| Project/Area Number |
18K16230
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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| Research Institution | Osaka University |
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Principal Investigator |
Hosokawa Yoshiya 大阪大学, 医学部附属病院, 特任助教(常勤) (10814569)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | MIN6 / iPS細胞 / 25HC / ch25h / 劇症1型糖尿病 / Ch25h / β細胞 |
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| Outline of Final Research Achievements |
The caspase-3 activity was significantly lower in both 25HC and cytokine treatment pancreatic cells included INSULIN positive cells induced from fulminant type 1 diabetes iPSCs than in only cytokine treatment.The proportion of cleaved caspase-3-positive cells among the induced INSULIN-positive cells was significantly lower in both 25HC and cytokine treatment fulminant type 1 diabetes iPSCs than in only cytokine treatment.
Plasma 25HC levels could be detected by GC-MS/MS and the measurement system of plasma 25HC levels from minutes amounts of blood sample could be in sight.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の研究により劇症1型糖尿病における膵β細胞のアポトーシスにch25hが関与していることが示唆され、他の1型糖尿病をふくめ膵β細胞傷害を抑制することでの糖尿病治療薬への応用が考えられる。また血中25HC測定系の樹立は劇症1型糖尿病の新規バイオマーカーとなりうる可能性が考えられる。
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