Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.4.1 (myosin ATPase)
 1,140 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postoperative pulmonary complication and respiratory failure, frequently seen in undernourished patients such as those with esophageal cancer, were suspected to be due to respiratory muscle wasting caused by nutritional depletion. Based on this idea, the respiratory muscles obtained by biopsies during operation from diaphragm, external intercostal muscle, and rectus abdominis muscle were assessed histochemically in 32 patients. The specimens were stained for myosin ATPase to differentiate the types of muscle fibers, and then the size and distribution of the muscle fibers of each type were measured. In diaphragm muscle, cross-sectional areas of type 1 & 2 and the ratio of the area occupied by each fiber were usually the same; in external intercostal muscle, however, type 1 fibers were dominant and in rectus abdominis muscle, type 2 fibers were dominant. The cross-sectional area of each respiratory muscle fiber well correlated with certain anthropometrical indexes, and the nutritionally depleted cases, the muscle fibers were of a smaller size suggesting less respiratory muscle strength. The ratio of the area occupied by type 1 fibers in diaphragm muscle was linearly related to serum albumin, total cholesterol, and PNI (prognostic nutritional index). Type 2 fibers were dominant in malnourished patients, suggesting greater fatigue compared to well-nourished cases. Opposite findings were obtained in external intercostal muscle and rectus abdominis muscle, and the ratio of the area occupied by type 2 fibers was smaller in the undernourished cases, suggesting reduced maximum strength of these muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Histochemical analysis of respiratory muscles of patients with esophageal cancer--with special reference to the preoperative nutritional state]. 214 8

Five patients with rapidly evolving, severe weakness had an unusual myopathy with virtually complete loss of myosin in 5 to 40% of muscle fibers. Three of the 5 patients began to develop weakness 1 to 2 weeks after lung transplantation. The fourth became weak after a febrile illness. The fifth presented with diabetic ketoacidosis and weakness. All patients had received corticosteroid therapy. In all cases the weakness was progressive and led to severe disability, with respiratory failure in 4 patients. Initial diagnostic testing did not localize an underlying cause for the weakness. Creatine kinase was normal or minimally elevated. Electromyography generally showed mildly myopathic or nondiagnostic changes. However, muscle biopsy revealed numerous small angular fibers with no myosin ATPase staining at any pH. Immunocytochemical staining and ultrastructural studies confirmed a severe loss of myosin in many fibers. This rapidly evolving myopathy with myosin-deficient muscle fibers appears to be different clinically and pathologically from previously described syndromes involving rapidly progressive weakness. Slow recovery over a period of months is the most common outcome.
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PMID:Rapidly evolving myopathy with myosin-deficient muscle fibers. 812 77