Prenatal stress is transmitted to infant development through cortisol, which imparts sex-specific effects on the development and connectivity of the amygdalae.

A novel, translational mouse model of prenatal methadone exposure was developed and a longitudinal assessment of offspring revealed impairments in physical, behavioral, and neuronal development.

Glucocorticoid receptor directly regulates the transcriptional activity of peroxisome proliferator-activated alpha (PPARα) before birth in anticipation of the sudden shifts in the postnatal nutrient source and metabolic demands.

mTORC1 inhibition by perinatal ER stress induces beta-cell growth arrest with subsequent development of diabetes.

In a randomized controlled trial in rural Bangladesh, an intensive, combined water, sanitation, handwashing, and nutrition intervention delivered to compounds of newborn children increased telomere length attrition during their first year of life.

Airborne PM2.5 exposure triggers oxidative stress and mitochondrial apoptosis in placental trophoblast cells via the KLF9/CYP1A1 transcriptional axis, ultimately leading to adverse pregnancy outcomes.

LDT-VTA dysfunction induced by prenatal glucocorticoid exposure leads to reward deficits that can be ameliorated by selective optogenetic activation of this circuit.

Although developing oocytes and sperm of mice both harbor the glucocorticoid receptor, fetal oocytes are resistant to differing levels of gluocorcorticoid stress hormones, while spermatogonia alter RNA splicing.

A nonlinear deep generative model can represent fetal–neonatal resting-state functional magnetic resonance imaging better than conventional linear models.

Vocal development in marmoset monkeys begins in utero.