Comparison of Labor and Delivery Complications and Delivery Methods Between Physicians and White-Collar Workers.

To evaluate labor and delivery complications and delivery modes between physicians and white-collar workers in Taiwan, this retrospective population-based study used data from Taiwan's National Health Insurance Research Database. We compared 1530 physicians aged 25 to 50 years old who worked and had singleton births between 2007 and 2013 with 3060 white-collar workers matched by age groups, groups of monthly insured payroll-related premiums, previous cesarean delivery, perinatal history anemia, and gestational diabetes mellitus. The logistic regression models were used to assess the labor and delivery complications between the two groups. Multivariate analysis revealed that physicians had a significantly higher risk of placenta previa (odds ratio (OR) 1.35, 95% confidence interval (CI) 1.08-1.69) and other malpresentation (OR 1.86, 95% CI 1.45-2.39) than white-collar workers, whereas they had a significantly lower risk of placental abruption (OR 0.53, 95% CI 0.40-0.71), preterm delivery (OR 0.75, 95% CI 0.61-0.92), and premature rupture of membranes (OR 0.72, 95% CI 0.59-0.88). Increased risks of some adverse labor and delivery complications were observed among physicians, when compared to white-collar workers. These findings suggest that working women should take preventative action to manage occupational risks during pregnancy.

Non-genomic immunosuppressive actions of progesterone inhibits PHA-induced alkalinization and activation in T cells.

Progesterone is an endogenous immunomodulator, and can suppress T-cell activation during pregnancy. When analyzed under a genome time scale, the classic steroid receptor pathway does not have any effect on ion fluxes. Therefore, the aim of this study was to investigate whether the non-genomic effects on ion fluxes by progesterone could immunosuppress phytohemagglutinin (PHA)-induced human peripheral T-cell activation. The new findings indicated that, first, only progesterone stimulated both [Ca2+]i elevation and pHi decrease; in contrast, estradiol or testosterone stimulated [Ca2+]i elevation and hydrocortisone or dexamethasone stimulated pHi decrease. Secondly, the [Ca2+]i increase by progesterone was dependent on Ca2+ influx, and the acidification was blocked by Na+/H+ exchange (NHE) inhibitor, 3-methylsulphonyl-4-piperidinobenzoyl, guanidine hydrochloride (HOE-694) but not by 5-(N,N-dimethyl)-amiloride (DMA). Thirdly, progesterone blocked phorbol 12-myristate 13-acetate (PMA) or PHA-induced alkalinization, but PHA did not prevent progesterone-induced acidification. Fourthly, progesterone did not induce T-cell proliferation; however, co-stimulation progesterone with PHA was able to suppress PHA-induced IL-2 or IL-4 secretion and proliferation. When progesterone was applied 72 h after PHA stimulation, progesterone could suppress PHA-induced T-cell proliferation. Finally, immobilization of progesterone by conjugation to a large carrier molecule (BSA) also stimulated a rapid [Ca2+]i elevation, pHi decrease, and suppressed PHA-induced proliferation. These results suggested that the non-genomic effects of progesterone, especially acidification, are exerted via plasma membrane sites and suppress the genomic responses to PHA. Progesterone might act directly through membrane specific nonclassical steroid receptors to cause immunomodulation and suppression of T-cell activation during pregnancy.