Analysis using knock-down methods for gene-associated receptor signaling in sepsis
| Project/Area Number |
23659843
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Emergency medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 敗血症 / セプシス / オートファジー / 蛋白異化 / 全身性炎症反応症候群 / TLR3 / TLR7 / TLR8 / TLR9 / TR3 / TRIF / NF-κB / 警笛細胞 / 転写因子 / 遺伝子治療 |
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| Research Abstract |
Sepsis is well known as a severe disease states corresponding emergency and intensive care. Sepsis is a systemic inflammatory reactions against viruses and bacteria, but effective therapy to control inflammation of the non-antibiotic still has not been established. In this study, to improve the survival rate of sepsis model mice by inhibiting gene transcription FADD, of TAK-1, such as by administering the siRNA, the manipulation reduced the LC3 expression level of lung, kidney, and aorta as gene recognition receptors. Subsequent analysis clarified the mechanism that inhibitions of both activation, autophagosome formation in sepsis pathology were not enhanced. The changeswere found as normalized functioning in electron microscope image. It can be said that it is considered by the suppression of gene-aware receptor signaling, leading to results that can reduce the organ inflammation associated bacterial infections, viral infections, in gene therapy, to have the significance of proposed new drug discovery in severe infection.
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Report
(3 results)
Research Products
(14 results)
