| Project/Area Number |
26293366
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Kondo Kenji 東京大学, 医学部附属病院, 准教授 (40334370)
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| Co-Investigator(Kenkyū-buntansha) |
菊田 周 東京大学, 医学部附属病院, 助教 (00555865)
有田 誠 国立研究開発法人理化学研究所, 統合生命医科学研究センター, チームリーダー (80292952)
野村 務 埼玉医科大学, 医学部, 講師 (20228365)
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| Research Collaborator |
YAMASOBA TATSUYA 東京大学, 医学部附属病院, 教授 (60251302)
BABA MIYUKI 東京逓信病院, 耳鼻咽喉科, 医長
UEHA RUMI 東京大学, 医学部附属病院, 助教 (10597131)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,380,000 (Direct Cost: ¥12,600,000、Indirect Cost: ¥3,780,000)
Fiscal Year 2016: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2014: ¥10,400,000 (Direct Cost: ¥8,000,000、Indirect Cost: ¥2,400,000)
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| Keywords | 嗅神経傷害 / 加齢変化 / 再生 / 脂質メディエーター / 嗅覚 / 脂肪酸 / 慢性副鼻腔炎 / CFD / 鼻科学 / 嗅覚医学 / 嗅神経障害 / 神経再生 |
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| Outline of Final Research Achievements |
(1) Caloric restriction exacerbated regeneration of the olfactory neuroepithelium after injury by methimazole. Downregulation of proliferative activity of basal cells in neuroepithelium by caloric restriction appeared to play important role in these findings. (2) During the regeneration of the olfactory neuroepithelium, lipid mediators generated through metabolism by 12/15 lipoxygenase (12/15 LOX) was increased. 12/15 LOX-positive cells were transiently infiltrated into the regenerating olfactory mucosa, suggesting that the composition of tissue fatty acid is associated with the regenerative process of the olfactory neuroepithelium. (3) Intranasal administration of cigarette smoke solution (CSS) suppressed the recovery of neuroepithelium after injury. CSS administration decreased the ORN injury-induced IGF-1 expression. Administration of recombinant human IGF-1 prevented the CSS-induced suppression of neuroepithelial recovery.
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