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In UC group, the content of CRP, FSTL1 and D-dimer was significantly higher than that in the control group (P less then 0.05). The DAI score was significantly higher (P less then 0.05), the content of MMP-2 and MMP-9 was remarkably raised (P less then 0.05), the platelet count, PT, APTT and fibrinogen level were all obviously increased (P less then 0.05), and the L/M ratio was notably lower (P less then 0.05) in the UC group than in the control group. In patients with active UC, MMP-2, MMP-9 and inflammatory factors were significantly increased, and there were changes in the blood coagulation factors and intestinal mucosal permeability, which further promote the occurrence and development of UC.Idiopathic inflammatory myopathies (IIMs) are a group of autoimmune inflammatory muscle diseases. Rapamycin has been shown to ameliorate inflammation and improve muscle function in a mouse model of experimental autoimmune myositis (EAM). In the present study, the therapeutic effect of rapamycin was compared with methylprednisolone (MP) on EAM. Mice were injected with myosin for 10 days to induce EAM and were subsequently treated with rapamycin (1.5 mg/kg), MP (40 mg/kg) or placebo (DMSO) for 14 days. The rapamycin-treated group exhibited significantly decreased severe inflammation and improved muscle strength compared with the MP-treated group. The plasma transforming growth factor-β (TGF-β) concentration in the rapamycin-treated group was significantly higher compared with the placebo group. However, both treatment groups exhibited significantly lower plasma interleukin-10 levels compared with the placebo group. Moreover, splenic regulatory T cell frequency in both the rapamycin- and MP-treated animals was significantly lower than that in the animals of the placebo group. Rapamycin showed better immune suppressive effects than MP in this model of EAM, and these effects were likely to be mediated by the TGF-β signaling pathway.In-stent restenosis (ISR) after drug-eluting stent (DES) placement has recently emerged as a major concern for cardiologists. Identification of biomarkers to predict ISR may be invaluable for tailored management strategies. The present study aimed to evaluate the prognostic utility of circulating S100 calcium-binding protein A12 (S100A12) for ISR. Out of 2,443 patients with DES-based percutaneous coronary intervention (PCI) and follow-up angiography at ~1 year after DES-based PCI, 258 patients were diagnosed with ISR and 258 patients without ISR were randomly selected as controls. Serum S100A12 levels were determined in the two subsets on admission. The association between ISR and the circulating levels of S100A12 was determined by constructing two multivariate stepwise logistic regression models. In addition, S100A12 was assessed for its ability to predict ISR using receiver operating characteristic (ROC) curve analysis. The serum levels of S100A12 at baseline were significantly elevated in patients in the ISR group compared with those in the non-ISR group (P less then 0.001). In the multivariate logistic regression analysis, after adjusting for conventional cardiovascular risk factors, laboratory parameters and medication after the procedure, the S100A12 level was revealed to be independently associated with ISR. When a cut-off for serum S100A12 levels of 34.75 ng/ml was used, the ROC curve was able to predict ISR with 72.8% sensitivity and 79.1% specificity, and the area under the ROC curve was 0.796 (95% CI 0.757 to 0.834, P less then 0.001). Furthermore, addition of S100A12 to established risk factors significantly improved the predictive power of reference models for ISR. S100A12 may serve as an independent marker to predict ISR in patients undergoing coronary DES implantation.Inflammation is considered as one of the major hallmarks of cancer and is associated with gastric cancer. Interleukin-22 (IL-22), a member of the IL-10 family, serves an important role in inflammatory diseases and tumors. The aim of the present study was to examine the effects of IL-22 on the proliferation of gastric cancer cells (AGS cells) in vitro and explore the associated molecular mechanism. The results of a Cell Counting kit-8 assay using AGS cells transfected with an IL-22-plasmid indicated that IL-22 could promote AGS cell viability. However, when IL-22 was knocked down by IL-22-short hairpin (sh)RNA, the viability of AGS cells was significantly impaired. Western blotting results indicated that IL-22 decreased the activation of the mitogen-activated protein kinase (MAPK) signaling pathway. Furthermore, IL-22-shRNA transfection increased the activation of MAPK, as evidenced by the upregulated phosphorylation of ERK and JNK. Taken together, the results of the present study suggest that IL-22 regulated the viability of gastric cancer cells through the JNK signaling pathway, suggesting a therapeutic approach for gastric cancer via targeting IL-22.Crystalized deposits of monosodium urate activate the Nod-like receptor protein 3 (NLRP3) inflammasome, resulting in kidney damage. The present study investigated whether the NLRP3 inflammasome is associated with the progression of hyperuricaemia and gouty nephropathy. Adult male patients were recruited at the Affiliated Baoan Hospital of Shenzhen and divided into three groups of 15 patients each The control group, the hyperuricaemia group and the gouty nephropathy group. General characteristics and organ function indicators were also measured for each patient. NLRP3, apoptosis-associated speck like protein (ASC) and caspase-1 mRNA and protein expressions in peripheral blood mononuclear cells were detected. The expression of certain downstream inflammatory factors, including interleukin (IL)-1β and IL-18 were also assessed in plasma. The results demonstrated that the concentration of uric acid and creatinine were increased in the hyperuricaemia and gouty nephropathy groups compared with the control group. AS101 research buy NLRP3, ASC and caspase-1 mRNA and protein expression, and IL-1β and IL-18 expression were increased in the hyperuricaemia and gouty nephropathy groups compared with the control group. In addition, ASC and caspase-1 mRNA and protein expression, and IL-1β expression were higher in the gouty nephropathy group compared with the hyperuricaemia group. In conclusion, the present results supported the hypothesis that the NLRP3 inflammasome signalling pathway is associated with gouty nephropathy leading to initiation of the inflammatory response and causing renal damage.