Cyclic adenosine 3',5'-monophosphate increases beta-adrenergic receptor concentration in cultured human fetal lung explants and type II cells.

cAMP regulates the maturation of many biochemical processes that occur during normal lung development, including the changing levels of surfactant proteins and phospholipids. We examined the effect of cAMP on the beta-adrenergic receptor concentration in the developing human lung. Isobutylmethylxanthine, a cAMP phosphodiesterase inhibitor, increased both the tissue cAMP content and beta-adrenergic receptor concentration in treated explants above those in untreated explants.

Exposure of human amnion to amniotic fluid obtained before labor causes a decrease in chorion/decidual prostaglandin release.

Prostaglandin (PG) production by fetal membranes has been implicated in the initiation of human parturition, but its regulation is not well understood. We used an in vitro system to study paracrine control of term, fetal membrane PG production. Using a modified Ussing chamber, full thickness fetal membranes with attached decidua were sealed into a chamber so that each hemichamber was a compartment for either the fetal (amnion) or maternal (chorion/decidua) side.

The epidemiology of premenstrual symptoms in a population-based sample of 2650 urban women: attributable risk and risk factors.

This epidemiologic survey achieved a reliable measure of the prevalence of premenstrual symptoms by avoiding the biases of small or selected samples, anamnestic error, and subjective expectation. From 6232 women (a 78.8% response), aged 20-49 years, identified through a random sample of urban households, the 24-hour prevalence of symptoms was obtained using the Moos' Menstrual Distress Questionnaire, administered without reference to the menstrual cycle.

Sera from preeclamptic women specifically activate human umbilical vein endothelial cells in vitro: morphological and biochemical evidence.

Endothelial cell dysfunction could explain many of the pathophysiological changes observed in preeclampsia. Markers of endothelial cell activation including increased circulating Von Willebrand factor (VWF) and cellular fibronectin (cFN) antedate clinically evident disease. We have therefore proposed that alteration of endothelial cell function by circulating agent(s) produced by the placenta initiates the clinical syndrome.