No abstract

This systematic review is to explore the prevalence of depression in patients with rheumatoid arthritis (RA) in China. Articles of prevalence rates for depression in adult RA patients published before October 2015 were identified from PubMed, Embase, The Cochrane Library, CNKI, CBM, VIP, and Wanfang database and other internet databases. Relevant journals and the recommendations of expert panels were also searched manually. Two independent reviewers searched and assessed the literature. Therelevant data were applied with Meta-Analyst 3.13 software, and the forest plot and funnel plot were performed. 21 studies with a total of 4447 patients were selected to be enrolled in this study. The prevalence of depression by analyzing the effect size was 48% [95% CI (41%, 56%)]. The prevalence of minor depression and dysthymic disorder was 30% [95%CI (23%, 38%)], and the moderate or major depression was 18% [95%CI (11%, 29%)], respectively. Subgroup analysis showed that the depression rate of female RA patients was higher than male. The depression rate in the central and western areas were higher than that of the eastern region of China, the prevalence level estimated by the Geriatric Depression Scale (GDS) was higher than estimated by other tools. Sensitivity analysis showed that the pooled effect size had good stability and reliability, To be conclusive, the prevalence rate of depression in RA patients is 48%, which suggesting that medical staff should pay more attention to depression in adult patients with RA.

BackgroundHepatocellular carcinoma (HCC) is the second leading cause of cancer death in Asia; however, the molecular mechanism in its tumorigenesis remains unclear. Abnormal expression of claudins (CLDNs), a family of tight junction (TJ) proteins, plays an important role in the metastatic phenotype of epithelial-derived tumors by affecting tight junction structure, function and related cellular signaling pathways. In a previous study, we used a tissue chip assay to identify CLDN17 as an upregulated gene in HCC. Here we aimed to use molecular biology technology to explore the effect of CLDN17 on the malignant phenotype of HCC and the underlying molecular mechanism, with the objective of identifying a new target for HCC treatment and the control of HCC metastasis.MethodThe expression levels of CLDN17 in HCC tissues and histologically non-neoplastic hepatic tissues were explored by immunohistochemistry. Stable transfection of the hepatocyte line HL7702 with CLDN17 was detected by real-time polymerase chain reaction (PCR), western blotting and immunofluorescence. The impact of CLDN17 on the malignant phenotype of HL7702 cells in vitro was assessed by a Cell Counting Kit-8 (CCK8) assay, a Transwell assay and a wound-healing experiment. Western blotting was utilized to detect the activation state of Tyrosine kinase 2 (Tyk2) / signal transducer and activator of transcription3 (Stat3) pathway. A Tyk2 RNA interference (RNAi) was utilized to determine the impact of the Tyk2/Stat3 signaling pathway on the malignant phenotype of hepatocytes.ResultsIn this work, our research group first found that CLDN17 was highly expressed in HCC tissues and was associated with poor prognosis. In addition, we demonstrated that CLDN17 affected the Stat3 signaling pathway via Tyk2 and ultimately enhanced the migration ability of hepatocytes.ConclusionIn conclusion, we confirmed that the upregulated expression of CLDN17 significantly enhances the migration ability of hepatocytes in vitro and we found that the activation of the Stat3 pathway by Tyk2 may an important mechanism by which CLDN17 promotes aggressiveness in hepatocytes.