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Kimihiko Hattori

Researcher at Johns Hopkins University

Publications -  8
Citations -  574

Kimihiko Hattori is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Social stress & Neuroprotection. The author has an hindex of 5, co-authored 8 publications receiving 543 citations. Previous affiliations of Kimihiko Hattori include Johns Hopkins University School of Medicine.

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Cognitive Deficits After Focal Cerebral Ischemia in Mice

TL;DR: Long-term cognitive deficits can be induced in mice by using a short duration of MCAO (60 minutes) that does not result in concomitant sensorimotor deficits.
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Social stress exacerbates stroke outcome by suppressing Bcl-2 expression

TL;DR: Modeling the effects of chronic social intimidation and stress on ischemia-induced bcl-2 expression and early neuronal cell loss resulting from cerebral artery occlusion in mice demonstrated that stressful prestroke social milieu strongly compromises an endogenous molecular mechanism of neuroprotection in injured brain and offer a new behavioral target for stroke therapy.
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Histopathological and behavioral characterization of a novel model of cardiac arrest and cardiopulmonary resuscitation in mice.

TL;DR: A dissociation between functional and histological outcome was found emphasizing the importance of combining both outcome measures for evaluation of neuroprotective strategies.
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Social Stress Exacerbates Focal Cerebral Ischemia in Mice

TL;DR: Prior exposure to social stress increases infarction volume and exacerbates cognitive deficits associated with transient cerebral ischemia and the mechanism underlying the effects of stress on stroke outcome likely involves corticosterone acting through glucocorticoid receptors to increase subsequent ischemIA-induced neuronal death.
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Nitric oxide production during cerebral ischemia and reperfusion in eNOS- and nNOS-knockout mice.

TL;DR: In vivo data suggest that NO production in the striatum after reperfusion is closely related to activities of both nN OS and eNOS, and is mainly related to nNOS following reperfusions.