| Project/Area Number |
26462343
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Anesthesiology
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| Research Institution | Nagoya City University |
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Principal Investigator |
So MinHye 名古屋市立大学, 大学院医学研究科, 助教 (60381886)
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| Co-Investigator(Kenkyū-buntansha) |
祖父江 和哉 名古屋市立大学, 大学院医学研究科, 教授 (90264738)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 水チャネル / 高次脳機能 / 敗血症 / 炎症 / 感染症 |
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| Outline of Final Research Achievements |
We aimed to elucidate the pathogenesis of higher brain dysfunction accompanying severe infection and establish a new treatment strategy.
The expression of aquaporin 9 (AQP 9), a water channel, was confirmed to be decreased by administration of inflammatory cytokine or endotoxin to cultured cells. In addition, we confirmed elevation of inflammatory cytokine and decreased expression of AQP9 in the brain of sepsis model mouse, and the decrease of AQP 9 could be suppressed by administration of dexamethasone. Next, behavioral experiments of sepsis model mice confirmed higher brain dysfunction, and an improvement trend was confirmed by administration of dexamethasone. Furthermore, endotoxin was administered to cultured astrocytes, cDNA microarray was performed, and many factors whose expression fluctuated were confirmed, so we will narrow down.
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