| Project/Area Number |
25462842
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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 |
Emergency medicine
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| Research Institution | Kurume University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAKASU Osamu 久留米大学, 医学部・救急医学講座, 教授 (90236216)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 敗血症 / 脳症 / エストロゲン / キヌレニン経路 / 盲腸結紮穿孔モデル / 重症敗血症 / 敗血症関連脳症 / CLPモデル / キヌレニン / 17βエストラジオール / L-キヌレニン / サイトカイン / 性ステロイドホルモン |
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| Outline of Final Research Achievements |
In recent years, tens of millions of people worldwide develop severe sepsis every year, with comorbid encephalopathy increasing mortality in particular. We developed a mouse sepsis model in an attempt to elucidate the mechanisms of sepsis-associated encephalopathy. The model we used was the cecal ligation and puncture (CLP) model. After confirming improvements of survival rate via estrogen and L-kynurenine administrations, detection of mRNA expressions of a kynurenine receptor, the aryl carbohydrate receptor, and a tryptophanase, the tryptophan 2,3-dioxygenase, in peritoneal exudate cells were determined, indicating the involvement of the kynurenine pathway. In this process, we successfully generated a modified model in which intraperitoneal abscess formation, which is considered to be a defect of the original model, can be highly-controlled.
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