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alanine/infarkt

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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
Plasma levels of glutamate, alanine, free fatty acids (FFA), citrate, glucose, insulin, lactate, creatine kinase and aspartate aminotransferase were determined frequently during the first 2-48 h after onset of chest pain in 10 patients who developed acute myocardial infarction (AMI) and in 8 who did

Threonine for alanine substitution in the eotaxin (CCL11) gene and the risk of incident myocardial infarction.

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Recent studies suggest that the chemokine eotaxin may participate in atherosclerosis. Threonine (T) for alanine (A) substitution at amino acid 23 in the eotaxin gene (CCL11) has been associated with risk of developing allergic-inflammatory disorders. However, no genetic-epidemiological data are
BACKGROUND Disorders of calcium homeostasis have been implicated in atherosclerosis. The calcium-sensing receptor (CASR) is crucial to the regulation of calcium metabolism. An alanine (A) to serine (S) polymorphism at codon 986 (A986S) of the CASR gene has been associated with higher calcium and
Early increases in the activity of alanine aminotransferase (ALT, EC 2.6.1.2) in plasma are observed in about 7% of patients with acute myocardial infarction (AMI), of whom about half die. Some type of liver injury, secondary to AMI, could be responsible for this phenomenon. However, quantitative

Is alanine release an early marker of acute myocardial infarction?

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We retrospectively examined the relationship between the genotype of the angiotensin-converting enzyme (ACE) gene or the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene, and the secondary cardiac events after myocardial infarction. The study population consisted of 176 patients (ACE genotype:
BACKGROUND Human or recombinant apolipoprotein A-I (apoA-I) has been shown to increase high-density lipoprotein-mediated cholesterol efflux capacity and to regress atherosclerotic disease in animal and clinical studies. CSL112 is an infusible, plasma-derived apoA-I that has been studied in normal

Effects of Muntingia calabura L. on isoproterenol-induced myocardial infarction.

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BACKGROUND This study was designed to scientifically evaluate the effects of an aqueous extract of Muntingia calabura L. (M. calabura), a medicinal herb, on isoproterenol-induced myocardial infarction (MI) in rat models. METHODS Six groups of Wistar albino rats, each comprising six animals, were

Effect of saturated, omega-3 and omega-6 polyunsaturated fatty acids on myocardial infarction.

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Dietary fatty acids have cholesterol lowering, antiatherogenic, and antiarrhythmic properties that decrease the risk of myocardial infarction (MI). This study was designed to study the effects of various oils rich in either polyunsaturated (omega-3 or omega-6) fatty acids (PUFA) or saturated fatty
Thrombolytic agents activate plasminogen and induce a systemic fibrinolytic and anticoagulant state. Two thrombolytic drugs are used frequently in practice: streptokinase (SK) and alteplase (t-PA). Streptokinase mainly undergoes renal elimination with a half-life of 11-17 min, while alteplase is
BACKGROUND In patients with ST-elevation myocardial infarction (STEMI), the relationship between transaminases and myocardial damage detected by cardiac magnetic resonance (CMR) imaging is unknown and the prognostic value incompletely investigated. METHODS CMR imaging was performed in 167 STEMI
BACKGROUND Research in rodents demonstrated that psychological stress increases circulating levels of alanine transaminase, aspartate transaminase, and alkaline phosphatase reflecting liver injury. Moreover, chronic posttraumatic stress disorder and transaminases predicted coronary heart
OBJECTIVE The objective of this study is to evaluate the effect of ethanolic extract of Urtica parviflora Roxb. in isoproterenol (ISO) induced myocardial infarction (MI) in rats. METHODS U. parviflora Roxb. (350 mg/kg and 500 mg/kg, p.o) was administered for 15 days in rats. MI was induced with a
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