Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026850 (muscular dystrophy)
5,870 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of the carcinoid syndrome associated with a proximal myopathy is reported. Histology showed advanced atrophy of type II muscle fibres but no inflammation. Perinuclear acid phosphatase was increased. Electron microscopy revealed persistence of the Z-line until the muscle fibre had been severely disrupted. Similar lesions have been observed in the hereditary muscular dystrophy in mice, and also in these animals and in rats when injected with 5-hydroxytryptamine (5-HT). Treatment with cyproheptadine caused a documented response in the patient's debilitating diarrhoea and also produced symptomatic improvement in her muscular power. We suggest that the myopathy is due to circulating 5-HT or is a non-metastatic complication of the carcinoid tumour.
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PMID:Carcinoid myopathy and treatment with cyproheptadine (Periactin). 427 14

Injection of serotonin (5-hydroxytryptamine) induced a marked decrease in the level of glucose 1,6-diphosphate (Glc-1,6-P2) in the rat tibialis anterior muscle. Concomitant to the decrease in Glc-1,6-P2, the potent activator of phosphofructokinase and phosphoglucomutase, the activities of both these enzymes were markedly reduced by serotonin. The level of Glc-1,6-P2 and the activities of phosphofructokinase and phosphoglucomutase increased with age in the tibialis anterior muscle and the effect of serotonin was more pronounced in the older animals. Serotonin also induced a significant increase in the level of cyclic GMP in muscle. The serotonin-induced changes in the normal muscle mimic the changes in carbohydrate metabolism we found previously in muscular dystrophy.
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PMID:Changes in the levels of glucose 1,6-diphosphate and cyclic GMP, and in the activities of phosphofructokinase and phosphoglucomutase induced by serotonin in muscle. 630 80

To investigate the "vascular" hypothesis of muscular dystrophy, the sensitivity and contractility of aortic spiral strips of dystrophic (BIO 14.6) and normal (FIB) hamsters have been determined to various smooth muscle agonists. The results obtained with cumulative dose-response curves show that there is no increase in the sensitivity of the dystrophic compared with the normal aorta to noradrenaline, phenylephrine, isoproterenol, histamine, or 5-hydroxytryptamine. However, there was a significant increase in the force generated by aortic strips of the dystrophic animals to all agonists. Determination of noncollagen and collagen protein showed that there was no difference in the relative proportions of these proteins in the aortas from the two strains. The results show that in this animal model of dystrophy an increased response to vasopressor amines occurs and is in accordance with that expected of the vascular hypothesis.
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PMID:Increased contractility in vascular smooth muscle of dystrophic hamsters. 683 16