Emily J. Camm

TL;DR: It is tested the hypothesis that oxidative stress in the fetal heart and vasculature underlies the molecular basis via which prenatal hypoxia programmes cardiovascular dysfunction in later life and possible targets for intervention against developmental origins of cardiac and peripheral vascular dysfunction in offspring of risky pregnancy.

TL;DR: This review examines the environmental regulation of the placental phenotype with particular emphasis on the impact of maternal nutritional challenges and oxygen scarcity in mice, rats and guinea pigs and the effects of such conditions on fetal growth and the developmental programming of disease postnatally.

TL;DR: The combined use of in vivo DTI and histopathology can assist in delineating normal developmental changes and postinjury modifications in the immature rodent brain.

TL;DR: It is shown that the HI lesion results in disruption of the normal radial glia architecture, which was paralleled by an increase in GFAP immunopositive reactive astrocytes, suggesting that glial responses are central to cortical tissue remodelling following neonatal ischemia and represent a potential target for therapeutic approaches.

TL;DR: The study shows that hypoxic pregnancy increased maternal circulating and placental molecular indices of oxidative stress and whether maternal treatment with vitamin C is protective and Maternal vitamin C treatment was protective and increased birth weight.