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arginase/infarction
Veza se sprema u međuspremnik
Stranica 1 iz 69 rezultatima
Association of arginase 1 gene polymorphisms with the risk of myocardial infarction and common carotid intima media thickness.
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BACKGROUND
Recently, it was suggested that arginase (ARG)1 plays an important role in atherogenesis. However, because of its complex functions depending on vascular cell type, its impact on atherogenesis remains unclear.
OBJECTIVE
To evaluate the association between ARG1 polymorphisms and phenotypes
Association of rs2781666 G/T polymorphism of arginase I gene with myocardial infarction in Tunisian male population.
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OBJECTIVE
The aim of this study was to investigate the association between rs2781666 G/T polymorphism of arginase I (ARG I) gene and myocardial infarction (MI) in the Tunisian male population.
METHODS
Three hundred eighteen patients with MI and 282 controls were recruited. The rs2781666 G/T
Arginase inhibition reduces infarct size via nitric oxide, protein kinase C epsilon and mitochondrial ATP-dependent K+ channels.
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Reduced bioavailability of nitric oxide (NO) contributes to the development of myocardial ischemia-reperfusion (I/R) injury. Increased activity of arginase is a potential factor that reduces NO bioavailability by competing for the substrate L-arginine. The aim of the study was to test the hypothesis
Serum levels of arginase I are associated with left ventricular function after myocardial infarction.
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OBJECTIVE
Upregulation of arginase redirects the arginine metabolism from nitric oxide (NO) synthesis to the formation of polyamine and proline, thus causing cardiac dysfunction. NO synthesis is also impaired by asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor. We
Early diagnosis of myocardial infarction by arginase activity determination.
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In blood serum of healthy persons the activity of arginase (EC 3.5.3.1) is very low, whereas in patients with myocardial infarction it increases within a few hours after the first attack of coronary pain, and returns to normal values after 3-5 days. No increase of arginase activity was observed in
Vagal nerve stimulation reduces infarct size via a mechanism involving the alpha-7 nicotinic acetylcholine receptor and downregulation of cardiac and vascular arginase.
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OBJECTIVE
Vagal nerve stimulation (VNS) protects from myocardial and vascular injury following myocardial ischaemia and reperfusion (IR) via a mechanism involving activation of alpha-7 nicotinic acetylcholine receptor (α7 nAChR) and reduced inflammation. Arginase is involved in development of
Arginase inhibition improves coronary microvascular function and reduces infarct size following ischaemia-reperfusion in a rat model.
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OBJECTIVE
Ischaemia-reperfusion injury is associated with reduced bioavailability of nitric oxide (NO) and microvascular dysfunction. One emerging mechanism behind reduced NO bioavailability is upregulation of arginase, which metabolizes the NO synthase substrate l-arginine. This study investigated
Occurrence of arginase in human blood serum in patients with myocardial infarction.
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[Usefulness of serum arginase activity determination in the diagnosis of acute myocardial infarct].
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[Clinical value of arginase activity determination in human blood serum: diagnosis of myocardial infarction].
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Inhibition of Rho kinase protects from ischaemia-reperfusion injury via regulation of arginase activity and nitric oxide synthase in type 1 diabetes.
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RhoA/Rho-associated kinase and arginase are implicated in vascular complications in diabetes. This study investigated whether RhoA/Rho-associated kinase and arginase inhibition protect from myocardial ischaemia-reperfusion injury in type 1 diabetes and the mechanisms behind these effects.
Rats with
Classically and alternatively activated macrophages contribute to tissue remodelling after myocardial infarction.
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An important goal in cardiology is to minimize myocardial necrosis and to support a discrete but resilient scar formation after myocardial infarction (MI). Macrophages are a type of cells that influence cardiac remodelling during MI. Therefore, the goal of the present study was to investigate their
Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis.
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We examined whether a shift in macrophage phenotype could be therapeutic for myocardial infarction (MI). The mouse macrophage cell line RAW264.7 was stimulated with peptidoglycan (PGN), with or without 5-azacytidine (5AZ) treatment. MI was induced by ligation of the left anterior descending coronary
Treatment of mice with a ligand binding blocking anti-CD28 monoclonal antibody improves healing after myocardial infarction.
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Both conventional and regulatory CD4+ T-cells rely on costimulatory signals mediated by cell surface receptors including CD28 for full activation. We showed previously that stimulation of CD4+ Foxp3+ regulatory T-cells by superagonistic anti-CD28 monoclonal antibodies (mAb) improves myocardial
Circulating CX3CR1 + CD163 + M2 monocytes markedly elevated and correlated with cardiac markers in patients with acute myocardial infarction
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Background: Vulnerable plaques have been generally recognized to play a role in the pathogenesis of acute myocardial infarction (AMI), however, the role of circulating CX3CR1+CD163+ M2 monocytes has not been studied
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