Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004093 (asthenia)
 2,650 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Weakness in inflammatory myopathy is commonly more prominent than is muscle fiber necrosis, suggesting additional explanations for its origin. Recent studies reveal that cell-mediated immune mechanisms are active in PMS-DMS. In experiments reported here, the effect of human mononuclear cell-derived mediator-rich supernatant upon calcium accumulation by SR membranes was examined. SR, by triggered binding and release of calcium in the vicinity of myofibrils, plays a key role in regulation of skeletal muscle contraction and relaxation. SR was derived from Lewis and Sprague-Dawley rat pelvic girdle muscles. Mediator-rich supernatants were generated by exposure of Hypaque-Ficoll-purified human mononuclear cells to PHA-P and Con-A during 72 hr of incubation in RPMl 1640 medium containing 10% autologous serum. Mitogens alone were without effect on SR. Suppression of ATP-dependent calcium accumulation was demonstrable within 40 min of exposure of SR to mediator-rich supernatants. The factor(s) producing suppression of calcium binding was nondialyzable, stable on storage at -70 degrees C, and active upon SR at physiologic calcium-loading levels. These findings may have important implications for understanding of the mechanism of weakness in inflammatory myopathies.
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PMID:Mitogen-activated human mononuclear cells suppress calcium binding by sarcoplasmic reticulum. 696 2