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1 orphological changes in a novel pig model of Becker muscular dystrophy.
2 individuals versus symptomatic patients with Becker muscular dystrophy.
3 for development as a therapy for Duchenne or Becker muscular dystrophy.
4 mice with mdx mice, a model for Duchenne and Becker muscular dystrophy.
5 ex mutants, including patients with Duchenne/Becker muscular dystrophy.
6 d upon reframing, similar to observations in Becker muscular dystrophy.
7 n order to detect deletions causing Duchenne/Becker muscular dystrophy.
8 trophin, the protein mutated in Duchenne and Becker muscular dystrophy.
9 r volume fraction in study participants with Becker muscular dystrophy.
10 g show promise as therapies for Duchenne and Becker muscular dystrophies.
12 rt failure is characteristic of Duchenne and Becker muscular dystrophies and X-linked dilated cardiom
14 Materials and Methods Eight patients with Becker muscular dystrophy and eight matched control subj
15 ive results for non-DMD disorders, including Becker muscular dystrophy and forms of limb-girdle and c
16 me pseudoexon mutations (one associated with Becker muscular dystrophy and one with DMD), mutation-in
17 ophin, the defective protein in Duchenne and Becker muscular dystrophies, and therapeutic utrophin de
21 ne muscular dystrophy (DMD) into less severe Becker muscular dystrophy (BMD) by altering pre-mRNA spl
25 henne muscular dystrophy (DMD) or the milder Becker muscular dystrophy (BMD), largely depending on wh
26 er disease (GD) type III, Duchenne (DMD) and Becker muscular dystrophy (BMD), Parkinson disease (PD),
27 D, Limb-girdle muscular dystrophy (LGMD) and Becker muscular dystrophy (BMD), strength-training impro
28 nclude Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), X-linked dilated cardio
34 s preserved in calf muscles of patients with Becker muscular dystrophy (BMD, n = 14) and limb-girdle
35 isruption of the reading frame often lead to Becker muscular dystrophy, but a genotype/phenotype corr
36 muscle protein dystrophin triggers Duchenne/Becker muscular dystrophy, but the structure-function re
39 l myopathy/muscular dystrophies and Duchenne/Becker muscular dystrophy) delivered a ~59% 'solved' and
41 ted progress in gene therapy of Duchenne and Becker muscular dystrophy (DMD and BMD) skeletal muscle
42 dystrophin gene result in both Duchenne and Becker muscular dystrophy (DMD and BMD), as well as X-li
45 tin, MYO-029, in adult muscular dystrophies (Becker muscular dystrophy, facioscapulohumeral dystrophy
46 n humans [Duchenne muscular dystrophy (DMD), Becker muscular dystrophy, facioscapulohumeral muscular
47 ity leads to dystrophinopathies like DMD and Becker muscular dystrophy, for which no cure is yet avai
48 d the clinical phenotype of 17 patients with Becker muscular dystrophy harbouring in-frame deletions
49 were reported in patients with Duchenne and Becker muscular dystrophies; improved understanding of t
50 Mutations in this locus cause Duchenne or Becker muscular dystrophies in human patients and are th
54 prednisone in patients with Limb Girdle and Becker muscular dystrophy (LGMD and BMD, respectively).
56 patients, missense mutations can cause DMD, Becker muscular dystrophy, or X-linked cardiomyopathy.
58 later phases of exercise, skeletal muscle in Becker muscular dystrophy patients was less acidic than
59 rate of proton efflux from muscle fibres of Becker muscular dystrophy patients was similar to that o
64 could benefit many patients with Duchenne or Becker muscular dystrophy, regardless of genotype, and c
65 enerative muscle diseases Duchenne (DMD) and Becker muscular dystrophy result from mutations in the D
68 hy phenotype to that of the milder disorder, Becker muscular dystrophy, typically caused by in-frame
69 s situation presents a striking analogy with Becker muscular dystrophy, where in-frame deletions in t
70 clinical trial of patients with Duchenne or Becker muscular dystrophy whose LVEF was preserved and M
71 sociated protein expression in patients with Becker muscular dystrophy with deletions relevant for on
72 ping the patients by deletion, patients with Becker muscular dystrophy with deletions with an end-poi