Objective To explore the induction of cardiomyogenesis of microRNA-129 (mir-129) in rat bone marrowmesenchymal stem cells (BM-MSCs) and its mechanism. Methods BM-MSCs were isolated from Sprague-Dawley rats and cultured in vitro. Overexpression of mir-129 or both mir-129 and glycogen synthase kinase-3β (GSK-3β) in BM-MSCs was produced with a lentiviral vector system. All the BM-MSCs were divided into four groups: control group (MSCs),Lentiviral vectors+MSCs group (Lv-MSCs),mir-129 transfection group (mir-129-MSCs),and mir-129+GSK-3βdouble transfection group (mir-129+GSK-3β-MSCs). Five-Azacytidine (5-Aza) (10 μmol/L) was used to induce BM-MSCsdifferentiation into cardiomyocytes. On the 1st,5 th,10 th,15 th and 20 th day after induction,realtime-PCR was performedto detect mRNA levels of GATA-4,Nkx2.5 and MEF-2C. On the 10 th,15 th and 20 th day after induction,Western blottingwas performed to examine expression levels of cTnI,Desmin,GSK-3β,phosphorylated β-catenin and dephosphorylated β-catenin. Results Compared with the control group,at respective time points,mRNA levels of cardiomyogenic genes and expression levels of cardiomyocyte-related proteins of mir-129 transfection group were significantly elevated,theexpression level of GSK-3β was significantly decreased,and the ratio of dephosphorylated/phosphorylated β-catenin was significantly elevated. When both mir-129 and GSK-3β were overexpressed in BM-MSCs,mRNA levels of cardiomyogenicgenes and expression levels of cardiomyocyte-related proteins were significantly lower than those of mir-129 transfection group,and the ratio of dephosphorylated/phosphorylated β-catenin was significantly decreased. Conclusion Overexpression of mir-129 can promote cardiomyogenesis of rat BM-MSCs possibly via inhibiting GSK-3β production and thus decreasing the inhibition of phosphorylation of β-catenin which then enters the nucleus and activates downstream signaling pathways that regulate cardiomyogenic differentiation of BM-MSCs.
Objective To investigate the application of sequential noninvasive ventilation (NIV) in weaning patients off mechanical ventilation after coronary artery bypass grafting (CABG). Methods From July 2007 to July 2009, 52 patients who underwent CABG with mechanical ventilation for no less than 24 hours and P/F Ratio lower than 150 mm Hg were divided into two groups with random number table. In the sequential NIV group (SNIV group), there were 19 patients including 16 males and 3 females whose ages were 69.26±8.10 years. In the prolonged mechanical ventilation group (PMV group), there were 33 patients including 28 males and 5 females whose ages were 70.06±7.09 years. Clinical data of these two groups were compared and the influence of NIV on the circulation and respiration of the patients were observed. Results The SNIV group weaned off mechanical ventilation earlier than the PMV group (26.46±3.66 h vs. 38.65±9.12 h, P=0.013). The SNIV group held shorter total ventilation time (29.26±21.56 h vs.54.45±86.57 h,P=0.016), ICU stay time (2.44±2.99 d vs. 4.89±7.42 d, P=0.028) and postoperative hospital time (10.82±4.31 d vs. 14.01±19.30 d, P=0.039) than the PMV group. Furthermore, the SNIV group had lower pneumonia rate (5.26% vs. 30.30%, P=0.033) and total postoperative complication rate (10.53% vs.45.45%, P=0.030) than the PMV group. However, there was no significant difference (Pgt;0.05) between the two groups in the successful weaning rate, repeated tracheal intubation rate, tracheotomy rate and mortality 30 days after operation. After NIV, SNIV group had no significant change in heart rate, central vein 〖CM(1585mm〗pressure, pulmonary arterial pressure and pulmonary arterial wedge pressure than the baseline value, while systolic pressure (129.66±19.11 mm Hg vs. 119.01±20.31 mm Hg, P=0.031), cardiacindex [3.01±0.30 L/(min.m2) vs. 2.78±0.36 L/(min.m2), P=0.043] and P/F Ratio (205.95±27.40 mm Hg vs. 141.33±9.98 mm Hg, P=0.001) were obviously elevated. Conclusion Sequential NIV is a effective and safe method to wean CABG patients off mechanical ventilation.
Abstract: Objective To summarize the experiences of treatment for prosthetic valve endocarditis (PVE), paying special emphasis on some interrelated conceptions of PVE, its microbiology, diagnosis, prevention and treatment. Methods From September 1979 to September 2009, 33 patients diagnosed to have PVE were treated in our department. There were 17 males and 16 females. Their age ranged from 19 to 57 years old with an average age of 34 years. The incidence of PVE was 1.48% (33/2 236)including 1.03%(16/1 551), 3.00%(7/233), 2.28%(10/438), and 0% of PVE in mitral valve replacement (MVR), aortic valve replacement (AVR), double valve replacement (DVR), tricuspid valve replacement (TVR), respectively. Pure medical treatment (Penicillin or Vancomycin with other broadspectrum antibiotics, Fluconazole and Amphotericin) was performed on 22 patients. Combined medical and surgical treatment was performed in 11 patients. The patients underwent operation after adequate antibiotics treatment and general condition improvement. The infective tissue and vegetation were completely debrided after the infective prosthetic valve was removed. Before the new valve was transplanted, paravalvular tissue was cleaned with antibiotics, iodine solution and normal saline. Results Hospital death occurred in 19 patients (86.36%) and only 3 patients (13.64%) recovered in the group with pure medical treatment. The main reasons for death were infective shock and cardiac failure in 9 patients, and cerebral complications including embolism, bleeding and multipleorgan failure in 10 patients. For the group with combined medical and surgical treatment, 10 patients (90.91%) survived and only one patient (9.09%) died of multipleorgan failure. Follow-up was done in 13 patients for 6 months to 15 years averaging 41 months. During the follow-up, only one patient was reoperated because of the paravalvular leak eight year later. There was no PVE recurrence in all the rest patients. Conclusion Compared with pure medical treatment, combined medical and surgical treatment is a better solution for PVE.
Objective To summarize the experiences of surgical treatment for partial atrioventricular canal defect. Methods The data of 66 patients of surgical treatment for partial atrioventricular canal defect from January 1984 to December 2007 were analyzed retrospectively. The cleft of mitral valve presented in all of those patients. There were 52 cases with direct suture on cleft, 8 cases with direct suture with commissurroplasty, 1 case with posterior leaflet plasty, 3 cases with direct suture St.Jude ring and 2 cases mitral valve replacement. The ostium primum atrial septal defects were repaired with patches of Dacron in 12 cases and autologous pericardium in 54 cases. Coronary sinus was situated on the left atrium in 5 and ostium primum atrial septal defects were repaired in Kirklin’s way; the others in MeGoon’way. Meanwhile other heart abnormalities were done. Results There were two early deaths (3.03%), one patient died of heart arrhythmia and one patient died of respiratory failure. Complications of total A-V block was in 2 cases. Both of them were replanted with pace makers.52 cases were followed up, followup time was 5 months to 22 years(mean follow-up 15 years). All patients had better life. Four patients have been re -operated for different reasons post primary operation. One had good result after re-mitral valve replacement. One case died of acute renal failure and the other two died of low cardiac output syndrome. Conclusions Early operation is definitely recommended when the diagnosis is confirmed. Because the structure or function of mitral valve is saved, pulmonary hypertension is avoided and the mortality is lower in the future. The key points of operation are to rectify the mitral insufficiency, repair ostium primum atrial septal defects and avoid atrioventricular block. The patients of mild regurgitation of mitral valve have good results. Provided in those have more than middle regurgitation of mitral valve then their longterm results are poor.
Objective To study the short and medium term effect of myocardial contractile force by implantation of endothelial progenitor cells (EPCs) in the myocardial infarction model. Methods Hundred and twenty SD rats were equally and randomly divided into experimental group and control group (60 rats in each group). Acute myocardial infarction model was created by ligation of LAD. Autologous EPCs were purified from peripheral blood then implanted into the acute myocardial infarct site via topical injection. IMDM were used in control group. Specimens and muscle strip were harvested at 3, 6 weeks, 6, 8 and 12 months after EPCs implantation for contractile force study and to detect the expression of vascular endothelial growth factor(VEGF), basic fibroblast growth factor (bFGF) and Ⅷ factor by immunohistology and video image digital analysis system. Results The expression of VEGF, bFGF and the microvessel counts in experimental group were much higher than those of control group(P〈 0.01) at 3, 6 weeks and 6 months after transplantation. The contractile force in experimental group was better than that in control group(P〈0.01) at the same time. But from 8 months after implantation, the contractile force and so on were not up in the experimental group. Conclusion EPCs, after being implanted into infarct myocardium, shows the ability of improvement of the contractile performance in infarcted myocardium by means of angiogenesis and vasculogenesis and the medium term results are persistent.
Objective To investigate the molecular mechanism of multiple cellular factors expressed shortly after ischemia reperfusion (IR) injury from the pathway of nuclear factor kappa B (NF κB). Methods The isolated heart models were established and sixty six rats were randomly divided into experimental group and control group. The deoxyribonucleic acid (DNA) binding activities of NF κB, the inhibitory kappa B (IκBα) levels in cytoplasm and tumor necrosis factor α (TNF α) messenger ribonucleic acid (mRNA) expressions were determined after 5, 15 min ischemia in experimental group, both after 0, 5, 15, 30 min ischemia and concomitantly 5, 15, 30, 45, 60 min reperfusion in control group. Results Augment of DNA binding activities of NF κB and reduction of IκBα in cytoplasm shortly after ischemia results were observed in control group. The level of IκBα was restored after reperfusion, the DNA binding activities of NF κB was further augmented. DNA binding activities of NF κB and TNF α mRNA expressions were lower in experimental group than those in control group. Conclusions NF κB in IR myocardium is activated by two different pathways: p65 p50 heterodimers and p50 p50 homodimers. In addition, the results suggest that early activation of NF κB induced by ischemia in the myocardium could be a signal mechanism for controlling and regulating immediate gene expressions during ischemia reperfusion.