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William Gibb

Researcher at University of Ottawa

Publications -  71
Citations -  4355

William Gibb is an academic researcher from University of Ottawa. The author has contributed to research in topics: Placenta & Fetus. The author has an hindex of 32, co-authored 71 publications receiving 4003 citations. Previous affiliations of William Gibb include Canadian Institutes of Health Research & University of Toronto.

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Endocrine and paracrine regulation of birth at term and preterm

TL;DR: In human pregnancy, it is argued that high circulating progesterone concentrations are required to effect regionalization of uterine activity, with predominantly relaxation in the lower uterine segment, allowing contractions in the fundal region to precipitate delivery.
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Prostaglandins and mechanisms of preterm birth

TL;DR: Increased uterine contractility at term and preterm results first from activation and then stimulation of the myometrium, resulting in increased concentrations of prostaglandin E2 (PGE2) in the fetal circulation and regulation of PGHS-2 at term is differentially controlled in fetal and maternal tissue.
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Expression of the multidrug resistance P-glycoprotein, (ABCB1 glycoprotein) in the human placenta decreases with advancing gestation.

TL;DR: Data indicate that with advancing gestation there is a decrease in the level of ABCB1/P-gp in the human placenta indicating that the fetus may be more susceptible to toxic insults in the latter part of gestation.
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The role of prostaglandins in human parturition

TL;DR: Prostaglandin formation is also important in infection-induced preterm labour and both phospholipase and PGHS-2 activities can be increased by various cytokines, and glucocorticoids may be important in regulating prostaglandsin formation within the human fetal membranes.
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Glucocorticoid Regulation of Human and Ovine Parturition: The Relationship Between Fetal Hypothalamic-Pituitary-Adrenal Axis Activation and Intrauterine Prostaglandin Production

TL;DR: It is suggested that in ovine pregnancy glucocorticoid-stimulated increases in intrauterine corticotropin-releasing hormone expression directly increase fetal placental prostaglandin production, and indirectly increase prostag landin production by maternal uterine tissues through the stimulation of placental estradiol synthesis.