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Ou HC, Lee WJ, Lee IT, Chiu TH, Tsai KL, Lin CY, Sheu WH. Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells.

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Three cases of primary hyperparathyroidism in pregnancy are described. Patient 1 developed left thigh pain and lower abdominal pain at 34 weeks' gestation. Patient 2 had right flank pain and lower abdominal pain at 32 weeks' gestation. Both patients accepted medical therapy initially, which resulted in poor control of hypercalcemia. Patient 1 delayed her parathyroidectomy until the postpartum period; she had maternal hypercalcemia and neonatal hypocalcemia. Patient 2 accepted parathyroidectomy at 32 weeks' gestation with an uneventful outcome for both mother and baby. Patient 3 was asymptomatic; her hyperparathyroidism was diagnosed postpartum after neonatal hypocalcemia and agreed to parathyroidectomy. All 3 patients had a parathyroid adenoma.

BackgroundWe examined the risk for Group B streptococcus (GBS)-related diseases in newborns born to mothers who participated in a universal GBS screening program and to determine whether differences are observed in factors affecting the morbidity for neonatal early-onset GBS-related diseases.MethodsThis is a retrospective study and the study subjects were women who had undergone GBS screening and who gave birth naturally and their newborns between April 15, 2012 and December 31, 2013. Data from the GBS screening system database and the National Health Insurance database were collected to calculate the GBS prevalence in pregnant women and morbidity of newborns with early-onset GBS-related diseases.ResultsThe GBS prevalence in pregnant women who gave birth naturally was 19.58%. The rate of early-onset infection caused by GBS in newborns decreased from the original 0.1% to 0.02%, a decrease of as high as 80%. After the implementation of the universal GBS screening program, only three factors, including positive GBS screening result (OR = 2.84), CCI (OR = 2.45), and preterm birth (OR = 4.81) affected the morbidity for neonatal early-onset GBS-related diseases, whereas other factors had no significant impact.ConclusionThe implementation of the universal GBS screening program decreased the infection rate of neonatal early-onset GBS diseases. The effects of socioeconomic factors and high-risk pregnancy on early-onset GBS infections were weakened.

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This study investigated whether mothers with prenatal environmental tobacco smoke (ETS) exposure increased the newborn genetic damage and adverse birth outcomes. Study participants were women receiving prenatal care at three hospitals in Central Taiwan and their newborns. Participants were divided into two groups (nonsmokers and ETS-exposed non-smokers) based on maternal ETSexposed status. Comet assay were performed for cord blood samples. Infants born to mothers with prenatal ETS exposure had the highest mean cord blood DNA damage score (69.7 Ϯ 42.3) and poorer birth outcomes. No negative fetal growth effects appeared among newborns with low DNA damage levels. Among newborns with high DNA damage levels (comet scores Ͼ50), those born to prenatal ETS exposure had an average reduction of 252.7 g in birth weight, 1.10 cm shorter in length and a 0.92-cm decrease in head circumference, compared to newborns with no smoking exposure. This study shows that the DNA damage scores can be used as an effect-modifier on the relationships between ETS exposure and adverse birth outcome. The association appears more apparent for the ETS exposure in relation with more severe DNA damage. S tudies have suggested adverse reproductive outcomes among newborns in relation to maternal cigarette smoking and environmental tobacco smoke (ETS) exposure during pregnancy. Most of these studies are based on self-reported smoking status, and serum or urinary cotinine levels as the exposure measures (1-6). Some studies failed to find a significant association (7-11). The discrepancy could be explained by the variability of study populations, sample size, study design, and individual susceptibility (12,13). Other markers linking the association between smoking and/or ETS and pregnant outcomes deserve exploration.Cigarette smoke contains more than 4000 chemicals (14), including carcinogens such as polycyclic aromatic hydrocarbons (PAHs), arylmines, N-nitrosamines (15,16), and aromatic amines. These compounds can cross the placenta and experimental animal studies have indicated that the fetus and newborn are more susceptible to carcinogens than adults (17)(18)(19). A study of white population showed that there is an increased susceptibility to DNA damage from PAHs and the diminished ability to clear ETS components for the fetus (20). de la Chica et al. found that maternal smoking exposure increase structural chromosomal abnormalities and chromosomal lesions in fetus (21). However, the effect of genotoxicity determined by comet assay for infants with prenatal smoking exposure has not been well documented. The comet assay is a sensitive technique allowing the detection of DNA damage at the single cell level. This assay is also effective in detecting DNA damage induced by tobacco smoke toxicants in white blood cells (22).The smoking prevalence among women in Taiwan has recently increased to 5.95%, and as many as 42.4% of women are daily exposed to ETS (23). Another studies in Taiwan showed that 58% of pregnant women and 57% of neversmoked wo...

Abstract.It is well known that the response of cancer cells to chemotherapeutic drugs involves the activation of apoptotic pathways. Benzyl isothiocyanate (BITC) is an important compound found in plant food and has been shown to have anti-cancer effects on human cancer cells, but its effect on prostate cancer cells in vitro remains unknown. The aim of the present study was to investigate the effects of BITC on DU 145 human prostate cancer cells in order to clarify whether a time/concentration range for optimal BITC-induced apoptosis exists and to find the associated signaling pathway. Cell morphological changes, percentage of cell viability, DNA damage and apoptosis in DU 145 cells were examined by phase-contrast microscopy, flow cytometric assay, 4',6-diamidine-20-phenylindole dihydrochloride staining, comet assay and Western blotting analysis. The results indicate that BITC induces cell morphological changes, decreases the percentage of viable cells (induction of cell cytotoxicity), and induces DNA damage and apoptosis in DU 145 cells in a time-and dose-dependent manner. Flow cytometric assays indicated that BITC promoted reactive oxygen species and Ca 2+ productions and decreased the levels of mitochondrial membrane potential (ΔΨm), while the pre-treatment with N-acetylcysteine caused an increase in the percentage of viable cells. BITC also promoted caspase-3, -8 and -9 activities. Furthermore, when cells were pre-treated with the caspase-3 inhibitor and then treated with BITC, this led to an increase in the percentage of viable cells. Confocal laser microscopy examination indicated that BITC promoted the expression of AIF and Endo G, which were released from the mitochondria in DU 145 cells. In conclusion, BITC induces apoptosis in DU 145 cells through the release of AIF and Endo G from the mitochondria and also promotes caspase-3 activation.