ライフサイエンスコーパス: neuromuscular

1 had a metabolic (14.3% vs 3.0%; P = .04) or neuromuscular (14.3% vs 3.6%; P = .05) condition, and mo

2 Adult ICU patients without preexisting neuromuscular abnormalities and a discharge diagnosis of

3 KEY POINTS: Neuromuscular acetylcholine (ACh) receptors have a high

4 ceptors play previously unsuspected roles in neuromuscular activity and elimination of excess synapti

5 t link between a robust biomarker of healthy neuromuscular age and a major axis of life span in model

6 evelopmental and neuropsychiatric disorders, neuromuscular and neurodegenerative diseases, and can of

7 has since expanded to include a spectrum of neuromuscular and ocular manifestations, including reduc

8 ease, the molecular pathology underlying the neuromuscular and sensory phenotypes is still not fully

9 cing analysis in two patients who had unique neuromuscular and skeletal symptoms, including progressi

10 ion emerges from the interaction between the neuromuscular and the musculoskeletal systems.

11 or decades, interactions between the enteric neuromuscular apparatus and the central nervous system h

12 oreal membrane oxygenation patients received neuromuscular blockade (46%) or were heavily sedated wit

13 Neuromuscular blockade alone does not cause hypothermia

14 more severely hypoxaemic patients with ARDS, neuromuscular blockade and prone positioning have furthe

15 y distress syndrome receiving treatment with neuromuscular blockade because they cannot shiver.

16 be a useful tool for monitoring the depth of neuromuscular blockade but only if it is incorporated in

17 To investigate whether partial neuromuscular blockade can facilitate lung-protective ve

18 Partial neuromuscular blockade facilitates lung-protective venti

19 6-37.3 degrees C), and fever occurred during neuromuscular blockade in 30 of 58 retrospective patient

20 in of four alone for monitoring the depth of neuromuscular blockade in patients receiving continuous

21 1) We make no recommendation as to whether neuromuscular blockade is beneficial or harmful when use

22 4) We make no recommendation on the use of neuromuscular blockade to improve the accuracy of intrav

23 Use of prone positioning and neuromuscular blockade was significantly more common in

24 can be managed with early short-term use of neuromuscular blockade, prone position ventilation, or e

25 ive drugs should be used prior to and during neuromuscular blockade, with the goal of achieving deep

26 iratory distress syndrome patients receiving neuromuscular blockade.

27 ients with PaO2/FIO2 less than 150 receiving neuromuscular blockade.

28 ria and PaO2/FIO2 less than 150 who received neuromuscular blockade.

29 pertoire [10/44 (23%) lacked BSACI compliant neuromuscular blocking agent (NMBA) panels and 17/44 (39

30 postulated cause of allergic anaphylaxis to neuromuscular blocking agents (NMBAs).

31 The relationship between neuromuscular blocking agents and neuromuscular dysfunct

32 alysis suggests a modest association between neuromuscular blocking agents and neuromuscular dysfunct

33 uscular disease, addiction, epilepsy and for neuromuscular blocking agents used during surgery.

34 s that a protocol should include guidance on neuromuscular-blocking agent administration in patients

35 practice suggests that a reduced dose of an neuromuscular-blocking agent be used for patients with m

36 10) We suggest that neuromuscular-blocking agents be discontinued at the end

37 ht or adjusted body weight) when calculating neuromuscular-blocking agents doses for obese patients.

38 make no recommendation on the routine use of neuromuscular-blocking agents for patients undergoing th

39 3) We suggest a trial of a neuromuscular-blocking agents in life-threatening situat

40 of less than 180 mg/dL in patients receiving neuromuscular-blocking agents.

41 in patients with myasthenia gravis receiving neuromuscular-blocking agents.

42 r patients receiving continuous infusions of neuromuscular-blocking agents.

43 unintended extubation in patients receiving neuromuscular-blocking agents.

44 in patients receiving continuous infusion of neuromuscular-blocking agents.

45 ebo-controlled, phase 2 study was done in 22 neuromuscular care centres in Belgium, France, Germany,

46 d Sept 20, 2016, we studied patients from 69 neuromuscular centres in North America, Europe, Israel,

47 have a diverse phenotype, with more frequent neuromuscular complications.

48 ce (FI) in women after menopause by altering neuromuscular continence mechanisms.

49 We investigated the neuromuscular contributions to kinematic variability and

50 terplay of morphological specializations and neuromuscular control mechanisms [1-3], and it is often

51 ovide a framework for future research on the neuromuscular control of mouse vocal production and for

52 enesis of OSA has been linked to a defect in neuromuscular control of the pharynx.

53 t, these same features arise in oscines from neuromuscular control of two labial sources [15-17].

54 odel successfully reproduced the retinal and neuromuscular defects observed in MLIV patients, indicat

55 Investigation of neuromuscular deficits and diseases such as SMA, as well

56 y be found in patients with low back pain or neuromuscular deficits.

57 that autophagy inhibition accelerated early neuromuscular denervation of the tibialis anterior muscl

58 hat Wnts may contribute to prepatterning and neuromuscular development in mammals.

59 This study provides the first description of neuromuscular development in the enigmatic ctenophores a

60 or collagen XV in motor axon pathfinding and neuromuscular development.

61 ay has significant potential for modeling of neuromuscular disease and regeneration.

62 Spinal muscular atrophy (SMA) is a neuromuscular disease caused by low levels of SMN protei

63 Spinal muscular atrophy (SMA) is a neuromuscular disease caused by reduced expression of su

64 Myotonic dystrophy type 2 is a genetic neuromuscular disease caused by the expression of expand

65 inal and bulbar muscular atrophy (SBMA) is a neuromuscular disease characterized by the loss of lower

66 ular dystrophy type 1A (MDC1A) is a dramatic neuromuscular disease in which crippling muscle weakness

67 expanded CUG repeats causes symptoms in the neuromuscular disease myotonic dystrophy.

68 h (U)-snRNAs, may contribute to the specific neuromuscular disease phenotype associated with SMA.

69 bulbar muscular atrophy (SBMA), an X-linked neuromuscular disease that is fully manifest only in mal

70 Duchenne muscular dystrophy (DMD) is a neuromuscular disease that predominantly affects boys as

71 otonic dystrophy type I (DM1) is a disabling neuromuscular disease with no causal treatment available

72 5 had encephalitis (3 with concomitant acute neuromuscular disease), 2 had transverse myelitis, and 1

73 eptors are important therapeutic targets for neuromuscular disease, addiction, epilepsy and for neuro

74 owing keywords: genome editing, CRISPR-Cas9, neuromuscular disease, Duchenne muscular dystrophy, spin

75 mon cause of early onset primary dystonia, a neuromuscular disease, is a glutamate deletion (DeltaE)

76 scular atrophy (SMA), an autosomal recessive neuromuscular disease, is the leading monogenic cause of

77 Muscle weakness, the most common symptom of neuromuscular disease, may result from muscle dysfunctio

78 rvous system (CNS) to treat neurological and neuromuscular disease.

79 motor function after spinal injury or during neuromuscular disease.

80 For many neuromuscular diseases (NMDs), cardiac disease represent

81 heir role in managing ventilatory failure in neuromuscular diseases and other chronic disorders.

82 -causing mutations responsible for monogenic neuromuscular diseases by genome editing.

83 postsynaptic AChRs, may underlie symptoms of neuromuscular diseases characterized by reduced AChRs, s

84 me-editing-meditated correction of monogenic neuromuscular diseases in cultured cells and animal mode

85 Dystrophinopathies are a group of distinct neuromuscular diseases that result from mutations in the

86 l myopathies define a heterogeneous group of neuromuscular diseases with neonatal or childhood hypoto

87 Articles describing neuromuscular diseases, including Duchenne muscular dyst

88 To date, more than 780 monogenic neuromuscular diseases, linked to 417 different genes, h

89 he Medical Research Council (MRC) Centre for Neuromuscular Diseases, National Hospital for Neurology

90 the identification of corrective therapy for neuromuscular diseases, such as spinal muscular atrophy

91 chenne muscular dystrophy and possibly other neuromuscular diseases.

92 chronic pain, epilepsy, certain cancers, and neuromuscular diseases.

93 ate to the potential correction of monogenic neuromuscular diseases; and to highlight scientific and

94 Spinal Muscular Atrophy (SMA) is a neuromuscular disorder caused by insufficient levels of

95 ar atrophy (SMA) is a common and often fatal neuromuscular disorder caused by low levels of the Survi

96 inal muscular atrophy (SMA) is a devastating neuromuscular disorder characterized by loss of spinal c

97 rrespective of the primary molecular defect, neuromuscular disorder pathological processes include di

98 The neuromuscular disorder spinal muscular atrophy (SMA), th

99 l muscular atrophy is an autosomal recessive neuromuscular disorder that is caused by an insufficient

100 ar dystrophy (FSHD) is an autosomal dominant neuromuscular disorder that is characterized by extreme

101 chondria, a condition linked to debilitating neuromuscular disorders in humans.

102 ide repeats produce several neurological and neuromuscular disorders including Huntington disease, mu

103 nt to progress in trials of new therapies in neuromuscular disorders is the absence of responsive out

104 ac troponin T (cTnT) levels in patients with neuromuscular disorders may erroneously lead to the diag

105 atic weakness is a main element, but in many neuromuscular disorders mechanical upper airway obstruct

106 TnT levels in Pompe disease and likely other neuromuscular disorders should be interpreted with cauti

107 s to restore motor function in patients with neuromuscular disorders that compromise movement.

108 ance as we develop therapies to treat severe neuromuscular disorders that compromise somatic motor be

109 in nerve-muscle signaling cause a variety of neuromuscular disorders with features of ataxia, paralys

110 en's Hospital of Philadelphia Infant Test of Neuromuscular Disorders) scale of motor function (rangin

111 cent findings in NMJ formation, maintenance, neuromuscular disorders, and aging of the NMJ, focusing

112 n's Hospital of Philadelphia Infant Test for Neuromuscular Disorders, and Alberta Infant Motor Score)

113 etagammadelta nAChRs, of use in treatment of neuromuscular disorders, have been hard to identify.

114 icits in NMJ formation and maintenance cause neuromuscular disorders, including congenital myasthenic

115 In human and animal trials for neuromuscular disorders, inconsistent electrode position

116 capacity in ALS.SIGNIFICANCE STATEMENT Since neuromuscular disorders, such as amyotrophic lateral scl

117 e for dysfunctional respiratory complex I in neuromuscular disorders.

118 veals COL15A1 as a candidate gene for orphan neuromuscular disorders.

119 as revealed two sigma-1R mutants involved in neuromuscular disorders.

120 ing has significant potential for therapy of neuromuscular disorders.

121 lowing training or during the progression of neuromuscular disorders.

122 ffect of interventions or the progression of neuromuscular disorders.

123 chondrial fusion and mitofusin-related human neuromuscular disorders.

124 ular junction, suggesting that mechanisms of neuromuscular disruption are distinct in these diseases.

125 ip between neuromuscular blocking agents and neuromuscular dysfunction acquired in critical illness r

126 on between neuromuscular blocking agents and neuromuscular dysfunction acquired in critical illness;

127 Aerobic exercise (AE) and non-aerobic neuromuscular electric stimulation (NMES) are common int

128 We assessed the effectiveness of neuromuscular electrical stimulation (NMES) as a home-ba

129 Neuromuscular electrical stimulation continually display

130 scles through a custom-built high-resolution neuromuscular electrical stimulation system.

131 Given that neuromuscular fatigue depends on interrelated factors, q

132 mic contractions (pumping) of the pharynx, a neuromuscular feeding organ.

133 al and regenerative potential, and increased neuromuscular fragmentation and occasional denervation.

134 sufficiently, they suffer an initial loss of neuromuscular function (chill coma) that is caused by de

135 myelination defects, significantly improved neuromuscular function and ameliorated neuromuscular jun

136 allows for a more accurate recapitulation of neuromuscular function for applications in disease inves

137 The majority of anthelmintics dysregulate neuromuscular function, a fact most prominent for drugs

138 end support for a protective role of VAPB in neuromuscular health.

139 tor neuron autophagy is required to maintain neuromuscular innervation early in disease but eventuall

140 Our study provides important mechanistic neuromuscular insight into walking balance control and i

141 x signalling and key roles in maintenance of neuromuscular integrity.

142 ments, anxiety, hippocampal LTP deficits and neuromuscular junction (NMJ) abnormalities, characterize

143 hR clustering, a complete reversal of normal neuromuscular junction (NMJ) development where AChR clus

144 anifesting deficits in coordinated movement, neuromuscular junction (NMJ) development, synaptic glyco

145 al of Motor Neuron (SMN) protein, leading to neuromuscular junction (NMJ) dysfunction and spinal moto

146 mulate the LRP4-MuSK receptor in muscles for neuromuscular junction (NMJ) formation.

147 ia, the terminal Schwann cells (SCs), at the neuromuscular junction (NMJ) in mice.

148 ed and retained at postsynaptic sites at the neuromuscular junction (NMJ) in vivo remains largely unk

149 The neuromuscular junction (NMJ) is a synapse formed between

150 The neuromuscular junction (NMJ) is a tripartite synapse tha

151 hether weakened synaptic transmission at the neuromuscular junction (NMJ) is an aspect of CMT2D.

152 SIGNIFICANCE STATEMENT: The neuromuscular junction (NMJ) is critical for all volunta

153 Here, we test the roles of Mmp at the neuromuscular junction (NMJ) model synapse in the reduct

154 Denervation of the neuromuscular junction (NMJ) precedes the loss of motor

155 The Drosophila larval glutamatergic neuromuscular junction (NMJ) represents a powerful synap

156 At the glutamatergic neuromuscular junction (NMJ) synapse, we find that Notum

157 is crucial for vesicle fusion at presynaptic neuromuscular junction (NMJ).

158 e morphogenic protein (BMP) signaling at the neuromuscular junction (NMJ).

159 dysfunction and progressive weakening of the neuromuscular junction (NMJ).

160 or may be caused indirectly by neuronal and neuromuscular junction abnormalities.

161 ential for normal synaptic plasticity at the neuromuscular junction and for muscle strength, enduranc

162 diate fast chemical neurotransmission at the neuromuscular junction and have diverse signalling roles

163 evelopment and evoked function of the larval neuromuscular junction are surprisingly normal, but the

164 Using Caenorhabditis elegans neuromuscular junction as a model synapse, we uncovered

165 its symptomatic treatment suggests that this neuromuscular junction assay has significant potential f

166 hed larval peristaltic contractions, loss of neuromuscular junction bouton structures, impaired olfac

167 However, it was not effective at preventing neuromuscular junction denervation in a mutant SOD1(G93A

168 equirement for MYO9A in the formation of the neuromuscular junction during development.

169 mmed cell and tissue death, neuromaturation, neuromuscular junction formation, and neuron cell fate d

170 as reduced motor axon branching and abnormal neuromuscular junction formation.

171 ein 4 (Lrp4), a protein that is critical for neuromuscular junction formation.

172 presynaptic neurotransmitter release at the neuromuscular junction in Drosophila.

173 Our studies at the Drosophila neuromuscular junction indicate that many synaptic defec

174 hat axon branch loss at the developing mouse neuromuscular junction is mediated by branch-specific mi

175 nd on the presynaptic nerve terminals at the neuromuscular junction level, but not on the axonal trac

176 sm underlying impaired neurotransmission and neuromuscular junction maintenance in SMA.

177 12 d to a mean of 456 d, with improvement in neuromuscular junction morphology, down-regulation of tr

178 local concentration of acetylcholine at the neuromuscular junction of frog cutaneous pectoris muscle

179 roved neuromuscular function and ameliorated neuromuscular junction pathology in SMA mice.

180 y, we examined the relative contributions of neuromuscular junction physiology and the motor program

181 on and motor defects, but not the defects in neuromuscular junction physiology.

182 targeted to synaptic sites at the vertebrate neuromuscular junction remains unclear.

183 Uptake at the neuromuscular junction represents a major unexpected pat

184 sted synaptic facilitation and depression in neuromuscular junction synapses that use exclusively CaV

185 of surviving motor units and instability of neuromuscular junction transmission.

186 lcholine receptor (AChR) clustering and NMJ (neuromuscular junction) formation.

187 g all Shank proteins and used the Drosophila neuromuscular junction, a model glutamatergic synapse, t

188 evels, the propriospinal projection network, neuromuscular junction, and central pattern generator, p

189 de preserved ganglioside distribution at the neuromuscular junction, delayed disease onset, improved

190 y autoantibodies that target proteins at the neuromuscular junction, primarily the acetylcholine rece

191 in SMA changes appeared concomitantly at the neuromuscular junction, suggesting that mechanisms of ne

192 At the neuromuscular junction, we showed mEPP amplitudes and fr

193 Here experiments at the Drosophila neuromuscular junction, where DCVs contain neuropeptides

194 endent synaptic remodeling at the Drosophila neuromuscular junction.

195 citatory synaptic transmission at the larval neuromuscular junction.

196 ue, probably around the nerve endings of the neuromuscular junction.

197 eostatic synaptic compensation at the larval neuromuscular junction.

198 ripheral cholinergic synapses, including the neuromuscular junction.

199 l synaptic-function at the Drosophila larval neuromuscular junction.

200 defects in the structure and function of the neuromuscular junction.

201 llite cells and within motor neurons via the neuromuscular junction.

202 locking acetylcholine receptors at the mouse neuromuscular junction.

203 endent synaptic plasticity at the Drosophila neuromuscular junction.

204 r structural modifications at the Drosophila neuromuscular junction.

205 echanism for graded locomotor control at the neuromuscular junction.

206 tamatergic synapses of the Drosophila larval neuromuscular junction.

207 We show that at larval neuromuscular junctions (NMJ), motor neuron expression o

208 Neuromuscular junctions (NMJs) are critical for survival

209 tical for the development and maintenance of neuromuscular junctions (NMJs) remains largely unknown.

210 ility of motor neurons and their output, the neuromuscular junctions (NMJs), has been considered a ke

211 e the morphology of their previously damaged neuromuscular junctions (NMJs), suggesting that the bene

212 pruning also occurs at embryonic Drosophila neuromuscular junctions (NMJs), where low-frequency Ca(2

213 ive disorders resulting from degeneration of neuromuscular junctions (NMJs), which form the connectio

214 f SMN deficiency are profound defects of the neuromuscular junctions (NMJs).

215 t the postsynaptic membrane of glutamatergic neuromuscular junctions and controls multiple parameters

216 ceptors (AChRs) mediate signalling at mature neuromuscular junctions and fetal-type AChRs are necessa

217 sympathetic neurons make close contact with neuromuscular junctions and form a network in skeletal m

218 er axonal elongation in an in vitro model of neuromuscular junctions and hastened recovery after peri

219 e respiratory rhythm generator and diaphragm neuromuscular junctions appeared normal.

220 eon mutants, postsynaptic specializations of neuromuscular junctions are dramatically expanded, inclu

221 use models of both diseases, suggesting that neuromuscular junctions are highly vulnerable from the v

222 Neuromuscular junctions are primary pathological targets

223 aterals to reinnervate previously denervated neuromuscular junctions concurrently with expression of

224 uency stimulation, both wild-type and mutant neuromuscular junctions depress to steady-state response

225 In rsu-1 mutants, neuromuscular junctions differentiate as in the wild typ

226 ction and preserved motor neurons as well as neuromuscular junctions from degeneration.

227 nervous system synapses and mouse diaphragm neuromuscular junctions fully intoxicated by BoNT seroty

228 ylcholine receptors for the establishment of neuromuscular junctions in vitro.

229 We show for the first time that neuromuscular junctions of the extraocular muscles (resp

230 Conversely, neuromuscular junctions of the lumbrical muscles of the

231 Loss of TMEM184b causes swellings at neuromuscular junctions that become more numerous with a

232 ophysiological and morphological deficits of neuromuscular junctions upon sympathectomy and in myasth

233 Green) uptake in the presynaptic terminal of neuromuscular junctions was restored to control levels i

234 Tongue muscle neuromuscular junctions were also spared in both animal

235 These formed 6618 synapses including 1772 neuromuscular junctions, augmented by 1206 gap junctions

236 earance occurred at motor nerve terminals of neuromuscular junctions, from where anti-ganglioside ant

237 e of exocytosis in isolated nerve terminals, neuromuscular junctions, neuroendocrine cells and in hip

238 vesicle recycling pathways at complexin null neuromuscular junctions, where spontaneous release is dr

239 that inhibits acetylcholine (ACh) release at neuromuscular junctions.

240 autoimmune disorder that selectively targets neuromuscular junctions.

241 ty at active zones of axon terminals at frog neuromuscular junctions.

242 inhibits nerve regeneration and destabilizes neuromuscular junctions.

243 functional defects at a subset of vulnerable neuromuscular junctions.

244 uggesting an effect on synaptogenesis beyond neuromuscular junctions.

245 rupts synaptic structure and function at the neuromuscular junctions.

246 ressive motor neuron loss and denervation of neuromuscular junctions.

247 nescent mitochondria in their motor axons or neuromuscular junctions; instead, they contain far fewer

248 The underlying neuromuscular mechanisms have been the subject of intens

249 Use-dependent fatigue accompanies many neuromuscular myasthenic syndromes, including muscle rap

250 Therefore, neuromuscular NMDA receptors play previously unsuspected

251 anipulations that decrease signaling through neuromuscular NMDA receptors, whereas application of exo

252 However, the first evidence of neuromuscular pathology occurred at different timepoints

253 Synaptic dysfunction contributes to impaired neuromuscular performance and disease progression.

254 synaptic efficacy were tested to see whether neuromuscular performance improved.

255 myelination, leading to nerve conduction and neuromuscular performance recovery in rodent models of d

256 We show that the neuromuscular phenotype observed in animals homozygous f

257 ion was part of an early-onset multisystemic neuromuscular phenotype with mental retardation, leading

258 combined respiratory-chain deficiency and a neuromuscular phenotype.

259 the duration over which numerous sensory and neuromuscular phenotypes manifest.

260 lder adult-onset forms, were collected in 17 neuromuscular referral centres in Europe and USA.

261 The neuromuscular reflex arc is the system that integrates t

262 benefit from the development of a functional neuromuscular reflex arc.

263 s, a large thigh muscle, undergoes extensive neuromuscular remodelling in healthy ageing, as characte

264 Emerging data promote neuromuscular signalling components, and especially G pr

265 ble link between SMN function and the distal neuromuscular SMA phenotype is an incorrectly spliced tr

266 hough how this is associated with changes to neuromuscular structure and function in terms of motor u

267 of axons and how the degenerative changes in neuromuscular structure that occur with ageing may contr

268 rmediate filaments in nerve terminals of the neuromuscular synapse and improves the innervation of mu

269 Despite these differences, neuromuscular synapse formation in zebrafish and mice sh

270 is likely to drive this wasting, and (4) the neuromuscular synapse is a primary subcellular target fo

271 anges during development and growth, yet the neuromuscular synapse maintains a remarkable fidelity of

272 dy weight and muscle size, but also inhibits neuromuscular synapse strength and composition in a Smad

273 , regulate the formation and function of the neuromuscular synapse, and their absence results in myas

274 e, complexity and functional capacity of the neuromuscular synapse.

275 In the lack of collagen XIII neuromuscular synapses do not reach full size, alignment

276 l synaptic transmission was unaltered in the neuromuscular synapses in IM-AA mice, we found reduced s

277 holine neurotransmission at both central and neuromuscular synapses, with important implications for

278 RG1 as a molecular determinant for SC-driven neuromuscular synaptic plasticity.

279 rrents in neurons are greatly decreased, and neuromuscular synaptic transmission is enhanced.

280 NSC transplantation can modulate the enteric neuromuscular syncytium to restore function, at the orga

281 es that distinguish it from other congenital neuromuscular syndromes.

282 cular cues and regulatory mechanisms for the neuromuscular system development.

283 ne potential and reduced excitability of the neuromuscular system.

284 characterised by progressive failure of the neuromuscular system.

285 level of coordination between the visual and neuromuscular systems.

286 study, we examined the relationship between neuromuscular transmission and skeletal muscle hyperexci

287 nd function of individual NMJs, we show that neuromuscular transmission at the most highly fragmented

288 NMJ maturation, led to NMJ fragmentation and neuromuscular transmission deficits.

289 avis (MG), an autoimmune disease that causes neuromuscular transmission dysfunction.

290 The depressed neuromuscular transmission in R6/2 muscle may help compe

291 Our examination of neuromuscular transmission in this study reveals defects

292 Neurophysiology showed abnormal neuromuscular transmission only in the affected muscles

293 remodelling is associated with impairment of neuromuscular transmission, and that this contributes to

294 henia gravis (MG), an autoimmune disorder of neuromuscular transmission, is treated by an array of im

295 to delay or reverse BoNT-induced blockade of neuromuscular transmission.

296 rtance of glycosylation for the integrity of neuromuscular transmission.

297 r se is not a reliable indicator of impaired neuromuscular transmission.

298 esponse, thus reducing the safety margin for neuromuscular transmission.

299 ides derived from ArPPLNP1 act as inhibitory neuromuscular transmitters in starfish, which contrasts

300 Neuromuscular weakness at the time of extubation was com

301 phy (DMD) is a severe, progressive, and rare neuromuscular, X-linked recessive disease.