In vivo estimation of muscle protein synthesis in myotonic dystrophy
β Scribed by David Halliday; G. C. Ford; Richard H. T. Edwards; Michael J. Rennie; Dr Robert C. Griggs
- Publisher
- John Wiley and Sons
- Year
- 1985
- Tongue
- English
- Weight
- 497 KB
- Volume
- 17
- Category
- Article
- ISSN
- 0364-5134
No coin nor oath required. For personal study only.
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Muscle fiber contractile dysfunction in myotonic dystrophy (MD) is poorly understood. We biopsied the tibialis anterior of two symptomatic and three asymptomatic subjects (aged 21-31 years) with the MD mutation. Biopsies were freeze dried. A total of 103 single muscle fibers were activated with Ca +
## Abstract Myotonic dystrophy is an inherited multiβsystem disease. Its pathophysiology leading to muscle malfunction and damage is not well understood. ^23^Na NMR spectroscopy was applied here for an __in vivo__ comparative study of the calf muscles of 7 myotonic dystrophy patients at various sta
Length of (CTG)n triplet repeats in myotonic dystrophy protein kinase gene (DMPK) was estimated in tumors, normal tissues of the same organs, muscles, and leukocytes from three myotonic dystrophy (DM) patients and a non-DM patient. Using cDNA 25 as a probe, a Southern blot analysis of EcoRI- and Bgl
In myotonic dystrophy (DM), the expansion of CTG triplet repeats in the 3'-untranslated region of DM-protein kinase (DMPK) is a causal gene mutation. However, the pathogenic molecular mechanism of CTG repeat expansion for DM phenotypic expression is unclear. To investigate this issue, we examined th