Our findings suggest that miR-23 plays a crucial role in controlling VSMCs proliferation and apoptosis by targeting BCL2L11.

The outcome of patients with acute type B aortic dissection (BAAD) is largely dictated by whether or not the case is “complicated.” The purpose of this study was to investigate the risk factors leading to in-hospital death among patients with BAAD and then to develop a predictive model to estimate individual risk of in-hospital death. A total of 188 patients with BAAD were enrolled. Risk factors for in-hospital death were investigated with univariate and multivariable logistic regression analysis. Significant risk factors were used to develop a predictive model. The in-hospital mortality rate was 9% (17 of 188 patients). Univariate analysis revealed 7 risk factors to be statistically significant predictors of in-hospital death ( P < .1). In multivariable analysis, the following variables at admission were independently associated with increased in-hospital mortality: hypotension (odds ratio [OR], 4.85; 95% confidence interval [CI], 1.12–18.90; P = .04), ischemic complications (OR, 8.24; 95% CI, 1.25–33.85; P < .001), renal dysfunction (OR, 12.32; 95% CI, 10.63–76.66; P < .001), and neutrophil percentage ≥80% (OR, 5.76; 95% CI, 2.58–12.56; P = .03). Based on these multivariable results, a reliable and simple prediction model was developed, a total score of 4 offered the best point value. Independent risk factors associated with in-hospital death can be predicted in BAAD patients. The prediction model could be used to identify the prognosis for BAAD patients and assist physicians in their choice of management.

Objective The aim of this study is to investigate the clinical value of long noncoding RNA growth arrest‐specific transcript 5 (LncRNA GAS5) in the diagnosis of coronary artery disease (CAD) and its protective effect on myocardial injury in rats with CAD. Methods Patients with CAD and healthy controls were selected to measure the expression of GAS5, and further to perform the correlation analysis and ROC curve. In addition, the rat models of CAD were also established to observe the effect of GAS5 on hyperlipidemia, myocardial injury, cardiomyocyte apoptosis, oxidative stress, and inflammatory injury of rats with CAD, and the effect of the Wnt/β‐catenin signaling pathway was also determined. Results Overexpression of GAS5 in CAD rats determines improvement of hyperlipidemia, attenuation of myocardial injury, inhibition of cardiomyocyte apoptosis, oxidative stress, inflammatory injury, and abnormal activation of the Wnt/β‐catenin signaling pathway in myocardial tissues. Conclusion Our study demonstrates that downregulation of GAS5 is found in CAD, and overexpression of GAS5 inhibits abnormal activation of the Wnt/β‐catenin signaling pathway in myocardial tissues of CAD rats.

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