The year 2019 witnessed an exponential growth of the e-commerce live streaming industry. Notably, competitions among live streamers have become increasingly fierce as more newcomers are marching in. To survive and thrive in the cut-throat market competitions, it is key for them to increase consumers’ repeat purchase rate and win customer loyalty. This study uses empirical research methods to probe into the influence of e-commerce live streaming on consumer repurchase intentions. According to this study, perceived entertainment and perceived similarity have a positive impact on consumer repurchase intentions, and this relationship is partially mediated by consumer satisfaction. In addition, perceived product quality, perceived interactivity, and perceived professionalism have a positive and indirect effect on consumer repurchase intentions, and this relationship is fully mediated by consumer satisfaction.
Background Nonalcoholic fatty liver disease (NAFLD) can lead to chronic liver diseases associated with mitochondrial damages. However, the exact mechanisms involved in the etiology of the disease are not clear. Methods To gain new insights, the changes affecting sirtuin 1 (SIRT-1) during liver fat accumulation was investigated in a NAFLD mouse model. In addition, the in vitro research investigated the regulation operated by SIRT-1 on mitochondrial structures, biogenesis, functions, and autophagy. Results In mice NAFLD, high-fat-diet (HFD) increased body weight gain, upregulated serum total cholesterol, triglycerides, aspartate aminotransferase, alanine aminotransferase, blood glucose, insulin levels, and liver malondialdehyde, and decreased liver superoxide dismutase activity. In liver, the levels of SIRT-1 and peroxisome proliferator-activated receptor-gamma coactivator -1α (PGC-1α) decreased. The expression of peroxisome proliferator-activated receptor-α and Beclin-1 proteins was also reduced, while p62/SQSTM1 expression increased. These results demonstrated SIRT-1 impairment in mouse NAFLD. In a well-established NAFLD cell model, exposure of the HepG2 hepatocyte cell line to oleic acid (OA) for 48 h caused viability reduction, apoptosis, lipid accumulation, and reactive oxygen species production. Disturbance of SIRT-1 expression affected mitochondria. Pre-treatment with Tenovin-6, a SIRT-1 inhibitor, aggravated the effect of OA on hepG2, while this effect was reversed by CAY10602, a SIRT-1 activator. Further investigation demonstrated that SIRT-1 activity was involved in mitochondrial biogenesis through PGC-1α and participated to the balance of autophagy regulatory proteins. Conclusion In conclusion, in high-fat conditions, SIRT-1 regulates multiple cellular properties by influencing on mitochondrial physiology and lipid autophagy via the PGC-1α pathway. The SIRT-1/PGC-1α pathway could be targeted to develop new NAFLD therapeutic strategies.
Background. Increased red cell distribution width (RDW) can predict the incidence and mortality of cardiovascular diseases. However, there are limited data on the relationship between RDW and altitude and the subtype of atrial fibrillation (AF). We investigated the effects of altitude on RDW in patients with different types of AF. Methods. A total of 303 patients with nonvalvular AF were included. Of these, 156 lived in low altitude (77 paroxysmal AF, PAF; 79 persistent AF, PeAF) and 147 in high altitude (77 paroxysmal AF, PAF; 70 persistent AF, PeAF). In these groups, baseline characteristics, complete blood counts, serum biochemistry, and echocardiography were evaluated. Multivariate logistic regression analysis was conducted to determine the independent predictors of AF at the different altitudes. Results. In both low and high altitudes, RDW and left atrial diameter (LAD) were higher in AF than control subjects (P<0.05) and higher in persistent AF than paroxysmal AF (P<0.05). Compared with any groups (PAF group, PeAF group, or control group) of low-altitude, RDW and LAD were found higher in high-altitude corresponding groups. Multivariate logistic regression analysis demonstrated that RDW, mean corpuscular volume (MCV), and LAD levels independently associated with AF patients in low altitude (RDW, OR 1.687, 95% CI 1.021–2.789; P<0.05), while in high altitude, RDW, MCV, creatinine (Cr), and LAD were independent predictors for AF patients (RDW, OR 1.755, 95% CI 1.179–2.613; P<0.05). Conclusion. Elevated RDW levels may be an independent risk marker for nonvalvular AF, affected by type of AF and altitude.
Mitochondria are key regulators of cell fate, maintaining self‐stability by a fine‐tuned quality‐control network including mitophagy, biogenesis, fission and fusion processes. Myocardial mitochondria can be impaired by hypercholesterolemia. Statins, such as atorvastatin, are considered the cornerstone in the management of hypercholesterolaemia primarily due to their marked cholesterol‐lowering ability. The direct effect of atorvastatin on myocardial mitochondria remains unclear. We aimed to explore whether atorvastatin could attenuate myocardial mitochondrial defects induced by high cholesterol, and whether cycloastragenol, a potent telomerase activator, could be used as a potential complementary bioactive compound for obesity and hypercholesterolaemia treatment. We found that atorvastatin at a low dose (3 mg/kg) did not reduce elevated serum cholesterol, but reversed cardiac remodelling and dysfunction in C57BL/6J mice fed with high‐fat diet (HFD). Atorvastatin reversed the upregulated mitophagy, mitochondrial fission and fusion, accompanied by mitochondrial biogenesis activation in HFD‐fed mice hearts. Mitochondrial structural impairments were attenuated by atorvastatin in HFD‐fed mice and oxidized low‐density lipoprotein (ox‐LDL) exposed HL‐1 cardiomyocytes. The depolarized mitochondrial membrane potential and increased mitochondrial oxygen consumption rates in ox‐LDL exposed HL‐1 cells were recovered by atorvastatin. Furthermore, atorvastatin co‐treated with cycloastragenol had better effects on reducing body weight, improving cardiac remodelling and dysfunction, and protecting mitochondria in high cholesterol. Conclusively, low‐dose atorvastatin exhibited a cholesterol‐independent cardioprotective effect through improving the mitochondrial quality‐control network and repairing mitochondrial ultrastructure in high cholesterol. Atorvastatin plus cycloastragenol supplement therapy has a better effect on treating obesity and hypercholesterolaemia.
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