myotonia/necrosis

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Myotonia, a new inherited muscle disease in mice.

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Electromyographic (EMG) and histological studies were carried out with the new mouse mutant myotonia (mto, autosomal recessive). Affected animals exhibited behavioral myotonia which was apparent at 2 weeks of age. EMG studies revealed myotonic discharges (prolonged repetitive discharges with

The RNA-binding protein CUGBP1 regulates stability of tumor necrosis factor mRNA in muscle cells: implications for myotonic dystrophy.

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Type I myotonic dystrophy (DM1) is caused by a triplet repeat expansion in the 3'-untranslated region (UTR) of the dystrophia myotonia protein kinase (DMPK) gene. Pathogenesis is closely linked with production of a toxic RNA from the mutant allele, which interferes with function of several

Mutual interference of myotonia and muscular dystrophy in the mouse: a study on ADR-MDX double mutants.

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For Duchenne muscular dystrophy (DMD, dystrophin deficiency) and Thomsen/Becker myotonia (muscular chloride channel deficiency) genetically homologous mouse models are available, the dystrophin-deficient MDX mouse and the myotonic ADR mouse. Whereas the latter shows more severe symptoms than human

Serum parvalbumin, an indicator of muscle disease in murine dystrophy and myotonia.

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The soluble Ca(++)-binding protein parvalbumin (PV) is highly concentrated in fast muscle fibers of the wild type mouse. Employing Sandwich ELISA, we have shown that PV is present in the serum of normal mice and that its level is indicative of the disease status of muscle. Elevated PV levels were

Concurrence of myotonic dystrophy and epilepsy: a case report.

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BACKGROUND Myotonic dystrophy is a clinically and genetically heterogeneous multisystem disorder with a prevalence of 1 in 8000 in the general population. METHODS A 25-year-old Ethiopian man presented with symptoms of myotonia, muscle wasting, gait problems, frontal baldness, and family history

The effect of topically applied n-butylester of 2,4-dichlorophenoxyacetic acid on the immune response in mice.

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Six-week-old female CD-1 mice were administered the n-butylester of 2,4-dichlorophenoxyacetic acid (2,4-D). The 2,4-D ester was applied dermally at dosages ranging from 0 to 500 mg/kg (2,4-D content) in the acute studies and 0 to 300 mg/kg in the 3 week subacute studies. Following acute exposure,

A new inherited muscular disorder in Japanese quails (Coturnix coturnix japonica).

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Thirteen adult mutant (LWC strain) Japanese quails (Coturnix coturnix japonica), between the ages of 8 and 60 weeks were examined for a progressive muscular disorder. The disorder, inherited as an autosomal dominant trait, was clinically apparent as early as 28 days of age; it was characterized by

[Muscular dystrophy in a cat].

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A case of muscular dystrophy in a 1-year-old male castrated Domestic Shorthair cat is presented. The most striking clinical features were regurgitation, a stiff gait, an increased muscle tone and exercise intolerance. Serum biochemistry panels showed a marked increase in the muscle specific enzyme

Myotonic dystrophy-like disease in a dog.

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A mature female Rhodesian Ridgeback was determined to have a progressive, degenerative myopathy associated with myotonia, dysphagia, and marked muscle wasting. Clinical findings revealed a diffuse muscular disease with percussion dimpling, dysphagia, and creatine kinase elevation. A paroxysmal

Myotonic ADR-MDX mutant mice show less severe muscular dystrophy than MDX mice.

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In Duchenne muscular dystrophy (DMD) and its murine model, the dystrophic mouse (MDX), the skeletal musculature lacks dystrophin. The presumed function of this cytoskeletal protein is to protect the sarcolemma against mechanical stress during muscle activity. To test this hypothesis in vivo, we bred

[Distal myopathy with rimmed vacuoles and sudden death--report of two siblings].

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We describe two siblings with distal myopathy with rimmed vacuoles, who died suddenly presumably due to fatal arrhythmia. Case 1. A 26-year-old man with a 4 year-history of progressive muscle weakness and wasting was hospitalized in April, 1989. The family history showed that his younger brother had

Skeletal muscle disorders and associated factors that limit exercise performance.

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The study of skeletal muscle disorders is providing potentially important insights into regulatory mechanisms in human exercise and fatigue and information useful for diagnostic and treatment purposes. This review primarily concerned the general metabolic and physiological factors which set upper

[Non-inflammatory muscle pain]

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Muscle pain as a common symptom in daily practice frequently occurs as a non-specific accompanying symptom in multiple internal and neurological diseases. Primarily inflammatory or autoimmune muscular diseases are causing muscle pain. However, a number of non-inflammatory causes of pain can also be

HMG-CoA Reductase Inhibitor Myopathy: Clinical, Electrophysiological, and Pathologic Data in Five Patients.

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OBJECTIVE To define the clinical, electrophysiological, and pathologic features of the myopathy associated with the use of HMG CoA reductase inhibitors. METHODS Five patients with myopathy associated with HMG CoA reductase inhibitors were evaluated. Complete histories, physical examinations, manual

Myopathy induced by HMG-CoA reductase inhibitors in rabbits: a pathological, electrophysiological, and biochemical study.

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A combination of electrophysiological, pathological, and biochemical studies were performed in myopathy induced by 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors. Simvastatin (a lipophilic inhibitor) or pravastatin (a hydrophilic inhibitor) were administered by gavage to

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