ライフサイエンスコーパス: neuromuscular

1 at over-expression of Oxr1 was able to delay neuromuscular abnormalities in the hSOD1G93A ALS mouse m

2 such as Paramecium [1, 2], to complex animal neuromuscular activity [3].

3 f several peptides that act as modulators of neuromuscular activity in A. japonicus were also identif

4 an example of a biohybrid robot implementing neuromuscular actuation and illustrates a path toward th

5 A (lamin A/C) gene have been associated with neuromuscular and cardiac manifestations, but the clinic

6 begf deletion also mimicked Galgt2-dependent neuromuscular and muscular dystrophy phenotypes.

7 transferase that is normally confined to the neuromuscular and myotendinous junction in adult skeleta

8 butes to the morbidity and mortality in many neuromuscular and respiratory diseases.

9 te geroprotectors affect cardiac, cognitive, neuromuscular, and metabolic health.

10 re idiopathic, 15 were congenital, four were neuromuscular, and two were neurofibromatosis.

11 Neuromuscular assessments were completed at baseline and

12 Myasthenia gravis (MG) is a neuromuscular, autoimmune disease caused by autoantibodi

13 vel, and tracheal intubations without use of neuromuscular blockade (p < 0.001).

14 or to a usual-care approach without routine neuromuscular blockade and with lighter sedation targets

15 The benefits of early continuous neuromuscular blockade in patients with acute respirator

16 on (odds ratio, 1.07, 95% CI, 0.90-1.26), or neuromuscular blockade use (odds ratio, 0.95; 95% CI, 0.

17 Continuous neuromuscular blockade was the most common, used in 31%,

18 x adjunctive therapies for PARDS: continuous neuromuscular blockade, corticosteroids, inhaled nitric

19 ntilation, spontaneous breathing trials, and neuromuscular blockade, respectively).

20 which is abolished by dorsal rhizotomy or by neuromuscular blockade.

21 s for anxiety relief; 3) against prescribing neuromuscular blockers during withdrawal of life support

22 luding low tidal volume, prone position, and neuromuscular blockers, demonstrating the negative effec

23 rarenes) as in vivo sequestration agents for neuromuscular blockers, drugs of abuse (methamphetamine

24 ents (17.0%) in the control group received a neuromuscular blocking agent (median dose, 38 mg).

25 om retrospective studies suggest that use of neuromuscular blocking agents during general anaesthesia

26 therefore aimed to assess whether the use of neuromuscular blocking agents is associated with postope

27 The use of neuromuscular blocking agents was associated with an inc

28 ing trials, lung-protective ventilation, and neuromuscular blocking agents).

29 piratory profiles were anaesthetised without neuromuscular blocking agents.

30 We showed that the use of neuromuscular blocking drugs in general anaesthesia is a

31 LGMD was helped by a collaborative effort of neuromuscular centres across Europe.

32 A total of 33 neuromuscular centres from 13 different European countri

33 red Dpr10 and DIP-alpha, for function in the neuromuscular circuit in flies, and reveal roles for hom

34 sted for such scaling in a Drosophila larval neuromuscular circuit, where the muscle receives synapti

35 nd balance beam tests have revealed abnormal neuromuscular co-ordination in ssTnT-knockout mice and a

36 rod and balance beam tests revealed impaired neuromuscular co-ordination in ssTnT-KO mice, indicating

37 isease 2019 (COVID-19) throughout the world, neuromuscular complications and rehabilitation concerns

38 ing that is present either as a feature of a neuromuscular condition or as part of a systemic disease

39 s in DMPK and FXN, which are associated with neuromuscular conditions, and in previously unknown loci

40 ), lipid disorders, cardiac complications of neuromuscular conditions, and vascular disease, includin

41 n technology or for use in the monitoring of neuromuscular conditions.

42 e intrinsic to the larynx rather than due to neuromuscular control.

43 nce of congenital vertebral malformations or neuromuscular defects [1].

44 ed neurotrophic factor (BDNF) correlate with neuromuscular deficits in mouse models of Kennedy's dise

45 inal extension and rescues mitochondrial and neuromuscular degeneration in a Parkinson's disease mode

46 agy and a mitochondrial deficit underlie the neuromuscular degeneration in SBMA and provide alternati

47 Dysregulated RNP granules drive neuromuscular degenerative disease but have not previous

48 G mutation result successively in diabetes, neuromuscular degenerative disease, and perinatal lethal

49 the development of the MitCHAP-60 and SPG13 neuromuscular degenerative disorders.

50 that blood-based RNA-seq is not adequate for neuromuscular diagnostics, whereas myotubes generated by

51 other muscle diseases (n = 265), and without neuromuscular disease (normal, n = 106), we identified a

52 Duchenne muscular dystrophy (DMD) is a fatal neuromuscular disease caused by deleterious mutations in

53 Spinal muscular atrophy (SMA) is a neuromuscular disease caused by deletions or mutations i

54 Spinal muscular atrophy (SMA) is a neuromuscular disease caused by mutations in survival mo

55 inal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) ex

56 ife-threatening and chronically debilitating neuromuscular disease caused by the expansion of a CTG t

57 Spinal muscular atrophy (SMA) is a neuromuscular disease causing the most frequent genetic

58 Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by loss of alpha-mot

59 yotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease characterized by motor neuron (MN)

60 hic lateral sclerosis (ALS) is a progressive neuromuscular disease involving motor neuron death, para

61 ated spinal muscular atrophy is a hereditary neuromuscular disease leading to progressive muscle weak

62 ion of glutamate E303 results in the genetic neuromuscular disease primary dystonia.

63 n (SMN) protein-the loss of which causes the neuromuscular disease spinal muscular atrophy (SMA)-bind

64 ne muscular dystrophy (DMD) is a devastating neuromuscular disease that causes progressive muscle was

65 onic dystrophy type 1 (DM1) is a multisystem neuromuscular disease without cure.

66 isruption of these pathways is implicated in neuromuscular disease, and the recent development of RNA

67 nary hypertension, home respiratory support, neuromuscular disease, immunodeficiency, or cancer were

68 t can be applied more generally to models of neuromuscular disease, such as spinal muscular atrophy,

69 p and administer systemic therapies for this neuromuscular disease.

70 ution about JNK antagonism in this pediatric neuromuscular disease.

71 ents from seven families presenting juvenile neuromuscular disease.

72 Inherited neuromuscular diseases are a heterogeneous group of deve

73 s and clinical abnormalities of a variety of neuromuscular diseases are well known, no curative thera

74 In sum, therapeutic strategies for neuromuscular diseases have shown encouraging results, r

75 apicomplexan parasite, is a leading cause of neuromuscular diseases in dogs as well as fetal abortion

76 hysiology of major human diseases, including neuromuscular diseases of childhood, ischaemia-reperfusi

77 mechanism by which these mutations lead the neuromuscular diseases remains unknown.

78 t content correlates with muscle function in neuromuscular diseases, and changes in fat content prece

79 atrophy, offers hope not only for additional neuromuscular diseases, but also for other disorders tha

80 thological behaviors associated with various neuromuscular diseases, such as regression of motor neur

81 ponsible for motor neuron disorders or other neuromuscular diseases, suggesting a broad phenotypic sp

82 needle electrical impedance to patients with neuromuscular diseases.

83 ept for gene therapy approaches for dominant neuromuscular diseases.

84 t cause multiple hereditary neurological and neuromuscular diseases.

85 n, but MuSK might also be protective in some neuromuscular diseases.

86 s may offer therapeutic promise for treating neuromuscular diseases.

87 apies are currently in clinical use to treat neuromuscular diseases.

88 ing mutations responsible for many monogenic neuromuscular diseases.

89 might prove useful for the treatment of some neuromuscular diseases.

90 tabolism have been reported for a variety of neuromuscular diseases.

91 sitive to change in rare, slowly progressive neuromuscular diseases.

92 tonic dystrophy type 1 (DM1) is an incurable neuromuscular disorder caused by an expanded CTG repeat

93 lbar muscular atrophy (SBMA) is a hereditary neuromuscular disorder caused by CAG trinucleotide expan

94 Spinal muscular atrophy (SMA) is a neuromuscular disorder caused by homozygous mutation or

95 uchenne muscular dystrophy (DMD) is a lethal neuromuscular disorder caused by loss of dystrophin.

96 multifactorial, multisystem pro-inflammatory neuromuscular disorder compromising muscle function resu

97 radation in cellular and mouse models of the neuromuscular disorder spinal bulbar muscular atrophy.

98 uscular dystrophy (DMD) is a severe X-linked neuromuscular disorder that affects males.

99 disease (CMT) is the most common peripheral neuromuscular disorder worldwide.

100 en's Hospital of Philadelphia Infant Test of Neuromuscular Disorders (CHOP INTEND) and the Hammersmit

101 mitter inhibitors that are used for treating neuromuscular disorders and are classified as essential

102 Neuromuscular disorders are often caused by heterogeneou

103 A sequencing (RNA-seq), by using monogenetic neuromuscular disorders as proof of principle.

104 backgrounds, the pathomechanisms underlying neuromuscular disorders might be attributed to the compl

105 lopment, how these pathways are disrupted in neuromuscular disorders, and advances in RNA-mediated th

106 iant class could have importance beyond rare neuromuscular disorders, given an increasing body of evi

107 tal muscles is a common feature of different neuromuscular disorders, which fall outside the mitochon

108 ber of causal genes identified for inherited neuromuscular disorders.

109 ed to advance the diagnosis and treatment of neuromuscular disorders.

110 ell as the complexity of the pathogenesis of neuromuscular disorders.

111 apse assembly and pathological mechanisms of neuromuscular disorders.

112 s potentially applicable to a broad range of neuromuscular disorders.

113 e receptor (AChR) cluster fragmentation, and neuromuscular dysfunction.

114 ole of enteric glial cells (EGCs) in colonic neuromuscular dysfunctions in a mouse model of high-fat

115 Neuromuscular electrical stimulation (NMES) of the lower

116 The application of neuromuscular electrical stimulation (NMES) to paretic l

117 ed controlled trials (nine on cycling, 14 on neuromuscular electrical stimulation alone and 20 on pro

118 d bidirectional communication with implanted neuromuscular electrodes.

119 ation-induced synaptic remodeling and causes neuromuscular endplate degeneration.

120 egulating muscle homeostasis and maintaining neuromuscular endplates after nerve injury.

121 heterozygous knock-in mice displayed smaller neuromuscular endplates that denervated before motor neu

122 toms of hypocalcemia can be due to increased neuromuscular excitation resulting in tetany, paresthesi

123 Neuron-targeted caveolin-1 improves neuromuscular function and extends survival in SOD1(G93A

124 Our goal was to define ASC-1 neuromuscular function and the phenotypical spectrum ass

125 Evidence suggests performance and neuromuscular function decline with age in this populati

126 All aspects of neuromuscular function deteriorated with age (P < 0.05)

127 We concluded that neuromuscular function significantly influenced breathin

128 ers athletes exhibit age-related declines in neuromuscular function that are largely equal across mal

129 of neurotrophic factors may optimally rescue neuromuscular function via effects on both pre- and post

130 f genes in muscle known to play key roles in neuromuscular function, including counteracting the expr

131 impaired endosomal retrograde transport and neuromuscular function, one of the symptoms of SCAR10.

132 entified 261 genes with phenotypes affecting neuromuscular function, tissue integrity, stem cell main

133 Alterations in K(+) regulation can lead to neuromuscular, gastrointestinal, and cardiac abnormaliti

134 into molecular mechanisms for maintenance of neuromuscular health and facilitate screening for therap

135 ng that enables rapid assessment of nematode neuromuscular health.

136 Neuromuscular impairment requires adherence to a rehabil

137 mities, and respiratory insufficiency due to neuromuscular incoordination.

138 Defects in neuromuscular innervation contribute significantly to th

139 Neuromuscular interfaces are required to translate bioel

140 Using the Drosophila larval neuromuscular junction (NMJ) as a model, we provide evid

141 inal Schwann cells (tSCs) at the adult mouse neuromuscular junction (NMJ) by using mice expressing di

142 heir application to the study of adult human neuromuscular junction (NMJ) development, a process requ

143 Neuromuscular junction (NMJ) disruption is an early path

144 Although the frog neuromuscular junction (NMJ) has long been a model synap

145 ptobrevin-2, are expressed at the developing neuromuscular junction (NMJ) in mice, but their specific

146 ces motor end plate volume without affecting neuromuscular junction (NMJ) integrity.

147 The Drosophila melanogaster larval neuromuscular junction (NMJ) is a model synapse with rob

148 The neuromuscular junction (NMJ) is a specialized synapse th

149 ectrical response.SIGNIFICANCE STATEMENT The neuromuscular junction (NMJ) is designed to faithfully e

150 The neuromuscular junction (NMJ) is the site of a number of

151 s suggest that pathological targeting of the neuromuscular junction (NMJ) may play a key role in cach

152 The neuromuscular junction (NMJ) provides the interface betw

153 utions of a macrophage-mediated response for neuromuscular junction (NMJ) reinnervation following ner

154 pled to skeletal muscles interacting via the neuromuscular junction (NMJ) within a microfluidic devic

155 Aging can also impact the neuromuscular junction (NMJ), a synapse that transmits s

156 At the neuromuscular junction (NMJ), early alterations in peris

157 of NAMPT on synaptic vesicle cycling in the neuromuscular junction (NMJ), end-plate structure of NMJ

158 n to be post-translationally modified at the neuromuscular junction (NMJ), hence increasing their sta

159 lized, non-myelinating, synaptic glia of the neuromuscular junction (NMJ), that participate in synaps

160 on of glial cell activity takes place at the neuromuscular junction (NMJ), the output of motor neuron

161 ed y+z+ agrin regulates the formation of the neuromuscular junction (NMJ), while y-z- agrin is widely

162 ators of synapse morphogenesis at the larval neuromuscular junction (NMJ).

163 in (BMP) signaling pathway at the Drosophila neuromuscular junction (NMJ).

164 naptic growth, structure and function at the neuromuscular junction (NMJ).

165 n has been extensively studied at the rodent neuromuscular junction (NMJ).

166 nd intensity of ACh receptor labeling at the neuromuscular junction (NMJ).

167 maintenance of the synaptic structure of the neuromuscular junction (NMJ).

168 eventually resulted in muscle fiber defects, neuromuscular junction abnormalities, compromised motor

169 NLP-12 directly modulates neuromuscular junction activity through the cholecystoki

170 nation, and gait and also related defects in neuromuscular junction architecture.

171 Skeletal muscle and the neuromuscular junction are the earliest sites to manifes

172 imary drivers of sarcopenia and identify the neuromuscular junction as a focal point of mTORC1-driven

173 Using the Drosophila neuromuscular junction as a model, we found that non-enz

174 Prevention of acetylcholine release at the neuromuscular junction causes long-lasting and potential

175 nregulated and gene expression indicators of neuromuscular junction denervation were diminished using

176 ATP) levels and a higher fatigability at the neuromuscular junction during high energy demand.

177 n pathway that coordinates muscle growth and neuromuscular junction expansion.

178 in subsynaptic nuclei and remodeling of the neuromuscular junction following ischemia-induced denerv

179 myofiber formation, long-term survival, and neuromuscular junction formation in vitro.

180 We found that Agrin, a factor critical for neuromuscular junction formation, is elevated in the hip

181 With dysfunction at the neuromuscular junction implicated as a key pathological

182 ed the effect of salbutamol treatment on the neuromuscular junction in the ColQ deficient mouse, a mo

183 Skeletal muscle morphology and neuromuscular junction integrity was not different betwe

184 Neuromuscular junction is a synapse between motoneurons

185 f the effect of adrenergic signalling on the neuromuscular junction is essential to facilitate the de

186 the less prominent role of COL13A1 once the neuromuscular junction is mature.

187 ynaptic compartment of the Drosophila larval neuromuscular junction is regulated by the conserved RNA

188 fn1 to rodents promoted axonal regeneration, neuromuscular junction maturation, and functional recove

189 ction, and the effect on muscle strength and neuromuscular junction morphology was analysed.

190 such as lethality, wing and eye morphology, neuromuscular junction morphology, bang sensitivity and

191 Neuromuscular junction number was unaltered in the media

192 ere alterations in synaptic growth using the neuromuscular junction of Drosophila melanogaster as a m

193 At the embryonic neuromuscular junction of Drosophila melanogaster, mutat

194 At the neuromuscular junction of female Drosophila larvae, we o

195 gnificant decrease in the denervation of the neuromuscular junction of the tibialis anterior muscle i

196 cluding increased motor neuron size, reduced neuromuscular junction pathology, increased muscle fiber

197 essing defects induced by SMN deficiency and neuromuscular junction pathology.

198 is an autoimmune disease in which Abs target neuromuscular junction proteins, in particular the acety

199 flexor digitorum superficialis atrophy, and neuromuscular junction reinnervation.

200 Salbutamol enhances neuromuscular junction synaptic structure by counteracti

201 uper-resolution microscopy at the Drosophila neuromuscular junction we quantitatively map vesicle:Ca(

202 At the Drosophila neuromuscular junction, a presynaptic GluR, DKaiR1D, loc

203 sHB-EGF expression was concentrated at the neuromuscular junction, and Hbegf deletion reduced Galgt

204 role in stabilizing the developing mammalian neuromuscular junction, but MuSK might also be protectiv

205 sexes for defects in synaptic growth at the neuromuscular junction, identifying 12 mutants with seve

206 tive as therapies for human disorders of the neuromuscular junction, in particular many subsets of co

207 At the Drosophila neuromuscular junction, inhibition of postsynaptic gluta

208 complement proteins that target muscle, the neuromuscular junction, peripheral nerves, the spinal co

209 changes to the structure and function of the neuromuscular junction, suggesting novel roles for MuSK

210 receptor (AChR) and inhibit signaling at the neuromuscular junction.

211 caffolding protein, rapsyn, as at the intact neuromuscular junction.

212 ptic boutons at the axon terminals of larval neuromuscular junction.

213 dies and immunohistochemical analysis of the neuromuscular junction.

214 oline receptor (AChR) is the hallmark of the neuromuscular junction.

215 r muscle channelopathies and diseases of the neuromuscular junction.

216 ctionally validated factors expressed at the neuromuscular junction.

217 ons in the spinal cord or denervation at the neuromuscular junction.

218 holinesterase inhibitors on the postsynaptic neuromuscular junction.

219 e and to long-term structural changes at the neuromuscular junction.

220 growth of synapses at the Drosophila larval neuromuscular junction.

221 By studying Drosophila neuromuscular junctions (NMJs) we show that AZs consist

222 At mammalian neuromuscular junctions (NMJs), prolonged inactivity lea

223 on and number of proprioceptive synapses and neuromuscular junctions (NMJs), while having no effects

224 vious loss of boutons and synapses at larval neuromuscular junctions (NMJs).

225 physiological and histological properties of neuromuscular junctions and muscle at P21 and motoric de

226 d muscle enables the formation of functional neuromuscular junctions in single organoids.

227 In addition, the neuromuscular junctions of salbutamol treated mice showe

228 Neuromuscular junctions on slow fibers became multiply i

229 orms of homeostatic plasticity at Drosophila neuromuscular junctions to stabilize synaptic communicat

230 plasticity (PHP) is induced at degenerating neuromuscular junctions, mediated by an evolutionarily c

231 motor function and improved the integrity of neuromuscular junctions, MOE-modified ASO10-29 (MOE10-29

232 n increased number of active zones in larval neuromuscular junctions, representing large glutamatergi

233 At GABAergic neuromuscular junctions, the short isoform MADD-4B binds

234 with kinesin, only on nuclei associated with neuromuscular junctions, whereas all adult cardiomyocyte

235 ects on synaptic innervation and function at neuromuscular junctions.

236 e A GABA receptors (GABA(A)Rs) at inhibitory neuromuscular junctions.

237 d to support the function of motoneurons and neuromuscular junctions.

238 e, but did improve axonal (re)innervation of neuromuscular junctions.

239 d axonal swellings in their spinal cords and neuromuscular junctions.

240 he postsynaptic regions of the glutamatergic neuromuscular junctions.

241 y 16, with an inflammatory infiltrate in the neuromuscular layers including eosinophils, CD3-positive

242 nd 51% of patients with combined cardiac and neuromuscular manifestations and 37% and 33% of those wi

243 Neuromuscular manifestations preceded cardiac signs by a

244 Neuromuscular manifestations were more frequent in this

245 The neuromuscular model consists of: 1.

246 The neuromuscular model counteracts friction to recover thes

247 e, and use it to develop a simple, reflexive neuromuscular model from physical principles.

248 We found that the neuromuscular modules of stepping and kicking differ sub

249 The use of neuromuscular monitoring (OR(adj) 1.31, 95% CI 1.15-1.49

250 icular strain information within the complex neuromuscular networks controlling posture and movement.

251 nematode Caenorhabditis elegans is a simple neuromuscular organ with a self-contained, autonomously

252 r data revealed the unexpected complexity of neuromuscular organization in this basal metazoan lineag

253 otor neurons, represent the primary locus of neuromuscular pathology in cancer cachexia.

254 that Col4a1 mutant mice develop progressive neuromuscular pathology that models human disease.

255 f skeletal muscle-derived BDNF in regulating neuromuscular physiology in vivo remains unclear.

256 four weeks of detraining, suggesting lasting neuromuscular re-training adaptations.

257 The pathogenic mechanism and the neuromuscular reflex-related phenotype (e.g. tremors acc

258 However, the neuromuscular reflex-related symptoms of ANM have not be

259 rience partial vascular occlusion or altered neuromuscular reflexes.

260 s conducted by the Cooperative International Neuromuscular Research Group (CINRG) and evaluated drug-

261 n steady-state and progressive metabolic and neuromuscular responses to exercise.

262 Gastric neuromuscular sections from adult female C57BL/6 J mice

263 in many cases via potent depression of human neuromuscular signaling by snake alpha-neurotoxins.

264 and nitrergic relaxation of circular gastric neuromuscular strips were assessed.

265 erve injury and its promotion might mitigate neuromuscular symptoms in mild SMA.

266 lved in the formation and maintenance of the neuromuscular synapse that appears independent of the Ag

267 Here, we examine how Drosophila neuromuscular synapses grow to match the size of their t

268 spontaneous neurotransmission at developing neuromuscular synapses in mice.

269 In addition, neuromuscular synapses in vezatin mutant mice display pr

270 Complex mechanisms are required to form neuromuscular synapses, direct their subsequent maturati

271 rotubules (MT) and actin, is concentrated at neuromuscular synapses, where it binds Rapsyn and serves

272 octopamine-mediated structural plasticity of neuromuscular synapses, whereas tyramine reduces locomot

273 on, and long-term stabilization of mammalian neuromuscular synapses.

274 aboration and postnatal maturation of murine neuromuscular synapses.

275 and then we monitor dendrite morphology and neuromuscular synaptic partnerships.

276 ipulation there are permanent alterations in neuromuscular synaptic partnerships.

277 three-dimensional locomotion challenges the neuromuscular system in a manner distinct from standard

278 ronal pathways in the brain, spinal cord and neuromuscular system of cats, rats and zebrafish, that t

279 The Drosophila larval neuromuscular system provides an ideal context in which

280 cnidarian polyp with an anatomically simple neuromuscular system that can offer evolutionary insight

281 Focusing on the Drosophila leg neuromuscular system, we show that the stereotyped termi

282 l for normal development and function of the neuromuscular system.

283 and likewise, affects the development of the neuromuscular system.

284 Here, we describe the organization of neuromuscular systems in eight ctenophore species focusi

285 pression and nitrergic relaxation in gastric neuromuscular tissues exposed to in-vitro hyperglycemia

286 he ErbB tyrosine kinase inhibitors to induce neuromuscular toxicity in a developing organism via a me

287 ur data thus support the hypothesis that the neuromuscular transformation changes over vocal developm

288 ur data thus support the hypothesis that the neuromuscular transformation changes over vocal developm

289 rogeneous collection of genetic disorders of neuromuscular transmission characterized by fatiguable m

290 stsynaptic membrane and may lead to enhanced neuromuscular transmission.

291 otransmitter release, which leads to minimal neuromuscular transmission.

292 tested had results consistent with abnormal neuromuscular transmission.

293 able muscle weakness resulting from impaired neuromuscular transmission.

294 athological conditions with reduced synaptic neuromuscular transmission.

295 have been recent developments in the use of neuromuscular ultrasound and MRI to aid in diagnosing MM

296 here a biohybrid swimmer driven by on-board neuromuscular units.

297 nsitive flagellar swimmers actuated by these neuromuscular units.

298 scle and innervate it, developing functional neuromuscular units.

299 pathophysiological features with a number of neuromuscular wasting conditions, including age-related

300 r data show Hb acts as a potent regulator of neuromuscular wiring decisions.