| Project/Area Number |
18591715
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
NAKAJIMA Yasufumi Kyoto Prefectural University of Medicine, Department of Anesthesiology, Assistant Professor (70326239)
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| Co-Investigator(Kenkyū-buntansha) |
MIZOBE Toshiki Kyoto Prefectural University of Medicine, Department of Anesthesiology, Associate Professor (50239266)
HASHIMOTO Satoru Kyoto Prefectural University of Medicine, Department of Anesthesiology, Associate Professor (90167578)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,820,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Venous Thromboembolism / RNA interference / Gene Therapy / RNAi法 / 炎症 / 凝固 / 相互作用 |
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| Research Abstract |
Orthopedic surgery, especially total knee and total hip arthroplasty, is considered a risk factor for perioperative venous thromboembolism. Our aim of the study was to evaluate how accelerated inflammatogenic cellular interactions and the subsequent production of tissue factor and CD40 ligand play an important role in the pathogenesis of venous thromboembolism. We have demonstrated that platelet, leukocyte and endothelium activities as well as their interactions are enhanced during the perioperative period of total knee arthroplasty, particularly in venous blood from the lower half of the bodies of patients, which consequently augments blood coagulability in the research paper. (J Thromb Haemost.5, 738-45.2007)
In the next project, we have demonstrated continuous perioperative milrinone infusion has the potential to prevent accelerated blood cell interactions and hypercoagulablility during the perioperative period of total knee arthroplasty via inhibition of intraplatelet p38 MAPK, 1VIEK/ERK, and PI3K/Akt signaling pathway. These contents will be submitted to the science journal.
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