| Project/Area Number |
21390433
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHITA Kouhei 京都大学, 医学研究科, 講師 (80402858)
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| Co-Investigator(Renkei-kenkyūsha) |
ENDO Nobuyuki 若狭湾エネルギー研究センター, 研究開発部, 主査研究員 (30359244)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥17,030,000 (Direct Cost: ¥13,100,000、Indirect Cost: ¥3,930,000)
Fiscal Year 2011: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2009: ¥9,360,000 (Direct Cost: ¥7,200,000、Indirect Cost: ¥2,160,000)
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| Keywords | 活性酸素 / 一重項酸素 / 細胞死 / 壊死型 / 自己貪食型 / アポトーシス / NETosis / 神経細胞 / グルタミン酸 / 細胞活性 / 好中球 / NETs / 神経様細胞 / オートファジー / エダラボン / プテリン化合物 / 新規一重項酸素消去剤 / 白血病細胞 / 組織傷害 |
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| Research Abstract |
The relation of reactive oxygen species(ROS) with cell injury was investigated. Among ROS, we noticed singlet oxygen(SO) that has not been much noticed yet. Human leukemia cell line NB4, rat neuronal cell line B50, mouse neuronal cell line MG6, human neutrophils and rat neuron were used. In NB4, produced SO induced vascular cell injury. In B50, extracellularly generated SO induced acute cell death by necrosis. In MG6, intracellularly generated SO induced subacute cell death by autophagy. In neutrophils, SO induced cell death with NETs formation. In neurons, SO was involved in cell death induced by glutamate. In above mentioned all experiments, SO was strongly involved in cell injury. Therefore, we speculated that SO is essential for cell injury induced by ROS.
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