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At least 253 records · Page 14Linked to original sources
PubMed1980

Simple electrophoretic technique for creatine kinase MM isozyme in neonatal Duchenne muscular disease screening using dried blood samples.

By increasing diadenosine pentaphosphate to a final concentration of 75 mumol to 100 mumol/l to inhibit excess adenylate kinase, a highly sensitive substrate in a gelatin matrix allowed the developement of a simple and cheap electrophoretic technique for creatine kinase MM isozyme in dried blood samples. The method is suitable for neonatal Duchenne muscular dystrophy screening, and it is an alternative method for a previously described bio-luminescent assay, which requires special equipment.

Adenine Nucleotides↗
PubMed1987

Influence of pressure on permeability of normal and diseased muscular arteries to horseradish peroxidase. A new catheter approach.

The effects of different distending pressures on permeability of dog and human arteries to horseradish peroxidase (HRP) were studied. A new catheter was employed to achieve the distention of defined vessel segments to the desired pressure. Normal dog brachial arteries were studied both post mortem and in vivo. Mildly to moderately diseased human coronary arteries were studied post mortem. A predictable linear relationship between pressure and penetration of HRP into the dog arterial media was found, using pressures of 0, 150, 300 and 500 mm Hg. Postmortem vessels were consistently less permeable than those studied in vivo. Full penetration of the media by HRP was achieved by application of 300 mm Hg pressure for 45 sec with the new catheter. When human coronary lesions were examined under these same conditions, plaques were readily demonstrated to be permeable to HRP, even to a depth of many hundreds of micrometer. Thus, penetration of arterial wall thickness by HRP (Mr 40,000 dalton) is related to the distending pressure applied. Human coronary plaques also show ready penetrance by HRP. The new catheter described allows the application of these pressures to defined segments of the arterial tree.

Adult↗
PubMed1999

[Macrophagic myofasciitis: description and etiopathogenic hypotheses. Study and Research Group on Acquired and Dysimmunity-related Muscular Diseases (GERMMAD) of the French Association against Myopathies (AFM)].

PURPOSE: A new type of inflammatory myopathy of unknown etiology has recently been described in France. The myopathy, called macrophagic myofasciitis, had never been described in the literature. METHODS: In December 1998, 35 cases of macrophagic myofasciitis were reported, showing an increase in its incidence since the description of the first case in 1993. The first 22 cases are described. RESULTS: The 22 patients were each referred with a presumptive diagnosis of either polymyositis (11 patients), polymyalgia rheumatica (5 patients), mitochondrial cytopathy (4 patients), or congenital myopathy or muscle dystrophy (1 patient for each). Clinical symptoms included myalgias (91%), arthralgias (68%), marked asthenia (55%), muscle weakness (45%), and fever (32%). Laboratory findings included elevated CK levels (50%) and a marked increased in the erythrocyte sedimentation rate (37%). Electromyographic recordings showed the existence of myopathy (35%). Muscle biopsy showed a unique pattern characterized by: (i) centripetal infiltration of the epimysium, perimysium and perifascicular endomysium by non epitheloid, cells of the monocyte/macrophage lineage (CD68+, CD1a-, S100-) with both large cytoplasm and PAS-positive content; (ii) absence of necrosis, of both epithelioid and giant cells, and of mitotic figures; (iii) occasional CD8+ T-cells; and, (iiii) minimal myocyte suffering. The disease symptoms were easily distinguishable from those of sarcoid myopathy and fasciitis-panniculitis syndromes. Infectious diseases known to be associated with reactive histiocytosis, including Whipple's disease, Mycobacterium avium intracellulare infection and malakoplakia, could not be documented. Patients' condition improved under corticosteroid therapy, associated or not with non-specific antibiotic therapy. CONCLUSION: A new inflammatory muscle disorder of unknown etiology, characterized by a distinctive pathological pattern of macrophagic myofasciitis, is emerging in France. Diagnosis is based on muscular biopsy. Numerous clinical, epidemiological and etiopathologic studies initiated by the GERMMAD (Groupe d'études et de recherche sur les maladies musculaires acquises) are in progress.

Adult↗
PubMed1999

Neurotrophic factors and neuro-muscular disease: II. GDNF, other neurotrophic factors, and future directions.

This is the second of two reviews in which we discuss the essential aspects of neurotrophic factor neurobiology, the characteristics of each neurotrophic factor, and their clinical relevance to neuromuscular diseases. The previous paper reviewed the neurotrophin family and neuropoietic cytokines. In the present article, we focus on the GDNF family and other neurotrophic factors and then consider future approaches that may be utilized in neurotrophic factor treatment.

Animals↗
PubMed1990

Cytochrome c oxidase deficient fibres in the limb muscle and diaphragm of man without muscular disease: an age-related alteration.

Cytochrome c oxidase (complex IV of the respiratory chain) was studied histochemically in human limb muscle (n = 109) and diaphragm (n = 115) obtained at autopsy revealing randomly distributed muscle fibres without enzyme activity. The defects were present both in normal type I and type II fibres and in ragged red like fibres with increased content of mitochondria. In both organs an age associated manifestation of the defect was observed. First defects occurred sporadically in the 3rd and 4th decade, but were present from the 6th to 9th decade in 66-83% of the limb muscles and 75-100% of the diaphragms. Also the number of defects/cm2 (defect density) increased with age from approx. 5, and 7 in limb muscle and diaphragm below the 6th decade to 54 and 60 defects in the 8th-9th decade (P = 0.000). Between both muscles no statistically significant difference in defect density (P greater than 0.15) existed. Irrespective of the defect density the defect typically affected isolated fibres showing normal histochemical reactivity for succinate dehydrogenase (complex II). The results indicate that cytochrome c oxidase deficient muscle fibres in normal skeletal muscle represent an age related phenomenon which probably results from cellular ageing and might be involved in the reduction of muscle mass and strength during senescence.

Adolescent↗