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Introduction Contrast-induced nephropathy (CIN) is a potential complication associated with the administration of intravenous contrast agents. The objective of this study was to evaluate the effectiveness of remote ischemic preconditioning (RIPC) and two pharmacological interventions in preventing CIN.Methods Randomized controlled trials (RCTs) examining the efficacy of RIPC, nicorandil, and trimetazidine in treating CIN were searched within databases such as PubMed, Cochrane Library, Embase, and Web of Science. The primary outcome was the incidence of CIN. The consistency model was used to address heterogeneity and enhance model fit. The assessment of consistency between direct and indirect evidence was conducted through the node-splitting method. Posterior probability estimates and surface under the cumulative ranking area (SUCRA) ranked interventions based on their effectiveness in preventing CIN. The Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) framework was used to grade the quality of evidence.Results Based on hydration therapy, RIPC, nicorandil, and trimetazidine all showed prophylactic effects on CIN compared to control groups. The SUCRA results showed that RIPC (SUCRA = 37.7%, PrBest = 0.4%), nicorandil (SUCRA = 91.2%, PrBest = 74.7%), and trimetazidine (SUCRA = 71.0%, PrBest = 24.9%). However, there were no significant differences between the nicorandil, RIPC, and trimetazidine groups. Subgroup analysis suggested that there was still a protective effect in populations with mean estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2 or with a high prevalence of diabetes mellitus.Conclusions Nicorandil, trimetazidine, and RIPC all showed renal protective effects. Based on hydration, nicorandil, trimetazidine, and RIPC may show better prophylaxis against CIN than hydration alone after intravenous contrast administration.

ABSTRACT Aims/Introduction The union of dipeptidyl peptidase‐4 inhibitors and insulin in patients with type 2 diabetes and chronic kidney disease provides satisfactory glucose management without increasing adverse events (AEs). This research appraised the therapeutic effect and safety of combination therapy in patients with type 2 diabetes and chronic kidney disease. Materials and Methods We carried out a meta‐analysis of randomized controlled trials to analyze AEs, hypoglycemia, serious AEs, severe hypoglycemia, estimated glomerular filtration rate, fasting plasma glucose, glycated hemoglobin, insulin dose, low‐density lipoprotein cholesterol, uric acid and weight between combination treatment groups and control groups by searching the Cochrane Library, Excerpta Medica Database (Embase), PubMed and Web of Science databanks until October 2020. Results Five studies (6 trials, 1,278 participants) met the inclusion criteria. The evidence quality ranged from moderate to high. Glycated hemoglobin (standardized mean difference −0.29, 95% confidence interval −0.44 to −0.14) and insulin dose (standardized mean difference −0.16, 95% confidence interval −0.29 to −0.02) were obviously smaller in the combination cure patients than in the control patients. Compared with the control groups, combination treatment did not increase AEs, hypoglycemia, serious AEs or severe hypoglycemia. Conclusions This study showed the effectiveness and safety of dipeptidyl peptidase‐4 inhibitors bonded with insulin in patients with type 2 diabetes and chronic kidney disease, but the protective actions of this cure on kidney and cardiovascular outcomes, as well as the functions of other dipeptidyl peptidase‐4 inhibitors, need to be affirmed by more good‐quality randomized controlled trials.

Background: Extensive evidence has shown that immune cell infiltration is associated with the pathogenesis of Crohn’s disease (CD). Methods: Differentially expressed genes (DEGs) from the GSE179285 dataset in the intestinal mucosa of CD patients and healthy individuals were then identified. The infiltration pattern of 22 immune cell types was assessed using the CIBERSORT algorithm. The DEGs and 22 immune cell types were combined to find the key gene network using weighted gene co-expression network analysis (WGCNA). A linear regression model for the relationship between the expression of the hub genes in CD patients and infiltration of immune cells was also developed. The utility and accuracy of the hub genes for CD diagnosis were assessed using receiver operating characteristic (ROC) analysis. The accuracy of the model was validated using the GSE20881 dataset. Results: There were 1135 DEGs between the intestinal mucosal tissue of CD patients and healthy individuals. Of these DEGs, 711 genes were upregulated, whereas 424 of them were downregulated. There was also a significant difference in the infiltration of immune cells to the intestinal mucosal between the CD patients and healthy individuals. WGCNA revealed that the turquoise module genes were strongly correlated with the infiltration of M1 macrophages (cor =0.68, p = 10 −16 ). Finally, the expression of GBP4, the identified hub gene, strongly correlated with the infiltration of M1 macrophages (adjusted r-squared =0.661, p < 2×10 −16 ), and is a relatively good marker for CD diagnostic prediction (AUC =0.736). The relationship between GBP4 expression and infiltration of M1 macrophages (adjusted r-squared =0.435, p < 2×10 −16 ) and diagnostic value of the gene (AUC =0.702) were verified using the GSE20881 validation dataset. Conclusion: The expression of GBP4 is associated with the infiltration of M1 macrophages to the intestinal mucosa of CD patients.

Pancreatic cancer (PCa) is a highly lethal and aggressive disease, characterized by high mortality rates. Although necroptosis plays a vital role in tumor progression, cancer metastasis, prognosis of cancer patients, necroptosis-related gene (NRG) sets have rarely been analyzed in PCa. Therefore, definition of novel necroptosis-related prognostic markers for PCa patients is urgently needed. Here, we screened 159 NRGs and identified 132 differentially expressed NRGs in The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) cohorts. Next, we employed univariate and multivariate Cox proportional regression models to establish a prognostic-related NRG signature comprising five NRGs that could stratify patients into high-risk and low-risk groups. Results from survival analysis showed that patients in the high-risk had dramatically shorter overall survival (OS) rates compared with their low-risk counterparts. Results from univariate and multivariate Cox regression analysis further confirmed the independent prognostic value of the established necroptosis-related signature, and the area under receiver (AUC) of the operating curve (ROC) for 1-, 3-, 5-years was 0.72, 0.74, and 0.75, respectively. Finally, we validated the signature efficacy using an independent cohort from the Gene Expression Omnibus (GEO) database. The ROC curve confirmed the predictive capacity of the five-gene signature. Furthermore, we validated expression of the signature proteins using the Human Protein Atlas (HPA) database. In conclusion, we successfully constructed a novel necroptosis-related signature for prognosis of patients with pancreatic cancer.

Renal fibrosis, in particular tubulointerstitial fibrosis, which is characterized by an increased extracellular matrix (ECM) formation and development in the interstitium, is the common end pathway for nearly all progressive kidney disorders. One of the sources for this matrix is the epithelial to mesenchymal transition (EMT) from the tabular epithelium. The driving force behind it is some profibrotic growth factors such as transforming growth factor-β (TGF-β) which is responsible for the formation of collagen in renal fibrosis. miR-29c, which is an antifibrotic microRNA, downregulates renal interstitial fibrosis by downregulating the TGF-β and collagen. However, it is not known whether miR-29c mediates the TGF-β1-driven PI3K-Akt pathway and Col-1 triggering within NRK-52E cultures. The main objective of this investigation was to examine the influence of miR-29c on the downregulation of the TGF-β1-driven PI3K-Akt pathway and Col-1 triggering in NRK-52E cultures. This study revealed that miR-29c inhibited TGF-β1 expression in NRK-52E cell cultures. Overexpression of miR-29c significantly inhibits NRK-52E culture proliferation mediated by TGF-β1. miR-29c inhibited the expression of Col-1 and decreased PI3K/Akt phosphorylation. These findings revealed a novel mechanism by which miR29c inhibits the proliferation of renal interstitial fibrotic cultures by downregulating the PI3k-Akt pathway, which is controlled by TGF-β1.