| Project/Area Number |
15K12507
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biomedical engineering/Biomaterial science and engineering
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| Research Institution | Kyoto University |
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Principal Investigator |
TABATA Yasuhiko 京都大学, ウイルス・再生医科学研究所, 教授 (50211371)
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| Co-Investigator(Kenkyū-buntansha) |
山本 雅哉 京都大学, ウイルス・再生医科学研究所, 准教授 (10332735)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | マクロファージ / 体内動態 / 細胞機能 / 徐放化 / ハイドロゲル / 細胞移動 / ピオグリタゾン / スフィンゴシン－1－リン酸レセプターアゴニスト |
|---|
| Outline of Final Research Achievements |
An agonist of sphigosin-1-phosphaie type1 receptor and pioglitazone were solubilized in water by the mix micelle formation with a hydrophobic derivative of gelatin. Following gelatin hydrogels incorporating water-solubilized micelles of drugs were applied to the skin defect of mice, the in vivo migration of macrophages (Mφ) and the Mφ biofunction, as well as the repairing of skin defect. The application of the agonist release hydrogel enhanced the in vivo Mφ migration while that of pioglitazone release promoted the number ratio of wound healing Mφto inflammation Mφ. The duel release of the agonist and pioglitazone significantly accelerated the repairing extent of skin defect.
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