ABSTRACT
no abstract available.
ABSTRACT
The authors report a successful thrombectomy using the AngioJet Rheolytic Thrombectomy System (AngioJet) and an embolic protection device in a patient with femorofemoral bypass graft occlusion. Lower extremity CT angiograms showed occlusion in the left-to-right femorofemoral bypass graft. A rheolytic thrombectomy using the AngioJet and balloon angioplasty restored blood flow to the right lower extremity, and distal embolization may be effectively prevented by placing an embolic protection device within the right superficial femoral artery during the procedure.
ABSTRACT
The authors report a successful thrombectomy using the AngioJet Rheolytic Thrombectomy System (AngioJet) and an embolic protection device in a patient with femorofemoral bypass graft occlusion. Lower extremity CT angiograms showed occlusion in the left-to-right femorofemoral bypass graft. A rheolytic thrombectomy using the AngioJet and balloon angioplasty restored blood flow to the right lower extremity, and distal embolization may be effectively prevented by placing an embolic protection device within the right superficial femoral artery during the procedure.
ABSTRACT
Cellular cardiomyoplasty has recently emerged as a potential new treatment of ischemic heart disease. Combining cellular cardiomyoplasty with gene therapy using myogenic transcription factor might facilitate myocardial regeneration. In this study, we engineered H9c2, L6 using plasmid vector to overexpress the transcription factor MEF2c, Nkx2.5 involved in cardiomyogenesis. We investigated 1) formation of intercellular junction in mono-culture and co-culture with cardiomyocyte for functional and structural synchronous contraction after transplantation, 2) differentiation into cardiomyocyte, 3) resistance to hypoxic condition. Each cell overexpressing MEF2 and Nkx2.5 was generated by gene transfection and clonal selection. CO-culture was performed that each cell line added over cultured cardiomyocyte. H9c2-MEF2c and H9c2-Nkx2.5 became long, spindle shape like cardiomyocyte. Troponin T, cardiac specific marker, was found spot-like pattern in H9c2-Nkx2.5. However, co-culture with cardiomyocyte did not induce differentiation all kinds of cells into cardiomyocyte. Connexin43, which is gap junction marker was increased in H9c2-MEF2c, H9c2-Nkx2.5, L6-MEF2c and L6-Nkx2.5. Especially, co-culture with cardiomyocyte resulted in elevation of connexin43 levels more than monoculture. Ultrastructurally, formations of gap junction and desmosome were found apparently in L6-Nkx2.5. Long-standing, strong, regular and more frequent contraction were observed in cardiomyocyte co-cultured with H9c2-MEF2c, H9c2-Nkx2.5, L6-MEF2c, L6-Nkx2.5, respectively. Neverthless, any cell did not have active contraction itself, but passive movement except cardiomyocyte. H9c2-MEF2c, L6-MEF2c and L6-Nkx2.5 had resistance to hypoxia compared with other groups. These results suggested that co-culture and overexpressions of MEF2c and Nkx2.5 induced differentiation into cardiomyocyte and played an important role on intercellular junction formation and hypoxic resistance. This would be a promising source of cellular cardiomyoplasty. Therefore, much more research would be essential for clinical application of cellular cardiomyoplasty and this study would be a basic source for further study of MEF2c and Nkx2.5 in cellular cardiomyoplasty.
Subject(s)
Animals , Rats , Hypoxia , Cardiomyoplasty , Cell Line , Cell Transplantation , Coculture Techniques , Connexin 43 , Desmosomes , Gap Junctions , Genetic Therapy , Intercellular Junctions , Myoblasts , Myoblasts, Cardiac , Myocardial Ischemia , Myocytes, Cardiac , Plasmids , Regeneration , Transcription Factors , Transfection , Troponin TABSTRACT
Recently, new treatments for human heart disease such as ischemia, infarction, cardiomyopathy, coronary heart disease have been developed. transplantation various kinds of cells from skeletal muscle, endothelium, mesenchyme, hemopoietic tissue to injured area after infarction were challenged. It's so called 'Cell Transplantation'. This therapeutic strategy already adopted and got a good result in clinical trial. But several limitations are still remained, including ethics, donor cell numbers, side effects, therapeutic efficiency. In this research, we investigated the formation of intercellular junction and synchronous contraction between cardiomyocyte and H9c2 cell line in co-culture to establish experimental model in vitro for cell transplantation. For this purpose, two kinds of cells, primary cultured cardiomyocyte and H9c2 (cardiomyoblast cell line) were used. Cultured cardiomyocytes had repetitive contraction-relaxation pattern along longitudinal axis both in single and coculture. But their contractions were slower, less regular, less strong in co-culture than in cardiomyocyte culture only. H9c2 cells did not contracted actively themselves, but moved toward cardiomyocyte passively coincided with contraction. In contact region between two kinds of cells, there was no signal after immunocytochemical staining labeled with connexin43 (gap junction), desmoplakin (desmosome), N-cadherin (adherent junction) even though they had membrane contact. Moreover, F-actin and striation were less developed. These results suggested that co-culture system interfere with remodelling of contractile apparatus, intercellular junction formation as well as contraction-relaxation. Furthermore cardiomyocyte could not induce H9c2 cells differentiation into cardiomyocyte. Therefore, much more research would be essential for clinical application of cell transplantation and this study would be the basic source for further study of new therapy of myocardial disease and building up in vitro model.
Subject(s)
Humans , Actins , Axis, Cervical Vertebra , Cadherins , Cardiomyopathies , Cell Count , Cell Line , Cell Transplantation , Coculture Techniques , Connexin 43 , Coronary Disease , Desmoplakins , Endothelium , Ethics , Heart Diseases , Infarction , Intercellular Junctions , Ischemia , Membranes , Mesoderm , Models, Theoretical , Muscle, Skeletal , Myocytes, Cardiac , Tissue Donors , TransplantsABSTRACT
BACKGROUND AND OBJECTIVE: Even though they are identified on the basis of their induction by elevated temperatures, heat shock proteins are induced by various stimuli. Such inducers include viral infection, exposure to ethanol, sodium arsenite, steroid hormones and heavy metals. They become involved under pathological conditions, such as anoxia/ischemia, reperfusion injury and oxidative stress in the heart. In this research, the cellular damages and changes of Hsp25 and alphaB crytallin were investigated under oxidative stress induced H2O2 treatment in a cultured cardiomyoblast cell line, H9c2. MATERIALS AND METHODS: The morphological changes of the H9c2, and the distributions of Hsp25 and alphaB crytallin, were examined with phase-contrast, confocal and electron microscopy. The levels of Hsp25 and alphaB crytallin expressions within the cells were also checked. RESULTS: After exposure to a low concentration (10 micrometer) of H2O2, the amounts of Hsp25 and alphaB crytallin were increased more than in the control and heat shock groups. They were particularly localized in the perinuclear region and along the actin filament. When exposed to a high concentration (more than 100 micrometer) of H2O2, many cells developed apoptotic features, such as vacuolization, blebbing and apoptotic body formations. The amounts of Hsp25 and alphaB crytallin were decreased more than in the control group. However, a weak reaction in the perinuclear region and along the actin filaments still remained when observed under confocal microscopy. CONCLUSION: These results suggest that the elevation of the expressions of Hsp25 and alphaB crytallin were dependent on the concentration of H2O2. Additionally, the redistribution of these small Hsps is closely associated with the actin filaments, as well as the nuclei. Therefore, much more research will be essential for the elucidation of roles of Hsp25 and alphaB crytallin in oxidative stress, such as ischemia or ischemic-reperfusion injury.