Dijana Tesic

TL;DR: Overall, it is shown that prenatal vitamin D-deficiency leads to alterations in fetal mouse brain morphology and genes related to neuronal survival, speech and language development, and dopamine synthesis.

TL;DR: It is shown that prenatal vitamin D deficiency leads to an increase in maternal corticosterone, alterations in genes indicative of increased fetal glucocorticoid exposure and impairment in placental vascular development, which may be due to alteration in direct vitamin D-related pathways.

TL;DR: Pravastatin-induced enhancement of fetal capillaries within the placenta and the resultant hemodynamic changes correspond with restored fetal cardiac function, highlighting the potential of statins to remedy placental vascular insufficiency and enhance fetal outcomes in compromised pregnancy.

TL;DR: As adults, males that had been exposed to vitamin D deficiency in early life exhibited decreased social behaviour, impaired learning and memory outcomes and increased grooming behaviour, but unaltered affective behaviours, highlighting that early life levels of vitamin D are an important consideration for maternal behavioural adaptations as well as offspring neuropsychiatry.

TL;DR: It is revealed that selective loss of neuronal AR actions impacts the kisspeptin/GnRH/LH cascade leading to compromised ovarian follicle dynamics.