valine/infarction

OBJECTIVE The aim of this study was to evaluate the pharmacogenetic role of the factor XIII (FXIII) valine 34 leucine (Val34Leu) polymorphism in the fibrinolytic therapy of acute myocardial infarction (MI). BACKGROUND Fibrinolytic therapy is an established treatment for acute MI, but up to 40% of

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 Heart-protecting musk pill (HMP), a traditional Chinese medicine prescription, has extensive cardioprotective effects against angina pectoris and myocardial infarction (MI), but the molecular mechanism behind such cardio protective effects still remains unclear. In this article, we aim to

Hyperhomocyst(e)inemia is associated with an increased risk of coronary artery disease and myocardial infarction. Both genetic and environmental factors influence the plasma level of homocysteine. One of the metabolic pathways for homocysteine involves the enzyme methylenetetrahydrofolate reductase

Hyperhomocysteinemia is thought to be an independent risk factor for coronary heart disease. Increased plasma homocysteine level can result from malnutrition (e.g. folate deficiency) and/or genetic-related disturbances. Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in the synthesis of

Inherited gene defects related to the coagulation system have been reported as risk factors for ischemic stroke. These gene defects include a G-A transition at nucleotide 1691 in exon 10 of the Factor V gene causing activated protein C resistance; a G-A transition in the 3' untranslated region of

The hemodynamic effects of valsartan ((S)-N-valeryl-N-¿[2'-(1H-tetrazol-5-yl)bipheneoyl-4-yl]meth yl¿valine, CAS 137862-53-4, CGP 48933), a new angiotensin II type 1 receptor antagonist, on rats with myocardial infarction induced by coronary artery ligation was examined. Four weeks after ligation,

Factor XIII is a transglutaminase that crosslinks fibrin in the last steps of the coagulation process. A few polymorphic sites have been identified in this gene, one of them being a point mutation (FXIII Val34Leu), leading to an amino acid change of valine to leucine. Recently, in British patients,

The hemoglobin S is a consequence of the substitution of valine for glutamic acid at position 6 of beta globin chain. The problem arises when some individuals with Hb S is moved to the mountains and exposed to hypoxia. The decrease in oxygen saturation distorts the red blood cell with HbS-shaped

Aims: Acute myocardial infarction (MI) is the major cause of chronic heart failure. The activity of blood coagulation factor XIII (FXIIIa) plays an important role in rodents as a healing factor after MI, whereas its role in healing and

BACKGROUND Hyperhomocysteinemia, an independent and graded risk factor for coronary artery disease, can result from both environmental and hereditary factors. C677T mutation of the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene [alanine/valine (A/V) polymorphism], one of the key enzymes

UNASSIGNED Acute cerebral infarction (ACI) and intracerebral hemorrhage (ICH) are potentially lethal cerebrovascular diseases that seriously impact public health. ACI and ICH share several common clinical manifestations but have totally divergent therapeutic strategies. A poor diagnosis can affect

Serum and cerebrospinal fluid (CSF) from 17 patients less than 3 days after brain infarction (measurement 1) and during recovery 7 +/- 2 days after infarction (measurement 2) were analysed for organic acids (energy metabolites, keto acids and amino acids). Clinical parameters improved by 32% over

Factor XIIIA (FXIIIA) levels are independent predictors of early prognosis after acute myocardial infarction (AMI) and the Valine-to-Leucine (V34L) single nucleotide polymorphism (SNP) seems associated with lower AMI risk. Since the long-term AMI prognosis merits deeper investigation, we performed

BACKGROUND Myocardial infarction (MI) increases the wall stress in the viable myocardium and initiates early adaptive remodeling in the left ventricle to maintain cardiac output. Later remodeling processes include fibrotic reorganization that eventually leads to cardiac failure. Understanding the