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Yuiko Morita-Fujimura

Researcher at Tohoku University

Publications -  40
Citations -  3650

Yuiko Morita-Fujimura is an academic researcher from Tohoku University. The author has contributed to research in topics: Ischemia & Apoptosis. The author has an hindex of 25, co-authored 40 publications receiving 3553 citations. Previous affiliations of Yuiko Morita-Fujimura include University of California, San Francisco & Stanford University.

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Early appearance of activated matrix metalloproteinase-9 after focal cerebral ischemia in mice: a possible role in blood-brain barrier dysfunction.

TL;DR: The appearance of activated MMP-9 after 4 hours of ischemia in correlation with BBB permeability alterations suggests that M MP-9 may play an active role in early vasogenic edema development after stroke.
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Early appearance of activated matrix metalloproteinase-9 and blood-brain barrier disruption in mice after focal cerebral ischemia and reperfusion

TL;DR: The early appearance of activated MMP-9, associated with evidence of BBB permeability alteration, suggests that activation of M MP-9 contributes to the early formation of vasogenic edema after transient FCI.
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Cytosolic redistribution of cytochrome c after transient focal cerebral ischemia in rats.

TL;DR: The results suggest the possibility that cytochrome c release may play a role in DNA-damaged neuronal cell death after transient focal cerebral ischemia in rats.
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Manganese superoxide dismutase mediates the early release of mitochondrial cytochrome C and subsequent DNA fragmentation after permanent focal cerebral ischemia in mice.

TL;DR: The subcellular distribution of the cytochrome c protein in both wild-type mice and heterozygous knock-outs of the Mn-SOD gene after permanent FCI is examined to suggest that Mn- SOD blocks cytosolic release of cy tochrome c and could thereby reduce apoptosis after permanentFCI.
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Overexpression of Copper/Zinc Superoxide Dismutase in Transgenic Rats Protects Vulnerable Neurons against Ischemic Damage by Blocking the Mitochondrial Pathway of Caspase Activation

TL;DR: The results suggest that overexpression of SOD1 reduced oxidative stress, thereby attenuating the mitochondrial release of cytochrome c and Smac, resulting in less caspase activation and apoptotic cell death in hippocampal CA1 neurons after global ischemia.