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glucose 6 phosphate dehydrogenase/infarkt

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Silent cerebral infarct (SCI) is the most commonly recognized cause of neurological injury in sickle cell anaemia (SCA). We tested the hypothesis that magnetic resonance angiography (MRA)-defined vasculopathy is associated with SCI. Furthermore, we examined genetic variations in glucose-6-phosphate
We report the case of an 82-year-old Sardinian woman affected by "favism" (i.e. intolerance to fava beans) with chest pain associated with persistent massive ST elevation in V2-V6 leads, admitted to our department after transfer from a rural hospital without catheterization facilities. On immediate

Study of glucose-6-phosphate dehydrogenase in acute myocardial infarction and in controls.

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[Enzyme activity in post-infarct aneurysm and in the myocardial zone outside the infarct in experimental infarct in rats].

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Activities of lactate dehydrogenase, glucose-6-phosphate dehydrogenase, transketolase and creatine phosphokinase were studied in tissue of aneurysm and in extrainfarctional part of rat heart muscle after experimental infarction. Activity of total LDH, content of its anode isoenzymes and creatine

[Activity of enzymes of tricarboxylic and pentose-phosphate cycles in dog brain with myocardial infarction].

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Under conditions of experimental myocardium infarction caused in dogs by ligation of the anterior descending branch of the left coronary artery, the activity of alpha-ketoglutarate dehydrogenase and succinate dehydrogenase in mitochondria of the cortex, cerebellum and medulla ablongata lowers most

Cardioprotective effects of aqueous extract of Oxalis corniculata in experimental myocardial infarction.

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The present study evaluated the protective potential of aqueous extract of Oxalis corniculata (OCE) against isoproterenol (ISO) induced myocardial infarction in rats. Myocardial infarction in rats was induced by isoproterenol (200 mg/kg) at an interval of 24 h for 2 days. OCE was given to rats as

[Glucose-6-phosphate dehydrogenase in normal human thrombocytes and in ischemic heart disease].

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Two zones, exhibiting glucose-6-phosphate dehydrogenase (G6PD) activity, were identified in lysates of thrombocytes from healthy persons by means of polyacrylamide gel disc electrophoresis; amount of the zones was increased up to 7 during the preinfarction period and up to II within the acute period

Early reductive stress and late onset overexpression of antioxidant enzymes in experimental myocardial infarction.

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Reductive stress is defined as a pathophysiological situation in which the cell becomes more reduced than in the normal, resting state. It represents a disturbance in the redox state that is harmful to biological systems. Our aim was to study the occurrence of reductive stress in the early phases of

[Clinical Features and Laboratory Data Analysis of Glucose-6- Phosphate Dehydrogenase Deficiency].

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OBJECTIVE To explore clinical features and laboratory data of glucose-6-phosphate dehydrogenase(G6PD)deficiency and to investigate the relationship between them. METHODS Clinical data of 43 patients with G6PD deficiency was analyzed, the statistical method was applied to investigate the relationship
Ischemic stroke is a leading cause of mortality and morbidity worldwide, and oxidative stress plays a significant role in the ischemia stage and reperfusion stage. Previous studies have indicated that both calcium/calmodulin-dependent protein kinase II (CaMKII) and glucose 6-phosphate dehydrogenase

Effects of acupuncture on glycometabolic enzymes in multi-infarct dementia rats.

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Acupuncture has exhibited therapeutic effects on vascular dementia in our previous research. The mechanism of its anti-dementia effects involves energy metabolism. For brain cells, glucose metabolism is almost the only source of energy, and glucose metabolism disorders are early signs of dementia.

Glucose-6-phosphate dehydrogenase deficiency protects against coronary heart disease.

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Previous studies suggest a reduction in cardiovascular risk among subjects expressing the glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) deficient phenotype. We aimed to test this hypothesis in male subjects expressing the G6PD-deficient phenotype vs wild type G6PD. In a case-control study we
BACKGROUND Glucose 6-phosphate dehydrogenase (G6PD) is the most common deficient enzyme in the world. In failing hearts, G6PD is upregulated and generates reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is used by the glutathione pathway to remove reactive oxygen species but also as

Impact of glucose-6-phosphate dehydrogenase deficiency on the pathophysiology of cardiovascular disease.

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Glucose-6-phosphate dehydrogenase (G6PD) catalyzes the rate-determining step in the pentose phosphate pathway and produces NADPH to fuel glutathione recycling. G6PD deficiency is the most common enzyme deficiency in humans and affects over 400 million people worldwide; however, its impact on
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