Objective: Placental fetal vessel thrombosis or vasculitis and retroplacental hematoma have been associated with adverse neonatal outcomes. The activation of thrombin may contribute to the development of thrombosis and inflammation, and can be assessed through the measurement of thrombin-inhibitor complexes.
Methods: A nested case-control study was performed within a cohort of women with singleton gestations.
Objective: This study was undertaken to determine whether the reduction in premature birth attributable to 17-alpha hydroxyprogesterone caproate occurs because of a greater affinity for progesterone or glucocorticoid receptors or by enhanced stimulation of progestogen responsive genes when compared with progesterone.
Study Design: We performed competitive steroid hormone receptor binding assays using cytosols expressing either recombinant human progesterone receptor-A or -B or rabbit uterine or thymic cytosols. We used 4 different carcinoma cell lines to assess transactivation of reporter genes or induction of alkaline phosphatase.
Objective: The purpose of this study was to determine whether progesterone, 17-alpha-hydroxyprogesterone, and 17-alpha hydroxyprogesterone caproate modulate the Toll-like receptor (TLR) pathway in the response of decidua to lipopolysaccharide.
Study Design: Cultured human decidual cells were incubated under control conditions, lipopolysaccharide alone, or pretreatment with each of the 3 progestins. Relative expression of 113 genes in the TLR pathway was determined by microarray.
Experimental Objectives: Activation of the oxytocin receptor (OTR) induces phospholipase C induced PIP(2) turnover in the human uterus. Relaxin (RLX), a polypeptide hormone produced in the corpus luteum of pregnancy as well as in the placenta and decidua inhibits PIP(2) turnover and subsequent signaling in human myometrium. The purpose of this study was to evaluate a possible effect of RLX on OTR regulation in human uterine smooth muscle cells.
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