| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Research Abstract |
1. Incidence of cardiovascular anomalies in bis-diamine treated rat embryos A bis-diamine administration to pregnant rats could induce cardiovascular anomalies including tetralogy of Fallot, ventral septal defect and patent truncus arteriosus. However, the incidence was different between Sprague-Dawley (SD) and Wister rats. When a single dose of 200 mg bis-diamine was administered to 9.5,10.5 and 11 pregnant day SD and Wister mother rats, the incidences of cardiovascular anomalies were 35.1%, 64.1% and 10.5%, and 100%, 92.8% and 45.6%, respectively.
2. Morphological and histological analysis of the heart in Bis-diamin treated and control rat embryos raised in whole embryo culture. Single dose of 200 mg bis-diamine was administered to the pregnant Wister rats on 10.5 pregnant day. The embryos were removed at 6 hours after bis-diamine administration and immediately cultured for 24 and 48 hours following the procedures described by New et al (1973). (1) Morphological analysis : There was n
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o difinite developmental and morphological difference between bis-diamine-treated and control embryos after 24 hours culture. However, poor development of the truncal ridges could be observed in bis-diamine treated embtryos after 48 hours culture, when compared with control embyos. (2) Histological analysis : In the poorly developed truncal ridges of the bis-diamine treated embryos after 48 hours culture, there were less HNK-1 or N-CAM immunoreactive mesenchymal cells in comparison with control embryos. Furthermore, a HNK-1 or N-CAM immunoreactive chain from the neural crest to the truncus arteriosus via the 3rd, 4th and 6th aortic arches, which was clearly recognized in the control embryos after 24 or 48 hours culture, could not be detected in the bis-diamine treated ones. These findings suggested that bis-diamine prevented neural crest cells from normal migration into the heart or transformation into truncal mesenchymal cells, inducing abnormal truncal division and subsequent cardiac defects with truncal anomalies. Less
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