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infarction/prolinas
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 101 rezultatus
Therapeutic potential of thymosin-beta4 and its derivative N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) in cardiac healing after infarction.
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Despite the numerous advances made in the prevention and treatment of cardiovascular diseases, there is a need for new strategies to repair and/or regenerate the myocardium after ischemia and infarction in order to prevent maladaptive remodeling and cardiac dysfunction. This article compiles and
Alanine for proline substitution in the peroxisome proliferator-activated receptor gamma-2 (PPARG2) gene and the risk of incident myocardial infarction.
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OBJECTIVE
Recent studies have implicated the potential importance of peroxisome proliferator-activated receptors as a molecular mechanism involved in atherothrombosis. A common alanine (A) for proline (P) substitution at codon 12 in the peroxisome proliferator activated receptor gamma-2 gene
Cardioprotective Effects of Metalloproteinase Inhibitor 1-({4-[(4-Chlorobenzoyl)amino]phenyl}sulfonyl-L-Proline in Modeled Acute Myocardial Infarction.
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Cardioprotective effect of 1-({4 [(4 chlorobenzoyl)amino]phenyl}sulfonyl-L-proline (compound AL-828) was studied in rats with modeled acute myocardial infarction. The test compound was administered intragastrically in a dose of 30 mg/kg/day for 3 days prior to infarction modeling. Metalloproteinase
Detection of secondary thalamic degeneration after cortical infarction using cis-4-18F-fluoro-D-proline.
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The amino acid cis-4-(18)F-fluoro-D-proline (D-cis-(18)F-FPro) exhibits preferential uptake in the brain compared with its L-isomer, but the clinical potential of the tracer is as yet unknown. In this study we explored the cerebral uptake of D-cis-(18)F-FPro in rats with focal cortical
Proline improves cardiac remodeling following myocardial infarction and attenuates cardiomyocyte apoptosis via redox regulation
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At present, ischemic heart failure (HF) caused by coronary heart disease (CHD) has a high morbidity and mortality, placing a heavy burden on global human health. L-Proline (Pro), a nonessential amino acid and the foundation of proteins in the human body, was found to be protective against oxidative
Stabilization of hypoxia inducible factor rather than modulation of collagen metabolism improves cardiac function after acute myocardial infarction in rats.
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Prolyl hydroxylase domain-containing enzymes (PHD) hydroxylate a proline residue that controls the degradation of hypoxia inducible factor (HIF). Hypoxia inhibits this hydroxylation thus increasing HIF levels. HIF is upregulated in ischemic tissues, growing tumors and in nonischemic, mechanically
Proline-rich protein is a glycoprotein and an acute phase reactant.
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Proline-rich protein (PRP) is a plasma protein associated with lipoproteins. In an attempt to clarify the biological significance of this protein, we isolated and characterized it and studied the biological role in plasma. PRP was isolated by immunosorber column chromatography and by gel filtration
Detection of remote neuronal reactions in the Thalamus and Hippocampus induced by rat glioma using the PET tracer cis-4-[¹⁸F]fluoro-D-proline.
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After cerebral ischemia or trauma, secondary neurodegeneration may occur in brain regions remote from the lesion. Little is known about the capacity of cerebral gliomas to induce secondary neurodegeneration. A previous study showed that cis-4-[(18)F]fluoro-D-proline (D-cis-[(18)F]FPro) detects
A new anti-fibrotic drug attenuates cardiac remodeling and systolic dysfunction following experimental myocardial infarction.
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BACKGROUND
Pathological deposition of extracellular matrix in the non-infarct zone (NIZ) of the ventricle post myocardial infarction (MI) is a key contributor to cardiac remodeling and heart failure. FT011, a novel antifibrotic compound, was evaluated for its efficacy in neonatal cardiac fibroblasts
Ac-SDKP reverses inflammation and fibrosis in rats with heart failure after myocardial infarction.
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Inflammation may play an important role in the pathogenesis of cardiac fibrosis in heart failure (HF) after myocardial infarction (MI). N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring antifibrotic peptide whose plasma concentration is increased 4- to 5-fold by
N-acetyl-seryl-aspartyl-lysyl-proline treatment protects heart against excessive myocardial injury and heart failure in mice.
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Myocardial infarction (MI) in mice results in cardiac rupture at 4-7 days after MI, whereas cardiac fibrosis and dysfunction occur later. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) has anti-inflammatory, anti-fibrotic, and pro-angiogenic properties. We hypothesized that Ac-SDKP reduces
Combination treatment with N-acetyl-seryl-aspartyl-lysyl-proline and tissue plasminogen activator provides potent neuroprotection in rats after stroke.
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OBJECTIVE
N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), an endogenously produced circulating peptide in humans and rodents, exerts anti-inflammatory and cardioprotective activities in various cardiovascular diseases.
METHODS
The present study evaluated the neuroprotective effect of AcSDKP alone
Leucine 7 to proline 7 polymorphism of the preproneuropeptide Y gene is not associated with restenosis after coronary stenting.
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OBJECTIVE
To identify if an association exists between the leucine 7 (Leu7) to proline 7 (Pro7) polymorphism located in the signal peptide of the preproneuropeptide Y (preproNPY) gene and restenosis after coronary stenting. The Pro7 allele of the preproNPY gene affects the plasma levels of human
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
Prolyl hydroxylase and collagen metabolism after experimental mycardial infarction.
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Mature male Sprague-Dawley rats were subjected to an isoproterenol-induced myocardial infarction. Animals were sacrificed on a daily basis in order to assess the temporal changes in prolyl hydroxylase activity and collagen metabolism during the acute stages of myocardial necrosis and repair. Total
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