Study on the association between ambient air pollution and daily cardiovascular death in Hefei, China.

Cardiovascular disease has always been the most serious public health problem in China. Although many studies have found that the risk of death caused by cardiovascular disease is related to air pollutants, the existing results are still inconsistent. The aim of this study was to investigate the effects of air pollutants on the risk of daily cardiovascular deaths in Hefei, China. Daily data on cardiovascular deaths, daily air pollutants, and meteorological factors from 2007 to 2016 were collected in this study. A time-series study design using a distributed lag nonlinear model was employed to evaluate the association between air pollutants and cardiovascular deaths. First, a single air pollutant model was established based on the minimum value of Akaike information criterion (AIC), and the single day lag effects and multi-day lag effects were discussed separately. Then, two-pollutant models were fitted. Subgroup analyses were conducted by gender (male and female), age (< 65 age and ≥ 65 age), and disease type (ischemic heart disease and cerebral vascular disease). There were 34,500 cases of cardiovascular deaths during the period 2007-2016, and the average concentrations of air pollutants (PM10, SO2, NO2, PM2.5, CO, O3) were 106.11, 20.34, 30.49, 72.59, 958.7, and 67.88 µg/m3, respectively. An increase of interquartile range (IQR) in PM10, SO2, NO2, PM2.5, CO, and O3 were associated with an increase of 4.34% (95%CI 1.54~7.23%) at lag 0-6, 5.79% (95%CI 2.43~9.27%) at lag 0-5, 4.47% (95%CI 1.64~7.37%) at lag 0-5, 3.14% (95%CI 0.03~6.36%) at lag 0-4, 3.11% (95%CI 0.21~6.10%) at lag 0-3, and 8.17% (95%CI 1.89~14.84%) at lag 0-5 in cardiovascular deaths, respectively. Females, older group (≥ 65 years) and deaths from cerebral vascular disease were more vulnerable to air pollution than males, younger individuals (< 65 years) and deaths from ischemic heart disease. Our results suggest that air pollution increased the risk of cardiovascular deaths in Hefei. These findings can provide evidence for effective air quality interventions in Hefei.

Impact of ambient temperature on hospital admissions for cardiovascular disease in Hefei City, China.

Many studies have quantified the hospitalization risk for cardiovascular disease (CVD) caused by temperature, but the results of most studies are not consistent. In this study, we evaluate the effect of temperature on CVD hospitalizations. We use a quasi-Poisson regression with a distributed-lag nonlinear model (DLNM) to evaluate the effect of temperature on CVD hospitalizations between July 1, 2015, and October 31, 2017, in Hefei City, China. We found that the cold effect and heat effect of temperature can impact CVD hospital admissions. Compared with the 25th percentile of temperature (10.3 °C), the cumulative relative risk (RR) of extremely low temperature (first percentile of temperature, 0.075 °C) over lags 0-27 days was 0.616 (95% CI 0.423-0.891), and the cumulative RR of moderate low temperature (10th percentile of temperature, 5.16 °C) was 1.081 (95% CI 1.019-1.147) over lags 0-7 days. Compared with the 75th percentile of temperature (25.6 °C), the cumulative RR of extremely high temperature (99th percentile of temperature, 33.7 °C) was 1.078 (95% CI 0.752-1.547) over lags 0-27 days, and the cumulative RR of moderate-high temperature (90th percentile of temperature, 29.0 °C) was 1.015 (95% CI 0.988-1.043) over lag 0 day. In the subgroup, the < 65-year group and male were more susceptible to low temperature; however, the ≥ 65-year group and female were more vulnerable to high temperature. The high temperature's impact on CVD hospital admissions was found to be more obvious in female and the ≥ 65-year group compared to male and the < 65-year group. However, the < 65-year group and men are more sensitive to low temperature.

RETRACTED: Ginsenoside Rg1 protects human retinal pigment epithelial ARPE-19 cells from toxicity of high glucose by up-regulation of miR-26a.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. Given the comments of Dr Elisabeth Bik regarding this article "… the Western blot bands in all 400+ papers are all very regularly spaced and have a smooth appearance in the shape of a dumbbell or tadpole, without any of the usual smudges or stains. All bands are placed on similar looking backgrounds, suggesting they were copy/pasted from other sources, or computer generated", the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article.

An increase of estrogen receptor α protein level regulates BDE-209-mediated blood-testis barrier disruption during spermatogenesis in F1 mice.

Deca-bromodiphenyl ether (BDE-209) regulates various aspects of spermatogenesis and male fertility through its effect on estrogen receptor α (ERα), but the underlying mechanism remains unclear. Because molecular mechanisms such as remodeling of the blood-testis barrier (BTB) play crucial roles in spermatogenesis, we investigated the disruptive effects of ERα agonists on the BTB in spermatogenesis. In this study, 0, 300, and 500 mg/kg/day of BDE-209 were administered to pregnant adult mice by oral gavage from gestation day 7 to postnatal day 21. SerW3 cells were treated with methylpiperidino pyrazole (MPP) for 30 min before being treated with 50 µg/mL of BDE-209. BDE-209 increases ERα in time- and dose-dependent manners and decreases formin 1 and BTB-associated protein in F1 male mice. Furthermore, BDE-209 impairs the structure and function of the BTB. Activation of ERα signaling could disrupt the BTB, leading to spermatogenesis dysfunction. The results identified the role of ERα in BTB disruption during spermatogenesis and suggested that BTB disruption occurs because of exposure to BDE-209, which could potentially affect spermatogenesis. In conclusion, Sertoli cells seem to be the primary target of BDE-209 in the perinatal period, and this period constitutes a critical window of susceptibility to BDE-209. Also, the SerW3 cell model may not be a particularly useful cell model for studying the function of the cytoskeleton.