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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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Incidence and Risk Factors of the Watershed Shift Phenomenon after Superficial Temporal Artery-Middle Cerebral Artery Anastomosis for Adult Moyamoya Disease.

TL;DR: Routine CBF measurement is recommended in the acute stage after revascularization surgery for adult MMD to avoid surgical complications, such as local CHP and cerebral ischemia, caused by the WS phenomenon.
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Surgical treatment of paraventricular cavernous angioma: fibre tracking for visualizing the corticospinal tract and determining surgical approach.

TL;DR: A patient with a paraventricular cavernous angioma manifesting as hemiparesis caused by haemorrhage is reported, with results that suggest fibre tracking is useful in surgical planning for procedures involving deep-seated lesions adjacent to the corticospinal tract, and may avoid postoperative morbidity due to corticOSPinal tract injury.
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Expression of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase (TIMP) in cerebral cavernous malformations: immunohistochemical analysis of MMP-2, -9 and TIMP-2.

TL;DR: It is found that CCM showed the increased endothelial expression of MMP-2, -9, and TIMP-2 that may affect the vascular matrix stability, and thus can contribute to hemorrhage from CCM.
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Hemodynamic analysis of the recipient parasylvian cortical arteries for predicting postoperative hyperperfusion during STA-MCA bypass in adult patients with moyamoya disease

TL;DR: This study revealed that direct anastomoses of PSCAs with anterograde hemodynamic sources from the MCA had a high risk of postoperative CHP during STA-MCA bypass in adult patients with MMD.
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Reduction of copper, zinc-superoxide dismutase in knockout mice does not affect edema or infarction volumes and the early release of mitochondrial cytochrome c after permanent focal cerebral ischemia.

TL;DR: The results indicate that the SOD1 enzyme does not appear to affect cerebral infarction, cerebral edema nor the mitochondrial signaling pathway for apoptosis following permanent focal cerebral ischemia where there is no reperfusion injury.