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Background: Frailty is associated with poor prognosis in patients undergoing transcatheter aortic valve replacement (TAVR). The red blood cell distribution width (RDW)-to-albumin ratio (RAR) reflects key components of frailty. This study aimed to evaluate the relationship between RAR and all-cause mortality in patients undergoing TAVR. Methods: The data were extracted from the Medical Information Mart for Intensive Care IV database. The RAR was computed by dividing the RDW by the albumin. The primary outcome was all-cause mortality within 1-year following TAVR. The association between RAR and the primary outcome was evaluated using the Kaplan-Meier survival curves, restricted cubic spline (RCS), and Cox proportional hazard regression models. Results: A total of 760 patients (52.9% male) with a median age of 84.0 years were assessed. The Kaplan-Meier survival curves showed that patients with higher RAR had higher mortality (log-rank P < 0.001). After adjustment for potential confounders, we found that a 1 unit increase in RAR was associated with a 46% increase in 1-year mortality (HR = 1.46, 95% CI:1.22–1.75, P < 0.001). According to the RAR tertiles, high RAR (RAR > 4.0) compared with the low RAR group (RAR < 3.5) significantly increased the risk of 1-year mortality (HR = 2.21, 95% CI: 1.23–3.95, P = 0.008). The RCS regression model revealed a continuous linear relationship between RAR and all-cause mortality. No significant interaction was observed in the subgroup analysis. Conclusion: The RAR is independently associated with all-cause mortality in patients treated with TAVR. The higher the RAR, the higher the mortality. This simple indicator may be helpful for risk stratification of TAVR patients. [ABSTRACT FROM AUTHOR]

Sample preparation is key to the success of proteomics studies. In the present study, two sample preparation methods were tested for their suitability on the mature, recalcitrant leaves of six representative perennial plants (grape, plum, pear, peach, orange, and ramie). An improved sample preparation method was obtained: Tris and Triton X-100 were added together instead of CHAPS to the lysis buffer, and a 20% TCA-water solution and 100% precooled acetone were added after the protein extraction for the further purification of protein. This method effectively eliminates nonprotein impurities and obtains a clear two-dimensional gel electrophoresis array. The method facilitates the separation of high-molecular-weight proteins and increases the resolution of low-abundance proteins. This method provides a widely applicable and economically feasible technology for the proteomic study of the mature, recalcitrant leaves of perennial plants.

OXPHOS is believed to play an important role in non-alcoholic fatty liver disease (NAFLD), however, precise mechanisms whereby OXPHOS influences lipid homeostasis are incompletely understood. We previously reported that ectopic expression of LRPPRC, a protein that increases cristae density and OXPHOS, promoted fatty acid oxidation in cultured primary hepatocytes. To determine the biological significance of that observation and define underlying mechanisms, we have ectopically expressed LRPPRC in mouse liver in the setting of NAFLD. Interestingly, ectopic expression of LRPPRC in mouse liver completely interdicted NAFLD, including inflammation. Consistent with mitigation of NAFLD, two markers of hepatic insulin resistance—ROS and PKCε activity—were both modestly reduced. As reported by others, improvement of NAFLD was associated with improved whole-body insulin sensitivity. Regarding hepatic lipid homeostasis, the ratio of NAD+ to NADH was dramatically increased in mouse liver replete with LRPPRC. Pharmacological activators and inhibitors of the cellular respiration respectively increased and decreased the [NAD+]/[NADH] ratio, indicating respiration-mediated control of the [NAD+]/[NADH] ratio. Supporting a prominent role for NAD+, increasing the concentration of NAD+ stimulated complete oxidation of fatty acids. Importantly, NAD+ rescued impaired fatty acid oxidation in hepatocytes deficient for either OXPHOS or SIRT3. These data are consistent with a model whereby augmented hepatic OXPHOS increases NAD+, which in turn promotes complete oxidation of fatty acids and protects against NAFLD. [ABSTRACT FROM AUTHOR]