The Combined Influence of Maternal Medical Conditions on the Risk of Primary Cesarean Delivery.

 Common maternal medical comorbidities such as hypertensive disorders, diabetes, tobacco use, and extremes of maternal age, body mass index, and gestational weight gain are known individually to influence the rate of cesarean delivery. Numerous studies have estimated the risk of individual conditions on cesarean delivery.  To examine the risk for primary cesarean delivery in women with multiple maternal medical comorbidities to determine the cumulative risk they pose on mode of delivery.

Placental nanoparticle gene therapy normalizes gene expression changes in the fetal liver associated with fetal growth restriction in a fetal sex-specific manner.

Fetal growth restriction (FGR) is associated with increased risk of developing non-communicable diseases. We have a placenta-specific nanoparticle gene therapy protocol that increases placental expression of (), for the treatment of FGR . We aimed to characterize the effects of FGR on hepatic gluconeogenesis pathways during early stages of FGR establishment, and determine whether placental nanoparticle-mediated therapy treatment could resolve differences in the FGR fetus.

Sexual dimorphisms in brain gene expression in the growth-restricted guinea pig can be modulated with intra-placental therapy.

Background: Fetal responses to adverse pregnancy environments are sex-specific. In fetal guinea pigs (GPs), we assessed morphology and messenger RNA (mRNA) expression in fetal growth-restricted (FGR) tissues at midpregnancy.

Methods: Female GPs were assigned either an ad libitum diet (C) or 30% restricted diet (R) prior to pregnancy to midpregnancy.

Nanoparticle mediated increased insulin-like growth factor 1 expression enhances human placenta syncytium function.

Introduction: Placental dysfunction is an underlying cause of many major obstetric diseases and treatment options for complications like fetal growth restriction (FGR) are limited .We previously demonstrated nanoparticle delivery of the human insulin-like growth factor 1 (hIGF1) transgene under control of the trophoblast-specific PLAC1 promoter maintains normal fetal growth in a surgically-induced FGR mouse model. However, uptake by human placental syncytiotrophoblast has yet to be determined.