Association of Pentachlorophenol with Fetal Risk of Prolonged Bradycardia: A Systematic Review and Meta-Analysis.

Objective: This study explored the systematic evaluation and meta-analysis of different concentrations of PCP on the risk of long-term bradycardia in fetuses. Methods: Cochrane Library, Embase, PubMed, China Biomedical Literature Service, CNCNKI, and Wanfang database were computerized to collect all case-control studies on the association between variety classes and different concentrations of environmental pollutant gas to fetal of prolonged bradycardia. After evaluating the quality of the inclusion study and extracting valid data, meta-analysis was performed using Stata15 software. Relative hazards were calculated using the Mantel-Haenszel method and the random effect model, and P values and I 2 values were used for heterogeneity evaluation. When heterogeneity occurs, subgroup analysis and sensitivity analysis were used to explore the sources. Results: A total of 15 studies were included, including 1202 patients with fetal of prolonged bradycardia and 1380 in the control population. Meta-analysis showed that there was no statistical difference in PCP < 0.1 mg/L between the experimental group and control group (OR = 1.03, 95% CI (0.62, 1.72), P=0.90, I 2 = 0%, Z = 0.13), but there was a statistical difference in PCP > 5 mg/L (OR = 1.73, 95% CI (1.15, 2.58), P=0.008, I 2 = 0%, Z = 2.65), PCP > 10 mg/L (OR = 1.75, 95% CI (1.19, 2.57), P=0.004, I 2 = 14%, Z = 2.85), and PCP >15 mg/L (OR = 2.02, 95% CI (1.38, 2.95), P=0.0003, I 2 = 77%, Z = 3.61). Conclusion: In this study, we found that different concentrations of PCP increased the risk of long-term bradycardia in fetuses, and the risk coefficient increased with the increase of PCP concentration.

LncRNA SNHG15 Knockdown Protects Against OGD/R-Induced Neuron Injury by Downregulating TP53INP1 Expression via Binding to miR-455-3p.

Cerebral ischemia-reperfusion (I/R) injury is the common symptom of ischemic stroke, which poses a heavy burden to human health. Long non-coding RNA (lncRNA) is indicated to be a critical regulator in cerebral ischemia. This study aims to reveal the effects of lncRNA small nucleolar RNA host gene 15 (SNHG15) on oxygen-glucose deprivation and reoxygenation (OGD/R)-induced neuron injury and underlying mechanism. The expression levels of SNHG15, microRNA-455-3p (miR-455-3p) and tumour protein p53 inducible nuclear protein 1 (TP53INP1) mRNA were determined by quantitative real time polymerase chain reaction in P12 cells. The protein levels of TP53INP1, cleaved caspase-3, caspase-3, B-cell lymphoma-2 and BCL2-associated x protein (Bax) were detected by western blot in P12 cells. Cell viability and apoptosis were revealed by cell counting kit-8 assay and flow cytometry analysis, respectively, in P12 cells. Caspase-3 activity, the levels of tumor necrosis factor-α and interleukin-1ß and the production of reactive oxygen species (ROS) were severally determined by caspase-3 activity assay, Enzyme-linked immunosorbent assay and ROS detection assay in P12 cells. The binding relationship between miR-455-3p and SNHG15 or TP53INP1 was predicted by starbase online database, and identified by dual-luciferase reporter, RNA pull-down or RNA immunoprecipitation assay. SNHG15 expression and the mRNA and protein levels of TP53INP1 were dramatically upregulated, while miR-455-3p expression was apparently downregulated in OGD/R-induced PC12 cells. SNHG15 silencing hindered the effects of OGD/R treatment on cell viability, apoptosis, inflammation and oxidative in PC12 cells; however, these impacts were restored after miR-455-3p inhibitor transfection. Additionally, SNHG15 acted as a sponge of miR-455-3p and miR-455-3p bound to TP53INP1. SNHG15 contributed to OGD/R-induced neuron injury by regulating miR-455-3p/TP53INP1 axis, which provided a novel insight to study lncRNA-directed therapy in ischemia stoke.