[Midterm outcome comparison between patients with bicuspid or tricuspid aortic stenosis undergoing transcatheter aortic valve replacement].

Objective: To compare the prognosis of transcatheter aortic valve replacement (TAVR) in patients with bicuspid aortic valve (BAV) or tricuspid aortic valve (TAV) stenosis. Methods: This was a retrospective study. Patients with symptomatic severe aortic stenosis, who underwent TAVR with follow-up time more than one year in Guangdong Provincial People's Hospital from April 2016 to August 2018, were included. According to aortic CT angiography, the patients were divided into BAV group and TAV group. The primary endpoint was the composite event of all-cause death and stroke, and the secondary endpoints were TAVR-related complications. Incidence of clinical endpoints and parameters derived from echocardiography were compared between the groups, and Kaplan-Meier survival analysis was used to compare the composite event between the two groups. Results: A total of 49 patients were included. The age was (73.6±6.3) years, and 25(51.0%) were male. There were 32 patients in BAV group and 17 in TAV group, the follow-up time was 466 (390, 664) days. The incidence of composite endpoint of death and stroke at one year were comparable in BAV and TAV groups (6.3% (2/32) vs. 5.9% (1/17), P=1.00). Kaplan-Meier curves also showed a similar risk of the composite endpoint(HR=1.03，95%CI 0.09-11.24，Log-rank P=0.98) between two groups. The incidence of all-cause death, stroke, myocardial infarction, severe bleeding, major vascular complications, new-onset atrial fibrillation or atrial flutter, and permanent pacemaker implantation were all similar between the two groups(all P>0.05), and there was no acute kidney injury (stage 2 or 3) in both groups. Echocardiographic parameters at one year were similar between the two groups (all P>0.05). Conclusions: The midterm prognosis of TAVR in patients with BAV and TAV stenosis is similar. Clinical trials of large sample size with long-term follow-up are warranted to verify our findings.

Study on molecular mechanism of MiRNA-29a in promoting proliferation and invasion of non-small-cell lung cancer by inhibiting MTSS1.

OBJECTIVE: To investigate the biological role of micro-ribonucleic acid (miR)-29a in non-small-cell lung cancer (NSCLC). PATIENTS AND METHODS: 55 cases of NSCLC tissue specimens and paired normal lung tissue specimens collected in the Department II of Oncology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine from July 2012 to April 2015 were randomly included. The fluorescent quantitative polymerase chain reaction, Western blotting, and immunohistochemistry were performed to detect the expression levels of miR-29a and metastasis suppressor 1 (MTSS1). Pearson correlation analysis was utilized to investigate the relationship between miR-29a expression and MTSS1 expression in NSCLC tissues, and the Kaplan-Meier survival curves were constructed to analyze the association of miR-29a expression with the survival time of NSCLC patients. A54 proliferation and invasion abilities were measured by means of plate clone formation assay, and transwell assay after the miR-29a was suppressed by miRNA inhibitor. Luciferase assay was used to detect the target gene of miR-29a. RESULTS: In NSCLC tissues, the miR-29a expression level was higher than that in normal lung tissues (p<0.05), while the expression level of MTSS1 protein was remarkably lower than that in normal lung tissues (p<0.05). The median survival time of the patients was 15.1 months in high miR-29a expression group and 18.3 months in low miR-29a expression group (p<0.05). The miR-29a expression was negatively correlated with the expression level of MTSS1 protein in NSCLC tissues (r=-0.762, p<0.05). Luciferase results suggest that miR-29a binds to the promoter region of MTSS1 and inhibits its transcription level. The expression of MTSS1 protein was up-regulated notably after miR-29a knockdown by an inhibitor. It was revealed in the results of transwell assay and plate clone formation assay that the proliferative and invasive capacity of A549 cells was significantly decreased after knockdown of miR-29a. CONCLUSIONS: The transcribed miR-29a down-regulates the protein level of MTSS1, suppressor of tumor proliferation and invasion, thereby promoting the proliferative and invasive capacity of NSCLC cells. Both miR-29a and MTSS1 are expected to become potential therapeutic targets for NSCLC.