| Project/Area Number |
25461650
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
MOMOI NOBUO 福島県立医科大学, 医学部, 教授 (10285033)
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| Co-Investigator(Kenkyū-buntansha) |
AOYAGI YOSHIMICHI 福島県立医科大学, 医学部, 助手 (30509469)
KANAI YUUJI 福島県立医科大学, 医学部, 助手 (60448628)
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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 |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | 胎児 / 心血行動態 / 低酸素 / フェニトイン / 胎児医学 |
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| Outline of Final Research Achievements |
We evaluated the effect of hypoxia on developing murine embryonic cardiovascular function using high-resolution echocardiography in utero. Because a specific potassium ion current (IKr) is of major importance for embryonic cardiac repolarization, phenytoin that inhibits Ikr has the potential to result in embryonic bradycardia. After making a hypoxic embryo model by phenytoin administration to the mother, we assessed the hypoxic status of the embryo using a hypoxia marker, pimonidazole. We also evaluated the blood redistribution in the fetus resulting from hypoxia by looking at the gene expression changes, which are transcriptionally activated by hypoxia inducible factor (HIF-1).
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