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Titlebook: Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma; Alexander Baethmann,Oliver S. Kempski,Frank Staub Conference proceed

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书目名称Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma
编辑Alexander Baethmann,Oliver S. Kempski,Frank Staub
视频video
丛书名称Acta Neurochirurgica Supplement
图书封面Titlebook: Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma;  Alexander Baethmann,Oliver S. Kempski,Frank Staub Conference proceed
描述The publication of the Vth International Symposium 1995 on "Mechanisms of Secondary Brain Damage" in Mauls/ltaly is a collection of focused reviews reaching from novel molecular- and cell biological findings to aspects of clinical management in head injury and cerebral ischemia. A specific purpose of these series of meetings introduced in 1984 is for an exchange on problems of mutual interest by international high ranking experts from the basic sciences and related clinical disciplines, such as intensive care medicine, neurology, or neurosurgery. The present volume covers three major areas: (a) Molecular and cell biological mechanisms including inflammation (b) Novel findings on mechanisms and treatment in cerebral ischemia (c) Secondary processes in head injury, regeneration and treatment Molecular-and cell biology is currently attracting attention towards activation of genomic processes associated with the demise of cells referred to as "programmed cell death" and "apoptosis" which, actually, might be distinguished from each other. Thus, the phenomenon of delayed neuronal death in selectively vulnerable brain areas following brief interruption of blood flow is scrutinized as to t
出版日期Conference proceedings 1996
关键词Alzheimer; Trauma; intensive care medicine; neurology; neurosurgery
版次1
doihttps://doi.org/10.1007/978-3-7091-9465-2
isbn_softcover978-3-7091-9467-6
isbn_ebook978-3-7091-9465-2Series ISSN 0065-1419 Series E-ISSN 2197-8395
issn_series 0065-1419
copyrightSpringer-Verlag/Wien 1996
The information of publication is updating

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Significance of the Inflammatory Response in Brain Ischemiaat leukocytes accumulate in focal zones of acute brain ischemia at a sufficiently early stage to participate in the process of progressive ischemic brain damage and that partial inhibition of that accumulation, by various measures, can attenuate ischemic brain injury. Mechanisms of leukocyte adhesio
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Three-Dimensional Metabolic and Hemodynamic Imaging of the Normal and Ischemic Rat Brainlopment of powerful image-processing techniques permitting three-dimensional (3D) autoradiographic image-averaging and analysis of replicate studies by a novel method termed “disparity analysis”. This method, based upon a linear affine transformation model, directly estimates scaling, translation an
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Origins of Glutamate Release in Ischaemiashown that the increase in extracellular glutamate under global penumbral conditions is minor. However, in the border of the ischaemic core, recurrent spreading depression is presumably associated with transient vesicular release of glutamate (exocytosis). With ischaemic insults severe enough to pro
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Swelling, Intracellular Acidosis, and Damage of Glial Cellsrobic glycolysis. Resulting metabolites, such as arachidonic- and lactic acid, can be expected to leak into perifocal brain areas, contributing there to cytotoxic swelling and damage of neurons and glia. Since elucidation of mechanisms underlying cell swelling and damage in the brain is difficult .,
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