Maternal blood serum and plasma human tumor-associated antigen RCAS1 during the course of uncomplicated pregnancies: a prospective study.

Problem: we aimed to investigate the expression of the tumor-associated RCAS1 protein in maternal blood of uncomplicated pregnancies.

Method Of Study: maternal blood was obtained from women with uncomplicated pregnancies (N = 43) at 11-13, 20-22, 32-34, 37-38 weeks of gestation, and immediately after delivery. Serum RCAS1 concentration was studied by ELISA, and plasma mRNA was subjected to real-time (RT)-PCR.

Nicotine restores endothelial dysfunction caused by excess sFlt1 and sEng in an in vitro model of preeclamptic vascular endothelium: a possible therapeutic role of nicotinic acetylcholine receptor (nAChR) agonists for preeclampsia.

Objective: In this study we tested the hypothesis that nicotine restores proangiogenic functions to endothelial cells pretreated with soluble fms-like tyrosine kinase 1 and/or soluble endoglin.

Study Design: Wound healing assay and tube formation assay were performed using human umbilical vein endothelial cells treated with nicotine (10(-9) to 10(-6) M), and with various combinations of soluble fms-like tyrosine kinase 1 (100 ng/mL), soluble endoglin (100 ng/mL), and nicotine (10(-7) M). Enzyme-linked immunosorbent assay was performed to measure vascular endothelial growth factor, placental growth factor, and transforming growth factor-beta1 concentrations in the conditioned media treated with nicotine (10(-9) to 10(-6) M).

Nicotine suppresses interleukin-6 production from vascular endothelial cells: a possible therapeutic role of nicotine for preeclampsia.

Normal pregnancy is the controlled state of inflammation and this systemic inflammatory response is reported to be more intense in preeclampsia. The current study tested the hypothesis that maternal serum stimulates interleukin 6 (IL-6) production from endothelial cells and that nicotine inhibits these effects. Human umbilical vein endothelial cells (HUVECs) were incubated with or without 0.