| Project/Area Number |
16K20009
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurosurgery
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| Research Institution | Kobe University |
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Principal Investigator |
otowa yasunori 神戸大学, 医学研究科, 医学研究員 (40647765)
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| Research Collaborator |
HIRASHIMA MASANORI 神戸大学, 医学研究科, 准教授
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Flt1 / Flk1 / 先天性水頭症 / 硬膜リンパ管 / 脳脊髄液 / 脈絡叢 / マウス / 遺伝子異常 / リンパ管 / 解剖学 |
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| Outline of Final Research Achievements |
We discovered that double hetero-deficient (Flt1 +/-; Flk1 +/-) mice of Flt1 and Flk1, receptors of the vascular endothelial growth factor VEGF-A, become lethal for congenital hydrocephalus about 2 months of age. Flt1 +/-; Flk1 +/- mice were analyzed with 1 month old mouse and the dura lymphatic vessels were confirmed around the sinus vein and dural lymphatic vessels and intravenous sinuses was considered as an excretion route. In Flk1 +/- mice, the number of lymphatic endothelial cells around the sinus vein was decreased, but no abnormality was found in the excretory function. In Flt1 +/- mice, edema of the choroid plexus was observed. Flt1 +/-; Flk1 +/- mice caused congenital hydrocephalus due to an increase in cerebrospinal fluid due to endothelial cell proliferation in the choroid plexus, no abnormality was observed in the excretory function. It was thought that the deficiency abnormality of Flt1 is more strongly reflected.
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