John R. G. Challis
University of Toronto
392 Papers
5.8K Citations
John R. G. Challis is an academic researcher from University of Toronto. The author has contributed to research in topics: Fetus & Placenta. The author has an hindex of 70, co-authored 392 publications. Previous affiliations of John R. G. Challis include McMaster University & Canadian Institutes of Health Research.
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Papers
Formation of Unconjugated Estrogens from Estrone Sulfate by Dispersed Cells from Human Fetal Membranes and Decidua
TL;DR: It is concluded that human amnion, chorion, and decidua possess the capability to hydrolyze E1S to free estrogen and that this activity in chorions and decidsua is increased after spontaneous vaginal delivery.
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Fetal sheep endocrine responses to sustained hypoxemic stress after chronic fetal placental embolization
TL;DR: PGE2 response to a sustained superimposed reduction in placental blood flow, leading to metabolic acidosis, is enhanced under conditions of chronic hypoxemia and may play an important role for the maintenance of the fetal cortisol response to an episode of superimposed acute stress.
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•Journal Article
Hormonal control of preterm and term parturition.
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Ovine surfactant protein cDNAs: use in studies on fetal lung growth and maturation after prolonged hypoxemia
Geert A. Braems,Geert A. Braems,Li-Juan Yao,Li-Juan Yao,Kevin Inchley,Kevin Inchley,Anne Brickenden,Victor K. M. Han,Allen Grolla,John R. G. Challis,John R. G. Challis,John R. G. Challis,Fred Possmayer +12 more
TL;DR: Mild prolonged fetal hypoxia produces alterations that could affect fetal cellular differentiation early in gestation and can induce changes consistent with lung maturation closer to term, which is suggested to be consistent with postnatal lung function.
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Effect of Pro-inflammatory Cytokines on Expression and Activity of 11β-Hydroxysteroid Dehydrogenase Type 2 in Cultured Human Term Placental Trophoblast and Human Choriocarcinoma JEG-3 Cells:
TL;DR: It is suggested that TNF-α and IL-1β may increase the amount of cortisol crossing to the placenta and fetal circulation by attenuating 11β-HSD2 activity, potentially contributing to preterm labor and altered fetal outcome in uterine infection.
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