| Project/Area Number |
26462757
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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 |
Emergency medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
Tashiro Takahiro 熊本大学, 医学部附属病院, 非常勤診療医師 (00613340)
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| Co-Investigator(Kenkyū-buntansha) |
木下 順弘 熊本大学, 大学院生命科学研究部(医), 教授 (30195341)
蒲原 英伸 熊本大学, 大学院生命科学研究部(医), 准教授 (90398222)
鷺島 克之 熊本大学, 医学部附属病院, 助教 (40336235)
廣佐古 進 熊本大学, 医学部附属病院, 非常勤診療医師 (70432995)
新森 大佑 熊本大学, 医学部附属病院, 診療助手 (70635789)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ARDS / Autophagy / microRNA / Exosome / Inflammation / Innate Immunity / Ｉｎｆｌａｍｍａｔｉｏｎ / autophagy / exosome |
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| Outline of Final Research Achievements |
Homeostasis is maintained by autophagy due to decomposition of cellular organelles under biological stress. Alveolar-derived cell line (A549) and monocyte-derived cell line (THP-1) were used to elucidate the defense mechanism by alveolar cells and infiltrating leukocytes autophagy due to excessive inflammation of ARDS. Cells were stimulated with TNFalpha, Il-1 beta, LPS and the expression of protein LC3-II in antophagy induction was confirmed. This reaction was suppressed by the autophagy inhibitor. MicroRNAs were also profiled using serum from ARDS patients and microRNAs attributed to ARDS and Autophagy were identified.
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