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Pagina 1 a partire dal 22 risultati
Thiamine deficiency activates hypoxia inducible factor-1α to facilitate pro-apoptotic responses in mouse primary astrocytes.
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Thiamine is an essential enzyme cofactor required for proper metabolic function and maintenance of metabolism and energy production in the brain. In developed countries, thiamine deficiency (TD) is most often manifested following chronic alcohol consumption leading to impaired mitochondrial
Hypoxia-ischemia and thiamine deficiency.
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In order to test the hypothesis that Wernicke's encephalopathy is of topographic rather than of pathogenetic specificity we examined the brains of 49 patients without any evidence of chronic alcoholism. They had died at least four days after an event of severe hypoxia-ischemia. They all showed
Stabilization of the hypoxia-inducible transcription Factor-1 alpha (HIF-1α) in thiamine deficiency is mediated by pyruvate accumulation.
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Vitamin B1, or thiamine is a critical enzyme cofactor required for metabolic function and energy production. Thiamine deficiency (TD) is common in various diseases, and results in severe neurological complications due to diminished mitochondrial function, oxidative stress, excitotoxicity and
Cardiac beriberi (shoshin beriberi) caused by excessive intake of isotonic drink.
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A 21 month old female had voluntarily ingested 0.5-1.51 of isotonic sports drink daily from 10 months of age. She developed hyponatremia and beriberi heart disease, which resulted in metabolic acidosis and cardiogenic shock (shoshin beriberi). Mechanical ventilation was applied for pulmonary edema.
Wernicke's encephalopathy-like lesions in global cerebral hypoxia.
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We report a patient with severe hypoxic encephalopathy after cardiac arrest, in which lesions depicted on MRI involved mainly the periaqueductal brainstem, hypothalamus and mamillary bodies, and medial thalami. Hypoxia usually causes cerebro-cerebellar cortical damage. However, it may also cause
Lactate dehydrogenase and isoenzyme changes in rats with experimental thiamine deficiency.
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Heat and liver lactate dehydrogenase (LDH) and isoenzyme distributions were studied in rats with experimental thiamine deficiency. No change in total heart LDH activity was observed on days 24 and 40 of a thiamine deficient diet. At the time of symptoms (average 53 days on diet), total heart muscle
Consideration of alternative causes of lactic acidosis: Thiamine deficiency in malignancy.
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Lactic acidosis is a common metabolic acidosis characterized by increased serum lactate and is usually associated with a decreased blood pH. Lactic acidosis has many different causes but has been differentiated into type A, hypoxic causes, and type B, non-hypoxic causes. Tissue hypoxia, type A, is
HIF1-α-mediated gene expression induced by vitamin B1 deficiency.
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It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the
[Thiamine deficiency as a cause of life threatening lactic acidosis in total parenteral nutrition].
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Two patients aged 37 and 44 years developed life-threatening lactic acidosis following abdominal surgery and a period of about 3 weeks of total parenteral nutrition. Septicaemia and hypoxia were excluded as possible causes. Conventional treatment including high doses of buffer agents was
Thiamine triphosphate and thiamine triphosphatase activities: from bacteria to mammals.
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In most organisms, the main form of thiamine is the coenzyme thiamine diphosphate. Thiamine triphosphate (ThTP) is also found in low amounts in most vertebrate tissues and can phosphorylate certain proteins. Here we show that ThTP exists not only in vertebrates but is present in bacteria, fungi,
Wernicke-Korsakoff syndrome following attempted hanging.
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The case of an alcoholic man is reported who survived a suicidal hanging attempt, and subsequently suffered of amnesia, dementia, apathy and behavioural abnormalities. A clinical diagnosis of hypoxic brain damage was made, but upon autopsy six years later, extensive pseudosystematic thalamic
[Case of infantile autism with pediatric Wernicke's encephalopathy due to severe eating disorder].
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Wernicke's encephalopathy (WE) or thiamine deficiency is fatal if left untreated. We report a case of a 3-year-old boy with infantile autism and a severe eating disorder who developed WE after 3 weeks of starvation without thiamine supplementation. The eating disorder started when he entered
Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia.
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We report the case of a 54-year-old alcoholic female patient who was hospitalized for neurologic alterations along with a severe hyponatremia (plasma Na+: 97 mEq/l). She suffered from potomania and was given, a few days before admission, a thiazide diuretic for hypertension. A careful correction of
An unusual cause of persisting hyperlactatemia in a neonate undergoing open heart surgery.
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Being a reflection of the degree of global tissue anoxia, serum lactate levels therefore can be used as a marker of organ damage and eventual outcome. A statistically significant association was observed between serum lactate levels and subsequent mortality and morbidity in critically ill adults,
Lactic acidosis update for critical care clinicians.
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Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must
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