Objective To discuss the correlation of serum TNFR level with renal function injury in patients with type 2 diabetes mellitus (T2DM)and normal albumin excretion.Methods 90 T2DMpatients with normal albu-min excretion(24h urine albumin excretion rate <20μg/min)were divided into three groups according to the esti-mated glomerular filtration rate level:eGFR >90mL · min -1 · (1.72m2 )-1 ,eGFR 60 -90mL · min -1 · (1.72m2 )-1 and eGFR <60mL·min -1 ·(1.72m2 )-1 ,30 cases in each group.The serum TNFRs level and related clinical data were measured and analyzed statistically.Results The levels of serum TNFR1,TNFR2 were negatively correlated with eGFR(r =-0.428,-0.335,all P <0.05),and positively correlated with Scr(r =0.476,0.225,all P <0.05)in patients with T2DM and normal albumin excretion.The course of disease and the levels of BUN,Scr, CysC,α1 -MG,β2 -MG were increased as the degree of renal function injury.All these index had statistically signifi-cant differences in three groups(F =3.758,5.851,71.738,25.751,7.530,13.735,all P <0.05).Logistic regres-sion analysis showed that the levels of serum TNFR1,TNFR2 were independent risk factors for renal impairment in patients with T2DMand normal albumin excretion(OR =2.009,1.143,all P <0.05).Conclusion TNFRs may be involved in the development and progression of renal impairment,and may become a new conventional indicator for DN because of reflecting the degree of renal function injury in some extent in T2DMpatients with normal albumin excretion.

Background/Aims: To evaluate the causal correlation between complement components and non-viral liver diseases and their potential use as druggable targets. Methods: We conducted Mendelian randomization (MR) to assess the causal role of circulating complements in the risk of non-viral liver diseases. A complement-centric protein interaction network was constructed to explore biological functions and identify potential therapeutic options. Results: In the MR analysis, genetically predicted levels of complement C1q C chain (C1QC) were positively associated with the risk of autoimmune hepatitis (odds ratio 1.125, 95% confidence interval 1.018–1.244), while complement factor H-related protein 5 (CFHR5) was positively associated with the risk of primary sclerosing cholangitis (PSC;1.193, 1.048– 1.357). On the other hand, CFHR1 (0.621, 0.497–0.776) and CFHR2 (0.824, 0.703–0.965) were inversely associated with the risk of alcohol-related cirrhosis. There were also significant inverse associations between C8 gamma chain (C8G) and PSC (0.832, 0.707–0.979), as well as the risk of metabolic dysfunction-associated steatotic liver disease (1.167, 1.036–1.314). Additionally, C1S (0.111, 0.018–0.672), C7 (1.631, 1.190–2.236), and CFHR2 (1.279, 1.059–1.546) were significantly associated with the risk of hepatocellular carcinoma. Proteins from the complement regulatory networks and various liver diseaserelated proteins share common biological processes. Furthermore, potential therapeutic drugs for various liver diseases were identified through drug repurposing based on the complement regulatory network. Conclusions Our study suggests that certain complement components, including C1S, C1QC, CFHR1, CFHR2, CFHR5, C7, and C8G, might play a role in non-viral liver diseases and could be potential targets for drug development.

Non-typhoid Salmonella(NTS)is widely distributed around the world, mainly infected children under 5 years of age.Salmonella Enteritidis and Salmonella Typhimurium are the main serotypes.NTS are major cause of acute gastroenteritis, but the invasive diseases such as bacteremia and meningitis are more serious.The antibiotic resis-tance of NTS is severe, and irrational use of antibiotics is ubiquitous.Now, the epidemiology, clinical characteristics, susceptible factor and antibiotic therapy of NTS infection in children were summarized, which helps early diagnose and rational antibiotic therapy.