| Project/Area Number |
21591630
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KUDO Toshifumi 東京医科歯科大学, 医学部・附属病院, 助教 (50431911)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Yoshinori 東京医科歯科大学, 医歯(薬)学総合研究科, 講師 (70280964)
JIBIKI Masatoshi 東京医科歯科大学, 医学部附属病院, 助教 (50422481)
菅野 範英 東京医科歯科大学, 医学部附属病院, 助教 (60332631)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 血管外科学 / Buerger病 / TLR / 歯周病 / 遺伝的多型 / Buerer病 / 遺伝子多型 / CD40 |
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| Research Abstract |
Myeloid differentiation primary-response protein 88(MyD88) is a key signaling adaptor for all Toll-like receptors. The frequency of GG genotype was significantly lower in the Buerger's disease patients than in the controls. The frequency of Formyl peptide receptors(FPR) 1 TCCCT haplotype was significantly higher in the Buerger's Disease patients than in the controls. The results of the current study suggest that TLR-MyD88 pathway and bacterial infection immunity play a role in the mechanism of pathogenesis of Buerger's disease as well as periodontal disease.
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