| Project/Area Number |
16K10728
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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 |
Neurosurgery
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| Research Institution | Saga University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
江良 択実 熊本大学, 発生医学研究所, 教授 (00273706)
北川 裕之 神戸薬科大学, 薬学部, 教授 (40221915)
島野 健仁郎 東京都市大学, 工学部, 教授 (90287475)
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| Research Collaborator |
Inoue Kouhei
Serigaya Syota
Nadanaka Satomi
Soga Minami
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | もやもや病 / 多能性幹細胞 / 血流剪断応力 / 血管内皮細胞 / 細胞外マトリックス / 血流剪断力 / 血流ストレス / 脳神経疾患 / 脳血管障害 / 多機能幹細胞 |
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| Outline of Final Research Achievements |
We demonstrated changed extracellular matrix of vascular endothelial cells in moyamoya disease. Extracellular matrix of vascular endothelium play an impotent role in protect endotheium against vascular shear stress. Thus, in moyamoya disease, vascular endothelium could become vulnerable to vascular shear stress. Since stenotic lesions in moyamoya disease exists in region where shear stress is high, endothelial damage would be caused first, then progressive thickening the vascular intima and narrowing the vascular lumen would occur during repair process.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究成果により、もやもや病の病態を明らかにすることができた。今後の治療介入のための新しい標的を定めることが可能となり、新しい治療法の開発につながると思われる。
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