Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The plasma level of atrial natriuretic factor and its relation to intracardiac and systemic hemodynamic parameters were examined in patients with coronary heart, rheumatic and mitral valvular diseases, neurocirculatory dystonia which were complicated by atrial fibrillation. The concentration of atrial natriuretic factor was found to vary with the left ventricular myocardial mass, left atrial contractility, antiarrhythmic therapy intensity and efficacy.
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PMID:[Structural and functional parameters of the myocardium and atrial natriuretic peptide in atrial fibrillation]. 140 69

Dystonin is a giant cytoskeletal protein belonging to the plakin protein family and is believed to crosslink the major filament systems in contractile cells. Previous work has demonstrated skeletal muscle defects in dystonin-deficient dystonia musculorum (dt) mice. In this study, we show that the dystonin muscle isoform is localized at the Z-disc, the H zone, the sarcolemma and intercalated discs in cardiac tissue. Based on this localization pattern, we tested whether dystonin-deficiency leads to structural defects in cardiac muscle. Desmin intermediate filament, microfilament, and microtubule subcellular organization appeared normal in dt hearts. Nevertheless, increased transcript levels of atrial natriuretic factor (ANF, 66%) beta-myosin heavy chain (beta-MHC, 95%) and decreased levels of sarcoplasmic reticulum calcium pump isoform 2A (SERCA2a, 26%), all signs of cardiac muscle stress, were noted in dt hearts. Hearts from two-week old dt mice were assessed for the presence of morphological and histological alterations. Heart to body weight ratios as well as left ventricular wall thickness and left chamber volume measurements were similar between dt and wild-type control mice. Hearts from dt mice also displayed no signs of fibrosis or calcification. Taken together, our data provide new insights into the intricate structure of the sarcomere by situating dystonin in cardiac muscle fibers and suggest that dystonin does not significantly influence the structural organization of cardiac muscle fibers during early postnatal development.
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PMID:Hearts of dystonia musculorum mice display normal morphological and histological features but show signs of cardiac stress. 2020 23