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beta galactosidase/infart
L'enllaç es desa al porta-retalls
Pàgina 1 des de 97 resultats
Serum and urinary beta-galactosidase and beta-glucuronidase activity in patients with acute myocardial infarction.
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To determine the effect of acute myocardial infarction (AMI) on serum and urinary activity of beta-galactosidase and beta-glucuronidase (lysosomal enzymes) 40 patients were studied. Eighteen patients had acute myocardial infarction and 22 were assigned as controls. Three of the 18 patients with
Neuron-derived neurotrophic factor ameliorates adverse cardiac remodeling after experimental myocardial infarction.
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BACKGROUND
Myocardial infarction (MI) is one of the major causes of death worldwide. Chronic heart failure is a serious complication of MI that leads to poor prognosis. We recently found that neuron-derived neurotrophic factor (NDNF) is a proangiogenic secretory protein that is upregulated in
Midkine gene transfer after myocardial infarction in rats prevents remodelling and ameliorates cardiac dysfunction.
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OBJECTIVE
We have previously reported that therapy with midkine (MK) has a protective effect in mouse models of myocardial infarction (MI) and ischemia/reperfusion. The underlying mechanism was proved to be anti-apoptosis and prevention of left ventricular (LV) remodelling following angiogenesis.
In vivo gene delivery of XIAP protects against myocardial apoptosis and infarction following ischemia/reperfusion in conscious rabbits.
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OBJECTIVE
We tested the hypothesis that an in vivo gene delivery of the pro-survival protein XIAP (X-chromosome linked inhibitor of apoptosis protein) protects against myocardial apoptosis and infarction following ischemia/reperfusion.
METHODS
Nineteen rabbits were chronically instrumented with a
Vascular endothelial growth factor-165 gene therapy promotes cardiomyogenesis in reperfused myocardial infarction.
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BACKGROUND
Vascular endothelial growth factor (VEGF)-165 promotes cardiomyogenesis in chronic myocardial ischemia and nonreperfused myocardial infarction (MI). It is unknown whether this effect is present in reperfused MI. We sought to investigate the effect of VEGF-165 gene therapy on
Cell transplantation for treatment of acute myocardial infarction: unique capacity for repair by skeletal muscle satellite cells.
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An adult heart injured by an ischemic episode has a limited capacity to regenerate. We administered three types of adult guinea pig cells [cardiomyocytes (CMs), cardiac fibroblasts (CFs), and skeletal myoblasts (Mbs)] to compare their suitability for repair of acute myocardial infarction. We used
Adenoviral-delivered angiopoietin-1 reduces the infarction and attenuates the progression of cardiac dysfunction in the rat model of acute myocardial infarction.
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In acute myocardial infarction (AMI), prognosis and mortality rate are closely related to the infarct size and the progression of postinfarction cardiac failure. Angiogenic gene therapy has presented a new approach for the treatment of AMI. Angiopoietin-1 (Ang1) is a critical angiogenic factor for
Selective spatiotemporal induction of matrix metalloproteinase-2 and matrix metalloproteinase-9 transcription after myocardial infarction.
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Myocardial remodeling after myocardial infarction (MI) is associated with increased levels of the matrix metalloproteinases (MMPs). Levels of two MMP species, MMP-2 and MMP-9, are increased after MI, and transgenic deletion of these MMPs attenuates post-MI left ventricular (LV) remodeling. This
Survival of grafts of genetically modified cardiac myocytes transfected with FITC-labeled oligodeoxynucleotides and the beta-galactosidase gene in the noninfarcted area, but not the myocardial infarcted area.
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Since one of the attractions of gene therapy in the heart is the implantation of genetically modified cultured cells, we employed genetically modified myocytes transfected with FITC-labeled oligodeoxynucleotides (ODN) and beta-galactosidase gene in this study, to investigate the cellular
[Glycosphingolipid content and beta-galacto- and beta-glucosidase activity of the blood in acute myocardial infarction and postinfarction cardiosclerosis].
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Content of acid and neutral glycosphingolipids was distinctly higher in blood plasma and cells of patients with acute myocardium infarction as compared with healthy persons. In leukocytes of the patients activity of beta-galactosidase, exhibiting pH optimum at pH 3.6, was decreased with simultaneous
Repair of myocardial infarction by epicardial deposition of bone-marrow-cell-coated muscle patch in a murine model.
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BACKGROUND
Myocardial infarction results in irreversible myocyte loss. In a murine model, we tested the feasibility of a novel repair technique combining bone marrow cell (BMC) transplantation and cardiomyoplasty.
METHODS
Myocardial infarction was induced cryogenically in backcrossed ROSA 26
Discordant activation of gene promoters for matrix metalloproteinases and tissue inhibitors of the metalloproteinases following myocardial infarction.
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BACKGROUND
Left ventricular (LV) remodeling following myocardial infarction (MI) is associated with increased levels of specific matrix metalloproteinases (MMPs) and relative reduction of endogenous tissue inhibitors of the MMPs (TIMPs). However, transcriptional mechanisms for the disparate post-MI
Acute myocardial infarction activates progenitor cells and increases Wnt signalling in the bone marrow.
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OBJECTIVE
We aimed to characterize the influence of acute myocardial infarction (AMI) on the metabolic activity of the bone marrow (BM) and on the composition and functional activity of BM-derived mononuclear cells (BMC). Acute ischaemia or other stressors induce the mobilization of progenitor cells
Efficient in vivo gene transfer into the heart in the rat myocardial infarction model using the HVJ (Hemagglutinating Virus of Japan)--liposome method.
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The lack of efficient treatment for myocardial infarction remains an unresolved problem in the field of cardiovascular disease. Gene therapy may be a potential therapeutic strategy for the treatment of myocardial infarction. However, current methods of in vivo gene transfer into the heart are
Intracoronary, adenovirus-mediated Akt gene transfer in heart limits infarct size following ischemia-reperfusion injury in vivo.
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BACKGROUND
Previous data have shown that enhanced Akt signaling inhibits cardiac myocyte apoptosis in vitro and in vivo. To elucidate the contribution of apoptosis to the pathogenesis of the infarct, we investigated whether intra-coronary Akt gene delivery could reduce gross infarct size following
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