The use of angiogenic factors in discriminating preeclampsia: are they ready for prime time?

Objectives: We sought to evaluate the association between soluble fms-like tyrosine kinase 1 (sFlt1) and endoglin (ENG) and preeclampsia in an urban population, to develop a discriminatory model, and evaluate the association of these biomarkers with small for gestational age (SGA).

Methods: Cases are prospectively identified with preeclampsia. Controls are term patients without preeclampsia.

Inflammation-induced preterm birth in a murine model is associated with increases in fetal macrophages and circulating erythroid precursors.

The presence of intrauterine inflammation has been associated with adverse neurologic outcomes in preterm infants, but the precise mechanisms of fetal brain injury remain unclear. We sought to evaluate inflammatory cell trafficking, fetal organ damage, and molecular regulation in the fetoplacental unit using an established mouse model of preterm birth associated with intrauterine inflammation. Gestational sacs were harvested 6 hours after intrauterine infusion of saline or lipopolysaccharide (LPS).

Beyond white matter damage: fetal neuronal injury in a mouse model of preterm birth.

Objective: The purpose of this study was to elucidate possible mechanisms of fetal neuronal injury in inflammation-induced preterm birth.

Study Design: With the use of a mouse model of preterm birth, the following primary cultures were prepared from fetal brains: (1) control neurons (CNs), (2) lipopolysaccharide-exposed neurons (LNs), (3) control coculture (CCC) that consisted of neurons and glia, and (4) lipopolysaccharide-exposed coculture (LCC) that consisted of lipopolysaccharide-exposed neurons and glia. CNs and LNs were treated with culture media from CN, LN, CCC, and LCC after 24 hours in vitro.

Preterm and term cervical ripening in CD1 Mice (Mus musculus): similar or divergent molecular mechanisms?

Premature cervical ripening is believed to contribute to preterm birth (PTB). Preterm cervical ripening may be due to an aberrant regulation in timing of the same processes that occur at term, or may result from unique molecular mechanisms. Using mouse models of PTB, this study sought to investigate if the molecular mechanisms that govern cervical ripening were similar between preterm and term.

Evaluating the association between all components of the metabolic syndrome and pre-eclampsia.

Objective: Hypothesising that metabolic syndrome may be associated with or useful in the prediction of pre-eclampsia, we investigated the association between all components of metabolic syndrome and C-reactive protein (CRP) in women with and without pre-eclampsia.

Methods: A case-control study was performed. Cases had gestational hypertension or pre-eclampsia and controls were term deliveries.

Maternal mortality from systemic illness: unraveling the contribution of the immune response.

Objective: Maternal morbidity and/or mortality (MM) is increased in pyelonephritis and influenza. Alterations in the immune response could account for the increase MM. We sought to determine whether the immune response is functionally different during pregnant and nonpregnant (NP) states.

Preventing cervical ripening: the primary mechanism by which progestational agents prevent preterm birth?

Objective: Recent clinical trials suggest that progestational agents may prevent preterm birth, specifically in women with short cervices. These studies sought to assess novel pathways by which progestational agents (PAs) may modify signal transduction pathways that are involved in cervical ripening.

Study Design: A microarray analysis was performed on pregnant mouse cervix that was exposed to a MPA.

Toll-like receptors in the uterus, cervix, and placenta: is pregnancy an immunosuppressed state?

Objective: These studies were performed to elucidate the expression of Toll-like receptors (TLRs) in the uterus, cervix, and placenta in pregnancy and across gestation.

Study Design: Message expressions of TLR-2, -3, -4, and -9 were investigated in nonpregnant mice and across gestation in CD-1 mice. Uterine, cervical, and placental tissues were harvested, and RNA was extracted.