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guanosine/fatigue

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Neurologic and psychiatric manifestations in a family with a mutation in exon 2 of the guanosine triphosphate-cyclohydrolase gene.

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OBJECTIVE To investigate the range of clinical features to correlate genotypic and phenotypic manifestations in hereditary progressive and/or levodopa-responsive dystonia due to a defect in the guanosine triphosphate-cyclohydrolase (GCH1) gene. METHODS A large family from Texas was studied in an

Investigation of anti-fatigue effect and simultaneous determination of eight nucleosides in different parts of velvet antler in red deer and sika deer.

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Velvet antler (VA) is crucial and precious nourishment in China and some countries in Southeast Asia. It has several pharmacological effects such as alleviating fatigue and strengthening the body. The incidence of fatigue syndrome has increased gradually. Thus, VA can be a potential source of

Nitric Oxide Regulates Skeletal Muscle Fatigue, Fiber Type, Microtubule Organization, and Mitochondrial ATP Synthesis Efficiency Through cGMP-Dependent Mechanisms.

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Skeletal muscle nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathways are impaired in Duchenne and Becker muscular dystrophy partly because of reduced nNOSμ and soluble guanylate cyclase (GC) activity. However, GC function and the consequences of reduced GC activity in skeletal muscle are

The hot water extract and active components nicotinamide and guanosine of the leather carp Cyprinus carpio nudis improve exercise performance in mice.

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We identified the main active, exercise performance-enhancing compounds in a hot water extract of the leather carp, Cyprinus carpio nudus, as nicotinamide and guanosine. Mice were fed casein (30 mg/ml) enriched with nicotinamide (0.1 mg/ml) and guanosine (0.05 mg/ml) once daily for a week at 10 µl/g

Are vasoactive neuropeptide autoimmune fatigue-related disorders mediated via G protein-coupled receptors?

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Vasoactive neuropeptides such as pituitary adenylate cyclase activating polypeptide (PACAP), calcitonin gene related peptide (CGRP) and vasoactive intestinal peptide (VIP) have been implicated in a number of fatigue-related conditions. Associations of these vasoactive neuropeptides with heat shock

Sildenafil increases muscle protein synthesis and reduces muscle fatigue.

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Reductions in skeletal muscle function occur during the course of healthy aging as well as with bed rest or diverse diseases such as cancer, muscular dystrophy, and heart failure. However, there are no accepted pharmacologic therapies to improve impaired skeletal muscle function. Nitric oxide may

A phase II trial of carboplatin and gemcitabine with exisulind (IND #65,056) in patients with advanced non-small cell lung cancer: an Eastern Cooperative Oncology Group study (E1501).

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BACKGROUND Carboplatin and gemcitabine are one standard regimen for patients with advanced non-small cell lung cancer (NSCLC). The oral proapoptotic agent exisulind is a cyclic guanosine monophosphate phosphodiesterase that increases apoptosis in vitro. We performed a phase II trial of carboplatin

Deficient nitric oxide signalling impairs skeletal muscle growth and performance: involvement of mitochondrial dysregulation.

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BACKGROUND Nitric oxide (NO), generated in skeletal muscle mostly by the neuronal NO synthases (nNOSμ), has profound effects on both mitochondrial bioenergetics and muscle development and function. The importance of NO for muscle repair emerges from the observation that nNOS signalling is defective

A pilot study of ribavirin therapy for recurrent hepatitis C virus infection after liver transplantation.

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Ribavirin is a guanosine analogue that normalizes serum liver enzymes in most nontransplant patients with chronic hepatitis C virus (HCV) infection. We conducted an uncontrolled pilot study of ribavirin in 9 liver transplantation recipients that had persistently elevated liver enzymes, active

Telomerase activity and cellular aging might be positively modified by a yoga-based lifestyle intervention.

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OBJECTIVE Recent studies showed that a brief yoga-based lifestyle intervention was efficacious in reducing levels of oxidative stress and cellular aging in obese men. The objective of this case report was to assess the efficacy of this intervention in reducing the levels of biochemical markers of

Clinical and electrophysiological evaluation of myasthenic features in an alpha-dystroglycanopathy cohort (FKRP-predominant).

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A postsynaptic dysfunction of the neuromuscular junction has been reported in patients with alpha-dystroglycanopathy associated with mutations in guanosine diphosphate (GDP)-mannose pyrophosphorylase B gene (GMPPB), some of whom benefit from symptomatic treatment. In this study, we determine the

PBC-AIH overlap syndrome with concomitant ITP and Hashimoto's disease with positivity for anti-centromere antibody.

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We report a case of primary biliary cirrhosis (PBC)-autoimmune hepatitis (AIH) overlap syndrome with concurrent idiopathic thrombocytopenic purpura (ITP) and Hashimoto's disease with positivity for anticentromere antibody. The patient was a 64-year-old woman with symptoms of jaundice and general

GCH1 variants contribute to the risk and earlier age-at-onset of Parkinson's disease: a two-cohort case-control study

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Background: Common and rare variants of guanosine triphosphate cyclohydrolase 1 (GCH1) gene may play important roles in Parkinson's disease (PD). However, there is a lack of comprehensive analysis of GCH1 genotypes, especially in

Chronic low-grade inflammation in elderly persons is associated with altered tryptophan and tyrosine metabolism: role in neuropsychiatric symptoms.

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BACKGROUND Neuropsychiatric symptoms are common complaints of elderly persons. Recent data suggest that chronic low-grade inflammation, a fundamental characteristic of aging, plays a role. Effects might rely on the influence of inflammation on the activity of two enzymatic pathways, the

Sildenafil reduces respiratory muscle weakness and fibrosis in the mdx mouse model of Duchenne muscular dystrophy.

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Duchenne muscular dystrophy (DMD) is the most common form of muscular dystrophy caused by mutations in the dystrophin gene. Loss of dystrophin initiates a progressive decline in skeletal muscle integrity and contractile capacity which weakens respiratory muscles including the diaphragm, culminating
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