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1 and Visual Analog Scales (VASs; Fatigue and Muscle Weakness).
2 C45B who exhibit childhood-onset progressive muscle weakness.
3 d by high myofilament Ca(2+)-sensitivity and muscle weakness.
4 mptom in most dystrophinopathies is skeletal muscle weakness.
5 topic neuronal positioning in the cortex and muscle weakness.
6 ith diaphragm fibrosis, a major cause of DMD muscle weakness.
7 responsible for the disease-associated fatal muscle weakness.
8 esenting with recurrent metabolic crises and muscle weakness.
9 nal Korean medicinal plant used to treat for muscle weakness.
10 energy expenditure, slow walking speed, and muscle weakness.
11 enital myopathy characterized by generalized muscle weakness.
12 disorders mainly characterized by fatigable muscle weakness.
13 to test therapeutic approaches to ameliorate muscle weakness.
14 trophy (DMD) is characterised by progressive muscle weakness.
15 dominal obesity, low energy expenditure, and muscle weakness.
16 els of serum creatine kinase but no or minor muscle weakness.
17 ng the earliest manifestation of respiratory muscle weakness.
18 mon treatment-related adverse event was mild muscle weakness.
19 mab who present with a cutaneous eruption or muscle weakness.
20 pe similar to human patients with late-onset muscle weakness.
21 r-bone microenvironment in cancer-associated muscle weakness.
22 ected subjects can also present with general muscle weakness.
23 diverse group of myopathies characterized by muscle weakness.
24 neuromuscular transmission, thereby causing muscle weakness.
25 sider in patients presenting with distal leg muscle weakness.
26 ized by abnormally centralized myonuclei and muscle weakness.
27 skeletal muscle mass, which causes profound muscle weakness.
28 S) characterized by a limb-girdle pattern of muscle weakness.
29 They are characterized by fatigable muscle weakness.
30 insufficient receptor clustering suffer from muscle weakness.
31 dition characterized by progressive proximal muscle weakness.
32 ation of anterior horn cells and progressive muscle weakness.
33 the prevalence of ICU-acquired delirium and muscle weakness.
34 thy (NM) patients with NEB mutations) causes muscle weakness.
35 mpound-Het mice are growth-retarded and have muscle weakness.
36 romuscular junction and result in fatiguable muscle weakness.
37 ions, were identified in patients exhibiting muscle weakness.
38 r neuron (SMN) protein and results in severe muscle weakness.
39 ver pathways that regulate heart failure and muscle weakness.
40 eading in many patients to fatal respiratory muscle weakness.
41 ther nonimmune mechanisms also contribute to muscle weakness.
42 required >/=3 abnormal CSMs, with or without muscle weakness.
43 f neuromuscular blocking agents and skeletal muscle weakness.
44 ein, is characterized by motoneuron loss and muscle weakness.
45 Seven patients also had axial muscle weakness.
46 predominant distal, proximal or respiratory muscle weakness.
47 Adult patients experience progressive muscle weakness.
48 f mice, prior to the development of skeletal muscle weakness.
49 lar transmission characterized by fatiguable muscle weakness.
50 ophy alone, underlies chronic sepsis-induced muscle weakness.
51 e-onset multisystem disease with progressive muscle weakness.
52 n was able to correct growth retardation and muscle weakness.
53 d- to adult-onset NM with slowly progressive muscle weakness.
54 ease muscle force and power in conditions of muscle weakness.
55 ses with neonatal or childhood hypotonia and muscle weakness.
56 respiratory distress syndrome survivors had muscle weakness.
57 ion; this may contribute to contractures and muscle weakness.
58 ) compared to a trajectory of maintaining no muscle weakness.
59 At discharge, 38% of patients had muscle weakness.
60 agitation (25%), behavioral disorders (25%), muscle weakness (23%), disorientation (21%), and neck ri
61 emonstrated a generalized slowly progressive muscle weakness accompanied by decreased vital capacitie
67 severe to profound intellectual disability, muscle weakness and abnormal tone, autistic features, be
68 NM) are congenital disorders associated with muscle weakness and abnormally located nuclei in skeleta
69 genital myopathies characterized by skeletal muscle weakness and an increase in the number of central
70 dinally evaluate the association of post-ICU muscle weakness and associated trajectories of weakness
71 molecular mechanisms of age-related skeletal muscle weakness and atrophy as well as new potential int
72 terozygous mutation in POLG, presenting with muscle weakness and atrophy at a young age aims to aid c
73 geneous group of disorders, characterized by muscle weakness and atrophy predominating at the distal
74 combining congenital myasthenia with distal muscle weakness and atrophy reminiscent of a distal myop
76 ceptor/Ca(2+) release channel (RyR1) display muscle weakness and atrophy, but the underlying mechanis
77 inical characteristics of progressive distal muscle weakness and atrophy, foot deformities, distal se
78 The axonal degeneration in CMT causes distal muscle weakness and atrophy, resulting in gait problems
83 set joint hypermobility, joint contractures, muscle weakness and bone dysplasia as well as high myopi
86 follow-up the patient showed improvement of muscle weakness and carpopedal spasm with near-normal bi
87 nuous spectrum of disorders characterized by muscle weakness and connective tissue abnormalities rang
89 h adverse outcomes and describes a status of muscle weakness and decreased physiological reserve lead
93 phy is characterized by progressive skeletal muscle weakness and dystrophic muscle exhibits degenerat
100 agm dysfunction is twice as frequent as limb muscle weakness and has a direct negative impact on wean
101 of myositis-prone mice with FHL1 aggravated muscle weakness and increased mortality, suggesting a di
102 clear myopathies (CNMs) are characterized by muscle weakness and increased numbers of central nuclei
103 wever, the effects of inactivity/activity on muscle weakness and increased susceptibility to muscle c
104 egenerative disorder that causes progressive muscle weakness and is the leading genetic cause of infa
105 rophy (SBMA) is characterized by adult-onset muscle weakness and lower motor neuron degeneration.
108 ion was delayed beyond infancy with proximal muscle weakness and most patients recall poor performanc
113 ere motor neuron (MN) loss, which results in muscle weakness and often infantile or childhood mortali
114 fore be applicable for treating more general muscle weakness and possibly other conditions that resul
115 f dystrophin protein, leading to progressive muscle weakness and premature death due to respiratory a
120 ubularin protein replacement can improve the muscle weakness and reverse the pathology that character
122 hy" (SMA) was used to investigate the severe muscle weakness and spasticity that precede the death of
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
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
136 Patients presented with more than 2 years of muscle weakness and with dystrophic or myopathic changes
137 naptopathy characterized by ataxia, skeletal muscles weakness and numbness of the extremities in expo
139 8.5% had weaning failure, 30.7% vs 23.8% had muscle weakness, and 90.9% vs 81.5% had hyperglycemia.
140 ing diseases including chronic inflammation, muscle weakness, and a severe combined immunodeficiency
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
151 d by congenital or early-onset hypotonia and muscle weakness, and specific pathological features on m
152 SMA could be corrected after development of muscle weakness, and the response of clinically relevant
153 affected members presenting with adult-onset muscle weakness, and we provide clinical, metabolic, his
154 t; predicted effects include energy deficit, muscle weakness, anomalies in cranial and skeletal devel
161 I preserved SC function and counteracted the muscle weakness associated with Duchenne-like dystrophy
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)
167 ypes including kyphosis, motor dysfunctions, muscle weakness/atrophy, motor neuron loss, and astrocyt
168 ential for the prevention of bone disorders, muscle weakness, autoimmune diseases, and possibly also
169 atients lack dystrophin from birth; however, muscle weakness becomes apparent only at 3-5 years of ag
171 e disease characterized by body weight loss, muscle weakness, brain atrophy, and motor impairment, wh
174 al TGF-beta release from bone contributes to muscle weakness by decreasing Ca(2+)-induced muscle forc
175 ertension by phosphodiesterase 5 inhibitors, muscle weakness by exercise training, sodium retention b
176 troponin activator, CK-2066260, counteracts muscle weakness by increasing troponin Ca(2+) affinity,
178 r myopathy (MFM) associated with progressive muscle weakness, cardiomyopathy, and respiratory failure
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
183 In motor neurone disease (MND), respiratory muscle weakness causes substantial morbidity, and death
184 d body weight loss, skeletal muscle atrophy, muscle weakness, contractile abnormalities, the loss 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
189 lateral sclerosis (ALS) presents with focal muscle weakness due to motor neuron degeneration that be
191 sleepiness and cataplexy, sudden episodes of muscle weakness during waking that are thought to be an
192 n their twenties, and these were followed by muscle weakness, dysphagia, and spino-cerebellar signs w
193 r dystrophy were easily identified by severe muscle weakness either preventing ambulation or resultin
195 y, characterized by exercise intolerance and muscle weakness even in the absence of sideroblastic ane
197 anging from severe disorders with congenital muscle weakness, eye and brain structural abnormalities
199 which presents with cardiomyopathy, skeletal muscle weakness, fatigue, and other symptoms, probably a
200 y diet or FDA-approved drugs can reverse the muscle weakness, fatigue-like physiology and pathology.
201 inine starts to decrease before the onset of muscle weakness, followed by the emergence of hand tremo
202 the analysis of five patients with skeletal muscle weakness for whom heterozygous mutations within A
205 herein that bumetanide protects against both muscle weakness from low K+ challenge in vitro and loss
206 urpurea, grade 2 nausea, grade 2 generalised muscle weakness, grade 2 infection, grade 1 fever, and g
209 persistent physical complications, including muscle weakness, impaired physical function, and decreas
210 es not lead to muscle atrophy but does cause muscle weakness in adult mice and suggest loss of CuZnSO
211 l for stratifying progression of respiratory muscle weakness in amyotrophic lateral sclerosis (ALS) w
213 membrane tubulation and may promote skeletal muscle weakness in CNM2 by disrupting machinery necessar
217 ed neuromuscular transmission contributes to muscle weakness in dystrophic myd mice and that the note
224 hy, but its role and mechanisms of action on muscle weakness in other conditions remains to be invest
226 f muscular dystrophy and leads to asymmetric muscle weakness in the facial, scapular, trunk and lower
227 (A)-binding protein nuclear 1 (PABPN1) cause muscle weakness in the late-onset disorder oculopharynge
229 neuromuscular disease leading to progressive muscle weakness in which fatigue occurs and affects qual
235 treatment for cardiomyopathy and respiratory muscle weakness is advocated because early treatment may
236 with other myasthenic syndromes, the general muscle weakness is also accompanied by use-dependent fat
241 and contractile dysfunction, and respiratory muscle weakness is thought to contribute significantly t
243 t with IVIG and related to clinical outcome: muscle weakness (measured by Medical Research Council su
245 s cognitive decline, seizures, parkinsonism, muscle weakness, neuropathy, spastic paraplegia, persona
246 d muscle ultrastructure likely contribute to muscle weakness observed in our flies and patients.
247 ntrations, which may explain some aspects of muscle weakness observed in patients with hypophosphatem
248 Persisting and resolving trajectories of muscle weakness, occurring in 50% of patients during fol
249 tes hypertrophic cardiomyopathy and skeletal muscle weakness of human IOPD, indicating its utility fo
251 applied mild, moderate, and severe levels of muscle weakness or contracture to either the soleus (SOL
253 eb cKO phenocopies important aspects of NEM (muscle weakness, oxidative fiber-type predominance, vari
254 their dysfunction and loss cause progressive muscle weakness, paralysis and eventually premature deat
255 urable motor neuron diseases associated with muscle weakness, paralysis and respiratory failure.
256 s of motor neurons, resulting in progressive muscle weakness, paralysis, and death within 5 years of
257 o determine the longitudinal epidemiology of muscle weakness, physical function, and health-related q
258 at were associated with a spectrum of severe muscle weakness ranging from a lethal antenatal form of
259 exhibited MG-associated symptoms, including muscle weakness, reduced compound muscle action potentia
263 ndromes (CMS) are characterized by fatigable muscle weakness resulting from impaired neuromuscular tr
264 model of sepsis can reproduce the long-term muscle weakness seen in patients who survive this life-t
265 ssion during infancy, profound hypotonia and muscle weakness, severe intellectual disability and prog
266 sive form of spastic paraplegia resulting in muscle weakness, short stature, and cognitive defects.
267 ne system damages their nerve cells, causing muscle weakness, sometimes paralysis, and infrequently d
268 related myopathy (SEPN1-RM) characterized by muscle weakness, spinal rigidity, and respiratory insuff
270 Ed 90-100 milliseconds: R = -0.44, P < .01), muscle weakness (TEd 90-100 milliseconds: R = -0.32, P <
272 eepiness and cataplexy, episodes of profound muscle weakness that are often triggered by strong, posi
273 c dysfunction (VIDD) refers to the diaphragm muscle weakness that occurs following prolonged controll
274 nd is responsible, at least in part, for the muscle weakness that occurs in the mouse model of myosit
275 ng condition associated with severe skeletal muscle weakness that persists in humans long after lung
277 f Friedreich's ataxia (FRDA) include ataxia, muscle weakness, type 2 diabetes and heart failure, whic
279 s a genetic disorder that causes progressive muscle weakness, ultimately leading to early mortality i
280 chronic stroke patients, with plantar flexor muscle weakness, using a randomized controlled crossover
282 a history of cardiomyopathy and progressive muscle weakness was admitted with cardiogenic shock.
283 higher ICU and hospital mortality, and limb muscle weakness was associated with longer duration of M
291 D phenotype with typical facial and scapular muscle weakness, whereas 20.1% present incomplete phenot
292 l presentation of flaccid and often profound muscle weakness (which can invoke respiratory failure an
293 associated diabetes in mice, but also causes muscle weakness, which suggests that mammals have retain
294 enital myasthenic syndrome exhibit fatigable muscle weakness with a variety of accompanying phenotype
295 members showed adult onset asymmetric distal muscle weakness with initial involvement of ankle dorsif
296 pinal muscular atrophy (SMA) presents severe muscle weakness with limited motor neuron (MN) loss at a
298 so characterised by various forms/degrees of muscle weakness with most cases being severe and resulti