ライフサイエンスコーパス: muscular

1 Results Median muscular (23)Na concentration was higher in patients wit

2 e day, through safe and sustainable types of muscular activity, will be the optimal way to create a h

3 ther body weight affects the augmentation of muscular and functional performance in response to PS in

4 inflammation, energy storage and metabolism, muscular and nervous systems, and scale/hair development

5 Mutations in mtDNA lead to muscular and neurological diseases and are linked to agi

6 the ventilator, the total pressure including muscular and ventilator pressure was calculated.

7 ogy involving the pulmonary, cardiovascular, muscular, and cellular oxidative systems.

8 morphology of the corpus bursa and the heavy muscular area of the ductus ejaculatorius simplex before

9 95% CI, 0.08-0.10; P = .049) and progressive muscular atrophy (HR, 0.17; 95% CI, 0.22-1.36; P = .10).

10 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease chara

11 s in the lethal motor neuron diseases spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis

12 SC3 cause pontocerebellar hypoplasia, spinal muscular atrophy (SMA) and central nervous system demyel

13 ative conditions of childhood such as spinal muscular atrophy (SMA) and neuronal ceroid lipofuscinosi

14 Spinal muscular atrophy (SMA) is a common and often fatal neuro

15 Spinal muscular atrophy (SMA) is a devastating neuromuscular di

16 Spinal muscular atrophy (SMA) is a hereditary neurodegenerative

17 Spinal muscular atrophy (SMA) is a major inherited cause of inf

18 Spinal muscular atrophy (SMA) is a motoneuron disease caused by

19 Spinal muscular atrophy (SMA) is a neurodegenerative disease ch

20 Spinal muscular atrophy (SMA) is a neuromuscular disease caused

21 Spinal Muscular Atrophy (SMA) is a neuromuscular disorder cause

22 Spinal muscular atrophy (SMA) is a progressive motor neuron dis

23 Spinal muscular atrophy (SMA) is a progressive neurodegenerativ

24 Spinal muscular atrophy (SMA) is an autosomal-recessive disorde

25 Spinal muscular atrophy (SMA) is caused by deficiency of SMN pr

26 Spinal muscular atrophy (SMA) is caused by deletions or mutatio

27 Spinal muscular atrophy (SMA) is caused by deletions or mutatio

28 Spinal muscular atrophy (SMA) is caused by depletion of the ubi

29 Spinal Muscular Atrophy (SMA) is caused by diminished Survival

30 Spinal muscular atrophy (SMA) is caused by homozygous mutations

31 Spinal muscular atrophy (SMA) is caused by low levels of surviv

32 The motoneuron disease spinal muscular atrophy (SMA) is caused by low levels of the su

33 Spinal muscular atrophy (SMA) is caused by mutation or deletion

34 pproach to SMA.SIGNIFICANCE STATEMENT Spinal muscular atrophy (SMA) is caused by the loss of motor ne

35 Spinal muscular atrophy (SMA) is caused by the low levels of su

36 Spinal muscular atrophy (SMA) is the leading genetic cause of i

37 Infantile-onset spinal muscular atrophy (SMA) is the most common genetic cause

38 myotonic dystrophy type 1 (CDM1) and spinal muscular atrophy (SMA) patients.

39 Spinal muscular atrophy (SMA), a leading genetic disease of chi

40 ere we show that, in a mouse model of spinal muscular atrophy (SMA), a reduction in proprioceptive sy

41 Spinal muscular atrophy (SMA), an autosomal recessive neuromusc

42 fish models of the motoneuron disease spinal muscular atrophy (SMA), motor axons fail to form the nor

43 Spinal muscular atrophy (SMA), the leading genetic cause of inf

44 The neuromuscular disorder spinal muscular atrophy (SMA), the most common inherited killer

45 Homozygous SMN1 loss causes spinal muscular atrophy (SMA), the most common lethal genetic c

46 es motor function in a mouse model of spinal muscular atrophy (SMA).

47 oving towards a potential therapy for spinal muscular atrophy (SMA).

48 Spinal muscular atrophy is an autosomal recessive neuromuscular

49 Spinal muscular atrophy is an untreatable potentially fatal her

50 Spinal muscular atrophy is the most common genetic killer of in

51 weeks and 7 months old with onset of spinal muscular atrophy symptoms between 3 weeks and 6 months,

52 Spinal muscular atrophy type 1 (SMA1) is a progressive, monogen

53 MT2D from the allelic disorder distal spinal muscular atrophy type V.

54 ions in cortical development (MCD) or spinal muscular atrophy with lower extremity predominance (SMAL

55 distal hereditary motor neuropathies, spinal muscular atrophy with parkinsonism and the later stages

56 ous familial hypercholesterolemia and spinal muscular atrophy) or as research tools to alter gene exp

57 ract associated with the disease spinobulbar muscular atrophy, also known as Kennedy disease.

58 disease, Duchenne muscular dystrophy, spinal muscular atrophy, amyotrophic lateral sclerosis, and myo

59 uch as amyotrophic lateral sclerosis, spinal muscular atrophy, and spinobulbar muscular atrophy.

60 d in patients with a dominant form of spinal muscular atrophy, but how these mutations cause disease

61 o adult care; (3) muscular dystrophy, spinal muscular atrophy, cystic fibrosis, haemophilia and sickl

62 tary causes are recognised, including spinal muscular atrophy, distal hereditary motor neuropathy and

63 Among infants with spinal muscular atrophy, those who received nusinersen were mor

64 treat Duchenne muscular dystrophy and spinal muscular atrophy, which are currently being tested in cl

65 bule motility in neurons may underlie spinal muscular atrophy.

66 is, spinal muscular atrophy, and spinobulbar muscular atrophy.

67 y trial of nusinersen in infants with spinal muscular atrophy.

68 in that is deficient in patients with spinal muscular atrophy.

69 may be one strategy in treating human spinal muscular atrophy.

70 Hypotheses for the muscular basis of this performance differential have inc

71 e also measured in one lamb undergoing Neuro-Muscular Blockade (NMB) and another undergoing lumbar sp

72 , or peroneal) in 243 patients (63.2%) and a muscular branch (soleus or gastrocnemius) in 215 (56.0%)

73 Features of SR EBW indicate that muscular connections between endo- and epicardium underl

74 s of each limb and used to compare vestibulo-muscular coupling between velocity-matched and unmatched

75 mary end point was endothelial integrity and muscular damage of the harvested vein.

76 uring dynamic muscle activity and to prevent muscular damage.

77 mitigate the oxidative damage caused by the muscular demands of flight.

78 ong the most common nondystrophic congenital muscular disorders, and are caused by mutations in genes

79 , cancer, organismal injury and skeletal and muscular disorders, as well as networks of upstream RNA

80 ee independent RNAi lines expressed by a pan-muscular driver elicited characteristic symptoms of VM,

81 y, ectodermal dysplasia with anhidrosis, and muscular dysplasia.

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

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

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

85 Muscular dystrophies (MDs) are often characterized by im

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

87 Muscular dystrophies are characterized by weakness and w

88 The muscular dystrophies are genetically diverse.

89 Congenital muscular dystrophies are hereditary disorders characteri

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

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

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

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

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

95 Congenital muscular dystrophies display a wide phenotypic and genet

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

97 Muscular dystrophies result from a defect in the linkage

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

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

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

101 n responsible for the majority of congenital muscular dystrophies when dysfunctional, has a function

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

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

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

105 alpha-dystroglycan gives rise to congenital muscular dystrophies.

106 Fibrosis is the main complication of muscular dystrophies.

107 omechanisms of neurological abnormalities in muscular dystrophies.

108 nsferase 1 (POMT1) and POMT2 underlie severe muscular dystrophies.

109 TMTC3 COB phenotype from typical congenital muscular dystrophies.

110 ex, is at the center of molecular studies of muscular dystrophies.

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

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

113 Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), X-linked dilated cardiomyopath

114 Dystrophinopathies include Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (

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

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

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

118 Duchenne muscular dystrophy (DMD) impacts 1 : 3500 boys and leads

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

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

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

122 Duchenne muscular dystrophy (DMD) is a severe and progressive mus

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

124 Duchenne muscular dystrophy (DMD) is a severe, degenerative muscl

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

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

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

128 Duchenne Muscular Dystrophy (DMD) is caused by a lack of dystroph

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

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

131 enhances exon-skipping activity in Duchenne muscular dystrophy (DMD) mdx mice.

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

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

134 ly tested the implication of ApN in Duchenne muscular dystrophy (DMD) using mdx mice, a model of DMD,

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

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

137 nt from the pathogenic mutation: in Duchenne muscular dystrophy (DMD), for instance, age at loss of a

138 gence of experimental therapies for Duchenne muscular dystrophy (DMD), it is fundamental to understan

139 In Duchenne muscular dystrophy (DMD), loss of dystrophin leads to th

140 treating genetic diseases, such as Duchenne muscular dystrophy (DMD), which is caused by mutations i

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

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

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

144 y and drive muscle deterioration in Duchenne muscular dystrophy (DMD).

145 Its absence leads to Duchenne muscular dystrophy (DMD).

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

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

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

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

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

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

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

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

154 Muscular dystrophy (MD) is associated with mutations in

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

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

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

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

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

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

161 in dysferlin are responsible for limb girdle muscular dystrophy 2B and Miyoshi myopathy.

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

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

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

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

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

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

168 tory role of COUP-TFII in the development of muscular dystrophy and open up a potential therapeutic o

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

170 velopment of SSOs designed to treat Duchenne muscular dystrophy and spinal muscular atrophy, which ar

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

172 a model that configures facioscapulohumeral muscular dystrophy as a "muscle-by-muscle" disease.

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

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

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

176 re linked to approximately 30% of congenital muscular dystrophy cases.

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

178 elated dystroglycanopathies, another form of muscular dystrophy characterized by weak interactions be

179 phic mesoangioblasts from a Golden Retriever muscular dystrophy dog were transfected with the large-s

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

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

182 Duchenne muscular dystrophy is a severe and progressive striated

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

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

185 Facioscapulohumeral muscular dystrophy is a slowly progressive but devastati

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

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

188 hesized that a reduction of Collagen VI in a muscular dystrophy model that presents with fibrosis wou

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

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

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

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

193 tic background, resulting in protection from muscular dystrophy pathogenesis that included reduced my

194 o the known contribution of myeloid cells to muscular dystrophy pathology.

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

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

197 integrin observed in mdx muscle and Duchenne muscular dystrophy patients.

198 ly, CD82 expression is decreased in Duchenne muscular dystrophy patients.

199 s progressive muscle pathology resembles the muscular dystrophy phenotype in humans and mice lacking

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

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

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

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

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

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

206 Congenital muscular dystrophy type MDC1A is caused by mutations in

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

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

209 or mouse Thbs4 rescues a Drosophila model of muscular dystrophy with augmented membrane residence of

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

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

212 niversal small molecule therapy for Duchenne muscular dystrophy would be an enormous advance for this

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

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

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

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

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

218 n and severe form among children is Duchenne muscular dystrophy, caused by mutations in the dystrophi

219 In preclinical models for Duchenne muscular dystrophy, dystrophin restoration during adeno-

220 In individuals exhibiting congenital muscular dystrophy, early-onset cataracts, and mild inte

221 INTERPRETATION: In patients with Duchenne muscular dystrophy, glucocorticoid treatment is associat

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

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

224 ment of fibrosis and chronic inflammation in muscular dystrophy, less is known about how they are mec

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

226 CRISPR-Cas9, neuromuscular disease, Duchenne muscular dystrophy, spinal muscular atrophy, amyotrophic

227 onal programs, transition to adult care; (3) muscular dystrophy, spinal muscular atrophy, cystic fibr

228 s to treat genetic diseases such as Duchenne muscular dystrophy, we propose that exon skipping of Fce

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

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

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

232 and accelerates disease in 2 mouse models of muscular dystrophy, while overexpression of mouse Thbs4

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

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

235 ed dystrophin restoration in mouse models of muscular dystrophy.

236 ass in models of osteogenesis imperfecta and muscular dystrophy.

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

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

239 lar dystrophy, including the lethal Duchenne muscular dystrophy.

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

241 agonist SR8278 could slow the progression of muscular dystrophy.

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

243 Thbs4 as a potential therapeutic target for muscular dystrophy.

244 ystrophic symptoms in this model of Duchenne muscular dystrophy.

245 d and likely contributes to the pathology of muscular dystrophy.

246 ic muscles in mdx mice, a model for Duchenne muscular dystrophy.

247 terstitial cells (PICs), play a dual role in muscular dystrophy.

248 reframing, similar to observations in Becker muscular dystrophy.

249 ogy, and a functional deficit reminiscent of muscular dystrophy.

250 e BM structure, and substantially ameliorate muscular dystrophy.

251 and underlies a recessive form of inherited muscular dystrophy.

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

253 espan and survival in patients with Duchenne muscular dystrophy.

254 dipogenic progenitors in facioscapulohumeral muscular dystrophy.Facioscapulohumeral muscular dystroph

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

256 nsects into two groups, depending on whether muscular energy is spent on moving fluid through the pro

257 ship between telomere length and aerobic and muscular fitness is not well characterized.

258 llowing a standardized submaximal step test; muscular fitness was assessed by means of a maximal isom

259 Hand grip strength is a widely used proxy of muscular fitness, a marker of frailty, and predictor of

260 ecifically improved long-term abdominal wall muscular function and quality of life.

261 tin cytoskeleton, implicating maintenance of muscular function.

262 Starting at a median age of 6 months, muscular hypotonia (91%) was seen, followed by progressi

263 th retardation, intellectual disability, and muscular hypotonia revealed biallelic mutations in IARS.

264 After muscular injection, all of the haploid viruses induced h

265 d between the muscularis mucosa and circular muscular layer of the human gut.

266 l scar was observed at the outer part of the muscular layer, whereas the mucosa and submucosa were no

267 mentation of the abdominal wall with a retro-muscular lightweight polypropylene mesh was compared wit

268 that this enables sex-specific regulation of muscular lipid metabolism and body weight by repressing

269 Inspired by cephalopod muscular morphology, we developed synthetic tissue group

270 Median muscular normalized (35)Cl signal intensity was higher i

271 l tool for the non-invasive investigation of muscular oxidative metabolism.

272 nd what mechanisms underlie neurological and muscular pathologies that toxoplasmosis patients present

273 an extension of the four-layer ventrolateral muscular patterning of the thorax and abdomen.

274 data suggests that chimpanzee mass-specific muscular performance is a more modest 1.5 times greater

275 Thus, the superior mass-specific muscular performance of chimpanzees does not stem from d

276 NAFLD); however, if this is due to increased muscular protein catabolism, obesity, and/or increased i

277 he human heart is continually operating as a muscular pump, contracting, on average, 80 times per min

278 ved systems for driving internal flows using muscular pumps or cilia.

279 Likewise, muscular secreted frizzled-related protein 2 expression

280 Muscular secreted frizzled-related protein 2 expression

281 Muscular secreted frizzled-related protein 2 is down-reg

282 fishes, the pelvic bones are suspended in a muscular sling or loosely attached to the pectoral girdl

283 Evidence shows an association between muscular strength (MS) and health among young people, ho

284 ) and health among young people, however low muscular strength cut points for the detection of high m

285 ings of grip strength and the causal role of muscular strength in age-related morbidities and mortali

286 s and policies should focus on improving the muscular strength of the population regardless of their

287 y, while simultaneously visualizing internal muscular structures at higher resolutions than confocal

288 ut the organization of ctenophore neural and muscular systems, and virtually nothing has been reporte

289 Defects within it, termed muscular ventricular septal defects (VSDs), are common,

290 The muscular ventricular septum separates the flow of oxygen

291 nd Sarcospan (Sspn) that affects the risk of muscular VSD in mice.

292 /Sspn(KO) mutants have a higher incidence of muscular VSD than Nkx2-5(+/-) mice.

293 ate into the septum even in the absence of a muscular VSD.

294 eotypical pattern that is disrupted around a muscular VSD.

295 hypothesized to be the mechanistic basis of muscular VSDs.

296 KX2-5 cause cardiac malformations, including muscular VSDs.

297 A detailed general description of muscular wave locomotion and its relationship with other

298 Muscular weakness in the first year after transplantatio

299 hic skeletal muscle disease characterized by muscular weakness of proximal dominance, hypotonia, and

300 cycle-related fluxes during an acute bout of muscular work.