45 Results for : infarct

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    The electrocardiogram (ECG) remains the most accessible and inexpensive diagnostic tool to evaluate the patient presenting with symptoms suggestive of acute myocardial ischemia. It plays a crucial role in decision making about the aggressiveness of therapy especially in relation to reperfusion therapy, because such therapy has resulted in a considerable reduction in mortality from acute myocardial infarction. Several factors play a role in the amount of myocardial tissue that can be salvaged by reperfusion therapy, such as the time interval between onset of coronary occlusion and reperfusion, site and size of the jeopardized area, type of reperfusion attempt (thrombolytic agent or an intracoronary catheter intervention), presence or absence of risk factors for thrombolytic agents, etc. Most important in decision making on reperfusion therapy and the type of intervention is to look for markers indicating a higher mortality rate from myocardial infarction. The ECG is a reliable, inexpensive, non-invasive instrument to obtain that information. Recently it has become clear that both in anterior and inferior myocardial infarction, the ECG frequently allows not only to identify the infarct related coronary artery, but also the site of occlusion in that artery and therefore the size of the jeopardized area. Obviously, the more proximal the occlusion, the larger the area at risk and the more aggressive the reperfusion attempt.
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    Ischemic Preconditioning: The Concept of Endogenous Cardioprotection consolidates, in one volume, both current knowledge and the most recent advances in ischemic preconditioning. The editors have invited investigators at the forefront of ongoing research to provide their scholarly and candid comments concerning each of these issues. This volume includes a comprehensive review of infarct size reduction with ischemic preconditioning, and the most recent data on the effects of preconditioning on ischemia and reperfusion-induced arrhythmias, myocardial metabolism, contractile function, and the coronary vasculature. The role of altered energy metabolism, stress-induced proteins, ATP-sensitive potassium channels, and adenosine -- the major hypotheses that have been proposed to explain the cardioprotective effects of ischemic preconditioning -- are critically reviewed by investigators who have been instrumental in developing these concepts. In addition, the editors raise the intriguing possibility that ischemic preconditioning may be more than simply a laboratory curiosity. Using a multidisciplinary approach, this volume challenges the readers to contribute their own expertise to address the unanswered questions concerning this endogenous, cardioprotective phenomenon.
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    Are there universal laws governing the persistence of weather, and is it possible to predict climate transitions as generated by natural or man-made perturbations? How can one quantify the roller-coaster dynamics of stock markets and anticipate mega-crashes? Can we diagnose the health condition of patients from heartbeat time-series analysis, which may even form the basis for infarct prevention? This book tackles these questions by applying advanced methods from statistical physics and related fields to all types of non-linear dynamics prone to disaster. The transdisciplinary analysis is organized in some dozen review articles written by world-class scientists.
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    Cell death is fast becoming one of the most dynamic areas of biological research-involving as it does the study of apoptosis and programmed cell death and the role these phenomena play in development and homeostasis on the one hand, and aging and disease on the other. The profound implications for medicine and agriculture from the manipulation of these processes have spawned a deluge of research papers, articles, approaches, and methods-making it difficult for scientists to get an overview of the field. When Cells Die II: A Comprehensive Evaluation of Apoptosis and Programmed Cell Death offers the most thorough, cutting-edge coverage of this field since publication of the acclaimed first edition. Leading international researchers present an up-to-date yet accessible survey ranging from the history of cell death science to its modern methodology. Extensively revised to include major advances in research, this new edition features relevant discussion of: * The impact of genomics and proteomics * Gene therapy and pharmacogenetics * The role of mitochondria * Caspase-independent and non-apoptotic cell death * Evolution of mechanisms With the manipulation of programmed cell death in clinical situations now in the foreseeable future, When Cells Die II also addresses the role of apoptosis in specific organ systems-the immune system, nervous system, and gastrointestinal tract-as well as different disease states, including viral infection, cancer, and myocardial infarct. Expertly edited to provide detailed cross-referencing, consistency of style, and a logical progression of topics, When Cells Die II is the definitive resource for understanding current cell death science. It will prove an invaluable text for advanced undergraduate, graduate, and medical students, postdoctoral fellows, scientists, and clinicians in cell biology, immunology, developmental biology, neuroscience, and cancer research.
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    Diffusion-weighted MR imaging is widely accepted as a means to identify stroke, thus enabling rapid and effective treatment. Over the past four years, these expert authors have presented over 30 exhibits and scientific reports on diffusion-weighted imaging at the RSNA and the American Society of Neuroradiology (ASNR), and more than 10 of these presentations have been recognized by specific awards. Diffusion-Weighted MR Imaging of the Brain's chapters range from basic principles to interpretation of diffusion-weighted MR imaging and specific disease. This is a valuable reference for radiologists, neurologists, neurosurgeons as well as residents, fellows, radiology technologists. TOC:Principles of diffusion-weighted imaging.- Normal brain and artifacts.- Brain edema: Classification. Cytotoxic edema. Edema of neuron and glial cell. Intramyelinic edema. Axonal edema. Vasogenic edema.- Infarction: Arterial infarction. Venous infarction.- Dementia: Alzheimer's. Multi-infarct dementia. Other dementias. HIV dementia.- Hemorrhage.- Vasculitis/Vasculopathy: Behcet. Systemic lupus erythematosus. Posterior reversal encephalopathy syndrome. Drug induced.- Epilepsy: Postictal encephalopathy. Status epilepticus.- Demyelinating and degenerative diseases: ADEM. Multiple sclerosis. Creutzfeldt-Jakob disease.- Toxic and metabolic diseases: Drug-induced encephalopathy. Mitochondrial encephalopathy. Phenylketonuria. Osmotic myelinolysis. Marchiafava-Bignami disease.- Infectious diseases: Brain abscess. Extra-axial abscess. Encephalitis. Septic emboli.- Trauma: Diffuse axonal injury. Brain contusion.- Brain neoplasm: Epidermoid. Meningioma. Lymphoma. GBM. Metastasis. PNET.- Pediatrics.
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