Ovarian reserve reflects a woman's fertility potential. The ABO blood group system is a very stable genetic marker. Although many recent studies have explored the relationship between ABO blood group and ovarian reserve, a consensus has not yet been reached. This paper is the first meta-analysis and systematic review of the relationship between ABO blood type and ovarian reserve. We analyzed seven cross-sectional studies evaluating follicle stimulating hormone (FSH) or anti-Mullerian hormone (AMH) levels in 55,113 participants to determine ovarian reserve. This study found no relationship between ABO blood type and ovarian reserve when FSH was used as an indicator of ovarian reserve (A vs non-A:OR=1.03, 95% CI:0.96-1.11; B vs non-B: OR=0.98, 95% CI:0.75-1.29; AB vs non-AB:OR=0.96, 95% CI:0.71-1.30; O vs non-O:OR=1.03, 95%CI:0.74-1.43).There was also no relationship between ABO blood type and ovarian reserve when AMH was used as an indicator (A vs non-A:OR=0.89, 95% CI:0.76-1.03; B vs non-B:OR=1.02, 95% CI:0.80-1.30; AB vs non-AB:OR=1.14, 95% CI:0.80-1.64, O vs non-O:OR=1.07, 95% CI:0.86-1.34). Overall, the current study found no relationship between ABO blood group and ovarian reserve. However, additional rigorous, high-quality and multi-indicator studies with large sample sizes are required for further verification.

Here we showed that dietary NiCl2 in excess of 300 mg/kg caused the G2/M cell cycle arrest and the reduction of cell proportion at S phase. The G2/M cell cycle arrest was accompanied by up-regulation of phosphorylated ataxia telangiectasia mutated (p-ATM), p53, p-Chk1, p-Chk2, p21 protein expression and ATM, p53, p21, Chk1, Chk2 mRNA expression, and down-regulation of p-cdc25C, cdc2, cyclinB and proliferating cell nuclear antigen (PCNA) protein expression and the cdc25, cdc2, cyclinB, PCNA mRNA expression.

It has been known that overexposure to Ni can induce nephrotoxicity. However, the mechanisms of underlying Ni nephrotoxicity are still elusive, and also Ni- and Ni compound-induced ER stress has been not reported in vivo at present. Our aim was to use broiler chickens as animal model to test whether the ER stress was induced and UPR was activated by NiCl2 in the kidney using histopathology, immunohistochemistry and qRT-PCR. Two hundred and eighty one-day-old broiler chickens were divided into 4 groups and fed on a control diet and the same basal diet supplemented with 300 mg/kg, 600mg/kg and 900mg/kg of NiCl2 for 42 days. We found that dietary NiCl2 in excess of 300 mg/kg induced ER stress, which was characterized by increasing protein and mRNA expression of ER stress markers, e.g., GRP78 and GRP94. Concurrently, all the three UPR pathways were activated by dietary NiCl2. Firstly, the PERK pathway was activated by increasing eIF2a and ATF4 mRNA expression. Secondly, the IRE1 pathway was activated duo to increase in IRE1 and XBP1 mRNA expression. And thirdly, the increase of ATF6 mRNA expression suggested that ATF6 pathway was activated. The findings clearly demonstrate that NiCl2 induces the ER stress through activating PERK, IRE1 and ATF6 UPR pathways, which is proved to be a kind of molecular mechanism of Ni- or/and Ni compound-induced nephrotoxicity.

Previous studies have addressed the involvement of phosphoinositide-specifc phospholipase γ1 (PLCγ1) and protein kinase B (PKB/Akt) in osteoarthritis (OA) pathogenesis, but it is not ascertained the possibility of them to be potential targets for OA therapy. Here, through local intra-articular injection of PLCγ or Akt inhibitor in a rat OA model induced by anterior cruciate ligament transaction plus medial meniscus resection, the architecture of chondrocyte and matrix organization of articular cartilage were observed using histopathological assays and Aggrecan, Col2, PLCγ1, and Akt levels were detected using immunohistochemistry assays. By treatment of Akt or PLCγ inhibitor and transfection of different PLCγ1- or Akt-expressing vectors in rat OA model chondrocytes, Aggrecan, Col2, PLCγ1, p-PLCγ1, Akt, and p-Akt levels were detected using western blotting analysis. The binding between PLCγ1 and Akt was assessed with co-immunoprecipitation assays in human OA chondrocytes. These results showed that PLCγ inhibition protected chondrocytes against OA, but Akt inhibition did not dramatically aggravate OA progression. There were mutual antagonism and binding between PLCγ1 and Akt that could be regulated by their phosphorylation levels. Consequently, the data reveal that the inhibition of PLCγ1 may provide an attractive therapeutic target for OA therapy, implicating its binding to Akt.

Urine HE4 has been reported as the potential novel diagnostic biomarker for ovarian cancer in several studies, but their results were inconsistent. Therefore, we conducted a systematic analysis to evaluate the diagnostic value of urine HE4 in detecting ovarian cancer. A comprehensive electronic and manual search was conducted for relevant literatures through several databases up to May 5, 2016. The quality of the studies included in the systematic review was assessed using the Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) tool. All analyses were conducted using Meta-DiSc 1.4 and STATA 12.0 software. A total of seven publications were included in this study, and these studies included 413 ovarian cancer patients and 573 controls. The summary estimates were: sensitivity 0.76 (95% confidence interval [CI]: 0.72-0.80), specificity 0.92 (95% CI: 0.89-0.94), positive likelihood ratio 8.39 (95%CI: 4.81-14.63), negative likelihood ratio 0.23 (95% CI: 0.13-0.39), diagnostic odds ratio 37.90 (95% CI: 18.69-76.83), and area under the curve 0.93. According to our results, urine HE4 has greater diagnostic value in detecting ovarian cancer. In addition, considering the high heterogeneity, further research studies with more well-designed and large sample sizes are needed in the future.

Ni, a metal with industrial and commercial uses, poses a serious hazard to human and animal health. In the present study, we used flow cytometry, immunohistochemistry and qRT-PCR to investigate the mechanisms of NiCl2-induced apoptosis in kidney cells. After treating 280 broiler chickens with 0, 300, 600 or 900 mg/kg NiCl2 for 42 days, we found that two caspase-dependent pathways were involved in the induced renal tubular cell apoptosis. In the mitochondria-mediated caspase-dependent apoptotic pathway, cyt-c, HtrA2/Omi, Smac/Diablo, apaf-1, PARP, and caspase-9, 3, 6 and 7 were all increased, while. XIAP transcription was decreased. Concurrently, in the Fas-mediated caspase-dependent apoptotic pathway, Fas, FasL, caspase-8, caspase-10 and Bid levels were all increased. These results indicate that dietary NiCl2 at 300+ mg/kg induces renal tubular cell apoptosis in broiler chickens, involving both mitochondrial and Fas-mediated caspase-dependent apoptotic pathways. Our results provide novel insight into Ni and Ni-compound toxicology evaluated in vitro and in vivo.