| Project/Area Number |
10671535
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Osaka University |
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Principal Investigator |
KIMURA Tadashi Osaka University, Graduate School of Medicine Assistant Professor, 医学系研究科, 助手 (90240845)
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| Co-Investigator(Kenkyū-buntansha) |
OOHASHI Kazutomo Osaka University, Graduate School of Medicine, Lecturer retire, 医学系研究科, 講師 (30203897)
AZUMA Chihiro Osaka University, Graduate School of Medicine, Lecturer, 医学系研究科, 講師 (20151061)
MURATA Yuji Osaka University, Graduate School of Medicine, Professor, 医学系研究科, 教授
HASHIMOTO Kazumasa Osaka University, Graduate School of Medicine Assistant Professor retire, 医学系研究科, 助手 (80301266)
TOKUGAWA Yoshihiro Osaka University, Graduate School of Medicine Assistant Professor, 医学系研究科, 助手 (70283786)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | fetal brain injury / oxidative stress / intrauterine growth retardation (IUGR) / preterm birth / knockout mice / 8-oxoグアニン / Mut-T |
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| Research Abstract |
The majour backgrounds for fetal central nerve injury during the course of pregnancy are intrauterine growth retardation (IUGR) and preterm birth. In order to elucidate the effect of oxidative stress on the pathogenesis of IUGR, we measured the amount of 8-oxodeoxyguanine (8-OHdG) in the samples of amniotic fluid and placental genomic DNA. We also examined the expression levels of enzymes Mut-T and Mut-Y, which deeply concern with elimination of 8OHdG from nucleotide pool. The concentration of 8OHdG in the amniotic fluid was lower in the IUGR group than control samples, whereas the 8OHdG amount in the placental chromosomal DNA was equivalent between two groups. The expression levels of Mut-T and Mut-Y mRNA, estimated by RT-PCR, were lower in the placental tissues of IUGR group These result suggested that fetus, rather than placenta are more affected by oxidative stress as pathogenesis of IUGR. Another background of fetal nerve injury should be preterm birth. One of pathophysiology of p
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reterm birth could be premature expression of oxytocin receptor in myometrium. To elucidate the mechanism of this expression, we attempted to clone DNA binding proteins to the oxytocin receptor gene. hMafF, a chicken MafF homologue, was obtained from Yeast one-hybrid screening which has the leucine zipper structure and binds specifically to the oxytocin receptor gene. hMafF mRNA as specifically expressed in term myometrium, whilst the expression during preterm myometrium should further be examined. The knock out mice model could also be an attractive model for investigation of the mechanism of preterm birth. We have literary reviewed the results of mice lacking the genes concerned as the important factor for preterm birth. Many kinds of knock out mice had developed, although most of them appears to be normal on their parturition, i. e., not informative for the investigation of preterm birth.
We have analysed several factors for the background of fetal neurological injury. However, we failed to show the direct pathophysiological relationship within the fetal brain. We should develop novel strategy to evaluate fetal brain directly. Less
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