A role of nitric oxide synthase in cerebral infarction and a new therapeutic strategy of stroke
| Project/Area Number |
24791605
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
KUBOTA Haruaki 琉球大学, 医学部附属病院, 助教 (10600421)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | マウス / 中大脳動脈閉塞 / 脳虚血 / 再灌流 / 一酸化窒素合成酵素 / nNOS / NOS / 硫化水素 / 脳梗塞 / 虚血再灌流 / 一酸化窒素合成酵素全欠損 / 性差 / 神経型NOS / eNOS / iNOS |
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| Outline of Final Research Achievements |
Nitric oxide (NO) is signaling gas molecule in vivo and there are three types of NO synthase (NOS). When animal lacking all three NOS, various pathological phenotype appears in many organ.
This time, in order to elucidate the role of nitric oxide in the pathogenesis of cerebral infarction, we perform the cerebral transient ischemia and reperfusion experiments with all three NOS deficient (mutant) mice and wild-type mice. Cerebral infarct size was smaller in mutant mice as compared with wild-type mice. Neurological deficit score was significantly reduced in mutant mice as compared with wild-type mice. Moreover, survival rate 24 hour after transient ischemia-reperfusion was significantly higher in mutant mice as compared with wild-type mice.
Although the mechanism of these phenomena is unknown, we are scheduled to clarify molecular biological and biochemical mechanism from now on.
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Report
(4 results)
Research Products
(4 results)
