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.

The human placenta has traditionally been viewed as sterile and microbial invasion of this organ has been associated with adverse pregnancy outcomes. However, recent studies utilizing DNA sequencing techniques have reported that the human placenta at term contains a unique microbiota.

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.

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.

Preeclampsia (PE) is a major obstetrical syndrome and is classified as early if it occurs prior to 34 weeks of gestation. Current prediction models for PE combine maternal risk factors, uterine artery Doppler velocimetry, and maternal blood proteins. Although the detection rate of such models to identify patients at risk for early/preterm PE is sufficient to allow preventive strategies, the contribution of biochemical markers in these models is limited.

Overlooked Immune Cells Trigger Preterm Labor

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.

Mechanisms of death in structurally normal stillbirths

Hypoxia secondary to placental dysfunction is believed to play an important role in most fetal deaths; however, evidence is indirect. Understanding the causes of hypoxia, and the intermediary steps between hypoxia and fetal death may allow identification of biomarkers that could be used to predict and prevent fetal death in women at risk for this complication.

Functional connectome of the fetal brain

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.

Fetal cerebral blood oxygenation status could be an important physiological parameter in identifying fetuses at risk of brain injury. Moreover, this allows the understanding of oxygen metabolism in the developing fetal brain in healthy homeostatic conditions.

Fetal cerebral blood perfusion could be a more sensitive biomarker of fetal “brain sparing” at early stages of growth restriction. Fractional moving blood volume (FMBV) provides an indirect but reliable estimate of tissue blood perfusion, and is more sensitive in detecting cerebral blood flow redistribution compared to Doppler indices in fetuses with growth restriction.