The collaboration and reporting quality of social welfare systematic reviews in the Campbell Collaboration online library.

BACKGROUND: To analyze the collaboration and reporting quality of the systematic reviews of social welfare in the Campbell collaboration online library. METHODS: The Campbell collaboration online library was searched for systematic reviews of social welfare and the basic information extracted in order to assess the reporting quality of systematic reviews using a MOOSE checklist. BICOMS-2 and UCINET software were used to produce the social network, and Comprehensive Meta Analysis (Version 2) and STATA 13.0 were used to analyze the related data. RESULTS: Fifty-seven systematic reviews of social welfare were included. Twenty-eight items of the included social welfare systematic reviews were rated as complete (≥70%). There were significant differences between ≤2013 and ≥ 2014 in five items. These differences were as follows: research published by one organization or more than one organization in one item, more than three authors or less than four authors in two items, and one country or more than one country in six items. It's completed about researches with more than one organization, three authors or more than one country. Some items were found to have a low reporting rate of studies published before 2014, by one organization, with less than four authors or one country, respectively. The social network of authors and organizations showed good collaboration. CONCLUSIONS: Some items could be further improved with regard to the rate of reporting systematic reviews of social welfare in the Campbell collaboration online library. This could improve the overall quality of social welfare systematic reviews.

ALDOB acts as a novel HBsAg-binding protein and its coexistence inhibits cisplatin-induced HepG2 cell apoptosis.

Chronic infection with hepatitis B virus is a cause of end-stage liver disease and hepatocellular carcinoma (HCC). We previously screened fructose-bisphosphate aldolase B (ALDOB) as a candidate binding protein of hepatitis B surface antigen (HBsAg) using a yeast 2-hybrid assay. In this study we aimed to confirm ALDOB as a binding protein of the S region of the HbsAg (HBs) and to investigate the function and involved mechanism between its interactions during HCC development. Our results demonstrated that both of exogenous and endogenous ALDOB proteins bind to HBs and colocalize in the cytoplasm in vitro. The coexistence of HBs and ALDOB inhibit apoptosis of cisplatin-induced HepG2 cells. Furthermore, western blot analysis showed the coexistence of HBs and ALDOB enhance the phosphorylations of AKT and its downstream of GSK-3ß (phosphorylation); decreased expression of the pro-apoptotic proteins Bax, Bid, Bim, and Puma; and increased expression of the prosurvival proteins Bcl-2, Bcl-xl, and Mcl-1 in HepG2 cells. These findings suggest that interaction between HBs and ALDOB might be applied as a potential therapeutic target during the treatment of HBV-related hepatitis or HCC.

Inhibitory effect of ARHI on pancreatic cancer cells and NF-κB activity.

The aim of this study was to investigate the effect of aplasia ras homolog member I (ARHI) on proliferation, apoptosis and the cell cycle in the pancreatic cancer cell line PANC-1. The study also aimed to examine the effect of ARHI on the activity of the nuclear factor (NF)-κB and to determine whether ARHI acts as a tumor suppressor in the development of pancreatic cancer by inhibiting the activity of NF-κB. A pIRES2­EGFP­ARHI vector, constructed by reverse transcrition (RT)­PCR, was transiently transfected into the PANC-1 cells and analyzed for the expression of the ARHI protein by western blotting. A MTT assay was used to quantify cell proliferation, and apoptosis was analyzed by flow cytometry. The NF­κB signaling pathway, specifically the pathway using the nuclear phosphorylated p65 isoform, was analyzed by western blotting. Expression of the ARHI protein was detected by western blotting subsequent to the PANC-1 cells being transiently transfected with the pIRES2­EGFP­ARHI construct. Cell proliferation was strongly inhibited in the PANC-1 cells transfected with pIRES2­EGFP­ARHI. The cell cycle assays indicated an increase in the number of cells at the G0/G1 phase and a decrease in the cells at the S phase, but the difference was not significant (P>0.05). Time course studies also indicated a marked increase in the apoptotic index following transient transfection, as well as a gradual decrease in the expression of the nuclear phosphorylated p65 protein. ARHI acts as a tumor suppressor by downregulating the NF­κB signaling pathway, which results in the inhibition of cell proliferation, apoptosis and the cell cycle in the pancreatic tumor PANC-1 cell line.