ライフサイエンスコーパス: muscle weakness

1 and Visual Analog Scales (VASs; Fatigue and Muscle Weakness).

2 e-onset multisystem disease with progressive muscle weakness.

3 ng the earliest manifestation of respiratory muscle weakness.

4 mon treatment-related adverse event was mild muscle weakness.

5 mab who present with a cutaneous eruption or muscle weakness.

6 pe similar to human patients with late-onset muscle weakness.

7 r-bone microenvironment in cancer-associated muscle weakness.

8 ected subjects can also present with general muscle weakness.

9 diverse group of myopathies characterized by muscle weakness.

10 neuromuscular transmission, thereby causing muscle weakness.

11 sider in patients presenting with distal leg muscle weakness.

12 d- to adult-onset NM with slowly progressive muscle weakness.

13 ized by abnormally centralized myonuclei and muscle weakness.

14 skeletal muscle mass, which causes profound muscle weakness.

15 S) characterized by a limb-girdle pattern of muscle weakness.

16 They are characterized by fatigable muscle weakness.

17 insufficient receptor clustering suffer from muscle weakness.

18 dition characterized by progressive proximal muscle weakness.

19 ation of anterior horn cells and progressive muscle weakness.

20 ease muscle force and power in conditions of muscle weakness.

21 the prevalence of ICU-acquired delirium and muscle weakness.

22 thy (NM) patients with NEB mutations) causes muscle weakness.

23 romuscular junction and result in fatiguable muscle weakness.

24 ions, were identified in patients exhibiting muscle weakness.

25 r neuron (SMN) protein and results in severe muscle weakness.

26 ver pathways that regulate heart failure and muscle weakness.

27 eading in many patients to fatal respiratory muscle weakness.

28 ses with neonatal or childhood hypotonia and muscle weakness.

29 ther nonimmune mechanisms also contribute to muscle weakness.

30 required >/=3 abnormal CSMs, with or without muscle weakness.

31 f neuromuscular blocking agents and skeletal muscle weakness.

32 ein, is characterized by motoneuron loss and muscle weakness.

33 Seven patients also had axial muscle weakness.

34 predominant distal, proximal or respiratory muscle weakness.

35 They are characterized by fatigable muscle weakness.

36 Adult patients experience progressive muscle weakness.

37 f mice, prior to the development of skeletal muscle weakness.

38 cterized by exercise intolerance, ptosis and muscle weakness.

39 rders characterized by motor neuron loss and muscle weakness.

40 patients who are at high risk of developing muscle weakness.

41 in the intensive care unit commonly develop muscle weakness.

42 iled postnatal maturation of motor units and muscle weakness.

43 respiratory distress syndrome survivors had muscle weakness.

44 aracterized by limb, diaphragm and laryngeal muscle weakness.

45 ndplate dysfunction and consequent fatigable muscle weakness.

46 ion; this may contribute to contractures and muscle weakness.

47 le and manifested in the patient as skeletal muscle weakness.

48 mal, distal or both proximal and distal limb muscle weakness.

49 (ALS) are challenging to investigate due to muscle weakness.

50 utoantibody-induced complement attack causes muscle weakness.

51 ) compared to a trajectory of maintaining no muscle weakness.

52 At discharge, 38% of patients had muscle weakness.

53 d by high myofilament Ca(2+)-sensitivity and muscle weakness.

54 mptom in most dystrophinopathies is skeletal muscle weakness.

55 n was able to correct growth retardation and muscle weakness.

56 topic neuronal positioning in the cortex and muscle weakness.

57 ith diaphragm fibrosis, a major cause of DMD muscle weakness.

58 responsible for the disease-associated fatal muscle weakness.

59 esenting with recurrent metabolic crises and muscle weakness.

60 energy expenditure, slow walking speed, and muscle weakness.

61 enital myopathy characterized by generalized muscle weakness.

62 disorders mainly characterized by fatigable muscle weakness.

63 to test therapeutic approaches to ameliorate muscle weakness.

64 trophy (DMD) is characterised by progressive muscle weakness.

65 dominal obesity, low energy expenditure, and muscle weakness.

66 agitation (25%), behavioral disorders (25%), muscle weakness (23%), disorientation (21%), and neck ri

67 emonstrated a generalized slowly progressive muscle weakness accompanied by decreased vital capacitie

68 Moreover, the pace and pattern of muscle weakness, along with onset of cardiomyopathy, is

69 Entry criteria included muscle weakness and >/=2 additional abnormal values on c

70 DMD is characterized by progressive muscle weakness and a shortened life span, and there is

71 NM) are congenital disorders associated with muscle weakness and abnormally located nuclei in skeleta

72 muscular dystrophies present in infancy with muscle weakness and are often associated with mental ret

73 dinally evaluate the association of post-ICU muscle weakness and associated trajectories of weakness

74 molecular mechanisms of age-related skeletal muscle weakness and atrophy as well as new potential int

75 terozygous mutation in POLG, presenting with muscle weakness and atrophy at a young age aims to aid c

76 geneous group of disorders, characterized by muscle weakness and atrophy predominating at the distal

77 combining congenital myasthenia with distal muscle weakness and atrophy reminiscent of a distal myop

78 Axial (86%) and periscapular (81%) muscle weakness and atrophy were frequent findings.

79 ceptor/Ca(2+) release channel (RyR1) display muscle weakness and atrophy, but the underlying mechanis

80 inical characteristics of progressive distal muscle weakness and atrophy, foot deformities, distal se

81 ATF4 as a potential mediator of age-related muscle weakness and atrophy.

82 investigate the pathogenesis of age-related muscle weakness and atrophy.

83 e ATF4 as a critical mediator of age-related muscle weakness and atrophy.

84 ed neuropathies characterized by distal limb muscle weakness and atrophy.

85 set joint hypermobility, joint contractures, muscle weakness and bone dysplasia as well as high myopi

86 As a result, DMD causes progressive limb muscle weakness and cardiac and respiratory failure.

87 storage myopathy associated with progressive muscle weakness and cardiomyopathy.

88 follow-up the patient showed improvement of muscle weakness and carpopedal spasm with near-normal bi

89 nuous spectrum of disorders characterized by muscle weakness and connective tissue abnormalities rang

90 as intermediate phenotypes characterized by muscle weakness and connective tissue abnormalities.

91 h adverse outcomes and describes a status of muscle weakness and decreased physiological reserve lead

92 Muscle weakness and dizziness were more common in the co

93 OPMD but also is a major contributor to the muscle weakness and dysfunction in this disease.

94 phy is characterized by progressive skeletal muscle weakness and dystrophic muscle exhibits degenerat

95 ar dystrophy is characterized by progressive muscle weakness and early death resulting from dystrophi

96 tedly, these mice display androgen-dependent muscle weakness and early death, show changes in muscle

97 oss, impaired myofiber development, profound muscle weakness and early mortality.

98 dings of dermatomyositis along with proximal muscle weakness and elevated muscle enzymes.

99 Muscle weakness and fatigue are common symptoms in multi

100 disorders often characterized by progressive muscle weakness and fragility.

101 agm dysfunction is twice as frequent as limb muscle weakness and has a direct negative impact on wean

102 of myositis-prone mice with FHL1 aggravated muscle weakness and increased mortality, suggesting a di

103 clear myopathies (CNMs) are characterized by muscle weakness and increased numbers of central nuclei

104 wever, the effects of inactivity/activity on muscle weakness and increased susceptibility to muscle c

105 imed at achieving rapid, complete control of muscle weakness and inflammation improves outcomes and r

106 temic autoimmune diseases defined by chronic muscle weakness and inflammation of unknown etiology and

107 eliably predict intensive care unit-acquired muscle weakness and its clinical consequences.

108 rophy (SBMA) is characterized by adult-onset muscle weakness and lower motor neuron degeneration.

109 Muscle weakness and metabolic disturbances were detectab

110 s, apoptosis, and necrosis leading to severe muscle weakness and minimal postnatal growth.

111 ion was delayed beyond infancy with proximal muscle weakness and most patients recall poor performanc

112 These heterozygous mice developed muscle weakness and myofibrillar instability, with forma

113 Muscle weakness and myopathy are observed in vitamin D d

114 odels corrected cyclin D3 levels and reduced muscle weakness and myotonia in DM1 mice.

115 The mice exhibit progressive muscle weakness and pathological examination of muscle s

116 phenotype in young mice, with rapid onset of muscle weakness and pathology.

117 muscle alpha-actin) are generalized skeletal muscle weakness and premature death.

118 tion occurs in many diseases and can lead to muscle weakness and premature muscle fatigue.

119 The elderly often suffer from progressive muscle weakness and regenerative failure.

120 Hypophosphatemia can lead to muscle weakness and respiratory and heart failure, but t

121 ubularin protein replacement can improve the muscle weakness and reverse the pathology that character

122 s group of disorders characterized by distal muscle weakness and sensory loss.

123 hy" (SMA) was used to investigate the severe muscle weakness and spasticity that precede the death of

124 Altogether, our study suggests that muscle weakness and susceptibility to contraction-induce

125 tivity (ie, leg immobilization) worsened the muscle weakness and the susceptibility to contraction-in

126 tributing factor to the progressive skeletal muscle weakness and wasting characteristic of myotonic d

127 s study suggest that approaches to alleviate muscle weakness and wasting in DMD patients should not o

128 Progressive skeletal muscle weakness and wasting is one of the most prominent

129 childhood marked by progressive debilitating muscle weakness and wasting, and ultimately death in the

130 -predominant, is characterized by lower limb muscle weakness and wasting, associated with reduced num

131 muscle disease was indicated by muscle pain, muscle weakness and wasting, significant fat replacement

132 disorders that produce progressive skeletal muscle weakness and wasting.

133 dystrophies are characterized by progressive muscle weakness and wasting.

134 group of genetic disorders characterized by muscle weakness and wasting.

135 Patients presented with more than 2 years of muscle weakness and with dystrophic or myopathic changes

136 naptopathy characterized by ataxia, skeletal muscles weakness and numbness of the extremities in expo

137 63% had diaphragm dysfunction, 34% had limb muscle weakness, and 21% had both.

138 8.5% had weaning failure, 30.7% vs 23.8% had muscle weakness, and 90.9% vs 81.5% had hyperglycemia.

139 ing diseases including chronic inflammation, muscle weakness, and a severe combined immunodeficiency

140 e ERK1/2 displayed stunted postnatal growth, muscle weakness, and a shorter life span.

141 elevated in chronic disease, correlate with muscle weakness, and are a predictor of morbidity and mo

142 in childhood, had progressive limb and axial muscle weakness, and experienced development of cardiomy

143 thenia, including severe NMJs dismantlement, muscle weakness, and fatigability.

144 nt of secondary infections, weaning failure, muscle weakness, and hyperglycemia (blood glucose level

145 symptoms, including abdominal pain, fatigue, muscle weakness, and low plasma levels of selenium.

146 ally heterogeneous conditions causing severe muscle weakness, and mutations in the ryanodine receptor

147 kin tightness, paresthesias, neck stiffness, muscle weakness, and neck pain.

148 nts, including impaired body balance, severe muscle weakness, and reduced life span.

149 ng, respectively, to pulmonary hypertension, muscle weakness, and sodium retention.

150 d by congenital or early-onset hypotonia and muscle weakness, and specific pathological features on m

151 SMA could be corrected after development of muscle weakness, and the response of clinically relevant

152 acterized by an exaggerated loss of skeletal muscle, weakness, and exercise intolerance, although the

153 t; predicted effects include energy deficit, muscle weakness, anomalies in cranial and skeletal devel

154 , geriatric conditions such as slow gait and muscle weakness are becoming increasingly common.

155 Chorea, rigidity, dystonia, and muscle weakness are characteristic motor defects of the

156 Mechanisms underlying muscle weakness are poorly understood, but might involve

157 of rare diseases with fluctuating fatigable muscle weakness as the clinical hallmark.

158 Their clinical hallmark is fatigable muscle weakness associated with a decremental muscle res

159 Mutant mice exhibited a progressive muscle weakness associated with an increased number of m

160 I preserved SC function and counteracted the muscle weakness associated with Duchenne-like dystrophy

161 skeletal muscle characterized by attacks of muscle weakness associated with low serum K+.

162 60 vs 6 [5.3%] of 114, P < .001), and severe muscle weakness at 4 weeks (Medical Research Council sum

163 nosed at age 1 year, she had onset of distal muscle weakness at age 2 years progressing to atrophy an

164 third of survivors had objective evidence of muscle weakness at hospital discharge, with most improvi

165 ary optic neuropathy (LHOND), and neurogenic muscle weakness, ataxia, and retinitis pigmentosa (NARP)

166 structure in a family expressing neurogenic muscle weakness, ataxia, and retinitis pigmentosa (NARP)

167 motor neurons in the spinal cord, leading to muscle weakness, atrophy and, in the majority of cases,

168 ypes including kyphosis, motor dysfunctions, muscle weakness/atrophy, motor neuron loss, and astrocyt

169 atients lack dystrophin from birth; however, muscle weakness becomes apparent only at 3-5 years of ag

170 heterozygous KI/KO mice were viable, but had muscle weakness; biochemically, they had respiratory cha

171 osphatase increase (five [1%]), colitis, and muscle weakness (both four [1%]).

172 e disease characterized by body weight loss, muscle weakness, brain atrophy, and motor impairment, wh

173 mice exhibit late-onset, slowly progressive muscle weakness but do not have a shortened lifespan, co

174 th relevant axial, proximal, and respiratory muscle weakness but without vocal cord palsy.

175 al TGF-beta release from bone contributes to muscle weakness by decreasing Ca(2+)-induced muscle forc

176 ertension by phosphodiesterase 5 inhibitors, muscle weakness by exercise training, sodium retention b

177 troponin activator, CK-2066260, counteracts muscle weakness by increasing troponin Ca(2+) affinity,

178 EEF1A2-deficient zebrafish had skeletal muscle weakness, cardiac failure and small heads.

179 dystrophin and characterized by progressive muscle weakness, cardiomyopathy, respiratory failure and

180 a 30-year-old male who came with symptoms of muscle weakness, carpopedal spasms and limitation of mov

181 trophy (DMD) is characterized by progressive muscle weakness caused by DMD gene mutations leading to

182 In motor neurone disease (MND), respiratory muscle weakness causes substantial morbidity, and death

183 d body weight loss, skeletal muscle atrophy, muscle weakness, contractile abnormalities, the loss of

184 Muscle weakness contributes to prolonged rehabilitation

185 ng and mild adult onset SMA characterized by muscle weakness, decreased activity and an alteration of

186 eriatric conditions assessed were slow gait, muscle weakness (defined as weak grip), cognitive impair

187 and the dy(W-/-) mouse model exhibit severe muscle weakness, demyelinating neuropathy, failed muscle

188 isorder characterized by severe, often fatal muscle weakness due to loss of motor neurons.

189 Profound muscle weakness during and after critical illness is ter

190 sleepiness and cataplexy, sudden episodes of muscle weakness during waking that are thought to be an

191 n their twenties, and these were followed by muscle weakness, dysphagia, and spino-cerebellar signs w

192 r dystrophy were easily identified by severe muscle weakness either preventing ambulation or resultin

193 tor neuron loss with concomitant progressive muscle weakness ending in paralysis and death.

194 y, characterized by exercise intolerance and muscle weakness even in the absence of sideroblastic ane

195 Recovery from ICU-acquired muscle weakness extends beyond hospital stay.

196 anging from severe disorders with congenital muscle weakness, eye and brain structural abnormalities

197 He had generalized muscle weakness, facial discomfort, recurrent episodes o

198 ific, subjective symptoms including proximal muscle weakness, fatigue, and reduced physical functiona

199 y diet or FDA-approved drugs can reverse the muscle weakness, fatigue-like physiology and pathology.

200 Respiratory muscle weakness frequently develops during mechanical ve

201 MDC1A patients exhibit severe muscle weakness from birth, are confined to a wheelchair

202 herein that bumetanide protects against both muscle weakness from low K+ challenge in vitro and loss

203 urpurea, grade 2 nausea, grade 2 generalised muscle weakness, grade 2 infection, grade 1 fever, and g

204 ry dysfunction is a hallmark of the disease, muscle weakness has been viewed as the underlying cause,

205 The two types of muscle weakness have only limited overlap.

206 ne in 3500 newborn boys, causing progressive muscle weakness, heart and respiratory failure and prema

207 erioration resulting in progressive skeletal muscle weakness, heart failure, and respiratory distress

208 ysferlinopathy) characterized by adult onset muscle weakness, high serum creatine kinase levels and a

209 inically the most important feature of NM is muscle weakness; however, the mechanisms underlying this

210 ession (HR: 1.23; 95% CI: 1.05 to 1.45), and muscle weakness (HR: 1.19; 95% CI: 1.00 to 1.42).

211 persistent physical complications, including muscle weakness, impaired physical function, and decreas

212 characterized by slowly progressive skeletal muscle weakness in a humero-peroneal distribution, early

213 es not lead to muscle atrophy but does cause muscle weakness in adult mice and suggest loss of CuZnSO

214 Clinical findings included progressive muscle weakness in an initially scapuloperoneal and dist

215 membrane tubulation and may promote skeletal muscle weakness in CNM2 by disrupting machinery necessar

216 r they are linked, and their contribution to muscle weakness in disease, are not known.

217 1 fibers associated with muscle atrophy and muscle weakness in DM1.

218 entification of new potential treatments for muscle weakness in DMD and other muscle disorders.

219 ed neuromuscular transmission contributes to muscle weakness in dystrophic myd mice and that the note

220 uscular synaptopathy might contribute to the muscle weakness in GBS patients.

221 a neuromuscular synaptopathy contributing to muscle weakness in GBS patients.

222 on, and that this contributes to age-related muscle weakness in mammals, including humans.

223 lity of myofibrillar Z-discs, explaining the muscle weakness in mice and humans.

224 erlie their dysfunctional conduction akin to muscle weakness in multiple sclerosis.

225 nel and calstabin-1 depletion contributes to muscle weakness in muscular dystrophy, and that preventi

226 P deaminase 1 (AMPD1) may be responsible for muscle weakness in myositis.

227 Limited neural input results in muscle weakness in neuromuscular disease because of a re

228 ited for elucidating the functional basis of muscle weakness in NM and for the development of treatme

229 egulated thin filament length contributes to muscle weakness in NM patients with nebulin mutations.

230 ile apoptosis is a major pathway that causes muscle weakness in OPMD, other cell death pathways may a

231 up of cytokines is a potential biomarker for muscle weakness in OPMD.

232 poptosis by over-expressing BCL2 ameliorates muscle weakness in our mouse model of OPMD (A17 mice).

233 ction and provide a mechanism for the severe muscle weakness in patients with nebulin-based nemaline

234 It is generally believed that muscle weakness in patients with polymyositis and dermat

235 effect of dutasteride on the progression of muscle weakness in SBMA, although there were secondary i

236 ian nerve is compressed, leading to pain and muscle weakness in the fingers and hand.

237 (A)-binding protein nuclear 1 (PABPN1) cause muscle weakness in the late-onset disorder oculopharynge

238 ollapse (EIC) in this breed is manifested by muscle weakness, incoordination and life-threatening col

239 Similarly, skeletal muscle weakness, increased Nox4 binding to RyR1 and oxid

240 Acquired diaphragm muscle weakness is a key feature in several chronic cond

241 Although respiratory muscle weakness is a known predictor of poor prognosis,

242 Cancer-associated muscle weakness is a poorly understood phenomenon, and t

243 treatment for cardiomyopathy and respiratory muscle weakness is advocated because early treatment may

244 with other myasthenic syndromes, the general muscle weakness is also accompanied by use-dependent fat

245 ssion on muscle weakness is transient, since muscle weakness is apparent in mice expressing both A17

246 This distal muscle weakness is associated with reduced numbers of mo

247 Muscle weakness is common after acute lung injury, usual

248 et the mechanism defining the development of muscle weakness is currently unclear.

249 tic neuromuscular disease in which crippling muscle weakness is evident from birth.

250 and contractile dysfunction, and respiratory muscle weakness is thought to contribute significantly t

251 The effect of BCL2 co-expression on muscle weakness is transient, since muscle weakness is a

252 t with IVIG and related to clinical outcome: muscle weakness (measured by Medical Research Council su

253 Patients had a predominantly distal muscle weakness, most severely affecting ankle and wrist

254 s cognitive decline, seizures, parkinsonism, muscle weakness, neuropathy, spastic paraplegia, persona

255 Rates of myalgia, muscle weakness, neuropsychiatric conditions, cancer, an

256 are, therefore, unlikely to account for the muscle weakness observed in affected patients.

257 d muscle ultrastructure likely contribute to muscle weakness observed in our flies and patients.

258 ntrations, which may explain some aspects of muscle weakness observed in patients with hypophosphatem

259 Persisting and resolving trajectories of muscle weakness, occurring in 50% of patients during fol

260 embers developed in utero- or neonatal-onset muscle weakness of variable severity.

261 In addition, a typical pattern of muscle weakness on manual muscle testing could be confir

262 erized by the sudden uncontrollable onset of muscle weakness or paralysis during wakefulness.

263 eb cKO phenocopies important aspects of NEM (muscle weakness, oxidative fiber-type predominance, vari

264 their dysfunction and loss cause progressive muscle weakness, paralysis and eventually premature deat

265 ive loss of lower motor neurons resulting in muscle weakness, paralysis and often death.

266 s of motor neurons, resulting in progressive muscle weakness, paralysis, and death within 5 years of

267 o determine the longitudinal epidemiology of muscle weakness, physical function, and health-related q

268 systems with the major symptoms being severe muscle weakness, progressive muscle wasting and myotonia

269 at were associated with a spectrum of severe muscle weakness ranging from a lethal antenatal form of

270 exhibited MG-associated symptoms, including muscle weakness, reduced compound muscle action potentia

271 MCT mimics loss of body weight and diaphragm muscle weakness reported in PH patients.

272 Deciphering mechanisms of muscle weakness requires sophisticated force protocols,

273 In seven cases, severe muscle weakness resulted in death during the third trime

274 ne system damages their nerve cells, causing muscle weakness, sometimes paralysis, and infrequently d

275 related myopathy (SEPN1-RM) characterized by muscle weakness, spinal rigidity, and respiratory insuff

276 Ed 90-100 milliseconds: R = -0.44, P < .01), muscle weakness (TEd 90-100 milliseconds: R = -0.32, P <

277 Defects in NMJ transmission cause muscle weakness, termed myasthenia.

278 eepiness and cataplexy, episodes of profound muscle weakness that are often triggered by strong, posi

279 pinal muscular atrophy (SMA) causes profound muscle weakness that most often leads to early death.

280 c dysfunction (VIDD) refers to the diaphragm muscle weakness that occurs following prolonged controll

281 nd is responsible, at least in part, for the muscle weakness that occurs in the mouse model of myosit

282 ich patients experience fluctuating skeletal muscle weakness that often affects selected muscle group

283 ng condition associated with severe skeletal muscle weakness that persists in humans long after lung

284 Importance: Muscle weakness, the most common symptom of neuromuscula

285 (HyperKPP) produces myotonia and attacks of muscle weakness triggered by rest after exercise or by K

286 s a genetic disorder that causes progressive muscle weakness, ultimately leading to early mortality i

287 Muscle Weakness VAS scores were significantly lower in t

288 a history of cardiomyopathy and progressive muscle weakness was admitted with cardiogenic shock.

289 higher ICU and hospital mortality, and limb muscle weakness was associated with longer duration of M

290 Limb muscle weakness was defined as a Medical Research Counci

291 Muscle weakness was earlier onset and more severe in the

292 Because muscle weakness was evident prior to loss of Fhl1 protei

293 Muscle weakness was generally milder than observed in li

294 on dysfunction and loss, rapidly progressive muscle weakness, wasting and death.

295 lts, muscle atrophy, muscle dysfunction, and muscle weakness were most frequent (74-84%).

296 associated diabetes in mice, but also causes muscle weakness, which suggests that mammals have retain

297 enital myasthenic syndrome exhibit fatigable muscle weakness with a variety of accompanying phenotype

298 pinal muscular atrophy (SMA) presents severe muscle weakness with limited motor neuron (MN) loss at a

299 so characterised by various forms/degrees of muscle weakness with most cases being severe and resulti

300 clinical phenotype is associated with distal muscle weakness with quadriceps sparing.