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1 mans with dystrophin gene mutations who have Duchenne muscular dystrophy.
2 nts a new treatment option for patients with Duchenne muscular dystrophy.
3 VL; ie, high-force contractions) accelerates Duchenne muscular dystrophy.
4 on 5 of the Acvr2b gene, in a mouse model of Duchenne muscular dystrophy.
5 protective therapy on event-free survival in Duchenne muscular dystrophy.
6 ory failure is the leading cause of death in Duchenne muscular dystrophy.
7 mitigated muscle damage in a murine model of Duchenne muscular dystrophy.
8 epresent a promising therapeutic approach in Duchenne muscular dystrophy.
9 skeletal and cardiac muscle degeneration in Duchenne muscular dystrophy.
10 ellite cell-like progenitors and a model for Duchenne Muscular Dystrophy.
11 dels of congenital muscular dystrophy 1A and Duchenne muscular dystrophy.
12 s the lifespan and survival in patients with Duchenne muscular dystrophy.
13 nse investigation as a potential therapy for Duchenne muscular dystrophy.
14 se loss of dystrophin expression and lead to Duchenne muscular dystrophy.
15 ogical relevance in an experimental model of Duchenne muscular dystrophy.
16 ytoskeletal protein, absence of which causes Duchenne muscular dystrophy.
17 ement of muscle function in a mouse model of Duchenne muscular dystrophy.
18 insight into cardiomyopathy associated with Duchenne muscular dystrophy.
19 efective nNOS homeostasis in dystrophin-null Duchenne muscular dystrophy.
20 y of the experimental studies are focused on Duchenne muscular dystrophy.
21 eneration occurring in a C. elegans model of Duchenne muscular dystrophy.
22 to the pathology of muscle diseases such as Duchenne muscular dystrophy.
23 d indicate that miR-206 slows progression of Duchenne muscular dystrophy.
24 linical trials for genetic disorders such as Duchenne muscular dystrophy.
25 tein due to mutations in the DMD gene causes Duchenne muscular dystrophy.
26 peptides may be considered for treatment of Duchenne muscular dystrophy.
27 recting frameshift and nonsense mutations in Duchenne muscular dystrophy.
28 the dystrophic phenotype in a mouse model of Duchenne muscular dystrophy.
29 elevant for on-going exon skipping trials in Duchenne muscular dystrophy.
30 ubstantial clinical benefit to patients with Duchenne muscular dystrophy.
31 -4658 to become a disease-modifying drug for Duchenne muscular dystrophy.
32 e morpholino oligomer (PMO) in patients with Duchenne muscular dystrophy.
33 ning muscle injury in the mdx mouse model of Duchenne muscular dystrophy.
34 ing SR Ca(2+) leak in the mdx mouse model of Duchenne muscular dystrophy.
35 cle and nerve-the prototypical example being Duchenne muscular dystrophy.
36 bute to the development of cardiomyopathy in Duchenne muscular dystrophy.
37 es in dystrophic mdx mice, a murine model of Duchenne muscular dystrophy.
38 s, both after injury and in a mouse model of Duchenne muscular dystrophy.
39 in muscular dystrophy, including the lethal Duchenne muscular dystrophy.
40 eat the dystrophic symptoms in this model of Duchenne muscular dystrophy.
41 dystrophic muscles in mdx mice, a model for Duchenne muscular dystrophy.
42 the effectiveness of potential therapies for Duchenne muscular dystrophy.
43 troglycan as a key event in the aetiology of Duchenne muscular dystrophy.
44 as therapeutic targets for the treatment of Duchenne muscular dystrophy.
45 muscles of mdx(5cv) mice, a mouse model for Duchenne muscular dystrophy.
46 Absence of the protein dystrophin causes Duchenne muscular dystrophy.
49 mg/kg bodyweight) in ambulant patients with Duchenne muscular dystrophy aged 5-15 years with amenabl
51 or planned exon skipping clinical trials for Duchenne muscular dystrophy and correlated it to the lev
52 is a leading cause of death in patients with Duchenne muscular dystrophy and myocardial damage preced
54 most common form of muscular dystrophy after Duchenne muscular dystrophy and one of the most common a
56 use, may open up new therapeutic avenues for Duchenne muscular dystrophy and possibly other neuromusc
59 ht the development of SSOs designed to treat Duchenne muscular dystrophy and spinal muscular atrophy,
60 k for providing information to patients with Duchenne muscular dystrophy and their families when intr
61 al merosin-deficient muscular dystrophy, and Duchenne muscular dystrophy, and 2 myotoxin (cardiotoxin
62 ts in this young population with early-stage Duchenne muscular dystrophy are encouraging but need to
64 rs of the inherited muscle wasting condition Duchenne muscular dystrophy, as they allow non-invasive
65 enrolled male patients aged 2-28 years with Duchenne muscular dystrophy at 20 centres in nine countr
66 to delay loss of ambulation in patients with Duchenne muscular dystrophy but are accompanied by promi
67 skipping is a strategy for the treatment of Duchenne muscular dystrophy, but has variable efficacy.
69 ost common and severe form among children is Duchenne muscular dystrophy, caused by mutations in the
70 normally increased in the mdx mouse model of Duchenne muscular dystrophy compared with the wild-type
71 pment of muscle pathology in mouse models of Duchenne muscular dystrophy, congenital muscular dystrop
72 g of which could rescue the largest group of Duchenne muscular dystrophy deletions) showed significan
73 oss underlying contraction-induced injury in Duchenne muscular dystrophy distinctly different from th
76 titative muscle ultrasound data in boys with Duchenne muscular dystrophy (DMD) and healthy controls t
78 th multiple inflammatory states, severity of Duchenne muscular dystrophy (DMD) and muscle size in hea
80 alization contributes to the pathogenesis of Duchenne muscular dystrophy (DMD) by promoting functiona
86 ish the deletion or duplication genotypes of Duchenne muscular dystrophy (DMD) due to different fluor
87 pment of novel therapeutics for treatment of Duchenne muscular dystrophy (DMD) has led to clinical tr
89 r the efficacy of experimental therapies for Duchenne Muscular Dystrophy (DMD) in clinical trials.
161 and is abnormally elevated in the muscle of Duchenne muscular dystrophy (DMD) patients and animal mo
162 myomiRs) are highly enriched in the serum of Duchenne Muscular Dystrophy (DMD) patients and dystrophi
165 presents a standard palliative treatment for Duchenne muscular dystrophy (DMD) patients, but various
166 -3 (MYOM3) are abnormally present in sera of Duchenne muscular dystrophy (DMD) patients, limb-girdle
167 e and were remarkably similar to muscle from Duchenne muscular dystrophy (DMD) patients, suggesting t
168 constitutes the principal cause of death in Duchenne muscular dystrophy (DMD) patients, yet the impl
169 As a marker for newborn screening, CK in Duchenne muscular dystrophy (DMD) results in false-posit
170 previously tested the implication of ApN in Duchenne muscular dystrophy (DMD) using mdx mice, a mode
171 is expected that serum protein biomarkers in Duchenne muscular dystrophy (DMD) will reflect disease p
172 o oligomer, enabled dystrophin production in Duchenne muscular dystrophy (DMD) with genetic mutations
173 tal muscle during the disease progression of Duchenne muscular dystrophy (DMD), a degenerative muscle
174 mon and severe form of muscular dystrophy is Duchenne muscular dystrophy (DMD), a disorder caused by
175 e athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle-wast
176 here is currently no effective treatment for Duchenne muscular dystrophy (DMD), a lethal monogenic di
177 rate these properties in two mouse models of Duchenne muscular dystrophy (DMD), a neurogenetic diseas
178 rophin gene to create mutations that lead to Duchenne muscular dystrophy (DMD), a recessive X-linked
185 ping is a promising therapeutic strategy for Duchenne muscular dystrophy (DMD), employing morpholino
186 independent from the pathogenic mutation: in Duchenne muscular dystrophy (DMD), for instance, age at
187 the emergence of experimental therapies for Duchenne muscular dystrophy (DMD), it is fundamental to
190 g in healthy muscle, but in diseases such as Duchenne muscular dystrophy (DMD), microtubule alteratio
192 Congenital neuromuscular disorders, such as Duchenne muscular dystrophy (DMD), spinal muscular atrop
193 of the muscle histopathology associated with Duchenne Muscular Dystrophy (DMD), the molecular and cel
195 ntial for treating genetic diseases, such as Duchenne muscular dystrophy (DMD), which is caused by mu
219 iously described in various animal models of Duchenne muscular dystrophy (DMD); however, the patholog
220 muscles of mdx mice (i.e., a mouse model of Duchenne Muscular Dystrophy [DMD]) could restore the mor
223 the most common forms of muscular dystrophy: Duchenne muscular dystrophy, facioscapulohumeral muscula
224 pecific genetic conditions; Cystic Fibrosis, Duchenne Muscular Dystrophy, Familial Adenomatous Polypo
225 Bisphosphonates have been used to treat Duchenne muscular dystrophy for prevention of osteoporos
226 of age; time to rise from floor </=7 s) with Duchenne muscular dystrophy from 13 specialist centres i
230 e gene was identified by positional cloning, Duchenne muscular dystrophy has served as a paradigm for
231 luated for the treatment of diseases such as Duchenne muscular dystrophy, hemophilia, heart failure,
232 ich have a point mutation in Dmd)-a model of Duchenne muscular dystrophy-Hippo deficiency protected a
233 ment is recommended as a standard of care in Duchenne muscular dystrophy; however, few studies have a
236 A cooperative effort of stakeholders in Duchenne muscular dystrophy-including representatives fr
253 king the protein dystrophin, as occurring in Duchenne muscular dystrophy, is a hypersensitivity to co
254 nts with Becker muscular dystrophy (BMD) and Duchenne muscular dystrophy lack neuronal nitric oxide s
255 the development of cell-based therapies for Duchenne muscular dystrophy, little is known regarding t
256 ct cardiac myocytes from the murine model of Duchenne muscular dystrophy (mdx) despite robust increas
259 for skeletal muscles in addition to heart in Duchenne muscular dystrophy mouse models and that minera
260 ophic phenotype in the mdx (a mouse model of Duchenne muscular dystrophy) mouse by blunting the regen
261 entres in the USA aged 7 years or older with Duchenne muscular dystrophy, myocardial damage by late g
263 nical trials for modifying splicing to treat Duchenne muscular dystrophy opens the door for the use o
264 uction of dystrophin expression in muscle of Duchenne muscular dystrophy patients by systemic adminis
266 ardiomyopathy is a leading cause of death in Duchenne muscular dystrophy patients, and currently no e
270 terventions currently being investigated for Duchenne muscular dystrophy, perhaps the most promising
272 t in regenerating myofibers of patients with Duchenne muscular dystrophy, polymyositis, and compartme
273 lly deleting S1PR3 in the mdx mouse model of Duchenne muscular dystrophy produced a less severe muscl
277 therapy has shown great clinical promise in Duchenne muscular dystrophy, resulting in the production
278 s identified 6 unique oxidized proteins from Duchenne muscular dystrophy samples (n = 6) (versus cont
280 editing, CRISPR-Cas9, neuromuscular disease, Duchenne muscular dystrophy, spinal muscular atrophy, am
281 describing neuromuscular diseases, including Duchenne muscular dystrophy, spinal muscular atrophy, am
282 rs, including neuromuscular diseases such as Duchenne muscular dystrophy, spinal muscular atrophy, am
283 id steroids affects muscle remodeling in non-Duchenne muscular dystrophies, suggesting a positive out
289 ively affected development of treatments for Duchenne muscular dystrophy; this approach could serve a
290 cal trials to treat genetic diseases such as Duchenne muscular dystrophy, we propose that exon skippi
291 the USA, patients (age 10-18 years old) with Duchenne muscular dystrophy were randomly assigned in a
292 cribed for chronic muscle conditions such as Duchenne muscular dystrophy, where their use is associat
294 d safety of idebenone in young patients with Duchenne muscular dystrophy who were not taking concomit
295 K of 360 boys aged 3-15 years with confirmed Duchenne muscular dystrophy who were treated with daily
296 ively studied in mdx mice, a murine model of Duchenne muscular dystrophy with dystrophin deficiency.
297 n top of background therapy in patients with Duchenne muscular dystrophy with early myocardial diseas
298 defective autophagy in mdx mice, a model of Duchenne muscular dystrophy, with the use of rapamycin-l
299 strophin-positive fibers in a mouse model of Duchenne muscular dystrophy without apparent toxicity.
300 ing and universal small molecule therapy for Duchenne muscular dystrophy would be an enormous advance
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