Evidence from Mendelian randomization: increased risk of miscarriage in patients with asthma.

OBJECTIVE: Several observational studies have revealed a possible association between asthma and miscarriage. However, inferring causal relationships from observational studies may be fraught with problems like bias, reverse causation, and residual confounding. Therefore, to assess the possible causal effect of asthma on miscarriage, we performed a two-sample Mendelian randomization (MR) analysis. MATERIALS AND METHODS: Asthma (56,167 cases and 352,255 controls) and miscarriage (9,113 cases and 89,340 controls) data from two GWAS of European ancestry were evaluated. Single nucleotide polymorphisms (SNPs) were used as instrumental variables (IVs). The random effect inverse-variance weighted (IVW) Mendelian randomization approach was used as the primary method, and MR-Egger, weighted-median, and MR-PRESSO approaches were replenished as sensitivity analysis to test the robustness of the results. RESULTS: In total, 70 SNPs were obtained using the SNP criteria. Additionally, the MR study found substantial evidence of the causality between asthma and miscarriage [IVW, OR=1.092; 95% CI=1.017-1.174; p<0.05]. The sensitivity analysis demonstrated the reliability of the MR findings [horizontal pleiotropy (MR-Egger, intercept=-0.0002; Standard error of mean, se=0.006; p=0.975)]. CONCLUSIONS: Asthma is a causal risk factor for miscarriage in European populations, according to MR evidence. Our results emphasize the significance of asthma management in reducing the risk of miscarriage in individuals with asthma.

[Toxic effect of trichloroethylene on liver cells with CYP3A4 gene defect].

OBJECTIVE: To investigate the toxic effect of trichloroethylene on liver cells with CYP3A4 gene defect. METHODS: The normal human liver cells (L02 cells) and liver cells with CYP3A4 gene defect were exposed to trichloroethylene at different doses (0.0, 0.4, 0.8, 1.6, 3.2, and 6.4 mmol/L). CCK8 assay and RT-qPCR were used to measure cell viability and changes in the expression of apoptosis genes and oncogenes. RESULTS: After being exposed to trichloroethylene at doses of 1.6, 3.2, and 6.4 mmol/L, the liver cells with CYP3A4 gene defect showed significantly higher cell viability than L02 cells (0.91±0.06/0.89±0.05/0.85±0.07 vs 0.80±0.04/0.73±0.06/0.67±0.07, P<0.05). The L02 cells in the 0.8~3.2 mmol/L trichloroethylene groups showed significant increases in the expression of the apoptosis genes caspase-3, caspase-8, and caspase-9 (P<0.05) , as well as the oncogenes c-myc, c-fos, and k-ras (P<0.05). Compared with the L02 cells, the cells with CYP3A4 gene defect showed significant reductions in the expression of the apoptosis genes caspase-3, caspase-8, and caspase-9 and the oncogenes c-myc, c-fos, and k-ras (P<0.05). CONCLUSION: Trichloroethylene exposure has a less effect on the expression of apoptosis genes and oncogenes in liver cells with CYP3A4 gene defect than in normal human liver cells, suggesting that CYP3A4 gene defect reduces the inductive effect of trichloroethylene on apoptosis genes and oncogenes.

Enhancement of bandgap emission of Pt-capped MgZnO films: important role of light extraction versus exciton-plasmon coupling.

We present on a systematic study of the contribution of surface plasmon (SP) coupling and light extraction toward emission enhancement of Platinum (Pt) nano-patterns capped MgZnO films. Time resolved Photoluminescence (PL) results indicate that the Pt coating can greatly reduces the non-radiative recombination rate by passivation of surface states, making the decay slow down. Temperature dependence of the integrated photoluminescence intensity reveals that the Pt nano-patterns can offer a large amount of light transfer and scattering, which enormously increase the light extraction efficiency up to 3.8-fold. These results indicate that the increased light extraction efficiency caused by surface modification via Pt coating rather than SP coupling plays a dominant role in increasing bandgap emission of MgZnO film.