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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
62 suggesting that variable gearing may explain muscle weakness after stroke.
63 suggesting that variable gearing may explain muscle weakness after stroke.
64            Moreover, the pace and pattern of muscle weakness, along with onset of cardiomyopathy, is
65                      Entry criteria included muscle weakness and >/=2 additional abnormal values on c
66          DMD is characterized by progressive muscle weakness and a shortened life span, and there is
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
75           Axial (86%) and periscapular (81%) muscle weakness and atrophy were frequent findings.
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
79  ATF4 as a potential mediator of age-related muscle weakness and atrophy.
80  investigate the pathogenesis of age-related muscle weakness and atrophy.
81 e ATF4 as a critical mediator of age-related muscle weakness and atrophy.
82 ed neuropathies characterized by distal limb muscle weakness and atrophy.
83 set joint hypermobility, joint contractures, muscle weakness and bone dysplasia as well as high myopi
84     As a result, DMD causes progressive limb muscle weakness and cardiac and respiratory failure.
85 storage myopathy associated with progressive muscle weakness and cardiomyopathy.
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
88  as intermediate phenotypes characterized by muscle weakness and connective tissue abnormalities.
89 h adverse outcomes and describes a status of muscle weakness and decreased physiological reserve lead
90            Survivors report chronic skeletal muscle weakness and development of new functional limita
91 hanical ventilation are at risk for profound muscle weakness and disability.
92                                              Muscle weakness and dizziness were more common in the co
93 phy is characterized by progressive skeletal muscle weakness and dystrophic muscle exhibits degenerat
94 dings of dermatomyositis along with proximal muscle weakness and elevated muscle enzymes.
95                                     Skeletal muscle weakness and eventual muscle degradation due to l
96  treatment to patients suffering from severe muscle weakness and exercise intolerance.
97 R1 frameshifting mutation complained of mild muscle weakness and fatigability.
98                                              Muscle weakness and fatigue are common symptoms in multi
99 disorders often characterized by progressive muscle weakness and fragility.
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.
106                                              Muscle weakness and metabolic disturbances were detectab
107 s, apoptosis, and necrosis leading to severe muscle weakness and minimal postnatal growth.
108 ion was delayed beyond infancy with proximal muscle weakness and most patients recall poor performanc
109 show HMN/CMT2 with slowly progressive distal muscle weakness and musculoskeletal deformities.
110            These heterozygous mice developed muscle weakness and myofibrillar instability, with forma
111                                              Muscle weakness and myopathy are observed in vitamin D d
112 odels corrected cyclin D3 levels and reduced muscle weakness and myotonia in DM1 mice.
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
116 muscle alpha-actin) are generalized skeletal muscle weakness and premature death.
117 tion occurs in many diseases and can lead to muscle weakness and premature muscle fatigue.
118    The elderly often suffer from progressive muscle weakness and regenerative failure.
119                 Hypophosphatemia can lead to muscle weakness and respiratory and heart failure, but t
120 ubularin protein replacement can improve the muscle weakness and reverse the pathology that character
121 s group of disorders characterized by distal muscle weakness and sensory loss.
122 hy" (SMA) was used to investigate the severe muscle weakness and spasticity that precede the death of
123          Altogether, our study suggests that muscle weakness and susceptibility to contraction-induce
124 ve impairment to AD associating with ongoing muscle weakness and the onset of muscle atrophy.
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 characterized by slowly progressive skeletal muscle weakness and wasting.
133  disorders that produce progressive skeletal muscle weakness and wasting.
134 dystrophies are characterized by progressive muscle weakness and wasting.
135 essive disorder characterized by progressive muscle weakness and wasting.
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
138  63% had diaphragm dysfunction, 34% had limb muscle weakness, and 21% had both.
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
141 e ERK1/2 displayed stunted postnatal growth, muscle weakness, and a shorter life span.
142 ty, diabetes mellitus, erectile dysfunction, muscle weakness, and all-cause mortality.
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 tabolism, resulting in exercise intolerance, muscle weakness, and myocyte apoptosis.
148 kin tightness, paresthesias, neck stiffness, muscle weakness, and neck pain.
149 nts, including impaired body balance, severe muscle weakness, and reduced life span.
150 ng, respectively, to pulmonary hypertension, muscle weakness, and sodium retention.
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
155 , geriatric conditions such as slow gait and muscle weakness are becoming increasingly common.
156              Chorea, rigidity, dystonia, and muscle weakness are characteristic motor defects of the
157             Loss of skeletal muscle mass and muscle weakness are common in a variety of clinical cond
158                        Mechanisms underlying muscle weakness are poorly understood, but might involve
159  of rare diseases with fluctuating fatigable muscle weakness as the clinical hallmark.
160         Their clinical hallmark is fatigable muscle weakness associated with a decremental muscle res
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)
166                  The symptoms of ANM include muscle weakness, atrophy, contracture and tremors accomp
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
170 osphatase increase (five [1%]), colitis, and muscle weakness (both four [1%]).
171 e disease characterized by body weight loss, muscle weakness, brain atrophy, and motor impairment, wh
172               The mice demonstrated skeletal muscle weakness but did not experience early mortality.
173 th relevant axial, proximal, and respiratory muscle weakness but without vocal cord palsy.
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,
177      EEF1A2-deficient zebrafish had skeletal muscle weakness, cardiac failure and small heads.
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
182 chondrial UPR activation effectively reduces muscle weakness caused by ethanol exposure.
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
185                                              Muscle weakness contributes to prolonged rehabilitation
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  lateral sclerosis (ALS) presents with focal muscle weakness due to motor neuron degeneration that be
190                                     Profound muscle weakness during and after critical illness is ter
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
194 tor neuron loss with concomitant progressive muscle weakness ending in paralysis and death.
195 y, characterized by exercise intolerance and muscle weakness even in the absence of sideroblastic ane
196                   Recovery from ICU-acquired muscle weakness extends beyond hospital stay.
197 anging from severe disorders with congenital muscle weakness, eye and brain structural abnormalities
198                           He had generalized muscle weakness, facial discomfort, recurrent episodes o
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
203                                  Respiratory muscle weakness frequently develops during mechanical ve
204                MDC1A patients exhibit severe muscle weakness from birth, are confined to a wheelchair
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
207                             The two types of muscle weakness have only limited overlap.
208 ession (HR: 1.23; 95% CI: 1.05 to 1.45), and muscle weakness (HR: 1.19; 95% CI: 1.00 to 1.42).
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
212       Clinical findings included progressive muscle weakness in an initially scapuloperoneal and dist
213 membrane tubulation and may promote skeletal muscle weakness in CNM2 by disrupting machinery necessar
214 r they are linked, and their contribution to muscle weakness in disease, are not known.
215  1 fibers associated with muscle atrophy and muscle weakness in DM1.
216 l anti-inflammatory therapy to alleviate the muscle weakness in DMD patients.
217 ed neuromuscular transmission contributes to muscle weakness in dystrophic myd mice and that the note
218 on, and that this contributes to age-related muscle weakness in mammals, including humans.
219 lity of myofibrillar Z-discs, explaining the muscle weakness in mice and humans.
220 erlie their dysfunctional conduction akin to muscle weakness in multiple sclerosis.
221 P deaminase 1 (AMPD1) may be responsible for muscle weakness in myositis.
222              Limited neural input results in muscle weakness in neuromuscular disease because of a re
223 up of cytokines is a potential biomarker for muscle weakness in OPMD.
224 hy, but its role and mechanisms of action on muscle weakness in other conditions remains to be invest
225                It is generally believed that muscle weakness in patients with polymyositis and dermat
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
228 ce, but mutant animals did not display gross muscle weakness in vivo.
229 neuromuscular disease leading to progressive muscle weakness in which fatigue occurs and affects qual
230                   The predominant pattern of muscle weakness included bilateral ptosis (non-fatigable
231                          Similarly, skeletal muscle weakness, increased Nox4 binding to RyR1 and oxid
232                           Acquired diaphragm muscle weakness is a key feature in several chronic cond
233                         Although respiratory muscle weakness is a known predictor of poor prognosis,
234                            Cancer-associated muscle weakness is a poorly understood phenomenon, and t
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
237                                              Muscle weakness is common after acute lung injury, usual
238 et the mechanism defining the development of muscle weakness is currently unclear.
239 tic neuromuscular disease in which crippling muscle weakness is evident from birth.
240                         Localized or general muscle weakness is the predominant symptom and is induce
241 and contractile dysfunction, and respiratory muscle weakness is thought to contribute significantly t
242                       Next, we predicted how muscle weakness may cause deviations from a normal walki
243 t with IVIG and related to clinical outcome: muscle weakness (measured by Medical Research Council su
244          Patients had a predominantly distal muscle weakness, most severely affecting ankle and wrist
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
250 embers developed in utero- or neonatal-onset muscle weakness of variable severity.
251 applied mild, moderate, and severe levels of muscle weakness or contracture to either the soleus (SOL
252 erized by the sudden uncontrollable onset of muscle weakness or paralysis during wakefulness.
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
260 MCT mimics loss of body weight and diaphragm muscle weakness reported in PH patients.
261                    Deciphering mechanisms of muscle weakness requires sophisticated force protocols,
262                       In seven cases, severe muscle weakness resulted in death during the third trime
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
269 including arthralgia, bone pain, generalised muscle weakness, syncope, and dyspnea.
270 Ed 90-100 milliseconds: R = -0.44, P < .01), muscle weakness (TEd 90-100 milliseconds: R = -0.32, P <
271            Defects in NMJ transmission cause muscle weakness, termed myasthenia.
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
276                                  Importance: Muscle weakness, the most common symptom of neuromuscula
277 f Friedreich's ataxia (FRDA) include ataxia, muscle weakness, type 2 diabetes and heart failure, whic
278  involvement, and proximal as well as distal muscle weakness (typical CIDP).
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
281                                              Muscle Weakness VAS scores were significantly lower in t
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
284                                         Limb muscle weakness was defined as a Medical Research Counci
285                                              Muscle weakness was earlier onset and more severe in the
286                                      Because muscle weakness was evident prior to loss of Fhl1 protei
287                                              Muscle weakness was generally milder than observed in li
288                                mylpfa mutant muscle weakness was most pronounced in an appendicular m
289              Mild skeletal myopathy/proximal muscle weakness was noted in 6 (29%) patients.
290                                              Muscle weakness was proximal with adulthood onset in mos
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
297 thy (NM), a muscle disorder characterized by muscle weakness with limited treatment options.
298 so characterised by various forms/degrees of muscle weakness with most cases being severe and resulti
299 clinical phenotype is associated with distal muscle weakness with quadriceps sparing.
300               These studies detail a primary muscle weakness (without a loss of muscle mass) in patie

 
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