| Project/Area Number |
24592228
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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 |
Orthopaedic surgery
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| Research Institution | Shinshu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Yukio 信州大学, 学術研究院医学系(医学部附属病院), 助教 (00549488)
UCHIYAMA Shigeharu 信州大学, 学術研究院医学系, 准教授 (10242679)
KATO Hiroyuki 信州大学, 学術研究院医学系, 教授 (40204490)
UEMURA Kazutaka 信州大学, 医学部附属病院, 医員 (50624706)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 狭窄性腱鞘炎 / 老化 / 糖尿病 / 滑膜内腱 / 腱細胞 / 軟骨細胞 / 軟骨化生 / Lubricin / 腱鞘炎 |
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| Outline of Final Research Achievements |
Tenosynovitis is common disorder in menopausal or perinatal women and diabetic patients. However, little is known about the pathogenic mechanism of tenosynovitis. We tried to clarify the pathogenesis of tenosynovitis with senescence-model mouse and diabetic model mouse. Gene expression analysis of senescence-model mouse showed that the expression of tenogenic marker in intrasynovial tendon decreased, while the expression of chondrogenic marker increased with aging. On the other hand, we could not find any difference in diabetic model mouse. Our results suggest that the shift of gene expression from tendon to cartilage, potentially developing with aging, is one of the causes of the pathogenesis of tenosynovitis.
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