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Titlebook: Mechanisms of Cerebral Hypoxia and Stroke; George Somjen Book 1988 Plenum Press, New York 1988 brain.cell.cell death.cortex.oxygen.paper.p

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书目名称Mechanisms of Cerebral Hypoxia and Stroke
编辑George Somjen
视频video
丛书名称Advances in Behavioral Biology
图书封面Titlebook: Mechanisms of Cerebral Hypoxia and Stroke;  George Somjen Book 1988 Plenum Press, New York 1988 brain.cell.cell death.cortex.oxygen.paper.p
描述The articles and short communications in this volume are based on papers pre­ sented to the Symposium on Cerebral Hypoxia and Stroke held in Budapest in August of 1987. Besides participants at the meeting, three scientists who were invited but could not attend have also contributed chapters to this volume. A synopsis of the general discussion at the conference and a review chapter conclude this volume. To the readers of this book it will not be news that stroke is a worldwide problem. Efforts to cope with this often devastating condition are worldwide also, as attested by the international membership of the conference. It has been said of oxygen deficiency that it not only stops the machine, it also wrecks the machinery. The paramount question in stroke research is this: why can‘t the brain be restarted after a hypoxic episode in much the same manner as a motor car can when its gas tank is refilled after it stalled because it ran out of fuel? Participants at the Symposium had been requested in advance of the meeting to especially consider a series of specific questions in relation to this general problem. Among these specific questions were: the mechanism of synaptic blockade in hy
出版日期Book 1988
关键词brain; cell; cell death; cortex; oxygen; paper; physiology; receptor; tissue
版次1
doihttps://doi.org/10.1007/978-1-4684-5562-5
isbn_softcover978-1-4684-5564-9
isbn_ebook978-1-4684-5562-5Series ISSN 0099-6246
issn_series 0099-6246
copyrightPlenum Press, New York 1988
The information of publication is updating

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Early and Late Neuronal Damage Following Cerebral Ischemiaect to neuronal death and “sclerosis” following only a brief period of ischemia of merely a few minutes. However, neurophysiologists have long been using the hippocampal slice method for their experiments. They know that their in vitro slice preparation of the hippocampus obtained mainly from rodent
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Possible Implications of Ischemic Damage to Dentate Hilar Somatostatin Neurons in the Ratns in the dorsal hippocampus. To further characterize the ischemia vulnerable CA-3c/hilar neurons we quantitated somatostatin (SS) and cholecystokinin (CCK) cell somata detected by immunocytochemistry in this zone before and at day 1, 2, 3 and 4 after the insult. A significant (p≺0.01) 60–80% loss o
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Regulation of Glutamate Receptors in Hippocampus after Cerebral Ischemia vulnerability): i.e. immediate upregulation of excitatory receptors could promote lethal hyperactivity (e.g. long-term potentiation in hippocampal CA-1) 2) Lowering of postischemic seizure threshold: i.e. delayed upregulation of excitatory receptors could result in seizure prone regions.
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Acidosis-Related Brain Damage: Immediate and Delayed Events. Tissue acidosis in form of an increased lactate formation during the period of ischemia in animals with hyperglycemia has been suggested as the cause for this increased vulnerability..To measure the acidosis during ischemia, and to evaluate and compare the brain damage incurred after the insult in
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Ischemic Damage of Rat Hippocampus and Basal Ganglia: Light Microscopical and Biochemical Changess of regional cerebral blood flow revealed injury of hippocampus and striatum. Morphological analysis showed a pattern of selective vulnerability in both structures. Concomitant immunohistochemical investigations revealed massive glial proliferation and extravasation of serum-albumin.
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Physiological Aspects of Brain Ischaemia in the Experimental Primate and Man analogies with man in the circumstances of subarachnoid haemorrhage or acute vascular occlusion during aneurysm surgery. This latter presents us with the closest approximation to experimental laboratory studies which we are likely to have in man.
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The Dependency of Cerebral Ischemic Damage on Duration and Severity of Ischemia: Studies of Single Cd postischemic reperfusion primarily in response to the degree of local blood flow reduction. However, other factors such as duration of ischemia, heterogeneity of residual blood flow, selective vulnerability of different neurons or brain regions, and remote deactivation caused by blood flow disturb
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