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Objective To study the regulatory effects of long non-coding RNA HIF1A-AS1 on the myocardial ischemia reperfusion (I/R) injury and the related mechanism. Methods Myocardial I/R injury model was established with SD rats, and hypoxia reoxygenation (H/R) model was established with rat cardiac myocytes. si-HIF1A-AS1 was used to inhibit HIF1A-AS1 expression in the cardiac myoctyes. Then the mRNA expression of HIF1A-AS1 was detected by real-time PCR, the growth vitality of cardiac myocytes was investigated by MTT assay, the concentration of lactate dehydrogenase (LDH) in the culture media was detected by ELISA, and the autophagy-associated protein Beclin-1 expression was observed by Western blotting analysis. Results HIF1A-AS1 expression was increased in cardiac muscle of rat I/R model and rat cardiac myocytes of H/R model. Inhibition of HIF1A-AS1 by siRNA protected the cardiomyocytes against H/R injuries, reversing the decreased growth vitality of cardiac myoctyes, increased LDH level in the culture media, and increased expression of autophagy-related protein Beclin-1 induced by H/R stimulation. Conclusion Inhibition of long non coding RNA HIF1A AS1 might play a protective role in I/R injury of cardiac myoctyes by inhibiting the excessive autophagy of cardiomyocytes.
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Objective To study the regulatory effect of urocortin (UCN) on ischemia/reperfusion (I/R)-induced myocardial autophagy, so as to explore the myocardial protection mechanism of UCN. Methods Cardiac I/R model was established with rats and hypoxia/reoxygenation(H/R) model was also established with neonatal rat cardiomyocytes. The injury was created by ischemic/hypoxia for 1 h plus reperfusion/reoxygenation for 2 h, and UCN pretreatment was given 1 h before ischemia/hypoxia. The I/R or H/R-induced myocardial injury, myocardial autophagy and autophagy-related gene expression were observed 2 h after reperfusion/reoxygenation. Results UCN pretreatment greatly reduced I/R-induced myocardial damage by decreasing the infarct size, serum creatine kinase (CK) and lactate dehydrogenase (LDH) concentration, increasing the vitality of H/R cardiomyocytes in vitro, and reducing LDH level in the culture supernatant. Moreover, UCN pretreatment also inhibited H/R-induced myocardial autophagy by reducing the ratio of LC3BII/LC3B I and inhibiting expression of autophagy-related genes (Beclin1 and Bnip3). Conclusion UCN can inhibit I/R-induced myocardial autophagy, which may play an important role in the protection against I/R injury.
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<p><b>OBJECTIVES</b>To explore the feature of the edge-to-edge technique and its effect for mitral regurgitation due to myxomatous degeneration.</p><p><b>METHODS</b>The in-patient data and follow-up outcomes of 58 patients after the edge-to-edge technique for mitral regurgitation due to myxomatous degeneration from January 2000 to January 2009 were analyzed retrospectively. Of the 58 patients, 32 patients were male and 26 patients were female, and the age range was from 43 years to 65 years with a mean of (56 ± 6) years, and moderate mitral regurgitation was observed in 18 patients and severe regurgitation in 40 patients, and the prolapse of the anterior leaflet was observed in 50 patients and the prolapse of the bileaflet in 8 patients. The edge-to-edge technique was performed in all patients and the annuloplasty was performed in 44 patients.</p><p><b>RESULTS</b>There was no perioperative death and serious complication. Postoperative transthoracic echocardiography of all the survivors indicated that the dimensions of left atrial and left ventricular were obviously decreased (P < 0.05) and mitral insufficiency was obviously improved (no regurgitation was observed in 9 patients and trace regurgitation in 30 patients and mild regurgitation in 19 patients) and there was no mitral stenosis. Totally 58 patients were followed up from 24 months to 95 months with a mean of (58 ± 20) months. During the follow-up, there were 2 deaths for noncardiac factors. Freedom from recurrent moderate or severe mitral regurgitation at 5 years after operations was 91.9%. According to undergoing combined annuloplasty or not, 58 patients were divided into the edge-to-edge technique group (14 cases) and the edge-to-edge technique + annuloplasty group (44 cases), and the survival analysis shows there was significant difference on freedom from long-term recurrent moderate or severe mitral regurgitation after operations between two groups (χ(2) = 4.034, P = 0.045) and long-term effect of the latter group was better.</p><p><b>CONCLUSIONS</b>The edge-to-edge technique can be conveniently used and bring about satisfactory perioperative and long-term effects for mitral regurgitation due to myxomatous degeneration. The combination of the edge-to-edge technique and the annuloplasty can improve the long-term effect significantly.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Follow-Up Studies , Mitral Valve , General Surgery , Mitral Valve Insufficiency , General Surgery , Mitral Valve Prolapse , General Surgery , Retrospective Studies , Suture Techniques , Treatment OutcomeABSTRACT
Objective: To evaluate the safety and efficacy of radiofrequecy ablation for atrial fibrillation during minimally invasive mitral valve surgery via right thoracotomy. Methods: From Jan. 2008 to Dec. 2011, 30 patients underwent radiofrequecy Maze EI procedure for atrial fibrillation during mini-invasive mitral valve surgery (study group). Another 30 patients with atrial fibrillation undergoing mitral valve surgery through median sternotomy without Maze procedure during the same period were taken as controls. The pre-treatment data of the patients were matchable between the two groups. The study group received mitral valve repair/replacement and radiofrequecy Maze HI procedure for atrial fibrillation. The operative outcome, postoperative complication and elimination rate of atrial fibrillation were compared between the two groups. Results: No patient in the study group was transferred to median sternotomy during operation, and there was no reoperation, prolonged incubation, failure of important organs, hemoglobinuria or death. Compared with the control group, the study group had significantly longer mean circulation arrest time and cardiopulmonary bypass time, significantly reduced chest drainage and blood transfusion volume, and significantly shortened hospital study (P<0. 05). The elimination rates of atrial fibrillation at immediately after operation,discharge and 6 months after operation were 96. 7%, 66. 7% and 73. 3% in the study group, and 50%, 23. 3% and 16. 7% in the control group, respectively, with significant difference found between the two groups (P< 0.01). Compared with the control group, better heart function recovery was achieved in the study group at 6 month after operation. Conclusion: Radiofrequecy ablation for atrial fibrillation during minimally invasive mitral valve surgery via right thoracotomy is safe and effective. Importantly, it does not increase risks and complications of surgery. The early and middle term effects are satisfactory.
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Objective: To investigate the inhibitory effects of RNA silencing via adenovirus-mediated vascular endothelial growth factor receptor (VEGFR) shRNA on proliferation of lung adenocarcinoma cells in vitro and in vivo. Methods: Ad-VEGFRshRNA adenovirus containing enhanced green fluorescent protein (EGFP) gene and VEGFRshRNA was constructed and was used to infect A549 cells; fluorescent microscopy was used to observe the infection efficiency. Western blotting assay was used to examine the expression of VEGFR protein in A549 cells. MTT method was used to examine the cell viability and the cell growth curve was drawn. The inhibition of cell growth was examined by cell cycle and colony-forming test. Meanwhile, nude mice were transplanted with A549 cells to establish tumor-bearing model, and the long term growth of tumor was observed. Results: Western blotting revealed that the expression of VEGFR was obviously decreased in the RNA interference group. The cell growth curve indicated that the cell growth was obviously inhibited after RNA interference. Cell cycle and colony-forming test indicated that the tumor growth was obviously inhibited after RNA interference. In vivo study with nude mice also indicated that RNA interference obviously inhibited tumor growth. Conclusion: The constructed VEGFR-targeted shRNA can effectively inhibit VEGFR expression in A549 cells and can suppress the growth of A549 cells.