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BACKGROUND: Previous studies have found that skeletal muscle satellite cell transplantation can induce angiogenesisin myocardial infarction area, reduce infarct size and improve cardiac function. But the overall effect is not satisfactory.OBJECTIVE: To observe the survival of basic fibroblast growth factor (bFGF) gene modified skeletal muscle satellitecells in acute myocardial infarction and to observe the expression of bFGF gene and the effect of cell transplantation onangiogenesis in myocardial infarction area.METHODS: Eighteen New Zealand white rabbits were divided into three groups by random: skeletal muscle satellite cellgroup (control group), bFGF gene enhanced skeletal muscle satellite cell group (experimental group) and blank controlgroup. The left anterior descending branch of the coronary artery of the rabbits was ligated so as to establish an animalmodel of acute myocardial infarction in the former two groups. After labeled by DAPI before transplantation, the skeletalmuscle satellite cells, bFGF gene modified skeletal muscle satellite cells and the equivalent amount of DMEM/F12 wereinjected into the local infarct myocardium correspondingly. Samples were taken 4 weeks after transplantation. Then, thesurvival of skeletal muscle satellite cells and the expression of bFGF gene were observed under light microscope andfluorescence microscope, and the neovascularization in the myocardial infarction area was examined byimmunohistochemical staining.RESULTS AND CONCLUSION: No DAPI-labeled cells were visible in the blank control group, but in the other twogroups, a large amount of DAPI-labeled skeletal muscle satellite cells were seen in the infarction area. Enhanced greenfluorescent protein was highly expressed in the experimental group. Microvessel density in the infarction area washighest in the experimental group followed by the control and blank control groups (P < 0.05). These findings indicatethat bFGF gene modified skeletal muscle satellite cells can survive and promote neovascularization in the acutemyocardial infarction area.
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Objective To compare the therapeutic effect of video-assisted thoracoscopic surgery and traditional thoracotomy in fixation of traumatic multiple rib fractures.Methods Clinical data of 56 patients with traumatic multiple rib fractures treated surgically between July 2005 and September 2012 were analyzed retrospectively.Based on the treatments,the patients were assigned to video-assisted thoracoscopy group (thoracoscopy group,n =27) and traditional thoracotomy group (thoracotomy group,n =29).A comparison was done on the variables including operation time,intraoperative blood loss,ventilator support rate,duration of mechanical ventilation,length of ICU stay,incidence of lung infections,visual analogue scale (VAS) at day 3 postinjury and mortality between the two groups.Results Operation time [(128.9 ± 21.1) min vs (140.7 ± 24.2) min],ventilator support rate (70％ vs 76％) and mortality (4％ vs 7％) in thoracoscopy group revealed no statistical differences compared with thoracotomy group (P ＞ 0.05),but intraoperative blood loss [(321.1 ± 30.1)ml vs (438.1 ± 43.2)ml],duration of mechanical ventilation [(4.3 ± 2.1) d vs (7.2 ± 1.6) d],length of ICU stay [(5.9 ± 21.1) d vs (8.5 ± 1.7) d],incidence of lung infection (33％ vs 90％),and VAS [(7.0 ± 1.4) points vs (8.3 ± 0.9) points] were significantly reduced in thoracoscopy group than in thoracotomy group (all P ＜ 0.01).Conclusion Video-assisted thoracoscopic surgery is characterized by fewer intraoperative bleeding,shorter duration of mechanical ventilation and ICU stay,and lower lung infection rate during treatment of traumatic multiple rib fractures compared to traditional thoracotomy.
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BACKGROUND:Skeletal muscle satel ite cells are totipotential stem cells with multi-directional differentiation potential, locate in skeletal muscle interstitium, have a certain tolerance to ischemia and hypoxia, and are important cells in stem cellengineering. OBJECTIVE:To establish a thrifty, convenient culture procedure and create a simple, efficient method to transfect skeletal muscle satel ite cells, and investigate genetic expression after the transfection for cellular cardiomyoplasty. METHODS:Skeletal muscle satel ite cells were isolated from rabbit thigh and cultured. Their growth curves were determined by CKK-8 method. Grouped by different proportions of the plasmid and liposome, skeletal muscle satel ite cells were transfered by the enhanced green fluorescent protein plasmid based on liposome. After transfection, the efficiency and character of target genetic expression was determined. RESULTS AND CONCLUSION:Satel ite cells were isolated, cultured and transfected successful y. In suitable ratio of plasmid and liposomes, the transfection efficiency reached up to above 35%. The target protein was expressed within 12 hours after transfection, reached maximum in 48-72 hours and decreased gradual y after one week. The expression stil could be observed two weeks latter. The enhanced green fluorescent protein plasmid conducted by cationic liposome could be transfered into skeletal muscle satel ite cells efficiently. The transfection efficiency was correlated closely to the ratio of plasmid and lipofectamine. The change of target gene expression depended on time.
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The primary function of cardiac mitochondria is the production of ATP to support heart contraction. Examination of the mitochondrial redox state is therefore crucially important to sensitively detect early signs of mitochondrial function in pathophysiological conditions, such as ischemia, diabetes and heart failure. We study fingerprinting of mitochondrial metabolic oxidative state in living cardiomyocytes with spectrally-resolved fluorescence lifetime spectroscopy of NAD(P)H, the principal electron donor in mitochondrial respiration responsible for vital ATP supply. Here NAD(P)H is studied as a marker for non-invasive fluorescent probing of the mitochondrial function. NAD(P) H fluorescence is recorded in cardiac cells following excitation with 375nm UV-light and detection by spectrally-resolved time-correlated single photon counting (TCSPC), based on the simultaneous measurement of the fluorescence spectra and fluorescence lifetimes. Modulation of NADH production and/or mitochondrial respiration is tested to study dynamic characteristics of NAD(P) H fluorescence decay. Our results show that at least a 3-exponential decay model, with 0.4-0.7ns, 1.2-1.9ns and 8.0-13. Ons lifetime pools is necessary to describe cardiomyocyte autofluorescence (AF) within 420-560nm spectral range. Increased mitochondrial NADH production by ketone bodies enhanced the fluorescence intensity, without significant change in fluorescent lifetimes. Rotenone, the inhibitor of Complex I of the mitochondrial respiratory chain, increased AF intensity and shortened the average fluorescence lifetime. Dinitrophenol (DNP), an uncoupling agent of the mitochondrial oxidative phosphorylation, lowered AF intensity, broadened the spectral shoulder at 520 nm and increased the average fluorescence lifetime. These effects are comparable to the study of NADH fluorescence decay in vitro. In the present contribution we demonstrated that spectrally-resolved fluorescence lifetime technique provides promising new tool for analysis of mitochondrial NAD(P) H fluorescence with good reproducibility in living cardiomyocytes. This approach will enhance our knowledge about cardiomyocyte oxidative metabolism and/or its dysfunction at a cellular level. In the future, this approach can prove helpful in the clinical diagnosis and treatment of mitochondrial disorder.