| Project/Area Number |
18K08529
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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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| Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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| Research Institution | Osaka Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
細川 吉弥 大阪大学, 医学部附属病院, 特任助教(常勤) (10814569)
佐野 寛行 大阪医科大学, 医学部, 助教 (20556435)
寺前 純吾 大阪医科大学, 医学部, 講師 (90351395)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 劇症１型糖尿病 / CD300e / １型糖尿病 |
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| Outline of Final Research Achievements |
We have established a method for measuring the expression rate of CD300e and mean fluorointensity (MFI) in peripheral blood monocytes in patients with fulminant type 1 diabetes and healthy subjects as controls. In addition, healthy human-derived iPS cells and fulminant type 1 diabetic iPS cells were induced to differentiate into insulin-positive cells, poly (I;C) -transfected, and only insulin-positive cells were isolated by flow cytometry and gene expression was examined.
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| Academic Significance and Societal Importance of the Research Achievements |
劇症１型糖尿病の発症メカニズムとして想定されている免疫制御機構の異常とウイルス感染の関与について、その研究をCD300eやiPS細胞の観点からさらに前進させたことが本研究の学術的意義である。劇症１型糖尿病は、非常に急激に膵β細胞が破壊され、それによる急激な血糖上昇と代謝異常が生命予後にも影響することから、成因解明を進めることは社会的意義も大きいと考える。
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