| Project/Area Number |
20790464
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Legal medicine
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
KATO Naho Fukushima Medical University, 医学部, 助教 (20457766)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 虚血再還流障害 / 挫滅症候群 / IL-6ノックアウトマウス / iNOSノックアウトマウス / リアルタイムPCR |
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| Research Abstract |
The mouse bilateral hind limb tourniquet-reperfusion model can be considered as an experimental animal model of crush syndrome. By using this model, we investigated mRNA expression levels of various inflammatory cytokines in the kidney, a damaged organ distant from the ischemic hind limb. So, we found that the expression level of kidney IL-6 mRNA increased and that of iNOS mRNA decreased after reperfusion. In contrast, survival rates 24 h after ischemia-reperfusion were in the order of iNOS-deficient mice≧C57Black/6J wild-type mice>IL-6-deficient mice. These results indicated that IL-6 plays an ameliorative role and that iNOS play a deteriorative role. This model shows a high mortality rate in mice, but morphological changes in the kidney, such as nuclear concentration of tubular epithelial cells and infiltration of inflammatory cells, were minor.
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