الصفحة 1 من عند 55 النتائج
Ensuring continuous intracellular supply of thiamine is essential to maintain metabolism. Cellular homeostasis requires the function of the membrane bound thiamine transporters THTR1 and THTR2. In the absence of increased dietary intake of thiamine, varying intracellular levels to meet metabolic
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
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
Aims: Although diabetic retinopathy has long been considered a microvascular complication, retinal neurodegeneration and inflammation may precede its clinical manifestations. Despite all research efforts, the primary treatment options
Previous studies have demonstrated that thiamine (vitamin B1) has a cytoprotective effect against ischemic damage to the heart, and that heat shock protein 70 (Hsp70) is capable of protecting cardiac cells from lethal ischemia/hypoxia. We show here that thiamine has a cytoprotective effect on
Adaptive responses within hypoxic tumor microenvironments require the altered expression of Solute Carrier (SLC) transporters to maintain nutrient uptake in support of cellular metabolism and biosynthesis. Using a real time PCR array strategy to further characterize changes in transporter expression
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
Rates of thiamin diphosphate accumulation in rat liver tissue and its subsequent depletion were decreased within the first hour after vitamin B1 administration into the animals with oxygen insufficiency. Hypoxia apparently inhibited simultaneously the processes of thiamin diphosphate biosynthesis
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,
The characteristics of normal thiamine transport across the intestine were studied in rats using intact intestinal loops and everted jejunal segments. In vivo studies with [35-S]-thiamine hydrochloride revealed, in all segments of small intestine, saturation kinetics for low thiamine concentrations
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
A thiamine (T) deficient state in rats was produced by feeding the rats a T deficient diet (TDD). At the stage of 13 days (TDD13 group), the number of red blood cells (RBC) and white blood cells (WBC), hematocrit (Ht) and hemoglobin (Hb) values decreased. On the other hand, after 30 days on the TDD