| Budget Amount *help |
¥48,750,000 (Direct Cost: ¥37,500,000、Indirect Cost: ¥11,250,000)
Fiscal Year 2012: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
Fiscal Year 2011: ¥15,210,000 (Direct Cost: ¥11,700,000、Indirect Cost: ¥3,510,000)
Fiscal Year 2010: ¥26,910,000 (Direct Cost: ¥20,700,000、Indirect Cost: ¥6,210,000)
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| Research Abstract |
Sepsis, known as a inducer of severe multiple organ diseases, has no established effective treatment except for antibiotics. Sepsis can lead multiple organ failure due to amid acid transformation to acute phase proteins such as inflammatory cytokines. In this study, I have found that some parts of autophagy-related gene family wereincreased at transcriptional and translated levels in the acute terms of sepsis of cultured human vascular endothelial cells and sepsis mouse models. LC3 was activated in particular, and promoted an autophagosome formation. It was concluded that FADD, TAK-1 andtranscriptional activity of NF-κB and AP-1 were significantly related with autophagy acceleration in the cultured human vascular endothelial cells and sepsis mouse model.
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