ganglia lying between the lateral

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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] Putaminal Hemorrhage: Bleeding into the putamen, a basal ganglia nucleus. This is a relatively common site of spontaneous intracranial hemorrhage and is associated with chronic hypertension and lipohyalinosis of small blood vessels in the putamen. Clinical manifestations vary with the size of hemorrhage, but include hemiparesis, headache, and alterations of consciousness. [NIH] Pyridoxal: 3-Hydroxy-5-(hydroxymethyl)-2-methyl-4- pyridinecarboxaldehyde. [NIH] Pyridoxal Phosphate: 3-Hydroxy-2-methyl-5-((phosphonooxy)methyl)-4pyridinecarboxaldehyde. An enzyme co-factor vitamin. [NIH] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and uracil) and form the basic structure of the barbiturates. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiopharmaceutical: Any medicinal product which, when ready for use, contains one or more radionuclides (radioactive isotopes) included for a medicinal purpose. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Reabsorption: 1. The act or process of absorbing again, as the selective absorption by the kidneys of substances (glucose, proteins, sodium, etc.) already secreted into the renal tubules, and their return to the circulating blood. 2. Resorption. [EU] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] 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]

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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] Recovery of Function: A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] 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] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [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] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] 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] 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

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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] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Reverberant: The sound field prevailing in a large enclosure with moderately reflecting surfaces. [NIH] Saline: A solution of salt and water. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] 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 as epilepsy or "seizure disorder." [NIH] Sella: A deep depression in the shape of a Turkish saddle in the upper surface of the body of the sphenoid bone in the deepest part of which is lodged the hypophysis cerebri. [NIH] Sella Turcica: A bony prominence situated on the upper surface of the body of the sphenoid bone. It houses the pituitary gland. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU]

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Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] 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] 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]

Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] 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] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]

Social Behavior: Any behavior caused by or affecting another individual, usually of the same species. [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]

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Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Sorbitol: A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Spatial disorientation: Loss of orientation in space where person does not know which way is up. [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] Spectrin: A high molecular weight (220-250 kDa) water-soluble protein which can be extracted from erythrocyte ghosts in low ionic strength buffers. The protein contains no lipids or carbohydrates, is the predominant species of peripheral erythrocyte membrane proteins, and exists as a fibrous coating on the inner, cytoplasmic surface of the membrane. [NIH]

Spectroscopic: The recognition of elements through their emission spectra. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] 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] Spinal Cord Injuries: Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., wounds, gunshot; whiplash injuries; etc.). [NIH] Status Epilepticus: Repeated and prolonged epileptic seizures without recovery of consciousness between attacks. [NIH] Stellate: Star shaped. [NIH] Stellate Ganglion: A paravertebral sympathetic ganglion formed by the fusion of the inferior cervical and first thoracic ganglia. [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] Stereotactic: Radiotherapy that treats brain tumors by using a special frame affixed directly to the patient's cranium. By aiming the X-ray source with respect to the rigid frame, technicians can position the beam extremely precisely during each treatment. [NIH] Stereotactic radiosurgery: A radiation therapy technique involving a rigid head frame that is attached to the skull; high-dose radiation is administered through openings in the head

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frame to the tumor while decreasing the amount of radiation given to normal brain tissue. This procedure does not involve surgery. Also called stereotaxic radiosurgery and stereotactic radiation therapy. [NIH] Sterile: Unable to produce children. [NIH] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Steroid therapy: Treatment with corticosteroid drugs to reduce swelling, pain, and other symptoms of inflammation. [NIH] 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] 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] 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] Stroma: The middle, thickest layer of tissue in the cornea. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Sudden death: Cardiac arrest caused by an irregular heartbeat. The term "death" is somewhat misleading, because some patients survive. [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

Dictionary 153

which the process of exclusion is not conscious. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] 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] 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] Systemic: Affecting the entire body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro. [NIH] 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] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalidomide: A pharmaceutical agent originally introduced as a non-barbiturate hypnotic, but withdrawn from the market because of its known tetratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of tumor necrosis factor alpha from monocytes, and modulates other cytokine action. [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] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Thoracic: Having to do with the chest. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or

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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] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombolytic Therapy: Use of infusions of fibrinolytic agents to destroy or dissolve thrombi in blood vessels or bypass grafts. [NIH] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]

Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tidal Volume: The volume of air inspired or expired during each normal, quiet respiratory cycle. Common abbreviations are TV or V with subscript T. [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] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU]

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Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] 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] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [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] Triad: Trivalent. [NIH] Tricuspid Atresia: Absence of the orifice between the right atrium and ventricle, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy because the right ventricle is absent or not functional. [NIH] Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] 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] Tumor-derived: Taken from an individual's own tumor tissue; may be used in the development of a vaccine that enhances the body's ability to build an immune response to the tumor. [NIH] Type 2 diabetes: Usually characterized by a gradual onset with minimal or no symptoms of metabolic disturbance and no requirement for exogenous insulin. The peak age of onset is 50 to 60 years. Obesity and possibly a genetic factor are usually present. [NIH] Typhoid fever: The most important member of the enteric group of fevers which also includes the paratyphoids. [NIH] Typhoid fever: The most important member of the enteric group of fevers which also includes the paratyphoids. [NIH] Umbilical Arteries: Either of a pair of arteries originating from the internal iliac artery and passing through the umbilical cord to carry blood from the fetus to the placenta. [NIH]

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Umbilical Cord: The flexible structure, giving passage to the umbilical arteries and vein, which connects the embryo or fetus to the placenta. [NIH] Uraemia: 1. An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. In current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]

Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]

Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [NIH]

Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] 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] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vascular Resistance: An expression of the resistance offered by the systemic arterioles, and to a lesser extent by the capillaries, to the flow of blood. [NIH] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoactive: Exerting an effect upon the calibre of blood vessels. [EU] Vasodilatation: A state of increased calibre of the blood vessels. [EU] Vasodilators: Any nerve or agent which induces dilatation of the blood vessels. [NIH] Vasogenic: Acute peripheral circulatory failure due to loss of capillary tone associated with a reduced circulating blood volume. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU]

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Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Ventriculostomy: Surgical creation of an opening in a cerebral ventricle. [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] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral Hepatitis: Hepatitis caused by a virus. Five different viruses (A, B, C, D, and E) most commonly cause this form of hepatitis. Other rare viruses may also cause hepatitis. [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] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] 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]

Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH]

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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] Wounds, Gunshot: Disruption of structural continuity of the body as a result of the discharge of firearms. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]

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INDEX A Abdomen, 103, 133, 141, 152 Abdominal, 103, 141, 142 Ablation, 17, 103 Acceptor, 103, 133, 140 Acetaminophen, 4, 32, 46, 103, 124 Acetylcholine, 103, 139 Acidemia, 7, 103 Acidosis, 5, 47, 103, 132 Actinin, 103, 120 Acute lymphoblastic leukemia, 27, 103 Acute lymphocytic leukemia, 103 Acute renal, 4, 103, 127 Adaptability, 103, 112 Adaptation, 10, 103, 143 Adenovirus, 44, 103 Adenylate Cyclase, 73, 77, 104 Adjustment, 103, 104 Adrenal Cortex, 104, 116, 144 Adverse Effect, 6, 104, 150 Aerospace Medicine, 26, 104 Affinity, 104, 107, 150 Agar, 104, 142 Age of Onset, 104, 110, 155 Agonist, 58, 104, 119 Air Embolism, 61, 104 Air Sacs, 104, 105 Albumin, 14, 24, 104, 142 Algorithms, 7, 104, 109 Alimentary, 3, 104, 131, 141 Alkaline, 103, 105, 111 Alpha Particles, 105, 147 Alternative medicine, 105 Alveoli, 105, 157 Amanita, 4, 105 Ameliorating, 18, 105 Amino Acid Sequence, 70, 105, 106 Amino Acids, 24, 67, 70, 105, 122, 134, 141, 143, 145, 150, 154, 156 Ammonia, 105, 125, 156 Amnesia, 6, 105 Amyloid, 105, 113 Anaesthesia, 105, 129 Analgesic, 103, 105, 137 Anatomical, 105, 108, 113, 129, 135, 149 Androgens, 104, 105, 116 Anemia, 105, 110 Anesthesia, 54, 105

Angiocardiography, 39, 105 Angiogenesis inhibitor, 74, 106, 121 Angiopathy, 106, 113 Animal model, 14, 106 Anions, 104, 106, 132, 152 Annealing, 106, 143 Anoxemia, 78, 106 Anterior Cerebral Artery, 106, 113 Antiallergic, 106, 116 Antibacterial, 106, 151 Antibiotic, 106, 151 Antibodies, 70, 106, 136, 142 Antibody, 70, 74, 104, 106, 114, 127, 130, 136, 147 Anticoagulant, 106, 145 Antidiuretic, 73, 77, 106 Antigen, 104, 106, 114, 127, 129, 130, 136 Anti-infective, 106, 128, 132 Anti-inflammatory, 13, 103, 107, 116, 118, 125 Anti-Inflammatory Agents, 107, 116 Antineoplastic, 107, 116 Antioxidant, 14, 107, 140 Antipyretic, 103, 107 Approximate, 17, 107 Aquaporins, 18, 107 Aqueous, 67, 107, 108, 117, 120, 128, 133 Arachidonic Acid, 107, 145 Arginine, 12, 20, 107, 139 Arterial, 12, 16, 24, 36, 50, 72, 106, 107, 110, 113, 116, 128, 131, 145, 153, 155 Arteries, 106, 107, 109, 112, 113, 116, 131, 132, 137, 146, 155 Arterioles, 107, 109, 111, 135, 137, 156 Arteriovenous, 107, 113, 135 Artery, 78, 106, 107, 116, 120, 131, 132, 136, 137, 148, 155 Aseptic, 66, 107 Asphyxia, 25, 29, 30, 107 Astrocytes, 14, 16, 17, 107, 134, 135 Asymptomatic, 107, 141 Ataxia, 46, 107, 128, 153 Atmospheric Pressure, 107, 128 Atrial, 70, 108, 116, 155 Atrioventricular, 108, 116 Atrium, 108, 116, 155, 157 Atrophy, 26, 108 Attenuated, 17, 18, 108, 119

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Attenuation, 17, 108 Autodigestion, 108, 141 Autoimmune disease, 108, 137 Autoradiography, 11, 21, 108 B Bacteria, 106, 108, 120, 121, 123, 135, 136, 147, 150, 151, 156 Bacterial Infections, 4, 108, 112 Bacterial Physiology, 103, 108 Bacterium, 108, 119, 127 Barbital, 71, 108 Barbiturate, 108, 153 Basal Ganglia, 107, 108, 110, 112, 124, 146, 147 Basal Ganglia Diseases, 107, 108 Base, 108, 118, 132, 153, 156 Benign, 108, 110, 124, 126, 147 Benzodiazepines, 72, 76, 108 Beta-Thromboglobulin, 109, 131 Bewilderment, 109, 115 Bile, 109, 133, 152 Biliary, 109, 141 Biliary Tract, 109, 141 Bilirubin, 104, 109 Biochemical, 11, 16, 20, 25, 35, 78, 109, 150 Biological therapy, 109, 126 Biological Transport, 109, 119 Biosynthesis, 107, 109, 117, 145, 150 Biotechnology, 22, 87, 109 Bladder, 73, 76, 109, 114, 129, 137, 156 Blood Coagulation, 109, 111, 154 Blood Flow Velocity, 25, 109 Blood Glucose, 4, 7, 109, 127, 130 Blood pressure, 5, 10, 72, 73, 109, 111, 128, 129, 136, 146, 150 Blood urea, 5, 109 Blood Viscosity, 8, 109 Blood Volume, 12, 33, 110, 156 Blood-Brain Barrier, 9, 12, 14, 15, 66, 71, 110 Blot, 11, 110 Body Fluids, 110, 123, 150 Bone Marrow, 44, 103, 110, 122, 124, 134, 136, 151 Brachytherapy, 110, 131, 147 Bradykinin, 110, 139, 142 Brain Hypoxia, 110, 153 Brain Infarction, 110, 131 Brain Injuries, 71, 110 Brain Ischemia, 13, 15, 47, 110, 113 Brain Neoplasms, 110, 128, 153 Brain Stem, 110, 112, 113

Bumetanide, 17, 110 Bypass, 110, 137, 154 C Calcium, 11, 36, 111, 114, 131, 134, 137 Capillary, 10, 15, 38, 66, 110, 111, 125, 146, 156, 157 Capillary Fragility, 66, 111 Capsules, 69, 111, 125 Carbohydrate, 8, 111, 116, 126, 143 Carbon Dioxide, 69, 111, 124, 128, 142, 146, 148, 157 Carcinogenic, 111, 152 Carcinoma, 30, 111 Cardiac, 52, 72, 73, 76, 78, 111, 116, 121, 122, 137, 152 Cardiac Glycosides, 52, 111 Cardiac Output, 111, 152 Cardiovascular, 74, 111, 122, 150 Cardiovascular disease, 74, 111 Cardiovascular System, 111, 122 Carnitine, 55, 111 Carotenoids, 67, 111 Case report, 5, 23, 37, 39, 42, 111, 112 Case series, 18, 112 Catheter, 19, 66, 77, 112 Cations, 112, 132 Caudal, 112, 129, 144 Cause of Death, 4, 72, 75, 112 Cell Death, 10, 17, 21, 67, 75, 112, 138 Cell Division, 11, 108, 112, 126, 142 Cell membrane, 70, 71, 109, 112, 118, 132 Cell motility, 112, 127 Cell Survival, 67, 112, 126 Central Nervous System Infections, 112, 126, 128 Cerebellar, 46, 107, 112, 148 Cerebellum, 110, 112, 113, 148 Cerebral Arteries, 112, 136 Cerebral Cortex, 107, 112 Cerebral hemispheres, 108, 110, 112, 113 Cerebral Hemorrhage, 14, 67, 112 Cerebral Infarction, 18, 24, 67, 69, 110, 113, 128 Cerebrospinal, 12, 24, 34, 46, 71, 75, 113, 128 Cerebrospinal fluid, 12, 24, 34, 46, 71, 75, 113, 128 Cerebrovascular, 7, 25, 68, 78, 108, 111, 113, 153 Cerebrovascular Disorders, 68, 113, 153 Cerebrum, 112, 113 Cervical, 113, 151

161

Chemokines, 16, 113 Chemotherapy, 44, 113 Chin, 58, 113, 135 Cholesterol, 109, 113, 116, 152 Chronic, 23, 25, 40, 48, 77, 110, 113, 118, 130, 133, 141, 143, 146, 147, 152, 153, 156 Circulatory system, 66, 104, 113 Cirrhosis, 52, 73, 113 Clinical trial, 5, 9, 20, 74, 87, 113, 147 Cloning, 109, 113 Clot Retraction, 114, 143 Collagen, 114, 123, 134, 143 Collapse, 114, 126 Colloidal, 104, 114 Complement, 114, 142 Complementary and alternative medicine, 61, 63, 114 Complementary medicine, 61, 114 Compliance, 8, 114 Computational Biology, 87, 114 Computed tomography, 23, 115 Computerized axial tomography, 115 Computerized tomography, 115 Concomitant, 7, 8, 24, 115 Confusion, 6, 115, 119, 156 Congestive heart failure, 72, 73, 76, 111, 115 Connective Tissue, 110, 114, 115, 124, 134, 153 Consciousness, 5, 6, 8, 69, 105, 115, 117, 127, 146, 147, 151 Constriction, 78, 115, 132, 146 Contraindications, ii, 115 Contralateral, 18, 115, 140, 148 Contrast medium, 105, 115 Contusions, 21, 50, 115 Conventional treatment, 19, 115 Convulsions, 108, 115, 120, 138 Convulsive, 26, 115 Coordination, 112, 115, 137 Cor, 54, 73, 76, 115 Cornea, 116, 152 Coronary, 72, 73, 76, 78, 111, 116, 128, 137 Coronary Arteriosclerosis, 116, 137 Coronary heart disease, 111, 116 Coronary Thrombosis, 116, 137 Coronary Vasospasm, 72, 73, 76, 116 Corpus, 116, 141, 144, 157 Corpus Luteum, 116, 144 Cortex, 21, 116, 136, 148 Cortical, 17, 116, 122, 138, 149, 153 Corticosteroid, 24, 116, 152

Cortisol, 104, 116 Cortisone, 116, 118 Cranial, 46, 112, 117, 126, 131, 141 Craniocerebral Trauma, 108, 113, 117, 126, 128, 153, 154 Craniotomy, 25, 55, 117 Curative, 117, 153 Cyclic, 104, 117, 126, 139, 145 Cystathionine beta-Synthase, 49, 117, 128 Cysteine, 113, 117 Cytokine, 10, 16, 21, 117, 131, 153 Cytoplasm, 112, 117, 134, 136, 137 Cytoskeletal Proteins, 117, 120 Cytostatic, 74, 117 Cytotoxic, 14, 25, 58, 71, 74, 117, 129, 147 D Deamination, 117, 156 Decompression, 46, 49, 117 Decompression Sickness, 117 Deferoxamine, 15, 117 Degenerative, 117, 127 Dehydration, 7, 8, 34, 39, 82, 117 Delirium, 117, 126 Demyelinating Diseases, 16, 118 Denaturation, 118, 143 Dendrites, 118, 138 Dendritic, 21, 118 Depolarization, 72, 118 Deprivation, 17, 118 Desensitization, 118, 129 Detoxification, 5, 118 Dexamethasone, 11, 62, 118 Diabetes Insipidus, 33, 118, 143 Diabetes Mellitus, 5, 6, 7, 118, 125, 127, 143 Diabetic Retinopathy, 74, 118 Diagnostic procedure, 65, 118 Dialyzer, 118, 126 Diastolic, 118, 128 Diffuse Axonal Injury, 110, 118 Diffusion, 11, 37, 109, 119, 130, 132, 139 Diffusivity, 67, 119 Digestion, 104, 109, 119, 133, 152 Dilation, 110, 119, 128 Dilution, 119, 122, 142 Direct, iii, 4, 14, 74, 119, 128, 148, 153 Disorientation, 5, 115, 117, 118, 119 Disposition, 82, 119 Distal, 12, 66, 72, 119, 146 Diuresis, 6, 71, 119 Diuretic, 19, 69, 110, 119, 134, 151 Dizziness, 5, 119, 157

162

Cerebral Edema

Dopamine, 119, 139 Dormancy, 74, 119 Dorsal, 119, 144 Drive, ii, vi, 11, 57, 119, 132 Drug Resistance, 74, 119 Drug Tolerance, 119 Dura mater, 120, 135, 140 Dystrophin, 18, 120 Dystrophy, 120 E Eclampsia, 29, 35, 109, 120 Efficacy, 5, 18, 19, 55, 120 Electrolyte, 6, 7, 8, 29, 116, 118, 120, 123, 136, 144, 150, 156 Electrons, 107, 108, 120, 132, 140, 147 Emboli, 69, 75, 120, 131 Embolism, 36, 120, 131, 146 Embolus, 120, 130, 131 Embryo, 120, 129, 156 Emollient, 120, 126 Emulsion, 108, 120 Encephalitis, 68, 120 Encephalitis, Viral, 120 Encephalopathy, 40, 45, 47, 121 Endogenous, 21, 119, 121, 122, 138 Endorphins, 121, 139 Endoscopy, 36, 121 Endostatin, 74, 121 Endothelial cell, 9, 14, 15, 16, 110, 121, 131, 154 Endothelium, 13, 16, 121, 139, 143 Endothelium, Lymphatic, 121 Endothelium, Vascular, 121 Endothelium-derived, 121, 139 Endotoxin, 121, 155 Enkephalins, 121, 139 Environmental Health, 86, 88, 121 Enzymatic, 11, 111, 114, 121, 123, 143, 149 Epidemiological, 37, 121 Epinephrine, 119, 121, 139 Epithelial, 13, 109, 122, 127 Epithelial Cells, 122, 127 Epithelium, 12, 121, 122 Erection, 122, 144 Erythrocyte Volume, 110, 122 Erythropoietin, 10, 122 Estrogen, 76, 122 Etomidate, 49, 122 Eukaryotic Cells, 117, 122, 129 Excipient, 70, 122 Excitability, 122, 138 Excitation, 122, 138

Excitatory, 13, 122, 125, 138 Excitatory Amino Acids, 13, 122, 138 Excitotoxicity, 20, 122 Exogenous, 121, 122, 155 Extensor, 122, 146 External-beam radiation, 122, 147 Extracellular, 12, 15, 17, 66, 105, 107, 115, 122, 123, 134, 135, 150 Extracellular Matrix, 115, 122, 123, 134 Extracellular Matrix Proteins, 122, 134 Extracellular Space, 15, 122, 123, 135 Extraction, 72, 123 Eye Infections, 103, 123 F Family Planning, 87, 123 Fat, 106, 107, 110, 115, 116, 120, 123, 132, 133, 137 Fatigue, 123, 126 Fatty acids, 104, 118, 123, 145 Femoral, 66, 123 Femur, 123 Fetus, 122, 123, 142, 155, 156 Fibrin, 109, 114, 123, 143, 154 Fibrinolytic, 123, 154 Fibrinolytic Agents, 123, 154 Fibroblasts, 123, 131 Flatus, 123, 124 Fluid Therapy, 7, 8, 123 Fluorescence, 14, 123 Fold, 12, 123 Foramen, 113, 123, 141 Forearm, 109, 123 Free Radicals, 71, 76, 107, 123, 137 Frontal Lobe, 106, 113, 124 Fulminant Hepatic Failure, 29, 30, 32, 34, 38, 46, 48, 124 G Galactosemia, 26, 35, 124 Gamma Rays, 124, 147 Ganglia, 103, 108, 124, 138, 141, 151 Ganglion, 124, 140, 151 Gas, 36, 105, 111, 117, 119, 123, 124, 128, 139, 146, 157 Gas exchange, 124, 157 Gastric, 108, 111, 124 Gastrin, 124, 127 Gastrointestinal, 4, 9, 110, 121, 124, 150, 152 Gastrointestinal Hemorrhage, 9, 124 Gastrointestinal tract, 124, 150 Gavage, 123, 124

163

Gene, 10, 13, 15, 36, 47, 74, 104, 109, 120, 124, 132, 139, 143 Gene Expression, 13, 15, 124 Gene Therapy, 74, 104, 124 Generator, 12, 124 Genetic testing, 125, 143 Genotype, 125, 142 Gestation, 125, 141, 142 Gland, 104, 116, 125, 134, 138, 141, 142, 149, 152, 154 Glioma, 47, 125 Glomerular, 5, 125, 131, 134, 148 Glomerular Filtration Rate, 5, 125, 134 Glomeruli, 125 Glomerulonephritis, 23, 125 Glomerulus, 125 Glucocorticoid, 118, 125 Glucose, 5, 6, 8, 9, 11, 17, 30, 109, 118, 124, 125, 126, 127, 130, 147, 149, 151 Glucose Intolerance, 118, 125 Glucuronic Acid, 125, 127 Glutamate, 11, 17, 58, 76, 122, 125, 135 Glutamic Acid, 125, 139 Glutamine, 24, 125 Glutathione Peroxidase, 15, 125 Glycerol, 37, 42, 47, 71, 107, 126 Glycine, 67, 126, 139, 150 Glycogen, 73, 76, 126 Glycolysis, 38, 126 Glycoprotein, 122, 126, 154, 155 Gonad, 126 Gonadal, 76, 126, 152 Governing Board, 126, 144 Grade, 40, 52, 126 Grafting, 49, 126 Growth factors, 11, 12, 21, 126, 136, 138 Guanylate Cyclase, 126, 139 H Headache, 5, 126, 128, 147 Headache Disorders, 126 Heart attack, 111, 126 Heart failure, 73, 126 Heartbeat, 126, 152 Heat Stroke, 68, 126 Hemiparesis, 110, 126, 147 Hemodialysis, 5, 25, 26, 29, 118, 126, 133 Hemodynamics, 20, 127 Hemoglobin, 14, 105, 127 Hemoglobinopathies, 124, 127 Hemolytic, 50, 127 Hemorrhage, 12, 14, 15, 39, 40, 45, 49, 75, 115, 117, 118, 126, 127, 137, 147, 152

Heparin, 9, 127, 143 Hepatic, 4, 5, 16, 23, 28, 30, 33, 40, 55, 73, 77, 104, 118, 127, 133 Hepatic Encephalopathy, 4, 23, 30, 127 Hepatitis, 26, 124, 127, 157 Hepatocyte, 4, 47, 127 Hepatocyte Growth Factor, 47, 127 Heredity, 124, 127 Hernia, 68, 127 Histology, 14, 23, 127 Homeostasis, 10, 17, 72, 127 Homodimer, 21, 127 Homologous, 124, 127, 153 Hormonal, 108, 116, 127 Hormone, 43, 73, 76, 116, 121, 122, 124, 127, 130, 132, 144, 153, 154 Hydrocephalus, 42, 71, 128, 131 Hydrogen, 103, 108, 111, 118, 122, 125, 128, 133, 136, 139, 140, 145, 152 Hydrogen Peroxide, 125, 128, 133, 152 Hydrogenation, 108, 128 Hydrolysis, 128, 132, 143, 145 Hyperbaric, 42, 62, 128 Hyperbaric oxygen, 42, 62, 128 Hypercapnia, 35, 128 Hyperglycemia, 4, 7, 8, 9, 47, 52, 128 Hyperhomocysteinemia, 117, 128 Hypertension, 19, 25, 31, 72, 73, 76, 111, 112, 128, 131, 144, 147, 156 Hyperthermia, 13, 128 Hypertrophy, 116, 128, 155 Hyperventilation, 19, 69, 128 Hypnotic, 108, 122, 128, 153 Hypoglycemia, 4, 7, 8, 16, 129 Hypotension, 5, 42, 115, 129 Hypotensive, 5, 129 Hypothalamus, 110, 129, 142 Hypothermia, 13, 19, 42, 129 Hypoxemia, 7, 50, 129 Hypoxia, 9, 10, 11, 12, 15, 16, 50, 52, 67, 75, 113, 118, 129 Hypoxic, 10, 11, 50, 69, 129 I Immune response, 20, 106, 108, 116, 129, 152, 155, 157 Immune system, 4, 109, 129, 134, 137, 156, 157 Immunosuppression, 50, 129, 134 Immunosuppressive, 125, 129, 153 Immunosuppressive Agents, 129 Impairment, 14, 20, 107, 109, 113, 118, 123, 129

164

Cerebral Edema

Implant radiation, 129, 131, 147 In situ, 10, 11, 129 In Situ Hybridization, 11, 129 In vitro, 13, 15, 16, 17, 19, 109, 124, 129, 143, 153, 154 In vivo, 10, 13, 15, 16, 18, 20, 124, 127, 129, 134, 135, 153 Incision, 129, 131 Incontinence, 128, 129 Induction, 51, 73, 76, 105, 122, 129 Infarction, 15, 75, 113, 130, 148 Infection, 7, 8, 47, 75, 107, 109, 118, 120, 123, 130, 134, 152, 157 Infiltration, 13, 125, 130 Inflammation, 13, 16, 104, 107, 120, 123, 127, 130, 135, 140, 141, 143, 152, 153, 156 Infusion, 45, 49, 55, 78, 130, 137 Ingestion, 4, 130, 137, 143 Inhalation, 130, 143 Innervation, 130, 140 Inositol, 130, 135 Insight, 13, 130 Insomnia, 66, 130 Insulator, 130, 137 Insulin, 5, 7, 8, 27, 82, 118, 130, 132, 155 Insulin-dependent diabetes mellitus, 5, 27, 130 Intensive Care, 4, 20, 23, 35, 130 Interleukin-1, 13, 130 Interleukin-2, 131 Interleukin-8, 70, 131 Intermittent, 123, 131, 141 Internal radiation, 131, 147 Interstitial, 66, 71, 110, 123, 131, 148 Intestines, 103, 124, 131 Intoxication, 118, 131, 158 Intracellular, 11, 13, 17, 130, 131, 135, 139, 144, 145 Intracranial Aneurysm, 39, 112, 131 Intracranial Arteriosclerosis, 112, 131 Intracranial Embolism, 113, 131 Intracranial Embolism and Thrombosis, 113, 131 Intracranial Hemorrhages, 128, 131, 153 Intracranial Hypertension, 26, 43, 45, 55, 126, 128, 131, 154 Intracranial tumors, 28, 131 Intramuscular, 131, 141 Intravenous, 7, 37, 66, 69, 130, 131, 141 Intrinsic, 78, 104, 107, 131 Inulin, 125, 131 Invasive, 11, 19, 131, 134

Iodine, 30, 132 Iodine-131, 30, 132 Ion Channels, 32, 107, 132 Ion Transport, 9, 132, 136 Ionization, 132 Ionizing, 19, 105, 132, 147 Ions, 71, 108, 120, 128, 132, 136 Ischemic stroke, 18, 21, 55, 69, 75, 132 Isopropyl, 68, 132 K Kb, 86, 132 Keratinocytes, 131, 132 Ketoacidosis, 4, 5, 7, 8, 24, 29, 30, 31, 32, 33, 34, 36, 37, 38, 39, 42, 43, 44, 45, 46, 48, 49, 50, 51, 81, 118, 132, 133 Ketone Bodies, 118, 132, 133 Ketosis, 118, 132, 133 Kidney Disease, 6, 47, 86, 133 Kidney Failure, 133, 134 Kinetic, 132, 133 L Lens, 107, 133 Lesion, 58, 66, 133 Lethal, 23, 24, 133 Lethargy, 128, 133 Leukemia, 124, 133 Ligaments, 116, 133 Linkages, 127, 133 Lipid, 44, 68, 75, 126, 130, 133, 137, 140 Lipid Peroxidation, 68, 133, 140 Liver Cirrhosis, 72, 73, 76, 133 Liver Transplantation, 4, 27, 32, 52, 133 Lobe, 106, 113, 133 Localization, 18, 22, 133 Localized, 9, 44, 110, 120, 130, 133, 142 Loop, 127, 133 Lupus, 133, 153 Lymph, 113, 121, 133, 134, 138 Lymph node, 113, 134, 138 Lymphatic, 121, 130, 133, 134, 143, 151 Lymphoblastic, 134 Lymphoblasts, 103, 134 Lymphocyte Depletion, 129, 134 Lymphocytes, 106, 130, 131, 134, 153, 157 Lymphoid, 106, 134 M Macroglia, 134, 135 Macrophage, 130, 134 Magnetic Resonance Imaging, 12, 18, 19, 21, 37, 41, 58, 134 Malignant, 8, 18, 25, 45, 47, 54, 55, 107, 110, 134, 147

165

Malnutrition, 104, 108, 134 Manifest, 58, 134 Mannitol, 18, 27, 52, 134 Maple Syrup Urine Disease, 29, 31, 134 Matrix metalloproteinase, 14, 16, 134 Mediate, 9, 13, 119, 135 Medicament, 67, 78, 135 MEDLINE, 87, 135 Membrane, 9, 30, 72, 73, 107, 112, 114, 118, 120, 122, 132, 135, 140, 148, 151, 155 Memory, 77, 105, 118, 135 Meninges, 112, 117, 120, 135 Meningioma, 28, 46, 135 Meningitis, 35, 63, 71, 135 Menstrual Cycle, 135, 144 Mental, iv, 5, 6, 9, 86, 88, 112, 113, 115, 117, 119, 123, 135, 138, 146, 149, 156 Mental Health, iv, 9, 86, 88, 135, 146 Metabolic acidosis, 8, 118, 135 Metabolic disorder, 4, 118, 135 Metabolite, 75, 135 Metabotropic, 58, 135 Metastasis, 70, 134, 135 Metastatic, 30, 110, 135 Microbe, 135, 154 Microbiology, 103, 135 Microcirculation, 77, 133, 135, 143 Microdialysis, 77, 135 Microglia, 13, 14, 76, 107, 135 Microorganism, 136, 157 Microscopy, 10, 11, 14, 21, 136 Middle Cerebral Artery, 18, 47, 136 Middle Cerebral Artery Infarction, 47, 136 Migration, 13, 136 Mineralocorticoids, 104, 116, 136 Mitochondrial Swelling, 136, 138 Molecular, 11, 12, 13, 15, 21, 66, 87, 89, 109, 115, 127, 136, 143, 151, 152, 155 Molecular Structure, 136, 155 Molecule, 106, 108, 114, 121, 122, 127, 128, 136, 140, 143, 147, 155, 156 Monitor, 48, 136, 139 Monoclonal, 17, 136, 147 Monoclonal antibodies, 17, 136 Monocytes, 130, 131, 136, 153 Mononuclear, 47, 136, 155 Morphological, 20, 34, 120, 137 Motion Sickness, 137, 138 Multiple sclerosis, 75, 137 Muscle Contraction, 120, 137 Mushroom Poisoning, 4, 137 Myelin, 118, 137

Myocardial infarction, 7, 8, 109, 116, 137 Myocardial Ischemia, 18, 137 Myocardial Reperfusion, 137, 148 Myocardial Reperfusion Injury, 137, 148 Myocardium, 137 Myofibrils, 120, 137 Myopathy, 47, 137 N N-acetyl, 78, 137 Nasogastric, 6, 137 Nausea, 5, 133, 138, 146, 156 Necrosis, 33, 66, 77, 110, 113, 130, 137, 138, 148 Neonatal, 24, 138 Nephrectomy, 25, 138 Nephropathy, 25, 133, 138 Nervous System, 8, 17, 20, 73, 75, 76, 103, 108, 110, 112, 113, 124, 125, 136, 137, 138, 141, 150 Nervousness, 5, 138 Neural, 15, 21, 105, 136, 138 Neurites, 67, 138 Neurobehavioral Manifestations, 110, 119, 138 Neurologic, 5, 45, 110, 128, 138, 155 Neuromuscular, 103, 138, 140, 156 Neuromuscular Junction, 103, 138, 140 Neuronal, 13, 14, 20, 67, 68, 72, 76, 138 Neurons, 15, 17, 67, 118, 122, 124, 138, 153 Neuropeptides, 12, 138 Neurophysiology, 38, 67, 118, 138 Neuroprotective Agents, 76, 138 Neurotoxicity, 11, 37, 138 Neurotransmitter, 76, 103, 110, 119, 122, 125, 126, 132, 138, 139, 152 Neutrons, 105, 139, 147 Neutrophil, 13, 139 Neutrophil Infiltration, 13, 139 Nitric Oxide, 11, 13, 14, 15, 16, 139 Nitrogen, 5, 14, 105, 117, 122, 125, 139 Norepinephrine, 119, 139 Nuclear, 10, 30, 48, 108, 120, 122, 124, 138, 139 Nuclei, 105, 106, 120, 124, 134, 139, 145 Nucleic acid, 129, 139, 146, 147 Nucleus, 106, 108, 117, 122, 124, 134, 136, 139, 145, 147, 152, 153 O Ocular, 139, 140 Oliguria, 133, 134, 139 Oncogene, 127, 139 Oncology, 29, 54, 139

166

Cerebral Edema

Oncology nurse, 54, 139 Ophthalmoplegia, 27, 140 Optic Chiasm, 129, 136, 140 Optic Disk, 118, 140 Osmolality, 7, 18, 73, 140 Osmolarity, 5, 19, 134, 140 Osmoles, 140 Osmosis, 140 Osmotic, 6, 18, 19, 43, 50, 71, 104, 136, 140 Osteonecrosis, 77, 140 Osteoporosis, 66, 140 Otitis, 8, 140 Overdose, 3, 4, 30, 45, 46, 124, 140 Overexpress, 15, 140 Ovum, 116, 125, 140, 144 Oxidation, 103, 107, 118, 125, 133, 140 Oxidative Stress, 15, 20, 140 Oxygenation, 117, 129, 140 P Pachymeningitis, 135, 140 Palliative, 141, 153 Pancreas, 103, 130, 141 Pancreatic, 111, 141 Pancreatitis, 7, 141 Parenteral, 69, 141 Pathologic, 6, 16, 37, 68, 75, 103, 116, 141, 146, 148 Pathophysiology, 12, 40, 41, 43, 48, 81, 141 Patient Education, 7, 96, 98, 101, 141 Penis, 141, 144 Peptide, 70, 73, 74, 76, 141, 143, 145 Perfusion, 7, 20, 34, 72, 129, 141 Pericardium, 141, 153 Perinatal, 11, 25, 29, 141 Peripheral Nervous System, 118, 121, 138, 141, 152 Peritoneal, 30, 66, 141 Peritoneal Cavity, 66, 141 Peritoneal Dialysis, 30, 141 Peritoneum, 141, 142 Perivascular, 18, 136, 142 Phagocytosis, 136, 142 Pharmacologic, 105, 142, 155 Phenotype, 16, 142 Phosphates, 72, 142 Phosphorus, 111, 142 Physical Examination, 7, 8, 142 Physiologic, 16, 104, 109, 131, 135, 142, 145, 147, 148 Physiology, 9, 16, 43, 50, 138, 142 Pilot study, 17, 142 Pituitary Gland, 73, 76, 116, 142, 149

Placenta, 142, 144, 155, 156 Plants, 111, 125, 131, 139, 142, 149, 155 Plaque, 75, 142 Plasma, 12, 18, 73, 104, 106, 109, 110, 112, 120, 121, 125, 127, 133, 136, 142 Plasma cells, 106, 142 Plasma protein, 104, 121, 142 Plasma Volume, 12, 110, 136, 142 Plasmin, 71, 123, 143, 154 Plasminogen Activators, 143 Plasticity, 10, 143 Platelet Aggregation, 73, 76, 139, 143 Platelet Factor 4, 131, 143 Platelets, 109, 139, 143, 150 Plethysmography, 11, 143 Plexus, 12, 143 Pneumonia, 115, 143 Poisoning, 71, 75, 118, 131, 137, 138, 143 Polydipsia, 23, 143 Polymerase, 13, 143 Polymerase Chain Reaction, 13, 143 Polypeptide, 67, 105, 114, 143, 145, 158 Polysaccharide, 70, 106, 143 Polyuria, 8, 143 Posterior, 53, 73, 76, 107, 112, 119, 141, 144 Postmenopausal, 140, 144 Postnatal, 11, 144, 151 Post-traumatic, 19, 52, 55, 110, 126, 144 Potassium, 5, 7, 8, 72, 136, 144 Potentiates, 130, 144 Practice Guidelines, 88, 144 Precipitating Factors, 7, 8, 126, 144 Precursor, 107, 119, 121, 139, 144 Pre-eclamptic, 120, 144 Presynaptic, 138, 144 Prevalence, 12, 144 Priapism, 27, 144 Probe, 135, 144 Progesterone, 20, 76, 144, 152 Prognostic factor, 4, 144 Progression, 69, 106, 144 Progressive, 46, 49, 113, 119, 138, 145, 148 Prone, 58, 145 Prostaglandin, 16, 145 Prostaglandins A, 145 Protease, 74, 145, 154 Protease Inhibitors, 74, 145 Protein C, 18, 104, 105, 145, 151, 156 Protein Conformation, 105, 145 Protein S, 109, 145 Proteolytic, 71, 114, 143, 145, 154 Protons, 105, 128, 132, 145, 147

167

Proximal, 6, 66, 119, 144, 146 Pseudotumor Cerebri, 131, 146 Psoriasis, 74, 146 Psychiatry, 146, 157 Psychic, 135, 146, 149 Psychoactive, 146, 158 Psychogenic, 23, 146 Public Health, 12, 88, 146 Public Policy, 87, 146 Publishing, 5, 22, 146 Pulmonary, 8, 12, 24, 26, 42, 109, 116, 128, 133, 146, 157 Pulmonary Artery, 109, 146, 157 Pulmonary Edema, 24, 42, 133, 146 Pulmonary Embolism, 8, 146 Pulmonary Gas Exchange, 12, 146 Pulmonary hypertension, 116, 146 Pulmonary Ventilation, 128, 146 Purifying, 78, 146 Purines, 146, 150 Putamen, 106, 108, 146, 147 Putaminal Hemorrhage, 25, 147 Pyridoxal, 117, 147 Pyridoxal Phosphate, 117, 147 Pyrimidines, 147, 150 R Race, 136, 147 Radiation, 19, 43, 108, 122, 123, 124, 128, 129, 131, 132, 147, 151, 158 Radiation therapy, 43, 122, 128, 131, 147, 151 Radioactive, 108, 128, 129, 131, 132, 136, 139, 147 Radiolabeled, 147 Radiopharmaceutical, 125, 147 Radiotherapy, 110, 147, 151 Randomized, 5, 120, 147 Reabsorption, 76, 147 Reactive Oxygen Species, 13, 16, 147 Receptor, 69, 70, 72, 73, 74, 76, 103, 106, 119, 127, 135, 147, 150 Recombinant, 21, 148, 156 Recombination, 124, 148 Recovery of Function, 20, 148 Rectum, 123, 124, 129, 148 Red blood cells, 127, 148, 149 Red Nucleus, 107, 148 Refer, 1, 114, 119, 121, 133, 138, 139, 148 Refraction, 148, 151 Refractory, 19, 35, 49, 148 Regeneration, 4, 148 Regimen, 61, 120, 148

Renal failure, 5, 25, 52, 72, 73, 76, 118, 148, 156 Reperfusion, 10, 14, 15, 69, 70, 71, 137, 148 Reperfusion Injury, 10, 69, 70, 71, 148 Resorption, 128, 147, 148 Respiration, 111, 136, 148 Respiratory distress syndrome, 7, 8, 9, 20, 148 Respiratory Physiology, 148, 157 Retina, 118, 133, 140, 148, 149 Retinal, 118, 140, 149 Retroviral vector, 124, 149 Reverberant, 119, 149 S Saline, 18, 42, 45, 55, 149 Saponins, 149, 152 Schizoid, 149, 158 Schizophrenia, 149, 158 Schizotypal Personality Disorder, 149, 158 Sclerosis, 131, 137, 149 Screening, 113, 149 Secretion, 73, 116, 130, 136, 149 Secretory, 13, 28, 149 Sedative, 108, 149 Seizures, 5, 26, 118, 149, 151 Sella, 142, 149 Sella Turcica, 142, 149 Semisynthetic, 111, 149 Senile, 140, 150 Sepsis, 4, 135, 150 Septic, 4, 107, 150 Sequencing, 143, 150 Serine, 67, 117, 150, 154 Serotonin, 139, 150 Serous, 121, 150 Serum, 7, 18, 71, 104, 114, 134, 136, 150, 155 Sex Characteristics, 105, 150, 153 Shock, 4, 39, 150, 155 Side effect, 18, 19, 66, 68, 74, 104, 109, 150, 154 Signs and Symptoms, 5, 6, 82, 150, 156 Skeleton, 123, 145, 150 Skull, 68, 117, 150, 151, 153 Small intestine, 128, 131, 137, 150, 157 Smooth muscle, 73, 76, 150, 151, 152 Social Behavior, 77, 150 Sodium, 30, 69, 72, 136, 147, 150 Solid tumor, 106, 121, 151 Solvent, 126, 140, 151 Sorbitol, 134, 151 Spasm, 115, 116, 151

168

Cerebral Edema

Spatial disorientation, 119, 151 Specialist, 4, 93, 119, 151 Species, 14, 105, 111, 121, 136, 147, 150, 151, 152, 155, 157, 158 Spectrin, 120, 151 Spectroscopic, 11, 151 Spectrum, 20, 136, 151 Spinal cord, 75, 107, 110, 112, 113, 120, 124, 135, 138, 140, 141, 144, 151 Spinal Cord Injuries, 75, 151 Status Epilepticus, 49, 151 Stellate, 54, 151 Stellate Ganglion, 54, 151 Stem Cells, 122, 151 Stereotactic, 43, 151 Stereotactic radiosurgery, 43, 151 Sterile, 69, 107, 152 Steroid, 51, 66, 71, 76, 111, 116, 149, 152 Steroid therapy, 51, 71, 152 Stimulus, 119, 122, 130, 131, 132, 152, 154 Stomach, 103, 108, 124, 127, 131, 133, 137, 138, 141, 150, 152 Strand, 143, 152 Stress, 10, 15, 16, 21, 73, 76, 111, 116, 138, 140, 152 Stroke Volume, 16, 111, 152 Stroma, 14, 152 Subacute, 130, 152 Subarachnoid, 12, 39, 40, 49, 75, 126, 131, 152 Subclinical, 130, 149, 152 Subcutaneous, 141, 152 Subspecies, 151, 152 Substance P, 135, 149, 152 Sudden death, 33, 152 Superoxide, 14, 15, 152 Superoxide Dismutase, 15, 152 Suppression, 116, 152 Symptomatic, 141, 153 Synapse, 21, 138, 144, 153, 155 Synaptic, 138, 153 Systemic, 4, 10, 18, 40, 43, 51, 66, 74, 109, 110, 118, 121, 127, 130, 131, 147, 153, 155, 156 Systemic lupus erythematosus, 40, 153 Systolic, 128, 153 T Tacrolimus, 50, 153 Temporal, 15, 21, 126, 153 Testosterone, 76, 153 Thalamic, 107, 153 Thalamic Diseases, 107, 153

Thalidomide, 74, 153 Therapeutics, 3, 24, 73, 153 Thermal, 139, 143, 153 Thigh, 123, 153 Thoracic, 134, 151, 153, 157 Threonine, 150, 153 Threshold, 6, 122, 128, 153 Thrombin, 123, 143, 145, 154 Thrombolytic, 14, 154 Thrombolytic Therapy, 14, 154 Thrombomodulin, 145, 154 Thrombosis, 8, 24, 72, 73, 76, 109, 131, 145, 152, 154 Thyroid, 30, 132, 154 Thyroxine, 104, 154 Tidal Volume, 128, 154 Tinnitus, 140, 146, 154 Tissue Culture, 138, 154 Tissue Plasminogen Activator, 72, 154 Tomography, 23, 35, 154 Tone, 154, 156 Tooth Preparation, 103, 154 Torsion, 130, 154 Toxic, iv, 4, 13, 39, 111, 137, 154, 155 Toxicity, 49, 154 Toxicology, 30, 88, 155 Toxins, 4, 5, 106, 120, 125, 130, 136, 155 Trachea, 154, 155 Transcriptase, 13, 155 Transfection, 109, 124, 155 Transient Ischemic Attacks, 69, 155 Translational, 18, 155 Transmitter, 103, 107, 119, 122, 132, 139, 155 Transplantation, 4, 5, 27, 32, 44, 45, 134, 155 Triad, 7, 155 Tricuspid Atresia, 116, 155 Tricyclic, 72, 73, 155 Tumor Necrosis Factor, 13, 153, 155 Tumor-derived, 74, 155 Type 2 diabetes, 7, 155 Typhoid fever, 23, 54, 155 U Umbilical Arteries, 155, 156 Umbilical Cord, 25, 155, 156 Uraemia, 141, 156 Urea, 26, 109, 156 Uremia, 5, 133, 148, 156 Ureters, 156 Urethra, 141, 156 Urinary, 8, 128, 129, 139, 143, 154, 156

169

Urinary tract, 8, 156 Urinary tract infection, 8, 156 Urine, 7, 71, 106, 109, 118, 119, 129, 132, 134, 139, 143, 156 Uterus, 113, 116, 144, 156 V Vaccine, 155, 156 Vascular endothelial growth factor, 11, 21, 35, 156 Vascular Resistance, 72, 73, 76, 156 Vasculitis, 113, 141, 156 Vasoactive, 20, 156 Vasodilatation, 72, 156 Vasodilators, 139, 156 Vasogenic, 10, 12, 15, 23, 35, 71, 156 Vector, 74, 156 Vein, 107, 131, 139, 156 Venous, 107, 109, 110, 113, 131, 145, 155, 156, 157 Venous blood, 110, 113, 157 Ventilation, 10, 12, 122, 157 Ventricle, 108, 116, 129, 146, 153, 155, 157 Ventricular, 42, 116, 128, 137, 155, 157 Ventriculostomy, 19, 157 Venules, 109, 111, 121, 135, 157 Vertebrae, 151, 157

Vertigo, 140, 157 Veterinary Medicine, 87, 157 Villi, 128, 157 Viral, 3, 4, 120, 157 Viral Hepatitis, 3, 4, 157 Virulence, 108, 154, 157 Virus, 112, 119, 142, 149, 157 Viscosity, 109, 157 Vitreous, 118, 133, 149, 157 Vitro, 127, 157 Vivo, 19, 20, 134, 157 W White blood cell, 103, 106, 134, 139, 142, 157 Windpipe, 154, 157 Withdrawal, 8, 18, 118, 158 Wound Healing, 134, 158 Wounds, Gunshot, 151, 158 X Xenograft, 106, 158 X-ray, 115, 123, 124, 139, 147, 151, 158 Y Yeasts, 142, 158 Z Zymogen, 145, 158

170

Cerebral Edema

171

172

Cerebral Edema