| Project/Area Number |
19K18375
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56010:Neurosurgery-related
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| Research Institution | Hirosaki University |
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Principal Investigator |
Matsuda Naoya 弘前大学, 医学部附属病院, 助教 (30587663)
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| Project Period (FY) |
2019-04-01 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2021: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 脳血管障害 / 脳神経疾患 |
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| Outline of Research at the Start |
Early Brain Injuryを引き起こす一大要因が酸化ストレスであることが示されており、それを最小限に抑えることで、予後向上に繋がることが期待される。Early Brain InjuryとLOX-1の関連に関する研究は未だ成されていない。酸化ストレスを介した両者の関係性につき証明し、LOX-1阻害によるEarly Brain Injury抑制効果を検討する。
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| Outline of Final Research Achievements |
Reducing oxidative stress that causes Early Brain Injury after subarachnoid hemorrhage is expected to improve patient prognosis. The aim of this study was to clarify the inhibitory effect of lectin-like oxidized LDL receptor-1 (LOX-1) inhibition on Early Brain Injury. We suggested that the expression of oxidized LDL and LOX-1 may be increased in the cerebral vascular wall of rat SAH model. The results are not reproducible and are still under investigation in terms of detection of apoptosis of neurons and vascular endothelial cells, disruption of blood-brain barrier, degree of brain edema, and measurement of cerebral microthrombi and intracerebral microvascular endothelial cell damage.
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| Academic Significance and Societal Importance of the Research Achievements |
くも膜下出血後の超急性期に生じる脳障害は、近年Early Brain Injuryと称され、超急性期の重症度を左右し、遅発性脳血管攣縮発生や予後に多大なる影響を与えることで注目されている。Early Brain Injuryを引き起こす一大要因が酸化ストレスであることが示されており、それを最小限に抑えることで、生命予後向上に繋がることが期待される。
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