| 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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| 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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