Elucidation of the mechanism of developmental fetal organ damage caused by stress-induced overmaturation
| Project/Area Number |
15H04881
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
MATSUDA TADASHI 東北大学, 医学系研究科, 非常勤講師 (50361100)
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| Co-Investigator(Kenkyū-buntansha) |
齋藤 昌利 東北大学, 大学病院, 講師 (00451584)
北西 龍太 東北大学, 医学系研究科, 非常勤講師 (20436116)
埴田 卓志 東北大学, 大学病院, 助教 (30400360)
渡邊 真平 東北大学, 大学病院, 助手 (70509413)
臼田 治夫 東北大学, 大学病院, 助手 (60722402)
秋山 志津子 東北大学, 大学病院, その他 (80466549)
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2018: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2017: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
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| Keywords | 過成熟 / 子宮内炎症 / コルチゾル / ヒツジ / 動脈管 / CRH / 胎仔 / 成熟 / 炎症 / 慢性低酸素 / グルココルチコイド / 人工胎盤 / 胎児 / ストレス / 虚血 / cortisol / コーチゾル |
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| Outline of Final Research Achievements |
The study was performed to analyze the influence of intrauterine inflammation to adrenocortical ability and to make clear that the inflammation could promote the maturation of fetal brain, adrenal cortex and ductus arteriosus using chronically instrumented premature fetal sheep. The fetuses were divided into two groups; control (n=9) and inflammation groups (n=11). We carried out CRH loading test. There was no difference between the two groups in the change of ACTH concentration (p=0.209) over time, but a significant difference in the change of cortisol (p=0.016). In the histological examination of ductus arteriosus, no difference was found between the two in the developmental score. The results could not suggest that the intrauterine inflammation would promote intimal thickening development of fetal ductus arteriosus. There is a need for further histological examination of the brain and adrenal cortex to make clear the intrauterine inflammation could promote the fetal overmaturation.
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| Academic Significance and Societal Importance of the Research Achievements |
新生児医療の進歩により，今日では極低出生体重児の合併症は組織損傷から成長障害へとその本態が移行してきていると言える．ストレス反応性のコルチゾルは胎児臓器組織の成熟を一過性に促進させるが，同時にその成長を抑制するため，長期的には臓器成長障害を誘導する危険性を有していることを本研究では検証した．今後の研究により，過度な成熟を適切に制御できれば極低出生体重児の合併症を減少させ，その長期予後を改善できる可能性がある．
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Report
(5 results)
Research Products
(13 results)
