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Maternal nutrition and fetal development.
There is growing evidence that maternal nutritional status can alter the epigenetic state (stable alterations of gene expression through DNA methylation and histone modifications) of the fetal genome, which may provide a molecular mechanism for the impact of maternal nutrition on both fetal programming and genomic imprinting.
Animal Model Systems for the Study of Alcohol Teratology
  • T. Cudd
  • Biology
    Experimental biology and medicine
  • 1 June 2005
Substantial progress in this field will require the judicious use of multiple scientific approaches that use different animal model systems, and animal models will play a significant role in the effort to develop these strategies.
Pharmacokinetics and safety of arginine supplementation in animals.
It is estimated that a 70-kg human subject should be able to tolerate long-term parenteral and enteral supplemental doses of 6 and 15 g/d arginine, respectively, in addition to a basal amount of arkinine from regular diets.
Third trimester binge ethanol exposure results in fetal hypercapnea and acidemia but not hypoxemia in pregnant sheep.
It is concluded that in an ovine model system, ethanol doses that create blood ethanol concentrations as high as 260 mg/dl do not result in fetal hypoxemia and whether neurodevelopmental injuries that are associated with maternal ethanol abuse are mediated by a reduction in fetal cerebral blood flow, fetal hypercapnea, or acidemia.
Parenteral administration of L-arginine enhances fetal survival and growth in sheep carrying multiple fetuses.
Improved pregnancy outcome was associated with an increase in maternal plasma concentrations of arginine, ornithine, cysteine, and proline, as well as a decrease in circulating levels of ammonia and β-hydroxybutyrate, and these novel results indicate that parenteral administration ofArginine to prolific ewes ameliorated fetal mortality and growth retardation.
Parenteral administration of L-arginine prevents fetal growth restriction in undernourished ewes.
Results indicate that parenteral administration of l-arginine to underfed ewes prevented fetal growth restriction and provide support for its clinical use to ameliorate IUGR in humans.
Chronic ethanol increases fetal cerebral blood flow specific to the ethanol‐sensitive cerebellum under normoxaemic, hypercapnic and acidaemic conditions: ovine model
It is concluded that repeated exposure to moderate doses of ethanol during the third trimester alters fetal cerebral vascular function and increases blood flow in brain regions that are vulnerable to ethanol in the presence of acidaemia and hypercapnia, and in the absence of hypoxia.
Maternal and neonatal plasma microRNA biomarkers for fetal alcohol exposure in an ovine model.
Shared profiles between pregnant dam and neonate suggest possible maternal-fetal miRNA transfer, and Cir miRNAs are biomarkers for alcohol exposure during pregnancy, in both mother and Neonate, and may constitute an important shared endocrine biomarker that is vulnerable to the maternal environment.
Alcohol-mediated Purkinje cell loss in the absence of hypoxemia during the third trimester in an ovine model system.
Neuronal loss can be observed after alcohol exposure during the third trimester equivalent in fetal sheep in the absence of alcohol-induced hypoxemia, indicating that the lack of gross brain volume deficits from magnetic resonance imaging techniques is not a reliable indication that the brain is unaffected by the alcohol exposure.
All three trimester binge alcohol exposure causes fetal cerebellar purkinje cell loss in the presence of maternal hypercapnea, acidemia, and normoxemia: ovine model.
Findings demonstrate in an ovine model where all 3 trimester equivalent of brain growth occur in utero that the fetal cerebellar Purkinje cells are more sensitive to the timing of alcohol exposure and less so to the duration of exposure, and concludes that alcohol-induced changes in maternal arterial pH may play a role in alcohol-mediated developmental brain injury.