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Page 1 od 33 rezultati
Reduced thiamine is a predictor for cognitive impairment of cerebral infarction
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Objective: Reduced thiamine (vitamin B1 ) had been reported to be associated with cognitive impairment caused by Alzheimer disease. Our study is to explore the association between thiamine and cognitive impairment after acute
Nerve Fiber Layer Infarcts in Thiamine Deficiency.
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Thiamine deficiency classically manifests as the triad of Wernicke encephalopathy: acute confusional state, ataxic gait, and ocular motor dysfunction. However, most patients do no present with this classic triad. Optic neuropathy in thiamine deficiency is a rare manifestation and is usually
Changes in myocardial thiamine in arteriosclerotic and non-arteriosclerotic rats subjected to isoprenaline induced myocardial infarction.
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Determination of DPN (TPN) thiamine, amino acids and amino sugars in blood of animals with experimental myocardial infarction.
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[Thiamine metabolism and transketolase activity of tissues in experimental myocardial infarct].
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The effect of thiamine deficiency on the structure and physiology of the rat forebrain.
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Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological
Sickle cell and thiamine deficiency: case report of a fetal death.
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The heterozygous state of the sickle cell trait is not known to be a cause of fetal death. This is a report of disseminated placental infarcts associated with thiamine deficiency in a patient with the sickle cell trait. This pathological association suggests an original physiopathological process.
No difference in blood thiamine diphosphate levels between Swedish Caucasian patients with congestive heart failure treated with furosemide and patients without heart failure.
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OBJECTIVE
To determine whether furosemide treatment in congestive heart failure (CHF) patients is associated with thiamine deficiency.
METHODS
Patients without heart failure and without diuretic treatment were included to compare with patients with CHF belonging to New York Heart Association (NYHA)
TRMA syndrome with a severe phenotype, cerebral infarction, and novel compound heterozygous SLC19A2 mutation: a case report.
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Wernicke's encephalopathy due to malnutrition and parenteral nutrition in a patient with cerebral infarction: A case report.
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Multivitamin use and the risk of myocardial infarction: a population-based cohort of Swedish women.
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BACKGROUND
Dietary supplements are widely used in industrialized countries.
OBJECTIVE
The objective was to examine the association between multivitamin use and myocardial infarction (MI) in a prospective, population-based cohort of women.
METHODS
The study included 31,671 women with no history of
Changes in ECG and enzyme activity in rat heart after myocardial infarction: effect of TPP and MnCl2.
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Heart infarction is one of the main causes of death in the human population. Assurance of a sufficient level of bioenergetic processes is very important for the heart after infarction. Mn2+ as well as thiamine pyrophosphate (TPP) are positive effectors of the pyruvate dehydrogenase complex (PDH) and
Beneficial effects of cocarboxylase in the treatment of experimental myocardial infarction in dogs.
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Cocarboxylase, or thiamine pyrophosphate, is an essential coenzyme in the catabolism of pyruvate. The authors evaluated the effects of a stable cocarboxylase solution in the treatment of an experimentally created acute myocardial infarction in 14 healthy mongrel dogs. The left anterior descending
Thiamine cardiotropism.
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Thiamine administration (200 mg/kg 2 hours before start of the experiment) substantially reduced the myocardial ischaemic lesion in a model of experimental myocardial infarction in the rat. As shown by stereometric analysis of histological heart preparations, the cytoprotective action of vitamin B1
Bilateral paramedian thalamic infarct in the presence of an unpaired thalamic perforating artery.
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Bilateral paramedian thalamic infarction is rare. The suggested mechanism is occlusion of a central unpaired thalamic perforating artery--an anatomic variant. In the few existing reports of this condition, the diagnosis was based on computed tomography (CT) or magnetic resonance imaging (MRI)
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