ライフサイエンスコーパス: muscular dystrophy

1 ions in SMCHD1 can cause facioscapulohumeral muscular dystrophy.

2 ercross strategy in mice to map modifiers of muscular dystrophy.

3 he clamp method in the mdx model of Duchenne muscular dystrophy.

4 celerates muscle loss and causes limb girdle muscular dystrophy.

5 ommonly deleted in individuals with Duchenne muscular dystrophy.

6 lacking for muscle diseases such as Duchenne muscular dystrophy.

7 activity in the setting of muscle growth and muscular dystrophy.

8 or developing intervention aimed at treating muscular dystrophy.

9 m) mouse is a murine model of human Duchenne muscular dystrophy.

10 esses to adult disorders including a form of muscular dystrophy.

11 s have been identified for treating Duchenne muscular dystrophy.

12 EMD encoding emerin cause cardiomyopathy and muscular dystrophy.

13 dystrophin-deficient mouse model of Duchenne muscular dystrophy.

14 ovel type of autosomal recessive limb girdle muscular dystrophy.

15 e BM structure, and substantially ameliorate muscular dystrophy.

16 trophic mdx mice, a murine model of Duchenne muscular dystrophy.

17 mutations in SMCHD1 contribute to a type of muscular dystrophy.

18 and underlies a recessive form of inherited muscular dystrophy.

19 elopment as a therapy for Duchenne or Becker muscular dystrophy.

20 espan and survival in patients with Duchenne muscular dystrophy.

21 ed dystrophin restoration in mouse models of muscular dystrophy.

22 ass in models of osteogenesis imperfecta and muscular dystrophy.

23 fter injury and in a mouse model of Duchenne muscular dystrophy.

24 model for ambulatory-type Lmalpha2-deficient muscular dystrophy.

25 lar dystrophy, including the lethal Duchenne muscular dystrophy.

26 ng the efficacy of therapeutics for Duchenne muscular dystrophy.

27 (DM1), the most common form of adult on-set muscular dystrophy.

28 as spinal muscular atrophy, NMJ disorder and muscular dystrophy.

29 may be effective in treating this inherited muscular dystrophy.

30 verity, including limb-girdle and congenital muscular dystrophy.

31 and following DUX4 expression that leads to muscular dystrophy.

32 diseases, including haemophilia and Duchenne muscular dystrophy.

33 em myopathy to the severe Ullrich congenital muscular dystrophy.

34 commonly used preclinical model for Duchenne muscular dystrophy.

35 ding cancer, neurodegenerative diseases, and muscular dystrophies.

36 alpha-dystroglycan gives rise to congenital muscular dystrophies.

37 Fibrosis is the main complication of muscular dystrophies.

38 omechanisms of neurological abnormalities in muscular dystrophies.

39 ing to the class of laminopathies, including muscular dystrophies.

40 me editing in preclinical models of Duchenne muscular dystrophy(1-6), however, the long-term persiste

41 lar dystrophy 2I (LGMD2I), severe congenital muscular dystrophy 1C (MDC1C), to Walker-Warburg Syndrom

42 enic muscle loss is a feature of limb girdle muscular dystrophy 2B (LGMD2B) - a disease caused by mut

43 ysferlin, the protein missing in limb girdle muscular dystrophy 2B and Miyoshi myopathy, concentrates

44 e range of pathologies from mild limb girdle muscular dystrophy 2I (LGMD2I), severe congenital muscul

45 In the most common form, Duchenne muscular dystrophy, a few personalised therapies have re

46 in a laminin-alpha2 knockout mouse model of muscular dystrophy, acting as a link between alpha-DG an

47 PMD) is a rare autosomal dominant late-onset muscular dystrophy affecting approximately 1:100 000 ind

48 hy (FSHD) is one of the most common types of muscular dystrophy, affecting roughly one in 8000 indivi

49 myoblasts involved in the pathophysiology of muscular dystrophies and confirmed our results in vivo b

50 in components of the DGC are responsible for muscular dystrophies and congenital myopathies.

51 ghts into the molecular pathology underlying muscular dystrophies and how the LINC complex may regula

52 (DMD) is the most common and severe form of muscular dystrophy and affects boys in infancy or early

53 In models of muscular dystrophy and cancer cachexia, combined inhibit

54 ted in a diverse range of diseases including muscular dystrophy and cancer metastasis.

55 Mutations in its gene have been linked to muscular dystrophy and cardiomyopathy.

56 was first discovered as a candidate gene for muscular dystrophy and cardiomyopathy.

57 n mouse models of acute muscle injury and in muscular dystrophy and determined that both regimens pro

58 with the clinical severity of milder Becker muscular dystrophy and DMD patients.

59 t in muscle lesions associated with Duchenne muscular dystrophy and dystrophin-deficient mdx mice tha

60 It is considered a late-onset form of muscular dystrophy and leads to asymmetric muscle weakne

61 s a therapeutic agent for patients with CMT, muscular dystrophy and other disorders with focal or asy

62 open up new therapeutic avenues for Duchenne muscular dystrophy and possibly other neuromuscular dise

63 This success, for Duchenne muscular dystrophy and spinal muscular atrophy, offers h

64 echnology to treat mouse models of diabetes, muscular dystrophy, and acute kidney disease.

65 nital muscular dystrophy, Ullrich congenital muscular dystrophy, and alpha-dystroglycanopathy).

66 ular disorders including Huntington disease, muscular dystrophy, and amyotrophic lateral sclerosis.

67 cated in the pathology of diseases including muscular dystrophy, and neurodegenerative diseases, such

68 (POMT2) are known to cause severe congenital muscular dystrophy, and recently, mutations in POMT2 hav

69 Muscular dystrophies are a heterogeneous group of geneti

70 Muscular dystrophies are characterized by weakness and w

71 Muscular dystrophies are debilitating disorders that res

72 The muscular dystrophies are genetically diverse.

73 Congenital muscular dystrophies are hereditary disorders characteri

74 linked to several of the Lmalpha2-deficient muscular dystrophies are predicted to compromise polymer

75 Muscular dystrophies are primary diseases of muscle due

76 tive effects of chronic steroid treatment in muscular dystrophy are paradoxical because these steroid

77 e chromosome 10 associated with body mass in muscular dystrophy as skeletal muscle contributes signif

78 Mutations in POMTs cause severe muscular dystrophies associated with pronounced neurolog

79 We describe a new muscular dystrophy associated with this gene.

80 sfunction before the onset of overt Duchenne muscular dystrophy-associated cardiomyopathy (DMDAC) may

81 male patients aged 2-28 years with Duchenne muscular dystrophy at 20 centres in nine countries.

82 Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), interventions reducing the pro

83 ne muscular dystrophy (DMD) or milder Becker muscular dystrophy (BMD).

84 ystroglycan complex (DGC) result in not only muscular dystrophy but also cognitive impairments.

85 loss of ambulation in patients with Duchenne muscular dystrophy but are accompanied by prominent adve

86 is a strategy for the treatment of Duchenne muscular dystrophy, but has variable efficacy.

87 hnology could offer a one-time treatment for muscular dystrophies by correcting the culprit genomic m

88 potential for, and challenges of, correcting muscular dystrophies by editing disease-causing mutation

89 sults, PDGF-BB may play a protective role in muscular dystrophies by enhancing muscle regeneration th

90 ilencing and indicate that lamin A-dependent muscular dystrophy can be ascribed to intrinsic epigenet

91 ver, the impact of this approach on Duchenne muscular dystrophy cardiac function has yet to be evalua

92 ular dystrophy is a severe inherited form of muscular dystrophy caused by mutations in the reading fr

93 o from iPSC, opening interesting avenues for muscular dystrophy cell therapy.

94 alpha-Dystroglycanopathies are a group of muscular dystrophies characterized by alpha-DG hypoglyco

95 n conditions such as cerebral palsy, stroke, muscular dystrophy, Charcot-Marie-Tooth disease, and sar

96 and POMT2, underlie a subgroup of congenital muscular dystrophies designated alpha-dystroglycanopathi

97 s are responsible for Cystinosis and Duchene Muscular Dystrophy diseases, respectively.

98 Like other single-gene disorders, muscular dystrophy displays a range of phenotypic hetero

99 of mice representing Duchenne and congenital muscular dystrophies (DMD and CMD, respectively) and dys

100 Duchenne muscular dystrophy (DMD) affects 1 in 3500 live male bir

101 In Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (

102 muscle ultrasound data in boys with Duchenne muscular dystrophy (DMD) and healthy controls to determi

103 y has been evaluated in humans with Duchenne Muscular Dystrophy (DMD) and in mouse models including t

104 ement of upper extremity muscles in Duchenne muscular dystrophy (DMD) and showed the feasibility of M

105 Duchenne muscular dystrophy (DMD) causes severe disability and de

106 onsidered to be outcome measures in Duchenne muscular dystrophy (DMD) clinical trials.

107 Patients affected by Duchenne muscular dystrophy (DMD) develop a progressive dilated c

108 The essential product of the Duchenne muscular dystrophy (DMD) gene is dystrophin(1), a rod-li

109 novel therapeutics for treatment of Duchenne muscular dystrophy (DMD) has led to clinical trials that

110 Duchenne muscular dystrophy (DMD) is a debilitating X-linked diso

111 Duchenne muscular dystrophy (DMD) is a devastating neuromuscular

112 Duchenne muscular dystrophy (DMD) is a devastating X-linked disea

113 Duchenne muscular dystrophy (DMD) is a fatal genetic disorder cau

114 Duchenne muscular dystrophy (DMD) is a fatal muscle disorder char

115 Duchenne muscular dystrophy (DMD) is a fatal muscle-wasting disea

116 Duchenne muscular dystrophy (DMD) is a fatal neuromuscular diseas

117 Duchenne muscular dystrophy (DMD) is a fatal X-linked disorder ca

118 Duchenne muscular dystrophy (DMD) is a genetic disorder caused by

119 Duchenne Muscular Dystrophy (DMD) is a lethal muscle disorder, ca

120 Duchenne muscular dystrophy (DMD) is a lethal neuromuscular disor

121 Duchenne muscular dystrophy (DMD) is a lethal, muscle degenerativ

122 Duchenne muscular dystrophy (DMD) is a lethal, X-linked disease c

123 Duchenne muscular dystrophy (DMD) is a monogenic disorder and a c

124 Duchenne muscular dystrophy (DMD) is a muscular dystrophy with hi

125 Duchenne muscular dystrophy (DMD) is a neuromuscular disease that

126 Duchenne muscular dystrophy (DMD) is a progressive muscle disease

127 Duchenne muscular dystrophy (DMD) is a rare genetic disease affec

128 Duchenne Muscular Dystrophy (DMD) is a severe muscle disorder cau

129 Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscu

130 Duchenne muscular dystrophy (DMD) is a severe, progressive, and r

131 Duchenne muscular dystrophy (DMD) is a uniformly fatal condition

132 The cardiomyopathy of Duchenne muscular dystrophy (DMD) is an important cause of morbid

133 Duchenne muscular dystrophy (DMD) is an incurable X-linked muscle

134 Duchenne muscular dystrophy (DMD) is an X-linked disorder with dy

135 Duchenne muscular dystrophy (DMD) is an X-linked genetic disease

136 Duchenne muscular dystrophy (DMD) is an X-linked, lethal muscle d

137 Duchenne muscular dystrophy (DMD) is caused by loss of dystrophin

138 Duchenne muscular dystrophy (DMD) is caused by loss of dystrophin

139 Duchenne muscular dystrophy (DMD) is caused by mutations in the D

140 Duchenne muscular dystrophy (DMD) is characterized by a progressi

141 Duchenne muscular dystrophy (DMD) is characterized by muscle dege

142 Duchenne muscular dystrophy (DMD) is characterized by progressive

143 Duchenne muscular dystrophy (DMD) is the most common and severe f

144 Patients with Duchenne muscular dystrophy (DMD) lack the protein dystrophin, wh

145 w preclinical efficacy for heart in Duchenne muscular dystrophy (DMD) models but also improve skeleta

146 whether they presented with severe Duchenne muscular dystrophy (DMD) or milder Becker muscular dystr

147 bnormally elevated in the muscle of Duchenne muscular dystrophy (DMD) patients and animal models.

148 corticosteroids is recommended for Duchenne muscular dystrophy (DMD) patients to slow the progressio

149 a standard palliative treatment for Duchenne muscular dystrophy (DMD) patients, but various adverse e

150 from most independent FSHD, DM2 or Duchenne muscular dystrophy (DMD) studies compared to control bio

151 urrently no effective treatment for Duchenne muscular dystrophy (DMD), a lethal monogenic disorder ca

152 promising therapeutic strategy for Duchenne muscular dystrophy (DMD), employing morpholino antisense

153 rged as a leading cause of death in Duchenne muscular dystrophy (DMD), limited studies and therapies

154 In the mdx mouse, a model of Duchenne muscular dystrophy (DMD), microtubules are mostly disord

155 promising therapeutic strategy for Duchenne muscular dystrophy (DMD), which should be applicable to

156 clinical study for the treatment of Duchenne muscular dystrophy (DMD).

157 reclinical models and subjects with Duchenne muscular dystrophy (DMD).

158 r contributors to muscle wasting in Duchenne muscular dystrophy (DMD).

159 y are needed for clinical trials in Duchenne muscular dystrophy (DMD).

160 ors hold great promise for treating Duchenne muscular dystrophy (DMD).

161 s contributes to the progression of Duchenne muscular dystrophy (DMD).

162 promising therapeutic approach for Duchenne muscular dystrophy (DMD).

163 c disease in the mdx mouse model of Duchenne muscular dystrophy (DMD); however, a mechanistic underst

164 ibroblasts of a patient affected by Duchenne Muscular Dystrophy (DMD, complete loss of dystrophin exp

165 of mdx mice (i.e., a mouse model of Duchenne Muscular Dystrophy [DMD]) could restore the morphology o

166 Muscular dystrophy-dystroglycanopathies comprise a heter

167 expression of genes linked to Emery-Dreifuss muscular dystrophy (EDMD) and centronuclear myopathy (CN

168 ients with autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD) as well as dilated cardiomyopa

169 Using a murine model of Emery-Dreifuss muscular dystrophy (EDMD), we show here that lamin A los

170 cross neurodevelopmental, neurodegenerative, muscular dystrophy, epilepsy, chronic pain and neoplasti

171 ival, and in the mdx mouse model of Duchenne muscular dystrophy, exosomes secreted by the engineered

172 dipogenic progenitors in facioscapulohumeral muscular dystrophy.Facioscapulohumeral muscular dystroph

173 sustained in the mdx mouse model of Duchenne muscular dystrophy for 1 year after a single intravenous

174 teins and its dysfunction leads to a form of muscular dystrophy frequently associated with neurodevel

175 Facioscapulohumeral muscular dystrophy (FSHD) is a common, dominantly inheri

176 Facioscapulohumeral muscular dystrophy (FSHD) is a myopathy with prevalence

177 Facioscapulohumeral muscular dystrophy (FSHD) is a prevalent, incurable myop

178 Facioscapulohumeral muscular dystrophy (FSHD) is a prevalent, incurable myop

179 Facioscapulohumeral muscular dystrophy (FSHD) is a prevalent, incurable skel

180 Facioscapulohumeral muscular dystrophy (FSHD) is a prevalent, inherited skel

181 Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant neuro

182 Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal-dominant myopa

183 Facioscapulohumeral muscular dystrophy (FSHD) is an incurable disorder linke

184 Facioscapulohumeral muscular dystrophy (FSHD) is caused by loss of repressio

185 Facioscapulohumeral muscular dystrophy (FSHD) is caused by the expression of

186 Facioscapulohumeral muscular dystrophy (FSHD) is characterized by sporadic d

187 Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common type

188 cles plays a key role in facioscapulohumeral muscular dystrophy (FSHD) pathogenesis, although the mol

189 Facioscapulohumeral muscular dystrophy (FSHD) results from expression of the

190 ave been associated with facioscapulohumeral muscular dystrophy (FSHD) type 2.

191 of diseases including facio-scapulo-humeral muscular dystrophy (FSHD), acute lymphoblastic leukemia,

192 is applied here to study facioscapulohumeral muscular dystrophy (FSHD), simultaneously recording the

193 n skeletal muscle causes facioscapulohumeral muscular dystrophy (FSHD).

194 ver, is toxic and causes facioscapulohumeral muscular dystrophy (FSHD).

195 disease progression in the golden retriever muscular dystrophy (GRMD) dog model of DMD.

196 ed on a total of 12 treated golden retriever muscular dystrophy (GRMD) dogs.

197 The degree to which exercise alters muscular dystrophy has been evaluated in humans with Duc

198 Cell-based therapies in muscular dystrophies have been pursued experimentally fo

199 ntribution of NFIX to muscle development and muscular dystrophies, hematopoiesis, cancer, and neural

200 a point mutation in Dmd)-a model of Duchenne muscular dystrophy-Hippo deficiency protected against ov

201 ecommended as a standard of care in Duchenne muscular dystrophy; however, few studies have assessed t

202 herapeutic with the potential to treat other muscular dystrophies in which there is defective muscle

203 cy does not provide sustained improvement of muscular dystrophy in mdx(5cv) mice.

204 GALGT2 overexpression in muscle can inhibit muscular dystrophy in mouse models of the disease by ind

205 us histological and physiological aspects of muscular dystrophy in small and large animal models.

206 Shared pathological features among muscular dystrophies include breakdown, or loss of muscl

207 of steroid administration in other types of muscular dystrophies, including limb-girdle muscular dys

208 DGC deficiency in humans results in muscular dystrophy, including the lethal Duchenne muscul

209 Duchenne muscular dystrophy is a deadly muscle-wasting disorder c

210 Duchenne muscular dystrophy is a genetic disorder that shows chro

211 RATIONALE: Duchenne muscular dystrophy is a severe inherited form of muscula

212 meral muscular dystrophy.Facioscapulohumeral muscular dystrophy is a severe myopathy that is caused b

213 Facioscapulohumeral muscular dystrophy is a slowly progressive but devastati

214 Additionally, muscular dystrophy is linked to mutations in genes that

215 proaches to restore dystrophin expression in muscular dystrophy is obtaining a sufficient quantity of

216 modifiers capable of altering the course of muscular dystrophy is one approach to deciphering gene-g

217 ystrophy type 1 (DM1), the most common adult muscular dystrophy, is an autosomal dominant disorder ca

218 hies type 2I (LGMD2I), a recessive autosomal muscular dystrophy, is caused by mutations in the Fukuti

219 In muscular dystrophies, it has been hypothesized that fibr

220 Laminin-alpha2 related congenital muscular dystrophy (LAMA2-CMD) is a fatal muscle disease

221 ave also been linked to a milder limb-girdle muscular dystrophy (LGMD) phenotype, named LGMD type 2N

222 LGMD2L is a subtype of limb-girdle muscular dystrophy (LGMD), caused by recessive mutations

223 h sarcoglycanopathies, which are limb-girdle muscular dystrophies (LGMD2C-2F) caused by mutations in

224 subtypes of autosomal recessive limb-girdle muscular dystrophies (LGMDR3, LGMDR4, LGMDR5 and LGMDR6)

225 muscular dystrophies, including limb-girdle muscular dystrophies (LGMDs).

226 rophin-deficient mdx mouse model of Duchenne muscular dystrophy, limb muscles are especially fragile.

227 enerative response is often provoked in many muscular dystrophies, little is known about whether a re

228 Muscular dystrophy (MD) is a group of genetic disorders

229 Muscular dystrophy (MD) is a group of progressive geneti

230 ardiomyopathy is a common complication among muscular dystrophy (MD) patients and often results in ad

231 Muscular dystrophies (MDs) are often characterized by im

232 Dystrophin proteomic regulation in muscular dystrophies (MDs) remains unclear.

233 esent an attractive cell source for treating muscular dystrophies (MDs) since they easily allow for t

234 iated with mitochondrial damage in different muscular dystrophies (MDs; Duchenne muscular dystrophy,

235 rom blood serum of a mouse model of Duchenne muscular dystrophy (mdx) and control mice.

236 uscle strength in mouse models of Duchenne's muscular dystrophy (mdx) and denervation-induce atrophy,

237 ifferent muscular dystrophies (MDs; Duchenne muscular dystrophy, megaconial congenital muscular dystr

238 uilds muscle and bone was tested in X-linked muscular dystrophy mice (mdx).

239 the haploinsufficiency of Dock3 in Duchenne muscular dystrophy mice improved dystrophic muscle patho

240 gitudinal studies in a large-animal Duchenne muscular dystrophy model in pigs, and then applied this

241 animal as well as in the C. elegans Duchenne muscular dystrophy model.

242 ury and reduced myofiber size decline in the muscular dystrophy model.

243 is finding to develop an facioscapulohumeral muscular dystrophy mouse model with muscle-specific doxy

244 muscle atrophy and dysfunction in a Duchenne muscular dystrophy mouse model.

245 d in skeletal muscle of classical congenital muscular dystrophy mouse models.

246 letal muscle regenerates, but with age or in muscular dystrophies, muscle is replaced by fat.

247 In muscular dystrophies, muscle membrane fragility results

248 Oculopharyngeal muscular dystrophy (OPMD) is a genetic disorder caused b

249 Oculopharyngeal muscular dystrophy (OPMD) is a late onset disease caused

250 Oculopharyngeal muscular dystrophy (OPMD) is a late-onset, primarily aut

251 Oculopharyngeal muscular dystrophy (OPMD) is a rare autosomal dominant l

252 Oculopharyngeal muscular dystrophy (OPMD) is a rare late onset genetic d

253 Oculopharyngeal muscular dystrophy (OPMD) is an autosomal dominant, late

254 of muscular dystrophy termed oculopharyngeal muscular dystrophy (OPMD).

255 at this mechanism is disrupted in congenital muscular dystrophy patient myotubes carrying a nonsense

256 an effective treatment for a select group of muscular dystrophy patients with end-stage heart failure

257 athy is a leading cause of death in Duchenne muscular dystrophy patients, and currently no effective

258 te that the restoration of TIPE2 ameliorates muscular dystrophy phenotype through a reduction in infl

259 mimicked Galgt2-dependent neuromuscular and muscular dystrophy phenotypes.

260 nerating myofibers of patients with Duchenne muscular dystrophy, polymyositis, and compartment syndro

261 Parent Project Muscular Dystrophy (PPMD) convened a workshop in Bethesd

262 Limb-girdle muscular dystrophy R1 (LGMD R1) is caused by mutations i

263 tion of recombinant annexin A6 in a model of muscular dystrophy reduced serum creatinine kinase, a bi

264 Muscular dystrophies result from a defect in the linkage

265 Dysferlinopathies are a group of muscular dystrophies resulting from a genetic deficiency

266 A limited number of DM2 and Duchenne muscular dystrophy samples were also sequenced.

267 date the etiology of neurological defects in muscular dystrophies.SIGNIFICANCE STATEMENT Protein O-ma

268 show that the endogenous facioscapulohumeral muscular dystrophy-specific DUX4 polyadenylation signal

269 utic purposes; and we will review its use in muscular dystrophy studies where considerable progress h

270 ds affects muscle remodeling in non-Duchenne muscular dystrophies, suggesting a positive outcome asso

271 that mutations in INPP5K cause a congenital muscular dystrophy syndrome with short stature, cataract

272 NA binding protein causes a specific form of muscular dystrophy termed oculopharyngeal muscular dystr

273 tein dystroglycan cause a form of congenital muscular dystrophy that is frequently associated with ne

274 These data link congenital muscular dystrophies to defective phosphoinositide 5-pho

275 the same pathway vary greatly, ranging from muscular dystrophy to spastic paraplegia to a childhood

276 Limb Girdle Muscular Dystrophies type 2I (LGMD2I), a recessive autos

277 Merosin-deficient congenital muscular dystrophy type 1A (MDC1A) is a dramatic neuromu

278 se-modifying gene associated with congenital muscular dystrophy type 1A (MDC1A) using the CRISPR acti

279 SMCHD1 mutations cause facioscapulohumeral muscular dystrophy type 2 (FSHD2) via a trans-acting los

280 ved cell lines for two diseases: limb-girdle muscular dystrophy type 2G (LGMD2G)(1) and Hermansky-Pud

281 parate diseases, one of which is Limb-girdle muscular dystrophy type 2H (LGMD2H).

282 late-onset muscle disease termed limb-girdle muscular dystrophy type D1 (LGMDD1), which is characteri

283 Congenital muscular dystrophy type MDC1A is caused by mutations in

284 ne muscular dystrophy, megaconial congenital muscular dystrophy, Ullrich congenital muscular dystroph

285 the potential beneficial effect of TIPE2 in muscular dystrophy, we performed intramuscular injection

286 r chronic muscle conditions such as Duchenne muscular dystrophy, where their use is associated with p

287 own for its role in a spectrum of congenital muscular dystrophies, which are often accompanied by res

288 For example, Duchenne muscular dystrophy, which is caused by mutations in the

289 (DM1) is the most common form of adult-onset muscular dystrophy, which is characterised by progressiv

290 l malformation and reproductive disorders to muscular dystrophy, which we speculate to be consistent

291 case control study of patients with Duchenne muscular dystrophy who underwent serial cardiac magnetic

292 al trial of patients with Duchenne or Becker muscular dystrophy whose LVEF was preserved and MF was p

293 s the most common autosomal dominant form of muscular dystrophy with a prevalence of ~1 in 8000 indiv

294 ng with variable clinical features including muscular dystrophy with a reduction in dystroglycan glyc

295 Patients with Duchenne muscular dystrophy with an LV ejection fraction >=55% on

296 Duchenne muscular dystrophy (DMD) is a muscular dystrophy with high incidence of learning and b

297 Congenital muscular dystrophy with megaconial myopathy (MDCMC) is a

298 arcot-Marie-Tooth disease (CMT) and Duchenne muscular dystrophy, with no evidence of systemic muscle

299 positive fibers in a mouse model of Duchenne muscular dystrophy without apparent toxicity.

300 The muscular dystrophy X-linked mouse (mdx) is the most comm