Application of graph auto-encoders based on regularization in recommendation algorithms.

Social networking has become a hot topic, in which recommendation algorithms are the most important. Recently, the combination of deep learning and recommendation algorithms has attracted considerable attention. The integration of autoencoders and graph convolutional neural networks, while providing an effective solution to the shortcomings of traditional algorithms, fails to take into account user preferences and risks over-smoothing as the number of encoder layers increases. Therefore, we introduce L1 and L2 regularization techniques and fuse them linearly to address user preferences and over-smoothing. In addition, the presence of a large amount of noisy data in the graph data has an impact on feature extraction. To our best knowledge, most existing models do not account for noise and address the problem of noisy data in graph data. Thus, we introduce the idea of denoising autoencoders into graph autoencoders, which can effectively address the noise problem. We demonstrate the capability of the proposed model on four widely used datasets and experimentally demonstrate that our model is more competitive by improving up to 1.3, 1.4, and 1.2, respectively, on the edge prediction task.

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1.

Acute pancreatitis (AP) is one of the most frequent gastrointestinal diseases and has no specific treatment. It has been shown that dysfunction of pancreatic acinar cells can lead to AP progression. Emodin is a natural product, which can alleviate the symptoms of AP. However, the mechanism by which emodin regulates the function of pancreatic acinar cells remains unclear. Thus, the present study aimed to investigate the mechanism by which emodin modulates the function of pancreatic acinar cells. To mimic AP in vitro, pancreatic acinar cells were cotreated with caerulein and lipopolysaccharide (LPS). Exosomes were isolated using the ExoQuick precipitation kit. Western blot analysis, Nanosight Tracking analysis and transmission electron microscopy were performed to detect the efficiency of exosome separation. Gene expression was detected by reverse transcription­quantitative PCR. The levels of IL­1ß and TNF­α were detected by ELISA. The data indicated that emodin significantly decreased the levels of IL­1ß and TNF­α in the supernatant samples derived from AR42J cells cotreated with caerulein and LPS. In addition, emodin significantly promoted the proliferation of AR42J cells cotreated with caerulein and LPS, and inhibited apoptosis, while the effect of emodin was reversed by long non­coding (lnc)RNA taurine upregulated 1 (TUG1) overexpression. The expression level of TUG1 in AR42J cells or exosomes derived from AR42J cells was significantly increased following treatment of the cells with LPS and caerulein, while this effect was notably reversed by emodin treatment. In addition, exosomes derived from caerulein and LPS cotreated AR42J cells inhibited the differentiation and anti­inflammatory function of regulatory T cells, while treatment of the cells with emodin significantly decreased this effect. In conclusion, the data indicated that emodin inhibited the induction of inflammation in AR42J cells by regulating the expression of cellular and exosomal lncRNA. Therefore, emodin may be used as a potential agent for the treatment of AP.

Inhibitory effect of tanshinone IIA on inflammatory response in rheumatoid arthritis through regulating ß-arrestin 2.

The current study aimed to investigate the inhibitory effect of tanshinone IIA (Tan IIA) on the inflammatory response in patients with rheumatoid arthritis (RA) and explore its mechanism. A total of 50 patients with RA were randomly separated into the control group (15 cases) and the research group (35 cases). The tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels in serum were determined, and peripheral blood mononuclear cells (PBMCs) were separated from patients with RA and cultured in vitro. The effects of the ß-arrestin 2 small interfering (si)RNA incubation, lipopolysaccharide (LPS) stimulation or Tan IIA incubation on TNF-α and IL-6 levels, and the expression levels of ß-arrestin 2, NAD-dependent protein deacetylase sirtuin-1 (SIRT1) and transcription factor p65 (p65) proteins were investigated. Prior to treatment, no significant differences in TNF-α and IL-6 levels in serum of patients with RA were identified between the research and control groups. Following treatment, the TNF-α and IL-6 levels in the serum of patients with RA in the research group were significantly lower compared with those in the research group prior to treatment and those in the control group following treatment (P<0.05). Tan IIA inhibited the LPS-induced secretion of TNF-α and IL-6, upregulated the LPS-inhibited expression of the ß-arrestin 2 and SIRT1 proteins, and downregulated the LPS-induced expression of the p65 protein in the PBMCs of patients with RA. The ß-arrestin 2 small interfering (si)RNA significantly upregulated the secretion of TNF-α and IL-6, inhibited the expression of the SIRT1 protein and upregulated the expression of the p65 protein in PBMCs of patients with RA. Tan II A effectively increased the weight of rats with rheumatoid arthritis, and reduced the circumference of the left posterior ankle, the posterior plantar metatarsal thickness, and the content of serum TNF-α and IL-6. Tan IIA did not significantly reverse these ß-arrestin 2 siRNA-induced changes. Tan IIA inhibited the inflammatory response in PBMCs of patients with RA by upregulating ß-arrestin 2 expression.

Mesh-preservation approach to treatment of mesh infection after large incisional ventral hernia repair-how I do it.

Mesh infection after large incisional ventral hernia repair is a clinical dilemma in abdominal wall hernia surgery. It is believed foreign material should be removed but it causes secondary trauma to the abdominal wall tissue and might be associated with a higher risk of complications. Currently, there is no consensus on mesh-preservation treatment in cases of mesh infection after hernia repair in general. Herein we present the case of a 27-year-old male who recovered well from mesh infection after large incisional ventral hernia repair by mesh-preservation approach. The path to success is choice of material of prosthetic mesh; surgical approach of hernia repair, sufficient wound irrigation and drainage, and acquiring sterility of the mesh surface by wound care techniques such as local iodophor packing and vacuum sealing drainage. Clinical cohorts are needed to verify the feasibility of mesh-preservation treatment of mesh infection after large incisional hernia repair.

[Effect of total flavones of hawthorn leafon (TFHL) on expression of UCP2 in liver of NASH rats].

OBJECTIVE: To study the expression of uncoupling protein 2 (UCP2) in liver of rats with nonalcoholic steatohepatitis (NASH) induced by fat-rich diet, and the effect of total flavones of hawthorn leafon (TFHL) on UCP2. METHOD: The NASH model of rat was induced by 12 weeks of fat-rich diet. Subsequently the rats were administrated with TFHL in accordance with 250, 125 mg x kg(-1) x d(-1) and the Essentiale N with 195.4 mg x kg(-1) x d(-1). The change of liver pathological. The levels of serum ALT and AST, the content of TG, CHOL, MDA and T-AOC activity of liver and were evaluated. The UCP2mRNA expression in liver was detected with RT-PCR, and the contents of UCP2 were examined with ELISA. RESULT: There are severe steatosis, inflammatory cellular infiltration in the liver of the NASH models. The levels of serum ALT, AST and the contents of TG, CHOL, MDA and UCP2 in the model group were higher than those of in the normal groop. The expression of UCP2mRNA was obviously enhanced and the activity of T-AOC decreased. The expression of UCP2 mRNA of rats was positively correlation with the contents of MDA, TNF-alpha. The inflammation activity in rat liver, the contents of MDA and UCP2, the expression of UCP2 mRNA in the administrated groups were obviously lower than those in the model group, while the activity of T-AOC was higher than that of model. CONCLUSION: TFHL may alleviate liver injury by means of the suppression of Oxidative stress/lipid peroxidation reaction and the overexpression of UCP2 in liver, which could prevent the further development of NASH.