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Objective:To study the expression of miR-496 in gastric cancer cells, and explore its role and mechanism in the proliferation and apoptosis of gastric cancer cells. Methods:Real-time fluorescence quantitative PCR (qPCR) was used to detect the expression of miR-496 in normal gastric epithelial cell lines and gastric cancer cell lines AGS and MKN45. miR-496 was knocked down in AGS cells with the lowest expression level, and a negative control group and a blank control group were set up. Cell proliferation and apoptosis were detected by CCK8 assay and flow cytometry. LYN, the target gene of miR-496, was screened using bioinformatics software, and the effect of transfection of miR-496 on LYN expression was detected by qPCR. Subsequently, rescure experiment was conducted to further study the mechanism of miR-496 on gastric cancer cells through regulation of LYN. Data were analyzed by GraphPad Prism 9 software. Measurement data were presented as mean ± standard deviation, and the comparison between the two groups was performed by t test. Results:The expression of miR-496 in AGS and MKN45 was significantly lower than that in normal gastric epithelial cells ( P<0.05). After overexpression of miR-496, the proliferation of AGS cells could be inhibited and the apoptosis ratio of AGS cells could be significantly increased ( P<0.05). QPCR results showed that miR-496 overexpression group could inhibit the expression of LYN ( P<0.05). Bioinformatics analysis showed that miR-496 binds to LYN kinase ( LYN) 3 ′UTR region, and overexpression of miR-496 can inhibit the expression of LYN in AGS cells, while CCK8 rescue experiment showed that overexpression of LYN could remove the inhibitory effect of miR-496 on cell proliferation. Flow cytometry showed that LYN expression could cancel the promoting effect of miR-496 on apoptosis ( P<0.05). Conclusion:miR-496 is low expressed in gastric cancer cells, and it inhibits the proliferation and promotes apoptosis of gastric cancer cells by targeting the expression of LYN in gastric cancer cells.
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Objective:This study was performed to assess the effect of glycemic control on atrial fibrillation recurrence rates after heart surgery concomitant with Cox-Maze Ⅳ ablation.Methods:A retrospective analysis was performed on 317 diabetic patients with atrial fibrillation who underwent cardiac surgery combined with Cox-Maze Ⅳ ablation in our hospital from May 2016 to February 2020. The patients were followed up for(37.7±27.7) months, and the data of atrial fibrillation recurrence and clinical outcome were collected and compared. The limited cubic spline model was used to analyze the dose-relationship between HbA1c level and the recurrence of atrial fibrillation. The univariate and multivariate Cox proportional regression analysis was used to explore the risk factors of recurrent atrial fibrillation after Cox-Maze Ⅳ ablation. Results:Higher glycated hemoglobin(HbA1c) at the time of ablation was associated with higher post-ablation recurrence rates. The cumulative survival freedom from atrial fibrillation recurrence for patients with HbA1c ≥7.4% at time of operation at 12, 24, 36 and 48 months were 96.3%、75.8%、52.7% and 35.7%, respectively( P<0.001). Besides, the rates of all-cause mortality, cardiac mortality and rehospitalization were significantly lower in patients with HbA1c<7.4%(1.7% vs. 6.3%, P=0.03; 1.1% vs. 5.6%, P=0.02 and 5.7% vs. 20.4%, P=0.01). The multivariate Cox regression model showed that HbA1c was an independent risk factor for atrial fibrillation recurrence( P<0.05). Conclusion:Higher preoperative HbA1c levels were associated with increased recurrence of atrial fibrillation and adverse clinical outcomes in patients undergoing cardiac surgery combined with Cox-Maze Ⅳ ablation.
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Objective:To investigate the difference between the short-term and long-term survival rates of patients undergoing tricuspid valve replacement with biological and mechanical valves.Methods:273 patients who received tricuspid valve replacement were selected from our Hospital from November 1993 to August 2018. The mean follow-up time was(8.2±5.6) years. The total follow-up rate was 95%. Kaplan-Meier method was used to make survival curves of the two groups and log rank test was used to compare the differences between the two groups. In addition, this study made the comparison of preoperative, intraoperative and postoperative information and long-term survival rate between these two groups.Results:There was no significant difference in demographic characteristics and baseline between mechanical valve group and biological valve group. 16 patients died in the mechanical valve group and 22 in the biological valve group. In the mechanical valve group, 14 cases died of postoperative low cardiac output syndrome and 2 cases died of gastrointestinal hemorrhage. 22 patients were died of low cardiac output syndrome. The auxiliary time in the mechanical valve group was longer than that in the biological valve group[(151.76±70.30)min vs.(131.62±60.25)min, P=0.013)]. There was no significant difference in long-term survival rate between the two groups in Kaplan- Meier survival curve( P=0.234). Conclusion:There is no difference in short-term and long-term survival rate between mechanical valve and biological valve in tricuspid valve replacement.
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Objective To investigate the role of hexosamine biosynthesis pathway (HBP) in the functionalalterationofmesangialcellstransinfectedwith glucose transporter 1 (GLUT1) gene. Methods Rat mesangial cells were transinfected with the human GLUT1 gene (MCGT1) by retrovirus vector. Mesangial cells transinfected with bacterial ?-galactosidase (MCLacZ) were used as control. Glucose uptake was detected with 2-deoxy-〔 3H〕-D-glucose (2-DG). Cell size, RNA/DNA ratio, protein/DNA ratio and the synthesis of fibronectin were evaluated by flow cytometry. The activity of glutamine: fructose-6-P aminotransferase (GFAT), which is the key enzyme of HBP, was assayed by spectrophotometry. The expression of GFAT gene was analyzed by RT-PCR. Results MCGT1 demonstrated higher 2-DG uptake than MCLacZ 〔(741.0?60.5)dpm/?g protein vs (92.2?9.0)dpm/?g protein,P