Correlation between Preoperative Serum Albumin-Globulin Ratio and Prognosis of Patients Undergoing Low Rectal Cancer Surgery.

BACKGROUND: To explore the correlation between preoperative serum albumin-globulin ratio (AGR) and the prognosis of patients undergoing low rectal cancer surgery. METHODS: A total of 152 patients treated from June 2013 to June 2015 were selected. They were divided into survival group (n = 128) and death group (n = 24). Their general clinical data and preoperative and postoperative serum albumin (ALB), globulin (GLB) levels, and AGR were compared. Multivariate logistic regression analysis was performed for influencing factors for postoperative death. A nomogram prediction model was established based on independent risk factors. The predictive value of AGR for clinical outcomes was analyzed by receiver operating characteristic (ROC) curve, and the optimal cut-off value was obtained. The correlation between AGR and postoperative clinical outcomes was analyzed. The patients were divided into group A and B according to cut-off value, survival curves were plotted by Kaplan-Meier method, and 5-year survival rates were compared. RESULTS: There were significant differences in tumor stage, cell differentiation, depth of tumor invasion, lymph node metastasis, chemotherapy, preoperative ALB, GLB, and AGR between the two groups, which were all independent risk factors for death. After operation, ALB and AGR significantly declined and were significantly lower in the death group than those in the survival group. The death group had significantly higher GLB level than that of the survival group. The optimal cut-off value of AGR for predicting death was 1.73. AGR was significantly correlated with postoperative clinical outcomes. The survival rate of patients with AGR > 1.73 significantly exceeded that of cases with AGR ≤ 1.73. CONCLUSIONS: The preoperative serum AGR is an independent risk factor for the postoperative clinical outcomes of patients with low rectal cancer and has a high predictive value. Lower AGR indicates higher risk of postoperative death.

A Nomogram Model that Predicts the Risk of Diabetic Nephropathy in Type 2 Diabetes Mellitus Patients: A Retrospective Study.

OBJECTIVE: To construct a novel nomogram model that predicts the risk of diabetic nephropathy (DN) incidence in Chinese patients with type 2 diabetes mellitus (T2DM). METHODS: Questionnaire surveys, physical examinations, routine blood tests, and biochemical index evaluations were conducted on 1095 patients with T2DM from Guilin. A least absolute contraction selection operator (LASSO) regression and multivariable logistic regression analysis were used to screen out DN risk factors. A logistic regression analysis incorporating the screened risk factors was used to establish a predictive nomogram model. The performance of the nomogram model was evaluated using the C-index, an area under the receiver operating characteristic curve (AUC), calibration plots, and a decision curve analysis. Bootstrapping was applied for internal validation. RESULTS: Independent predictors for DN incidence risk included gender, age, hypertension, medicine use, duration of diabetes, body mass index, blood urea nitrogen level, serum creatinine level, neutrophil to lymphocyte ratio, and red blood cell distribution width. The nomogram model exhibited moderate prediction ability with a C-index of 0.819 (95% confidence interval (CI): 0.783-0.853) and an AUC of 0.813 (95%CI: 0.778-0.848). The C-index from internal validation reached 0.796 (95%CI: 0.763-0.829). The decision curve analysis displayed that the DN risk nomogram was clinically applicable when the risk threshold was between 1 and 83%. CONCLUSION: Our novel and simple nomogram containing 10 factors may be useful in predicting DN incidence risk in T2DM patients.

Diosgenin and GSK126 Produce Synergistic Effects on Epithelial-Mesenchymal Transition in Gastric Cancer Cells by Mediating EZH2 via the Rho/ROCK Signaling Pathway.

BACKGROUND: Diosgenin, a natural steroidal saponin isolated from Trigonella foenum-graecum, has been reported to exert anti-cancer effects. Inhibitors of enhancer of zeste homology 2 (EZH2) have been widely used in treatment of cancers. However, the effects of combined treatment with diosgenin and an EZH2 inhibitor on gastric cancer (GC) cells, and the mechanism for those effects are not fully understood. METHODS: AGS and SGC-7901 gastric cancer cells were treated with diosgenin (0 to 8 µM), followed by treatment with either diosgenin or an EZH2 inhibitor, GSK126 alone. Afterwards, an EZH2 overexpression plasmid and Rho inhibitor, GSK429286A was involved in cells. Cell proliferation, cell cycle distribution, and cell apoptosis, migration, and invasion were examined by CCK-8 assays, flow cytometry, and transwell assays. Western blotting was performed to detect the relative levels of protein expression. RESULTS: Treatment with diosgenin alone caused a dose-dependent decrease in the cell viability, and combined treatment with an EZH2 inhibitor plus GSK126 caused a further significant decrease. A further analysis revealed that treatment with either diosgenin or GSK126 alone induced significant increases in G0/G1 cell cycle arrest and apoptosis, and combined treatment with both agents induced further increases in those parameters. In addition, combined treatment with diosgenin and GSK126 synergistically induced even stronger effects on impaired cell proliferation, G0/G1 phase arrest, and cell apoptosis when compared to treatment with either diosgenin or GSK126 treatment alone. At the molecular level, we demonstrated that inhibition of Rho/ROCK signaling by combined treatment with diosgenin and GSK126 could downregulate the expression of epithelial-mesenchymal transition (EMT)-related molecules. We also found that EZH2 overexpression reversed the anti-tumor effect of diosgenin by inducing cell survival, blocking G1-phase arrest, and promoted EMT. While, these biological properties were further reversed by GSK429286A. CONCLUSION: Collectively, combined treatment with diosgenin and GSK126 produced even more significant effects on GC cell inhibition by targeting EZH2 via Rho/ROCK signaling-mediated EMT, which might be a therapeutic strategy for improving the poor therapeutic outcomes obtained with GSK126 monotherapy.