ライフサイエンスコーパス: muscle fibre

1 ontact between motor axons and each skeletal muscle fibre.

2 reparation or a skinned slow-twitch skeletal muscle fibre.

3 n the basal lamina and the sarcolemma of the muscle fibre.

4 hanced electrical signalling over the entire muscle fibre.

5 ins co-localize to costameric regions of the muscle fibre.

6 etween the sensory neuron and the intrafusal muscle fibre.

7 osin regulatory light chain in demembranated muscle fibres.

8 voltage range relevant for AP initiation in muscle fibres.

9 eurons, the neuromuscular junction (NMJ) and muscle fibres.

10 ysiological signals and metabolic demands on muscle fibres.

11 brane of many cell types, including skeletal muscle fibres.

12 nd in the proximity of mitochondria in adult muscle fibres.

13 nduced myopathy in both cardiac and skeletal muscle fibres.

14 (MC) decreased in both type 1 and 2A skinned muscle fibres.

15 vasoactive agents or contraction of adjacent muscle fibres.

16 n of both types of mtDNA deletions in single muscle fibres.

17 g the resting membrane potential of skeletal muscle fibres.

18 ein abundance in large numbers of individual muscle fibres.

19 oxidase (COX)-deficient regions in skeletal muscle fibres.

20 ct action of radially oriented diaphragmatic muscle fibres.

21 ically beneficial, especially in slow-twitch muscle fibres.

22 l death due to an absence of multi-nucleated muscle fibres.

23 oth these situations, there is a net loss of muscle fibres.

24 dependent electrical properties of mammalian muscle fibres.

25 lasmic surface of the sarcolemma of striated muscle fibres.

26 sential for the formation of multi-nucleated muscle fibres.

27 cellular sites for ROS and RNS production in muscle fibres.

28 imize blood flow to the metabolically active muscle fibres.

29 tructure of the DGC causing severe damage to muscle fibres.

30 addition, nau mutant embryos display thinner muscle fibres.

31 remodelling of the triads in adult skeletal muscle fibres.

32 tes and fast-twitch and slow-twitch skeletal muscle fibres.

33 imilar between cardiac myocytes and skeletal muscle fibres.

34 s and from intact and skinned fast mammalian muscle fibres.

35 ow, CS were composed of >/= 69% Type IIb/d/x muscle fibres.

36 ruitment) in predominantly highly glycolytic muscle fibres.

37 soluble aggregates in the nuclei of skeletal muscle fibres.

38 to record sodium currents from intact mouse muscle fibres.

39 MBD2 in vitro, in myotubes, and in isolated muscle fibres.

40 of force production in fast twitch skeletal muscle fibres.

41 ogical functions in adult mammalian skeletal muscle fibres.

42 ctions in isolated intact mammalian skeletal muscle fibres.

43 sponses to step current pulses in individual muscle fibres.

44 he somite, by contrast, elongate into medial muscle fibres.

45 of Ca(2+) spark appearance in permeabilized muscle fibres.

46 itochondrial proteins in thousands of single muscle fibres.

47 lasts, whereas mef2c expression commences in muscle fibres.

48 T-jump) in shortening and lengthening active muscle fibres.

49 g the role of potassium released by skeletal muscle fibres.

50 dult stages that had stopped recruiting fast muscle fibres.

51 deletions in approximately one-third of all muscle fibres.

52 ological PO2 in intact single mouse skeletal muscle fibres.

53 ng SR Ca(2+) pumping rate in single skeletal muscle fibres.

54 regated in the central regions of intrafusal muscle fibres.

55 [Ca(2)(+) ] during contractions of isolated muscle fibres.

56 and demonstrate a marked reduction in fused muscle fibres.

57 y a lack of dystrophin expression in patient muscle fibres.

58 y the intrinsic force-generating capacity of muscle fibres.

59 maintenance of excitability in active human muscle fibres.

60 the dominant cause of insulin resistance in muscle fibres.

61 ed by high-resolution respirometry on single muscle fibres.

62 c force in fast- and slow-twitch muscles and muscle fibres.

63 to mitochondrial ROS generation in skeletal muscle fibres.

64 icated in structure and function of skeletal muscle fibres (ACTG1), neuronal maintenance and signal t

65 on electrical properties is not regulated by muscle fibre activity but rather by a retrograde signall

66 leaves open the possibility that the loss of muscle fibre activity underlies the observed effects.

67 Single mouse muscle fibres acutely treated with nitrite had a lower f

68 al muscle fibres, the contribution of single muscle fibre adaptations to ageing-induced atrophy and f

69 emote dilatations to contraction of skeletal muscle fibres also occur.

70 ldtype androgen receptor (AR) exclusively in muscle fibres and a knockin (KI) model expressing a huma

71 tributable to K(+) released from contracting muscle fibres and acting extraluminally on arterioles.

72 has primarily come from in vitro studies of muscle fibres and analysis of optical diffraction patter

73 structural myopathy with numerous lobulated muscle fibres and considerable myofibrillar alterations

74 cy did not have the negative consequences to muscle fibres and extracellular matrix observed in mouse

75 h larger cross-sectional area of fast-twitch muscle fibres and favoured strength/power vs. endurance/

76 es of ANM such as atrophy of extrafusal slow muscle fibres and increased fatigability.

77 in are influenced by the interaction between muscle fibres and motor nerves.

78 This suggests that PGE(2) released from muscle fibres and PGI(2) released from capillaries and v

79 specific events in SMA, including atrophy of muscle fibres and post-synaptic motor endplates, loss of

80 Isolated intact single mouse muscle fibres and rat muscles in-situ treated with CK-20

81 s underneath the basal lamina that surrounds muscle fibres and respond to damage by giving rise to tr

82 in isoforms of class II myosins are found in muscle fibres and show a large variety of different mech

83 strongly associated with larger fast-twitch muscle fibres and strength/power performance versus endu

84 ation between CP and highly oxidative type I muscle fibres and that muscle metabolic steady-state is

85 n-alpha2, which compromises the stability of muscle fibres and the myelination of peripheral nerves.

86 ROS production in both cardiac and skeletal muscle fibres and the prevention of DOX-induced increase

87 ranscripts in perifascicular capillaries and muscle fibres, and occlusion of larger perimysial blood

88 e of extensive proliferation, contributes to muscle fibres, and Pax7(+)luciferase(+) mononucleated ce

89 stration of ClC-1 inhibition in active human muscle fibres, and we determine the changes in ClC-1 gat

90 icularly to identify the mechanisms by which muscle fibres are completely lost with increasing age.

91 These data show that mdx muscle fibres are depolarized after an injurious bout of

92 Muscle fibres are multinucleated post-mitotic cells that

93 muscle and stabilizes Ca(2+) transients when muscle fibres are subjected to osmotic shock injury (OSI

94 ctions of glucocorticoids, in adult skeletal muscle fibres, are mediated by a glucocorticoid receptor

95 vatives of which--both slow--and fast-twitch muscle fibres--are themselves significantly disorganised

96 and composition, leg lean mass and skeletal muscle fibre area all remained unchanged following the a

97 triguingly, we also observed changes in slow muscle fibre arrangement; previously, Dok-7 has not been

98 ulations of the electrical properties of the muscle fibre as long as Kir channels were assumed to be

99 ed muscle mass, hypotrophy and hypoplasia of muscle fibres, as well as an increase in oxidative fibre

100 an indication of the structural registry in muscle fibres, as well as the contractile strains produc

101 the start of electrical stimulation in frog muscle fibres at 4 degrees C.

102 the start of electrical stimulation in frog muscle fibres at 4 degrees C.

103 ) in maximally Ca(2+)-activated rabbit psoas muscle fibres at 8-9 degrees C (the fibre length (L(0))

104 NO in isolated single mature mouse skeletal muscle fibres at rest and following a period of contract

105 that likely reflects the gastric sling/clasp muscle fibres at the OCJ.

106 ATP is released into the interstitium from muscle fibres, at least in part through cystic fibrosis

107 ain the pathological basis of perifascicular muscle fibre atrophy in dermatomyositis.

108 in maximum muscle fibre force and preceding muscle fibre atrophy was observed in the diaphragm in re

109 nt of myosin molecules to actin monomers and muscle fibre atrophy.

110 d in the rate of clonal expansion throughout muscle fibres between mtDNA deletions of different sizes

111 itively with their percentage type IIb + d/x muscle fibres (blood flow: r = 0.74, vascular conductanc

112 metabolism in isolated, intact long skeletal muscle fibre bundles from adult mice.

113 t of cellular respiration in intact skeletal muscle fibre bundles obtained from the extensor digitoru

114 Detergent-skinned cardiac muscle fibre bundles were used to study how the interpla

115 Treating small skeletal muscle fibre bundles with the synthetic glucocorticoid b

116 itochondrial parameters in isolated skeletal muscle fibre bundles.

117 nction and fuel utilisation in live skeletal muscle fibre bundles.

118 oduction in isolated, intact, mouse skeletal muscle fibre bundles.

119 ions in mouse fast- and slow-twitch skeletal muscle fibre bundles.

120 l role in isolated intact mammalian skeletal muscle fibre bundles.

121 and the proportional abundance of oxidative muscle fibres, but in highlanders, these traits were unc

122 myosin-containing thick filaments in nascent muscle fibres, but not for the earlier steps of skeletal

123 e furthest longitudinally through individual muscle fibres by means of a greater rate of clonal expan

124 ensures increased oxygen delivery to active muscle fibres by reducing upstream resistance via comple

125 s, whereas acute knock-down of RYR1 in mouse muscle fibres by siRNA caused up-regulation of HDAC-4/HD

126 mplete loss of large supervillin isoforms in muscle fibres by western blot and immunohistochemical an

127 They consist of specialized skeletal muscle fibres, called intrafusal fibres, which are inner

128 hich accumulate to high levels in individual muscle fibres causing a respiratory defect.

129 s contraction that affects a small number of muscle fibres, causing a flicker of movement under the s

130 ed limb, whereas metamorphosed newts recruit muscle fibre cells in the stump for the same purpose.

131 More severe muscle fibre coagulation and denaturation were observed

132 amyloid beta (A4) precursor protein (APP) in muscle fibres coincides with symptom onset in both spora

133 was enhanced in S1PR3-null mice, with bigger muscle fibres compared to control mice.

134 n to define the influence loss of the VDR on muscle fibre composition, protein synthesis, anabolic an

135 measure of the strength of intrafusal bag(2) muscle fibre contacts, but not to a measure of bag(1) co

136 COX-deficient skeletal muscle fibres contained supra-threshold levels of multip

137 rophin glycoprotein complex were restored in muscle fibres containing donor-derived dystrophin.

138 uscle fiber analysis showed that, the type I muscle fibre content was substantially higher in Jeju ho

139 s, including motor unit activation patterns, muscle fibre contractile properties and bioenergetic fun

140 K(+) released from active skeletal muscle fibres could facilitate vasodilatation in proport

141 associated with abnormal oxygen transport to muscle fibres critically depends on the objective charac

142 Muscle fibre cross sectional area and protein synthesis

143 KEY POINTS: Muscle fibre cross sectional area is enhanced with massa

144 Muscle fibre cross sectional area was enhanced by 18% wi

145 te cells impaired post-burn recovery of both muscle fibre cross-sectional area and volume (P < 0.05).

146 e deacetylases (HDACs) move between skeletal muscle fibre cytoplasm and nuclei in response to various

147 ex (DGC) provides an essential link from the muscle fibre cytoskeleton to the extracellular matrix.

148 rt the hypotheses that the specific force of muscle fibres decreased following unilateral lower limb

149 ly altered in the absence of caspase-12, but muscle fibre degeneration found in the mdx mouse was red

150 tic deletion in mice results in a paucity of muscle fibres demonstrating its requirement for normal m

151 Growth and maintenance of skeletal muscle fibres depend on coordinated activation and retur

152 In muscle fibres derived from cells that had been transduce

153 reduced muscle fibrosis, earlier increase in muscle fibre diameter and a short-term benefit in reduci

154 fibrillar and sarcoplasmic proteins, smaller muscle fibre diameter and lower myofibril fragmentation

155 By contrast, mouse muscle fibres did not respond unless channel-opening dru

156 s, but not for the earlier steps of skeletal muscle fibre differentiation, elongation, fusion or thin

157 eral aspects of fetal development, including muscle fibre differentiation.

158 d cessation (V(o)(2)off)) in single skeletal muscle fibres differing in oxdidative capacity, and acro

159 set ( ) and cessation ( ) in single skeletal muscle fibres differing in oxidative capacity, and acros

160 Whether this reflects the recruitment of muscle fibres differing in oxidative capacity, or slowed

161 will be correlated with type I and type IIx muscle fibre distributions, respectively.

162 escribed to illustrate how ROS released from muscle fibres during exercise may help maintain the inte

163 During 10 Hz trains of muscle fibre electrical stimulation, the nuclear efflux

164 te that the aged muscle stem cell niche, the muscle fibre, expresses Fgf2 under homeostatic condition

165 it (MU) remodelling acts to minimise loss of muscle fibres following denervation in older age, which

166 ease is enhanced in isolated single skeletal muscle fibres following NO(3) (-) supplementation or NO(

167 urrents from intact murine (C67BL6) skeletal muscle fibres for the first time.

168 A rapid and early decline in maximum muscle fibre force and preceding muscle fibre atrophy wa

169 At the cellular level, single muscle fibre force production was reduced in OA patients

170 (P < 0.05) with the proportion of oxidative muscle fibres found in the individual muscles or muscle

171 Muscle fibres from a patient harbouring the R1135H mutat

172 ible for force transduction and protects the muscle fibres from contraction induced damage.

173 We proposed that in muscle fibres from patients with mtDNA maintenance disor

174 tion Facility from small bundles of skeletal muscle fibres from Rana esculenta at sarcomere lengths b

175 reported that flexor digitorum brevis (FDB) muscle fibres from S100A1 knock-out (KO) mice exhibit a

176 Cardiac muscle fibres from these mice contained approximately 80

177 ts in isolated flexor digitorum brevis (FDB) muscle fibres from wild-type and S100A1 knock-out (KO) m

178 Following disuse, muscle fibre function goes through adaptations such as a

179 It is generally assumed that muscle fibres go through atrophy following disuse with a

180 d subsequent recruitment of poorly efficient muscle fibres has been proposed to mediate this decline.

181 The contractile properties of muscle fibres have been extensively investigated by fast

182 Here we show that different muscle fibres have distinct regulatory roles during rege

183 brane of many cell types, including skeletal muscle fibres; however, the exact localisation of these

184 It has been debated whether muscle fibre hypertrophy requires activation and fusion

185 onstrate that hemidiaphragm paralysis causes muscle fibre hypertrophy, maintaining global oxygen supp

186 2 or disruption of the Dio2 gene in skeletal muscle fibres impaired acute exercise-induced PGC-1a exp

187 ing reduced the myofibril fractional area of muscle fibres in both groups.

188 rmatomyositis, lupus nephritis, and necrotic muscle fibres in Duchenne dystrophy.

189 SV2) protein for the structural integrity of muscle fibres in humans and show that recessive loss-of-

190 ration in quiescent and contracting skeletal muscle fibres in real time, although peroxynitrite and o

191 mutations produce depolarization of skeletal muscle fibres in response to reduced extracellular potas

192 onse to 3 kHz oscillations imposed on single muscle fibres in rigor.

193 ng a novel ecological context for glycolytic muscle fibres in small birds.

194 Striated muscle fibres in the urethral rhabdosphincter are innerv

195 raction, adenosine is released from skeletal muscle fibres independently of NO and acts directly on A

196 work shows that the metabolic property of a muscle fibre is a key factor in regulating the expressio

197 ctions of DHT in isolated mammalian skeletal muscle fibres is to stimulate amino acid uptake.

198 charge movements (Q) and SR Ca2+ release of muscle fibres isolated from adult mice.

199 es) and the joint angle at which the optimum muscle fibre length occurred (phi).

200 joint range of motion and therefore range of muscle fibre lengths only part of the force-length curve

201 geing on structure and functions of skeletal muscle fibres, likely to be due to a complex interplay b

202 tization, bone fracture, muscle fibrosis and muscle fibre loss.

203 ith advancing age, probably acting to reduce muscle fibre loss.

204 sted to represent a mechanism by which human muscle fibres maintain their excitability during sustain

205 All muscle fibres maintained a longitudinal, fibre parallel

206 ing misregulation of DMD exon 78 compromises muscle fibre maintenance and contributes to the progress

207 s that additional recruitment of inefficient muscle fibres may not be the sole mechanism contributing

208 evere flaccid muscle paralysis, in which the muscle fibre membrane becomes electrically inexcitable,

209 this ratio and whole body oxygen uptake and muscle fibre mitochondrial content.

210 separated by 5 min of rest in intact single muscle fibres (n = 7) isolated from Xenopus laevis.

211 ed body mass gain and food intake, increased muscle fibre necrosis, plasma creatine kinase levels, mu

212 oesophagus including functional epithelium, muscle fibres, nerves and vasculature.

213 ression is localized along the length of the muscle fibre, not just at the synapse, and is fibre-type

214 tion of denervated fibres acting to preserve muscle fibre number, but little data are available in fe

215 mitochondrial parameters of intact skeletal muscle fibres obtained from adult mice.

216 ng, structural and functional alterations of muscle fibres occur.

217 random coils and aromatic side chains in the muscle fibres of both muscles.

218 rmonic frequencies of light generated in the muscle fibres of live mice and humans.

219 tudy, we show that Nogo-A levels increase in muscle fibres of SOD1(G93A) mice along with the elevatio

220 mechanisms, namely, the force applied by the muscle fibres on the ribs into which they insert (insert

221 were: the ratio of tendon resting length to muscle fibre optimum length (L(TR):L(F.OPT)) (varied fro

222 PT)) (varied from 0.5 to 11.5), the ratio of muscle fibre optimum length to average moment arm (L(F.O

223 volving alterations in somitic structure and muscle fibre organization as well as defects in developi

224 Transgenic mouse muscle fibres over-expressing HDAC-4/HDAC-5 exhibited de

225 muscle parts consisting of 35% type IIb+d/x muscle fibres (P < 0.05).

226 ory infiltrate with invasion of non-necrotic muscle fibres (partial invasion) and amyloid or 15-18 nm

227 etric force (c) (varied from 0 to 0.08), the muscle fibre pennation angle (theta) (varied from 0 degr

228 his study we investigated connection between muscle fibre phenotype and the DGC.

229 tion respirometry performed in permeabilized muscle fibres prepared from muscle biopsies.

230 eceptor (AChR) clusters in the middle of the muscle fibre prior to motor neuron contact.

231 Available evidence supports the idea that muscle fibres provide retrograde signals that enable the

232 and above CS would support that the greatest muscle fibre recruitment above, relative to below, CS oc

233 mechanism linking local vasodilatation with muscle fibre recruitment during exercise.

234 tation during exercise which demands greater muscle fibre recruitment independent of the total amount

235 ipants performed two exercise bouts in which muscle fibre recruitment was manipulated while total con

236 nnels underlies vasodilatation with elevated muscle fibre recruitment when work rate is increased (Pr

237 asodilatation in proportion to the degree of muscle fibre recruitment.

238 ve skeletal muscle is augmented with greater muscle fibre recruitment.

239 determined via immunohistochemistry, as were muscle fibre regeneration and myonuclear apoptosis.

240 s revealed that miR-133b deletion influences muscle fibre regeneration, satellite cell proliferation

241 t regulation of excitability of active human muscle fibres relies on PKC-dependent ClC-1 inhibition v

242 d exon 78 missplicing switch in mice induces muscle fibre remodelling and ultrastructural abnormaliti

243 icrospectroscopy on connective tissue and in muscle fibres rigorously identified for sub-type.

244 Recent studies in rat muscle fibres show that repetitive firing of action pote

245 Thus, quantitative changes in muscle fibre size and contractile proteins are not the d

246 saged limb exhibited a comparable 17% higher muscle fibre size compared to reloading alone, and myofi

247 sing microcomputed tomagraphic scanning, and muscle fibre size distribution and fibrosis were followe

248 Skeletal muscle fibre size is highly variable, and while diffusio

249 nia, fibrosis and a shift to smaller average muscle fibre size lasting up to 5 weeks from injury.

250 ges occurred without alterations in skeletal muscle fibre size or type.

251 Detailed tissue geometry, such as muscle fibre size, has been incorporated into such measu

252 ns of whole muscle size and strength, single muscle fibre size, ultrastructure and tension and myosin

253 By contrast to extrafusal muscle fibres, spindle intrafusal fibres of normal mice

254 sults indicate that impairment of individual muscle fibre structure and function is a major feature o

255 n intact loose-patch clamped murine skeletal muscle fibres subject to a double pulse procedure.

256 c characteristics of highly oxidative type I muscle fibres, such that a muscle metabolic steady-state

257 tructural protein, dystrophin, which renders muscle fibres susceptible to injury and degeneration.

258 series of anatomically distinct slow twitch muscle fibres that characteristically express genes enco

259 OS balance is compromised in intact skeletal muscle fibres that underwent osmotic shock and whether t

260 In striated muscle fibres, the binding of myosin motors to actin fil

261 tudies on the impact of ageing on individual muscle fibres, the contribution of single muscle fibre a

262 f most of the properties of IKir in skeletal muscle fibres, the model demonstrates that a substantial

263 ex36 mutation and suggests that in skeletal muscle fibres there is a functional reserve of RyR1.

264 ughout muscle development and that, in adult muscle fibres, they were localised in the extracellular

265 The first slow twitch muscle fibres to differentiate, which are specified by t

266 for the first time in single human skeletal muscle fibres to measure muscle mechanics, including cro

267 system of mechanically skinned rat skeletal muscle fibres to measure SOCE during intracellular Ca2+

268 from the accumulation of metabolites within muscle fibres to the generation of an inadequate motor c

269 skeletal muscle shifted toward an oxidative muscle fibre type and, in parallel, increased myofibre s

270 2 week aerobic training protocol on skeletal muscle fibre type distribution and satellite cell conten

271 We show that the W' is not correlated with muscle fibre type distribution and that it represents an

272 ole-body exercise and their relationships to muscle fibre type.

273 elationship between W' (19.4 +/- 6.3 kJ) and muscle fibre type.

274 n was associated with the discovery of mixed muscle fibre types (i.e. both fast glycolytic and fast o

275 ueous suspensions of myofibrils according to muscle fibre types and cellular compounds (oxidants and

276 he bioenergetic characteristics of different muscle fibre types and the power-duration relationship.

277 between the bioenergetic characteristics of muscle fibre types and the power-time relationship for h

278 uced (>60%) in both glycolytic and oxidative muscle fibre types despite an increase in a major regula

279 Both muscle fibre types expressed a cytosolic GCR.

280 e differentiation of several early zebrafish muscle fibre types.

281 mouse flexor digitorum brevis (FDB) skeletal muscle fibres under voltage clamp, using confocal micros

282 3) respiration was measured in permeabilized muscle fibres using high-resolution respirometry with se

283 It was studied on isolated muscle fibres using synthetic localized increases in Ca2

284 Contraction of skeletal muscle fibres via electrical field stimulation produced

285 firing leads to substantial changes in both muscle fibre volume and Ri.

286 the specific cytosolic resistivity (Ri) and muscle fibre volume remained constant during the repeate

287 Each muscle fibre was perfused with Tyrode solution pre-equil

288 The average growth in diameter of fast muscle fibres was checked with fasting and significant f

289 In small bundles and single muscle fibres, we demonstrate automated recordings of (i

290 n (HDAC4-GFP) expressed in isolated skeletal muscle fibres, we now show that activation of PKA by the

291 Furthermore, muscle fibres went through extensive qualitative changes

292 tendon force were significantly lower; (ii) muscle fibres went through significant atrophy and impai

293 Isolated single mouse muscle fibres were fatigued by 100 repeated 350 ms contr

294 However, skeletal muscle fibres were hypotrophic and their nuclei were mor

295 Muscle fibres were isolated from the flexor digitorum br

296 ndingly, the passive mechanics of individual muscle fibres were not altered.

297 actin ratio and myosin content in individual muscle fibres were not altered; (iv) the muscle proteome

298 ed large-scale mtDNA deletions in individual muscle fibres with 20% of cytochrome c oxidase-deficient

299 kness associated with an increased number of muscle fibres with central nuclei at the perimysium and

300 c physiological sphincter of circular smooth-muscle fibres within the abdominal oesophagus.