BackgroundDue to the high prevalence in pregnant women and potential association with pregnancy complications or perinatal outcomes, sleep-disordered breathing (SDB) has become an increasing concern.MethodsPubmed and Embase were retrieved from inception until 2017 to conduct a meta-analysis to explore the association of SDB and several outcomes during gestation. A stratified analysis differentiated by the type of SDB [snoring alone/obstructive sleep apnea (OSA)] was also performed. Pooled odds ratios were produced for binary outcomes. Weighted mean differences were also produced for continuous outcomes. Sensitivity analysis was performed to identify the impact of individual studies on summary results and estimation of publication bias was performed by funnel plot.Results35 studies with a total of 56,751,837 subjects were included. SDB during pregnancy was associated with a significantly increased risk of gestational diabetes mellitus (GDM), pregnancy-induced hypertension (PIH), and preeclampsia (PEC), but not significantly associated with fetal maternal outcomes, namely APGAR score and birth weight. Moreover, OSA was linked with an increasing risk of GDM, PIH, PEC and preterm birth while snoring appeared to increase the risk of GDM, PIH, and PEC.ConclusionThe finding provided potential evidence for association between SDB and adverse perinatal outcomes. SDB increased the risk of some pregnancy complications while its influence to fetal outcomes was not clear.

Endothelial cells are thought to play a key role in sepsis pathogenesis: vascular endothelial damage occurs in severe sepsis and multiple organ dysfunction. Soluble vascular endothelial cadherin (VE-cadherin) levels were investigated in a prospective study involving 28 consecutive critically ill patients with or without severe sepsis who were admitted to surgical intensive care; 13 healthy age-matched volunteers were included as controls. Soluble VE-cadherin levels increased significantly in patients with severe sepsis compared with ill patients without severe sepsis and healthy controls. There was a significant linear correlation between soluble VE-cadherin levels and illness severity scores. Soluble VE-cadherin levels were significantly higher in patients who died compared with survivors. In vitro cell culture showed that serum from patients with severe sepsis greatly decreased VE-cadherin staining at intercellular junctions and total VE-cadherin expression in human umbilical cord vein endothelial cells. These findings suggest that endothelial cells play an important role in the poor outcome of patients with severe sepsis.

Quinocetone (QCT), a new quinoxaline 1,4-dioxides, has been used as antimicrobial feed additive in China. Potential genotoxicity of QCT was concerned as a public health problem. This study aimed to investigate the protective effect of curcumin on QCT-induced oxidative stress and genotoxicity in human hepatocyte L02 cells. Cell viability and intracellular reactive oxygen species (ROS), biomarkers of oxidative stress including superoxide dismutase (SOD) activity and glutathione (GSH) level were measured. Meanwhile, comet assay and micronucleus assay were carried out to evaluate genotoxicity. The results showed that, compared to the control group, QCT at the concentration ranges of 2-16 μg/mL significantly decreased L02 cell viability, which was significantly attenuated with curcumin pretreatment (2.5 and 5 μM). In addition, QCT significantly increased cell oxidative stress, characterized by increases of intracellular ROS level, while decreased endogenous antioxidant biomarkers GSH level and SOD activity (all p < 0.05 or 0.01). Curcumin pretreatment significantly attenuated ROS formation, inhibited the decreases of SOD activity and GSH level. Furthermore, curcumin significantly reduced QCT-induced DNA fragments and micronuclei formation. These data suggest that curcumin could attenuate QCT-induced cytotoxicity and genotoxicity in L02 cells, which may be attributed to ROS scavenging and anti-oxidative ability of curcumin. Importantly, consumption of curcumin may be a plausible way to prevent quinoxaline 1,4-dioxides-mediated oxidative stress and genotoxicity in human or animals.