M
Miki Fujimura
Researcher at Tohoku University
Publications - 338
Citations - 13058
Miki Fujimura is an academic researcher from Tohoku University. The author has contributed to research in topics: Moyamoya disease & Cerebral blood flow. The author has an hindex of 50, co-authored 289 publications receiving 11341 citations. Previous affiliations of Miki Fujimura include Stanford University.
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Subarachnoid hemolysate produces DNA fragmentation in a pattern similar to apoptosis in mouse brain
TL;DR: Evidence is provided that the presence of subarachnoid blood products is associated with DNA fragmentation and apoptotic cell death and that apoptosis was present after cortical exposure to subarachesnoid hemolysate.
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Delayed intracerebral hemorrhage after superficial temporal artery-middle cerebral artery anastomosis in a patient with moyamoya disease: possible involvement of cerebral hyperperfusion and increased vascular permeability.
TL;DR: Early increase in CBF associated with vasogenic edema formation at the site of the anastomosis could be the warning sign for subsequent hemorrhagic complication, and intensive blood pressure control is warranted in such patients.
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Copper-Zinc Superoxide Dismutase Prevents the Early Decrease of Apurinic/Apyrimidinic Endonuclease and Subsequent DNA Fragmentation After Transient Focal Cerebral Ischemia in Mice
Miki Fujimura,Yuiko Morita-Fujimura,Purnima Narasimhan,Jean-Christophe Copin,Makoto Kawase,Pak H. Chan +5 more
TL;DR: Examination of the expression of APE/Ref-1 and DNA damage after FCI in wild-type and transgenic mice overexpressing copper-zinc superoxide dismutase suggests that reactive oxygen species contribute to the early decrease of apurinic/apyrimidinic endonuclease and thereby exacerbate DNA fragmentation after transientFCI in mice.
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Reduction of Apurinic/Apyrimidinic Endonuclease Expression After Transient Global Cerebral Ischemia in Rats: Implication of the Failure of DNA Repair in Neuronal Apoptosis
TL;DR: Evidence is provided that APE/Ref-1 decreased in hippocampal CA1 neurons after transient global ischemia and that this reduction precedes DNA fragmentation, which is destined to cause apoptosis.
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Increased Cytochrome c–Mediated DNA Fragmentation and Cell Death in Manganese–Superoxide Dismutase–Deficient Mice After Exposure to Subarachnoid Hemolysate
TL;DR: It appears that Mn–superoxide dismutase plays a role in preventing cell death after exposure to subarachnoid blood products, and the presence of cytochrome c in the cytosol and subsequent cell death in neurons is demonstrated.