Titlebook: Maturation Phenomenon in Cerebral Ischemia II; Neuronal Recovery an Umeo Ito,Takaaki Kirino,Igor Klatzo (Former Chief Conference proceedin

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高尔夫

Stress Response and Ischemic Tolerance in the Brainhe cultured astrocytes exposed to hypoxia—reoxygenation (H—R). In a separate in vivo study, we examined the inducibility of ischemic tolerance and heat shock protein 72 (HSP72) in moderately symptomatic gerbils by unilateral preconditioning ischemia. In the former studies, we first attempted to clar

Minutes

Preconditioning Depresses Excitatory Cell Signaling Following the Second Ischemic Insult3 days of interischemic interval protected the brain from a subsequent period of lethal ischemia of 10–15 min duration. Calcium-calmodulin protein kinase II (CaMKII) is translocated from its cytosolic form to the membrane-bound form during ischemia. In the CA1 region the translocated protein is boun

GNAW

Electrophysiological Evaluation of Ischemic Tolerance Phenomenonice preparations. Firstly, the capacity for long-term potentiation triggered by tetanic stimulation, which is a putative synaptic background of memory, was examined in hippocampal slices from gerbils subjected to double ischemia. Capacity for long-term potentiation was transiently inhibited 2 days f

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Transient Ischemia Depletes Free Ubiquitin in the Gerbil Hippocampal CA1 Neuronsippocampus was strongly dependent on the antibodies used. Using rabbit polyclonal antibody U-5379, immunoreactivity disappeared from the hippocampus in the early reperfusion period, and reappeared in the dentate granule cells and CA3 pyramidal cells, but never in the CA1 pyramidal cells. In contrast

沉积物

Insight into the Protective Mechanisms of Cortical Spreading Depression in Cardiac Arrest Cerebral Ige if elicited prior to ischemia. The present study was undertaken to investigate pathomechanisms of neuronal protection conferred by cortical spreading depression (CSD) elicited by the topical application of 5. KCl to the occipital cortex in Sprague-Dawley rats. Autoradiographic analysis on brain t

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谁在削木头

Features and Threshold of Infarct Development in Ischemic Maturation Phenomenonnecrosis in the cerebral cortex without inducing focal infarction. Furthermore, we investigated the threshold for induction of focal infarction in the cerebral cortex by changing the number and interval between repetitive ischemic insults. We found that with an increase in number of these insults an

irreparable

Impending Cerebral Infarction and Inflammatory Response: A Possible Target for Therapeutic Interventee of ischemia, the changes become irreversible and the tissues undergo pan-necrosis. This activates a cascade of inflammatory response which scavenges the damaged cells in areas of impending infarction through liquification and phagocytosis. Induction of the immune response further accelerates disi

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