Comparison of three nutritional screening tools for predicting mortality in maintenance hemodialysis patients.

OBJECTIVES: The aim of this study was to compare the effect of different nutritional screening tools on predicting the risk for mortality in patients on maintenance hemodialysis (MHD). METHODS: A cohort of 1025 patients on MHD were enrolled from eight hospitals. The malnutrition-inflammation score (MIS), objective score of nutrition on dialysis (OSND), and geriatric nutritional risk index (GNRI) were measured at baseline. All-cause mortality and cardiovascular (CV) mortality were the major study outcomes. RESULTS: The median follow-up duration was 28.1 mo. The MIS (per SD increase, hazard ratio [HR], 1.35; 95% confidence interval [CI], 1.18-1.55), the OSND (per SD decrease, HR, 1.24; 95% CI, 1.09-1.42), and the GNRI (per SD decrease, HR, 1.26; 95% CI, 1.10-1.43) were significantly associated with the risk for all-cause mortality. More importantly, the mortality predictability of the MIS appears similar to the GNRI (P = 0.182) and greater than the OSND (MIS versus OSND: P = 0.001; GNRI versus OSND: P = 0.045). Similar results were found for CV mortality. CONCLUSIONS: Each of the three nutritional screening tools was significantly associated with an increased risk for all-cause and CV mortality. The mortality predictability of the MIS was similar to the GNRI and greater than the OSND.

Sonic hedgehog improves ischemia-induced neovascularization by enhancing endothelial progenitor cell function in type 1 diabetes.

The Sonic hedgehog (Shh) pathway is downregulated in type 1 diabetes, and it has been reported that augmentation of this pathway may alleviate diabetic complications. However, the cellular mechanisms underlying these protective effects are poorly understood. Recent studies indicate that impaired function of endothelial progenitor cells (EPCs) may contribute to cardiovascular problems in diabetes. We hypothesized that impaired Shh signaling contribute to endothelial progenitor cell dysfunction and that activating the Shh signaling pathway may rescue EPC function and promote diabetic neovascularization. Adult male C57/B6 mice and streptozotocin (STZ)-induced type 1 diabetic mice were used. Gli1 and Ptc1 protein levels were reduced in EPCs from diabetic mice, indicating inhibition of the Shh signaling pathway. EPC migration, tube formation ability, and mobilization were impaired in diabetic mice compared with non-diabetic controls (p < 0.05 vs control), and all were improved by in vivo administration of the Shh pathway receptor agonist SAG (p < 0.05 vs diabetes). SAG significantly increased capillary density and blood perfusion in the ischemic hindlimbs of diabetic mice (p < 0.05 vs diabetes). The AKT activity was lower in EPCs from diabetic mice than those from non-diabetic controls (p < 0.05 vs control). This decreased AKT activity led to an increased GSK-3ß activity and degradation of the Shh pathway transcription factor Gli1/Gli2. SAG significantly increased the activity of AKT in EPCs. Our data clearly demonstrate that an impaired Shh pathway mediated by the AKT/GSK-3ß pathway can contribute to EPC dysfunction in diabetes and thus activating the Shh signaling pathway can restore both the number and function of EPCs and increase neovascularization in type 1 diabetic mice.

Resveratrol inhibits proliferation and induces apoptosis of nasopharyngeal carcinoma cell line C666-1 through AMPK activation.

BACKGROUND: Resveratrol, a natural phenolic compound found in red grapes, has been reported to inhibit proliferation and induce apoptosis via regulation of AMPK signaling pathways in several cancer cell types. However, little is known about the effect of resveratrol on the human Nasopharyngeal carcinoma (NPC) cell line C666-1. Moreover, the molecular mechanisms of resveratrol-mediated apoptosis in C666-1 cells remain to be clarified. METHODS: Cell proliferation was measured by CCK8 assay, cell apoptosis rate was evaluated by flow cytometric analysis, and the protein expression alterations of AMPK signaling pathways were detected by Western blotting. RESULTS: Treatment of resveratrol inhibited cell viability and promote apoptosis of C666-1 cells. In addition, we showed that resveratrol could also activate caspase-3 and alter the Bax/Bcl-2 apoptotic signaling. Furthermore, all these changes may be due to the activation of AMPK activity by resveratrol treatment, and we also found that the p70S6K and s6 activities, downstream factors of AMPK, were also blocked by resveratrol. CONCLUSION: Our results revealed that resveratrol can be regarded as a new effective and chemopreventive compound for human NPC treatment.