Nonalcoholic fatty liver disease (NAFLD) has emerged globally and is associated with inflammatory signaling. The underlying mechanisms remain poorly delineated, although NAFLD has attracted considerable attention and been extensively investigated. Recent publications have determined that angiotensin II (Ang II) plays an important role in stimulating NAFLD progression by causing lipid metabolism disorder and insulin resistance through its main receptor, Ang II type 1 receptor (AT1R). Herein, we explored the effect of supplementary S-adenosylmethionine (SAM), which is the main biological methyl donor in mammalian cells, in regulating AT1R-associated protein (ATRAP), which is the negative regulator of AT1R. We found that SAM was depleted in NAFLD and that SAM supplementation ameliorated steatosis. In addition, in both high-fat diet-fed C57BL/6 rats and L02 cells treated with oleic acid (OA), ATRAP expression was downregulated at lower SAM concentrations. Mechanistically, we found that the subcellular localization of human antigen R (HuR) was determined by the SAM concentration due to protein methylation modification. Moreover, HuR was demonstrated to directly bind ATRAP mRNA and control its nucleocytoplasmic shuttling. Thus, SAM was suggested to upregulate ATRAP protein expression by maintaining the export of its mRNA from the nucleus. Taken together, our findings suggest that SAM can positively regulate ATRAP in NAFLD and may have various potential benefits for the treatment of NAFLD.

To evaluate the effects of different surgical dressings in reducing surgical site infection (SSI) and identify the optimal dressings. Randomized controlled trials investigating the application of surgical dressings were retrieved from electronic databases, including MEDLINE, EMBASE, and the Cochrane Library. The odds ratios (ORs) of the SSI rate were compared by direct meta-analysis, and the surface under the cumulative ranking (SUCRA) curve values were calculated based on the Bayesian theorem. A node-splitting model was applied to analyse the consistency of the comprehensive comparison results. Twenty-two studies containing 5487 participants were pooled for the comprehensive comparison. Among all the studies included, 9 types of surgical dressings were identified for comparison. The results of the direct meta-analysis revealed that novel dressings significantly reduced the overall SSI rate with an OR of 1.026 (95% CI: 1.013-1.040, p < 0.001), which was determined to have low heterogeneity (I² = 32.1%). Specifically, 3 types of dressings presented significant effects in reducing SSI, namely, mupirocin-containing (OR = 1.076, 95% CI: 1.014-1.142, p = 0.015), dialkylcarbamoyl-chloride-containing (OR = 1.047, 95% CI: 1.012-1.083, p = 0.008) and vitamin E (VE)-silicone-containing (OR = 1.129, 95% CI: 1.016-1.255, p = 0.025) dressings. Network meta-analysis demonstrated that the VE-silicone dressing (SUCRA = 0.37) was the optimal dressing, followed by the mupirocin dressing, with a SUCRA of 0.31. The present network meta-analysis identified the superiority of VE-silicone and mupirocin dressings in preventing SSI. The evidence-based results provide suggestions and directions for future investigations on surgical dressings. More large-scale trials with rigorous designs are warranted to clarify the clinical value of novel dressings in surgical incision management.

Background and Aims: Currently, the Barcelona Clinic Liver Cancer staging system remains huge controversies in the management of hepatocellular carcinoma. To determine the best therapeutic strategy for patients at each stage, we conducted a network meta-analysis and aimed to provide a new treatment concept.

The mechanisms by which the tumor behaviors of hepatocellular carcinoma (HCC) support growth and metastasis remain largely unknown, and it has become increasingly apparent that molecular dysregulation is of considerable importance for cellular signaling pathways. Recently, RNA-binding motif protein 47 (RBM47) has been suggested to function as a tumor regulator by acting as an RNA binding protein (RBP), but its role in HCC remains ambiguous. Here, in HCC, we identified that RBM47 had an inhibitory influence on tumor behaviors in vitro and accordingly suppressed the growth and metastasis of xenograft tumors in vivo. Additionally, RBM47 was verified to positively regulate Upframeshift 1 (UPF1), which is a crucial protein involved in the nonsense-mediated RNA decay (NMD) process and was previously determined to be an HCC suppressor. Mechanistically, the stability of UPF1 mRNA was demonstrated to be enhanced with its 3’UTR bound by RBM47, which acted as an RNA binding protein. Meanwhile, RBM47 was also proven to promote the transcription of UPF1 as a transcription factor. Taken together, we concluded that RBM47 functioned as a tumor suppressor by upregulating UPF1, acting as a DNA/RNA binding protein at the transcriptional and posttranscriptional levels.