phosphorylase/fatigue

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Phosphorylase re-expression, increase in the force of contraction and decreased fatigue following notexin-induced muscle damage and regeneration in the ovine model of McArdle disease.

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McArdle disease is caused by a deficiency of myophosphorylase and currently a satisfactory treatment is not available. The injection of notexin into, or the layering of notexin onto, the muscles of affected sheep resulted in necrosis followed by regeneration of muscle fibres with the expression of

[Influence of adrenalin on muscle phosphorylase activity and its significance in the mechanism of fatigue inhibition].

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[Influence of adrenal in muscle phosphorylase activity and its significance in the mechanism of the fatigue-inhibiting action].

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Differential histochemical effects of muscle contractions on phosphorylase and glycogen in various types of fibres: relation to fatigue.

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Metabolic capacity, fibre type area and capillarization of rat plantaris muscle. Effects of age, overload and training and relationship with fatigue resistance.

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1. The influences of age (5, 13 and 25-month-old rats), overload as obtained by denervation of synergists, and training on the metabolic capacity, relative muscle cross-sectional area occupied by each fibre type, capillarization and fatigue resistance of the rat m. plantaris were investigated. 2.

Phase I dose-escalating trial of Escherichia coli purine nucleoside phosphorylase and fludarabine gene therapy for advanced solid tumors.

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BACKGROUND The use of Escherichia coli purine nucleoside phosphorylase (PNP) to activate fludarabine has demonstrated safety and antitumor activity during preclinical analysis and has been approved for clinical investigation. METHODS A first-in-human phase I clinical trial (NCT 01310179; IND 14271)

The experimental type 2 diabetes therapy glycogen phosphorylase inhibition can impair aerobic muscle function during prolonged contraction.

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Glycogen phosphorylase inhibition represents a promising strategy to suppress inappropriate hepatic glucose output, while muscle glycogen is a major source of fuel during contraction. Glycogen phosphorylase inhibitors (GPi) currently being investigated for the treatment of type 2 diabetes do not

Muscle fatigue in McArdle's disease studied by 31P-NMR: effect of glucose infusion.

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In muscle phosphorylase deficiency (McArdle's disease) there is an abnormally rapid fatigue during strenuous exercise. Increasing substrate availability to working muscle can improve exercise tolerance but the effect on muscle energy metabolism has not been studied. Using phosphorus-31 nuclear

Genetic evaluation of AMPD1, CPT2, and PGYM metabolic enzymes in patients with chronic fatigue syndrome.

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Chronic fatigue syndrome (CFS) is a disease that can seriously impair one's quality of life; patients complain of excessive fatigue and myalgia following physical exertion. This disease may be associated with abnormalities in genes affecting exercise tolerance and physical performance. Adenosine

Thymidine phosphorylase expression is associated with time to progression in patients receiving low-dose, docetaxel-modulated capecitabine for metastatic breast cancer.

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BACKGROUND Preclinical data have indicated a synergistic interaction between docetaxel and capecitabine by means of taxane-induced up-regulation of thymidine phosphorylase (TP). On the basis of such premises, we conducted a phase II trial to determine the activity and tolerability of weekly

Metabolic and energy correlates of intracellular pH in progressive fatigue of squid (L. brevis) mantle muscle.

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Squid (Lolliguncula brevis) were exercised at increasing swimming speeds to allow us to analyze the correlated changes in intracellular metabolic, acid-base, and energy status of the mantle musculature. Beyond a critical swimming velocity of 1.5 mantle lengths/s, an intracellular acidosis developed

Chronic fatigue and myalgia syndrome: mitochondrial and glycolytic studies in skeletal muscle.

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Clinical and biochemical findings in skeletal muscle in 11 patients with chronic fatigue myalgia syndromes of unknown aetiology are reported. All patients had severe asthenia for from one to 10 years with greatly limited exercise capacity and protracted exhaustion after minor exercise. Diffuse

Phase I clinical and pharmacological studies of benzylacyclouridine, a uridine phosphorylase inhibitor.

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Benzylacyclouridine (BAU, IND 039655) is a potent and specific inhibitor of uridine phosphorylase (UrdPase; EC 2.4.2.3). This enzyme plays a major role in regulating uridine homeostasis and also catalyzes the conversion of fluoropyrimidine nucleosides to their respective bases. Inhibition of UrdPase

Reversal of phosphorylase activation in muscle despite continued contractile activity.

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During studies of the regulation of phosphorylase activity and glycogenolysis in contracting muscle, it was found that conversion of phosphorlyase beta to alpha is transient. Reversal of phosphorylase activation during both continuous and intermittent stimulation in the plantaris might, in part,

Calcium-dependent regulation of phosphorylase activation in a fast-twitch oxidative-glycolytic skeletal muscle.

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Calcium-mediated phosphorylase kinase activation has been studied in the rat flexor digitorum brevis, a fast-twitch oxidative-glycolytic skeletal muscle that exhibits a robust inward Ca2+ current [Can J. Physiol. Pharmacol. 63:958-965, 1985]. This system provided an opportunity to compare the

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