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Chronic ethanol increases fetal cerebral blood flow specific to the ethanol‐sensitive cerebellum under normoxaemic, hypercapnic and acidaemic conditions: ovine model
Cerebral hypoxia has been proposed as a mechanism by which prenatal ethanol exposure causes fetal alcohol spectrum disorder (FASD) in children, but no study had tested this hypothesis using a chronicExpand
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Estrogen receptor-α and estrogen receptor-β in the uterine vascular endothelium during pregnancy: functional implications for regulating uterine blood flow.
The steroid hormone estrogen and its classical estrogen receptors (ERs), ER-α and ER-β, have been shown to be partly responsible for the short- and long-term uterine endothelial adaptations duringExpand
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All three trimester binge alcohol exposure causes fetal cerebellar purkinje cell loss in the presence of maternal hypercapnea, acidemia, and normoxemia: ovine model.
BACKGROUND The third trimester equivalent has been identified, both in rat and sheep models, as a period of cerebellar vulnerability to alcohol-mediated injury. We wished to determine whether alcoholExpand
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A Novel Role for an Endothelial Adrenergic Receptor System in Mediating Catecholestradiol-Induced Proliferation of Uterine Artery Endothelial Cells
Sequential conversion of estradiol-17&bgr; to its biologically active catecholestradiols, 2-hydroxyestradiol (OHE2) and 4-OHE2, contributes importantly to its angiogenic effects on uterine arteryExpand
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Estradiol-17&bgr; and its Cytochrome P450- and Catechol-O-Methyltransferase–Derived Metabolites Selectively Stimulate Production of Prostacyclin in Uterine Artery Endothelial Cells: Role of Estrogen
Metabolism of estradiol-17&bgr; to 2-hydroxyestradiol, 4-hydroxyestradiol, 2-methoxyestradiol, and 4-methoxyestradiol contributes importantly to the vascular effects of estradiol-17&bgr; in severalExpand
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Estradiol-17&bgr; and Its Cytochrome P450- and Catechol-O-Methyltransferase–Derived Metabolites Stimulate Proliferation in Uterine Artery Endothelial Cells: Role of Estrogen Receptor-&agr; Versus
Estradiol-17&bgr; (E2&bgr;) and its metabolites, which are sequentially synthesized by cytochrome P450s and catechol-O-methyltransferase to form 2 and 4-hydroxyestradiol (OHE2) and 2- andExpand
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Alcohol-Induced Developmental Origins of Adult-Onset Diseases.
Fetal alcohol exposure may impair growth, development, and function of multiple organ systems and is encompassed by the term fetal alcohol spectrum disorders (FASD). Research has so far focused onExpand
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Binge alcohol exposure during all three trimesters alters bone strength and growth in fetal sheep.
Women who drink while pregnant are at a high risk of giving birth to children with neurodevelopmental disorders. Heavy consumption of alcohol during pregnancy is also known to be deleterious to fetalExpand
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Proteomic profile of uterine luminal fluid from early pregnant ewes.
Embryonic development is a time-sensitive period that requires a synchronized uterine environment, which is created by the secretion of proteins from both the embryo and uterus. Numerous studies haveExpand
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Chronic binge ethanol-mediated acidemia reduces availability of glutamine and related amino acids in maternal plasma of pregnant sheep.
Heavy drinking during pregnancy can result in fetal alcohol syndrome (FAS), of which, fetal and postnatal growth retardation and central nervous system deficits are cardinal features. Although aExpand
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