| Project/Area Number |
12671750
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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 |
Plastic surgery
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| Research Institution | NAGASAKI UNIV |
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Principal Investigator |
TANAKA Katsumi Nagasaki University, School of Medicine, senior assistant professor (lecturer), 医学部・附属病院, 講師 (70244069)
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Tohru Nagasaki University, School of Medicine, professor, 医学部, 教授 (60136661)
AKITA Sadanori Nagasaki University, Medical School Hospital, assistant professor, 医学部・附属病院, 助手 (90315250)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | cytokine / angiogensis / apoptpsis / Insulin-like growth factor-1, IGF-1 / flap survival / signaling pathway / 抗体中和療法 / 軸性皮弁 / 分子生物学 / 受容体中和抗体 / 微小血管象影 / 分子生物解析 |
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| Research Abstract |
In order to further obtain the molecular mechanisms of the optimal flap survival, the signal transduction pathways of the cytokines were primarily investigate. In the primary culture model for human keloid-derived fibroblasts, Insulin-like Growth Factor-1 and its receptor involved in the keloid-derived fibroblasts resistance against the ceramide-induced apoptosis, therefore they are concluded as the primary cause of the cellar hyper-expression and the possible excessive production of the extracelluar matrix seen in keloid patients. In the further experiment, the axial-pattern epigastric flap was adopted as the flap survival model. In the modified epigastric flap, the cytokine-dependent gp130 receptor submit was strongly attributed to the flap survival, the pedicle blood flow, the microangiography and the angiogenesis transcript expression represented By VEGF. Therefore, the cytokine signaling via receptor was the major component for the flap angiogenesis as well as the flap blood flow.
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