| Project/Area Number |
15591559
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | National Cardiovascular Center Research Institute |
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Principal Investigator |
YOKOTA Chiaki National Cardiovascular Center, Cerebrovascular Division, Seniro Staff, 内科脳血管部門, 医長 (80300979)
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| Co-Investigator(Kenkyū-buntansha) |
KUGE Yuji Kyoto University Graduate School of Pharmaceutical Science, Department of Patho-Functional Bioanalysis, Associate Professor, 大学院・薬学研究科病態機能分析学, 助教授 (70321958)
INOUE Hiroyasu Nara Women's University, Department of Food Science and Nutrition Faculty of Human Life and Environment, Professor, 生活環境学部・生活環境学科食物科学専攻, 教授 (40183743)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Cyclooxygenase-2 / Spreading depression / Rat / S100A9 / JTE-522 / Prostaglandin / RAT / Focal ischemia / Environmental enrichment / Neurogenesis / MAPK phosphatase / cyclooxygenase-2 / focal ischemia / rat / cerebral blood flow / iomazenil / neuronal viability / benzodiazepine receptor |
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| Research Abstract |
Temporal and topographic profiles of cyclooxygenase-2 (COX-2) expression and prostaglandins as well as [^<123>I]iomazenil distribution during 24 hours of focal brain ischemia in rats were examined. We demonstrated that prostaglandin production as well as COX-2 expression in ischemic tissues depended on the degree and duration of the reduction in cerebral blood flow (Yokota C, et al.,2004). We also confirmed that [^<123>I]iomazenil should be a useful marker of neuronal viability using histopathological findings (Kaji T, et al.2004).
COX-2 was reported to be induced in the infarcted human brain. Spreading depression (SD) is thought to play a role in this induction. Thus, we correlated the expression of SD-associat.ed genes with COX-2 production in brains after SD. We showed that the bilateral induction of expression of the S-100A9 gene in response to SD was associated with COX-2 activation (Yokota C. et al.2005).
We hypothesized that SD, evoked after ischemic insult, might contribute to the process of reconstitution of neural networks via the activation of SD-associated genes as a result of COX-2 production in the hemisphere contralateral to the ischemia.
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