More than 135 million births occur each year; yet, the molecular underpinnings of human parturition in gestational tissues, and in particular the placenta, are still poorly understood.
The brain is organized as a complex network of functionally communicating regions, a network also known as the functional connectome. The fetal to neonatal period is well known as a critical stage in brain development.
Microbial invasion of the amniotic cavity resulting in intra-amniotic infection (IAI) is associated with obstetrical complications such as preterm labor with intact or ruptured membranes, cervical insufficiency, as well as clinical and histological chorioamnionitis.
Any baby born less than 37 weeks after conception is considered premature, but not all premature births have the same root cause. In a new study, IRP researchers have detailed how a particular component of the immune system can trigger premature labor, which could help doctors prevent more preterm births.
Prematurity is the leading cause of perinatal morbidity and mortality worldwide. In most cases, preterm birth is preceded by spontaneous preterm labor (PTL), a syndrome that is associated with intra-amniotic inflammation, the most studied etiology. However, the remaining etiologies of PTL are poorly understood; therefore, most preterm birth are categorized as idiopathic. Whether fetal T cell activation occurs
during idiopathic PTL is unknown.