| Project/Area Number |
22591548
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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 |
Thoracic surgery
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
SAIKAWA Satoko 琉球大学, 大学院・医学研究科, 助教 (20404569)
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| Co-Investigator(Kenkyū-buntansha) |
KAKINOHANA Manabu 琉球大学, 大学院・医学研究科, 准教授 (20274897)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 硫化水素 / 遅発性対麻痺 / 脊髄虚血 / アポトーシス / 遅発性麻痺 / エピジェネティクス / 神経変性 / 虚血性脊髄障害 / 対麻痺 / ヒストン脱アセチル化酵素 / 脊髄運動神経細胞 |
|---|
| Research Abstract |
We investigated whether inhibition of histon-deacetylation (HDAC) can exert neuroprotective effect against delayed paraplegia after spinal cord ische mia in mice. Treatment groups were divided into 3 groups in corresponding to duration of HDAC treatment (7 days before, 3 days before, and 1 day before spinal cord ischemia). Saline treatment was defined as control group. As a result from our experiments, any animal treated with inhibition of HDAC could not show significantly improve neurological outcome in comparison with control group. Histopathological and immunohistopathological analysis also failed to show any differences among all groups. According to our data, modulation of HDAC is unlikely to be associated with delayed neurological degeneration in spinal ventral horn in mice spinal cord ischemic model.
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