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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.

// Dao-Jun Chen 1, 2 , Lan-Ju Li 1, 2 , Xiao-Ke Yang 1, 2 , Tao Yu 1, 2 , Rui-Xue Leng 1, 2 , Hai-Feng Pan 1, 2 and Dong-Qing Ye 1, 2 1 Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China 2 Anhui Province Key Laboratory of Major Autoimmune Diseases, Hefei, Anhui, China Correspondence to: Dong-Qing Ye, email: ydqahmu@gmail.com , ydq@ahmu.edu.cn Keywords: microRNA, vitamin D, SLE, T cells Received: August 15, 2016 Accepted: May 31, 2017 Published: July 07, 2017 ABSTRACT Vitamin D has been recognized as a potent immunomodulator and its deficiency is common in different population groups including patients with SLE. As miRNAs regulation plays a significant role in SLE, the present study aimed to evaluate the association between vitamin D status and miRNAs levels in patients with SLE. The serum concentrations of vitamin D (25-hydroxyvitamin D) and the levels of six miRNAs in T cells from patients with SLE were measured in 42 SLE cases and 48 healthy controls. Vitamin D treatment was also performed in isolated and cultured T cells from SLE patients in different times and doses. Vitamin D insufficiency (25-hydroxyvitamin D concentration

Epidemiological studies demonstrate a linkage between morbidity and mortality and particulate matter (PM), particularly fine particulate matter (PM2.5) that can readily penetrate into the lungs and are therefore more likely to increase the incidence of respiratory and cardiovascular diseases. The present study investigated the compositions of cooking oil fume (COF)-derived PM2.5, which is the major source of indoor pollution in China. Furthermore, oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest induced by COF-derived PM2.5 in primary fetal alveolar type II epithelial cells (AEC II cells) were also detected. N-acetyl-L-cysteine (NAC), a radical scavenger, was used to identify the role of oxidative stress in the abovementioned processes. Our results suggested that compositions of COF-derived PM2.5 are obviously different to PM2.5 derived from other sources, and COF-derived PM2.5 led to cell death, oxidative stress, apoptosis, and G0/G1 cell arrest in primary fetal AEC II cells. Furthermore, the results also showed that COF-derived PM2.5 induced apoptosis through the endoplasmic reticulum (ER) stress pathway, which is indicated by the increased expression of ER stress-related apoptotic markers, namely GRP78 and caspase-12. Besides, the induction of oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest was reversed by pretreatment with NAC. These findings strongly suggested that COF-derived PM2.5-induced toxicity in primary fetal AEC II cells is mediated by increased oxidative stress, accompanied by ER stress which results in apoptosis.

Epidemiological studies indicated that there is an increased risk of respiratory tract cancer among cooks and bakers. The cooking oil fumes are believed to conduct this risk, and many studies have focused on evaluating the mutagenicity and finding the mutagenic components in oil fumes. COFs contains two major classes of compounds. One class consists of polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene, benzo[b]fluoranthene, fluoranthene, and benzo[g,h,i]perylene. BaP is a known immunosuppressant. It can also alter cell cycle progression, induce inflammation, and impair DNA repair and apoptotic processes leading to aberrant cellular functioning. This study investigates the effect of toxicity of cooking oil fumes (COFs) in primary ICR mice' fetal lung type II-like epithelium cells (AEC II). The cells were cultured in different concentrations (0, 12.5, 25, 50, 100, and 200μg/ml) of COFs for different time periods. The results showed that cell viability decreased in a dose- and time- dependent manner, which is accompanied by increased malondialdehyde (MDA) level and decreased superoxide dismutase (SOD) and glutathione (GSH) activities. Moreover, comet assay suggested DNA damage, as well as increased production of DNA adducts induced by PAHs. The present study also shows that COFs may disturb cell cycles even at a very low dose. In summary, the present study indicates that COFs may lead to toxicity in AEC II cells.

Systemic lupus erythematosus (SLE) is an autoimmune disease. Cytokine-mediated immunity plays an important role in the pathogenesis of SLE. TNF-like ligand 1A (TL1A) belongs to the TNF superfamily of cytokines and has been found to perform significantly in autoimmune diseases, such as rheumatoid arthritis and inflammatory bowel disease. To date, no study has discussed the expression levels of TL1A in SLE. We found that plasma levels of TL1A were significantly higher in newly diagnosed SLE patients compared with controls. Correlation analysis showed that plasma levels of TL1A were positively associated with SLE disease activity index. These data indicated that TL1A may play a role in SLE and may reflect the disease activity for SLE.

The Ubiquitin carboxy-terminal hydrolase-L1 (UCHL1) is a candidate risk gene for Parkinson’ disease (PD), and a function SNP (rs5030732) in the coding region of this gene has been studied for the association with the disease extensively among worldwide populations, but the results were inconsistent and controversial. Here, to estimate the association between UCHL1 S18Y polymorphism and risk of PD in general population, we conducted a systematic meta-analysis by combining all available case–control subjects in Asian, European, and American populations, with a total of 7742 PD cases and 8850 healthy controls, and the pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for UCHL1 S18Y polymorphism and PD were calculated using the Mantel–Haenszel method with a fixed- or random-effects model. Subgroup analysis was also performed in different onset age-matched groups. Among high-quality studies, UCHL1 S18Y polymorphism was moderately associated with the risk of PD (allele contrasts, OR = 1.063, 95 % CI 1.008–1.122; p = 0.024; regressive genetic model, OR = 1.078, 95 % CI 1.005–1.157; p = 0.035). When stratifying for ethnicity, none association were observed in subgroups. Analysis of early-onset PD (EOPD) and late-onset PD (LOPD) revealed that the polymorphism was not associated with the risk of PD. In conclusion, our meta-analysis suggests that UCHL1 S18Y polymorphism is moderately associated with susceptibility to PD, and more studies are needed to confirm our conclusion.

The aim of this study was to explore the association between follicle stimulating hormone receptor (FSHR) Thr307Ala and Asn680Ser polymorphisms and susceptibility to polycystic ovary syndrome (PCOS). A comprehensive literature search for relevant studies was conducted on Google Scholar, PubMed, the Chinese National Knowledge Infrastructure (CNKI) and the Chinese Biomedical Literature Database (CBM). This meta-analysis was performed using the STATA 11.0 software and the pooled odds ratio (OR) with 95% confidence interval (CI) was calculated. Ten case-control studies were included in this meta-analysis. However, meta-analysis results showed no association between both FSHR Thr307Ala polymorphism and Asn680Ser polymorphism and susceptibility to PCOS. Stratified analysis of ethnicities also showed no association. In conclusion, the present study suggested that the FSHR polymorphisms were not associated with an increased risk of PCOS and larger-scale studies of populations are needed to explore the roles played by FSHR polymorphisms during the pathogenesis of PCOS.

To explore the effects of mitogen activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK) on kidney injury in female BALB/c mice exposed to cadmium.Twenty-one female BALB/c mice were randomly divided into 3 groups, i.e. control group, low Cd exposure group (2.5 µmol/kg) and high Cd exposure group (10 µmol/kg) were exposed to normal saline, 2.5, 10 µmol/kg Cd, respectively, 3 times a week for 14 weeks. The kidney slice were stained by HE, PAS and Masson staining to observe the morphological changes. The expression levels of pERK, ERK, pp38, p38, pJNK and JNK proteins in kidneys were tested by Western blot assay.The ratios of pERK/ERK, pp38/p38, pJNK/JNK in high Cd group were higher than those in the control group (P0.05). The ratio of pERK/ERK in low Cd group was higher than control group (P0.05). The expression levels of bcl-2, bax proteins and the ratio of bcl-2 to bax in Cd exposure groups decreased significantly, as compared with the control group (P0.05). The impairment of renal glomeruli and tubules were observed in HE, PAS and Masson staining slices of kidneys in mice exposed to Cd.CdCl2 may induced renal injury by affecting the expression levels of MAPK.

To investigate the relationship between polymorphism of NAD(P)H quinone oxidoreductase 1 (NQO1) and X-ray repair cross-complementing group1 (XRCC1) and their correlation with smoking on the susceptibility to gastric cancer.A 1:1 case-control study of 334 patients with primary gastric cancer, with non-cancer or alimentary inpatients as control group (matched for ages ± 5 years, sex and region) in Anhui province was conducted to analyze the NQO1(C609T) and XRCC1(G28152A). Gene types by PCR-based restriction fragment length polymorphism techniques. Interaction index (γ) was calculated to determine the type of gene-environment interaction.The average age of 334 cases of gastric cancer patients was 57 years, with 65.3% of them were male. Smoking rate in the case group (55.09%) was significantly higher than in the control group (36.53%). The consequence showing that it carried the heterozygous variant (CT) or homozygous variant (TT) of NQO1 could enhance the risk of gastric cancer (OR = 1.507, 3.050), but not the XRCC1(G28152A) gene polymorphism or the susceptibility to gastric cancer. At the same time, individuals that carrying XRCC1AG and NQO1TT could increase 2.789 times the incidence of gastric cancer than those who carrying the XRCC1AG or NQO1CC. The gastric cancer risk of XRCC1GG individuals that carrying NQO1TT was 4.448 times higher than those who carrying XRCC1GG or NQO1 CC. The positive interactions of NQO1 homozygous variant (TT), XRCC1 homozygous variant (GG) and smoking were revealed in the occurrence rates of gastric cancer (OR=3.094, γ=2.070).Our research findings showed that the significant interactions between genetic polymorphisms of NQO1, XRCC1 and smoking added the risk of gastric cancer, while genetic and environmental hazardous factors co-effecting the development of gastric cancer.

To study the effect of multiglycosides of Tripterygium wilfordii (MTW) for treatment of proteinuria in kidney transplant recipients.Forty-five kidney transplant recipients with proternuria were randomized into 3 groups (n=15) and received full daily dose (1 mg/kg) MTW, half dose (0.5 mg/kg) MTW or no MTW (control) in addition to immunosuppressant therapy. The 24-hour urinary protein (24 h Upro), blood urea nitrogen (BUN), serum creatinine (Scr), dose of ciclosporin and the adverse effects of MTW were recorded.MTW at both the full dose and half dose significantly reduced the 24 h Upro as compared to exclusive immunosuppressant therapy (P0.05). The therapeutic dose of ciclosporin in patients with full and half dose of MTW was significantly lower than that in the control group (P0.05), and the patients receiving full dose MTW showed greater adverse effects than those having half dose MTW (P0.05).MTW can significantly ameliorate proteinuria, reduce the therapeutic dose of ciclosporin and protect the renal function in kidney transplant recipients. While producing similar therapeutic effect to routine full dose, long-term use of half dose MTW may reduce the adverse effect associated with MTW.