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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書目名稱Mechanisms of Cerebral Hypoxia and Stroke影響因子(影響力)




書目名稱Mechanisms of Cerebral Hypoxia and Stroke影響因子(影響力)學(xué)科排名




書目名稱Mechanisms of Cerebral Hypoxia and Stroke網(wǎng)絡(luò)公開度




書目名稱Mechanisms of Cerebral Hypoxia and Stroke網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Mechanisms of Cerebral Hypoxia and Stroke被引頻次




書目名稱Mechanisms of Cerebral Hypoxia and Stroke被引頻次學(xué)科排名




書目名稱Mechanisms of Cerebral Hypoxia and Stroke年度引用




書目名稱Mechanisms of Cerebral Hypoxia and Stroke年度引用學(xué)科排名




書目名稱Mechanisms of Cerebral Hypoxia and Stroke讀者反饋




書目名稱Mechanisms of Cerebral Hypoxia and Stroke讀者反饋學(xué)科排名

GLUE

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

謙卑

absolve

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

賞心悅目

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.

TOXIC

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

小鹿

JADED

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.

強(qiáng)化

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.

adjacent

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