My research investigates the molecular mechanisms contributing to variable fetal responsiveness to antenatal corticosteroids (ACS), a treatment routinely recommended to mothers at risk of preterm birth. ACS use had greatly reduced risk of respiratory issues and mortality but, despite over five decades of clinical use, there is limited understanding of the underlying mechanisms contributing to reduced fetal response.

Using sheep as a preclinical model of preterm birth, my research integrates molecular analyses with lung ventilation function outcomes to investigate the impact of ACS on fetal lung maturation.