IMPORTANCEThe association between obesity, an established risk factor for atrial fibrillation (AF), and response to antiarrhythmic drugs (AADs) remains unclear.OBJECTIVE To test the hypothesis that obesity differentially mediates response to AADs in patients with symptomatic AF and in mice with diet-induced obesity (DIO) and pacing induced AF. DESIGN, SETTING, AND PARTICIPANTSAn observational cohort study was conducted including 311 patients enrolled in a clinical-genetic registry. Mice fed a high-fat diet for 10 weeks were also evaluated. The study was conducted from January 1, 2018, to June 2, 2019.MAIN OUTCOMES AND MEASURES Symptomatic response was defined as continuation of the same AAD for at least 3 months. Nonresponse was defined as discontinuation of the AAD within 3 months of initiation because of poor symptomatic control of AF necessitating alternative rhythm control therapy. Outcome measures in DIO mice were pacing-induced AF and suppression of AF after 2 weeks of treatment with flecainide acetate or sotalol hydrochloride.RESULTS A total of 311 patients (mean [SD] age, 65 [12] years; 120 women [38.6%]) met the entry criteria and were treated with a class I or III AAD for symptomatic AF. Nonresponse to class I AADs in patients with obesity was less than in those without obesity (30% [obese] vs 6% [nonobese]; difference, 0.24; 95% CI, 0.11-0.37; P = .001). Both groups had similar symptomatic response to a potassium channel blocker AAD. On multivariate analysis, obesity, AAD class (class I vs III AAD [obese] odds ratio [OR], 4.54; 95% Wald CI, 1.84-11.20; P = .001), female vs male sex (OR, 2.31; 95% Wald CI, 1.07-4.99; P = .03), and hyperthyroidism (OR, 4.95; 95% Wald CI, 1.23-20.00; P = .02) were significant indicators of the probability of failure to respond to AADs. Pacing induced AF in 100% of DIO mice vs 30% (P < .001) in controls. Furthermore, DIO mice showed a greater reduction in AF burden when treated with sotalol compared with flecainide (85% vs 25%; P < .01). CONCLUSIONS AND RELEVANCEResults suggest that obesity differentially mediates response to AADs in patients and in mice with AF, possibly reducing the therapeutic effectiveness of sodium channel blockers. These findings may have implications for the management of AF in patients with obesity.

The rapid increasing number of automobile products has brought great convenience to people’s living, but it has also caused serious environmental issues, waste of resources and energy shortage during its whole lifecycle. Corporate Environmental Responsibility (CER) refers to the company’s responsibility to avoid damage to the natural environment derived from its corporate social responsibility (CSR), and it plays an important role in solving resource and environmental problems. However, due to various internal and external reasons, it is difficult for the automobile manufacturing industry to find the key drivers for the implementation of CER. This research proposes a model framework that uses the fuzzy decision-making test and evaluation laboratory (fuzzy DEMATEL) method to analyze the drivers of CER from the perspective of the triple bottom line (TBL) of economy, environment and society. Firstly, the common drivers of CER are collected using literature review and questionnaire survey methods. Secondly, the key drivers are analyzed by using the fuzzy DEMATEL. Finally, the proposed approach was verified through a case study. The research results show that some effective measures to implement CER can be provided for the government, the automobile manufacturing industry and the public to promote sustainable development of Chinese Auto Manufacturing Industry (CAMI).

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MicroRNA (miR)-126 is known to inhibit inflammatory responses in various inflammatory-related diseases, but its role during the cerebral ischemia/reperfusion (I/R) injury remains unknown. The present study aimed to examine the interaction between miR-126 and RAB3A interacting protein (RAB3IP), and explore its potential protective effects during I/R injury. The human neuroblastoma cell line SH-SY5Y was cultured in an oxygen-glucose deprivation/reoxygenation (OGD/R) environment to simulate I/R injury to assess miR-126 expression and cell viability. SH-SY5Y cells cultured in normal conditions were used as a negative control (NC) group. SH-SY5Y cells were transfected with a miR-126 mimic or an NC mimic, then cultured in OGD/R conditions; in rescue experiments, SH-SY5Y cells were co-transfected with RAB3IP overexpression or NC plasmid together with mimic-NC or mimic-miR, and then maintained in an OGD/R environment to evaluate miR-126, RAB3IP expression, cell viability and apoptosis. Cell viability was reduced in the Model group compared with the NC group, suggesting the successful construction of the OGD/R model. miR-126 expression was downregulated in the Model group compared with the NC group. However, following transfection with mimic-miR, cell viability increased compared with the mimic-NC group. Annexin V and PI staining and Hoechst/PI assays also indicated that apoptosis was reduced in the mimic-miR group compared with the mimic-NC group. RAB3IP expression was reduced following mimic-miR transfection. In rescue experiments, miR-126 negatively regulated RAB3IP expression; by contrast, RAB3IP did not affect that of miR-126. In addition, RAB3IP overexpression attenuated the protective effect of miR-126 on OGD/R-induced apoptosis. These findings suggest that miR-126 protects against cerebral I/R injury by targeting RAB3IP.