Judith A. Wubah

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BACKGROUND Many birth defects are believed to involve gene-environment interactions, although the mechanisms involved are poorly understood. Apoptosis is a common effect of many kinds of environmental stresses on the developing embryo; therefore, mechanisms of teratogenesis may be approached within the context of the cell death program. The p53 tumor(More)
BACKGROUND Treatment of pregnant mice with 2-chloro-2'-deoxyadenosine (2CdA) on day 8 of gestation induces microphthalmia through a mechanism coupled to the p53 tumor suppressor gene. The present study defines 2CdA dosimetry with respect to exposure (pharmacokinetics), p53 protein induction, and disease (microphthalmia). METHODS Pregnant CD-1 mice dosed(More)
Inactivation of the tumor suppressor p53 is associated with neural tube defects and altered teratogenicity in early embryos. To gain insight into the function of p53 during early embryogenesis, RNA profiles of wild-type p53(+/+) and p53(-/-) null mutant mouse embryos were compared at the head-fold stage (day 8 post coitum) using HPLC-based mRNA differential(More)
BACKGROUND The purine analog 2-chloro-2'-deoxyadenosine (2-CdA) caused ocular and limb defects in the mouse and rabbit. The current study examined the teratogenic potential of this drug in the rat and compared the adverse developmental outcomes with the other species. METHODS Timed-pregnant Sprague-Dawley rats were given a single intraperitoneal injection(More)
Adenosine is a short-range signal molecule that surges in the mouse uterus immediately after blastocyst implantation (Blackburn et al. [1992] Dev. Dyn. 194:155-168). The present study has investigated patterns of uterine adenosine receptor expression during early post-implantation development. Strong expression of the A2b adenosine receptor was observed.(More)
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