| Project/Area Number |
18K08930
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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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| Review Section |
Basic Section 55060:Emergency medicine-related
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| Research Institution | Fukuoka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
山浦 健 九州大学, 医学研究院, 教授 (70264041)
根本 隆行 福岡大学, 医学部, 准教授 (90506833)
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| Project Period (FY) |
2018-04-01 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2022: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2021: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2020: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 虚血再灌流障害 / 脳障害 / 腎障害 / 心肺蘇生後臓器障害 / 遅発性細胞死 / 遅発型細胞死 / 腎不全 / 遅発性神経細胞死 / 心肺蘇生後脳症 / ミクログリア / アストロサイト / TNF-α / 心肺停止 |
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| Outline of Final Research Achievements |
While the rate of cardiopulmonary resuscitation of patients suffering from cardiopulmonary arrest has improved, it has become a serious problem that post-resuscitation patients develop organ damage such as encephalopathy and renal failure. The pathogenesis of these diseases is still unclear, and at present no effective treatment method has been established. It has been suggested that activation of inflammatory cells caused by cardiopulmonary resuscitation may induce cell death in various organs, but the detailed mechanism is unknown. In this study, we revealed that activation of inflammatory cells after cardiopulmonary resuscitation or ischemia-reperfusion is dependent on Ca 2+ signals with relevant cells.
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| Academic Significance and Societal Importance of the Research Achievements |
蘇生後脳症の患者の中には記憶障害のみが残存し社会復帰が困難な場合がある。この様な記憶障害を持つ患者数が増加することは、社会的損失となる可能性がある。また蘇生後の腎機能障害も同様であり、特に末期腎不全に至る場合には社会復帰に大きな障害となる。本研究では、心肺停止蘇生後の脳および腎機能障害に対する新規治療法の開発を目指すべく、脳・腎臓における蘇生後病態発症機構の分子基盤を明らかにすることを目的としている。
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