Abstract
Preterm neonates exposed in utero to magnesium sulfate (MgSO4) and corticosteroids have a lower incidence of neurodevelopmental disabilities. The efficacy of MgSO4/betamethasone (BMTZ) remains poor particularly in male offspring, suggesting a differential response with fetal sex. The mechanisms by which MgSO4/BTMZ confers neuroprotection in only some patients and its relation to fetal sex is unknown. Our objective was to examine sex-specific responses to MgSO4/BMTZ in brain and placental tissue in a murine model of preterm birth and fetal neuroinflammatory injury.
Published Version
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