ライフサイエンスコーパス: muscle fibre

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

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

3 hanced electrical signalling over the entire muscle fibre.

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

5 h) to an otherwise isometrically contracting muscle fibre.

6 ontact between motor axons and each skeletal muscle fibre.

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

8 ct action of radially oriented diaphragmatic muscle fibres.

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

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

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

12 dependent electrical properties of mammalian muscle fibres.

13 lasmic surface of the sarcolemma of striated muscle fibres.

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

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

16 imize blood flow to the metabolically active muscle fibres.

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

18 addition, nau mutant embryos display thinner muscle fibres.

19 remodelling of the triads in adult skeletal muscle fibres.

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

21 imilar between cardiac myocytes and skeletal muscle fibres.

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

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

24 and demonstrate a marked reduction in fused muscle fibres.

25 ruitment) in predominantly highly glycolytic muscle fibres.

26 soluble aggregates in the nuclei of skeletal muscle fibres.

27 to record sodium currents from intact mouse muscle fibres.

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

29 of force production in fast twitch skeletal muscle fibres.

30 ogical functions in adult mammalian skeletal muscle fibres.

31 ctions in isolated intact mammalian skeletal muscle fibres.

32 sponses to step current pulses in individual muscle fibres.

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

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

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

36 lasts, whereas mef2c expression commences in muscle fibres.

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

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

39 dult stages that had stopped recruiting fast muscle fibres.

40 f SR refilling of 1-2 min measured in intact muscle fibres.

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

42 force must reflect impaired processes in the muscle fibres.

43 TnT(E162DEL) and cTnT(K211DEL) reconstituted muscle fibres.

44 stigated in resting Rana temporaria striated muscle fibres.

45 luence of bag1 (b1) and bag2 (b2) intrafusal muscle fibres.

46 rms aggregates within the nuclei of skeletal muscle fibres.

47 effects of P(i) and temperature on force in muscle fibres.

48 invade ICOS-L- and MHC class I-co-expressing muscle fibres.

49 maintenance of excitability in active human muscle fibres.

50 the dominant cause of insulin resistance in muscle fibres.

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

52 to mitochondrial ROS generation in skeletal muscle fibres.

53 osin regulatory light chain in demembranated muscle fibres.

54 voltage range relevant for AP initiation in muscle fibres.

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

56 ysiological signals and metabolic demands on muscle fibres.

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

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

59 nduced myopathy in both cardiac and skeletal muscle fibres.

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

61 vasoactive agents or contraction of adjacent muscle fibres.

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

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

64 g the resting membrane potential of skeletal muscle fibres.

65 ein abundance in large numbers of individual muscle fibres.

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

67 d re-activation of muscle, but in this study muscle fibre activity and evoked acetylcholine release w

68 s recovered to normal despite the absence of muscle fibre activity and evoked release.

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

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

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

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

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

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

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

76 from AMP that is released from the skeletal muscle fibres and dephosphorylated by ecto 5'nucleotidas

77 II content is elevated in fatigue resistant muscle fibres and exercise trained muscle.

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

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

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

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

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

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

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

85 ia the provision of mechanical links between muscle fibres and the basement membrane.

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 Approximating the muscle fibres as a single sarcomere in both muscles and

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

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

102 and peak power in rat fast- and slow-twitch muscle fibres at 15 degrees C and 30 degrees C.

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

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

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

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

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

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

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

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

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

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

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

114 (0.1-10 L(0) s(-1)) of tetanized intact rat muscle fibre bundles (L0 approximately 2 mm) with a rest

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

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

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

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

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

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

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

122 itochondrial parameters in isolated skeletal muscle fibre bundles.

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

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

125 ectively removed from bovine cardiac skinned muscle fibres by gelsolin, and the actin filament was re

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

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

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

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

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

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

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

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

136 these two cTnT mutants were reconstituted in muscle fibres containing beta-MHC; by approximately 24%

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

138 d (BRE) men to examine slow- and fast-twitch muscle fibre contractile function.

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

140 ases in tension cost in alpha-MHC-containing muscle fibres corresponded to 17% (P < 0.01) and 23% (P

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 During the unloading period, soleus muscle fibre cross-section decreased by 38%.

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

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

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

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

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

151 ents were used because our previous study on muscle fibres demonstrated that the temperature effect w

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

153 In muscle fibres derived from cells that had been transduce

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

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

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

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

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

162 clei of cultured dissociated adult mouse FDB muscle fibres during slow-twitch fibre type electrical s

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

164 cay of nuclear NFATc1-GFP after cessation of muscle fibre electrical stimulation, whereas inhibition

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

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

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

168 Slow muscle fibres form and commence normal migration in the

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

170 Muscle fibres from a patient harbouring the R1135H mutat

171 Intact skeletal muscle fibres from adult mammals exhibit neither spontan

172 otein (GFP) in flexor digitorum brevis (FDB) muscle fibres from adult mouse.

173 Muscle fibres from normal and PTU-treated rat hearts wer

174 ynamic analysis of cTnT mutant reconstituted muscle fibres from normal and PTU-treated rat hearts.

175 tension and ATPase activity were measured in muscle fibres from normal rat hearts containing alpha-MH

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

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

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

179 Cardiac muscle fibres from these mice contained approximately 80

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

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

182 n to be involved in turning on slow skeletal muscle fibre gene expression.

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

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

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

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

187 upport previous suggestions that in IBM, the muscle fibres have the capacity for antigen presentation

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

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

190 2 or disruption of the Dio2 gene in skeletal muscle fibres impaired acute exercise-induced PGC-1a exp

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

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

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

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

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

196 Striated muscle fibres in the urethral rhabdosphincter are innerv

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

198 Weight loss was correlated with the loss of muscle fibres, indicating that progressive muscle wastin

199 st-terminals were larger and more complex in muscle fibres injected with IGF-1-TTC, compared to the o

200 the other groups, suggesting preservation of muscle fibre innervation.

201 dependent residual population of medial fast muscle fibres is not Hedgehog dependent.

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

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

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

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

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

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

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

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

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

211 that macrophages play a significant role in muscle fibre membrane repair, regeneration and growth du

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

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

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

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

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

217 to the removal of NFATc1 that accumulates in muscle fibre nuclei during muscle activity, and that GSK

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

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

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

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

222 excitation-contraction coupling in skeletal muscle fibres of the mdx mouse, a model of the human dis

223 gous to the superficial slow and medial fast muscle fibres of zebrafish.

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

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

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

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

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

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

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

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

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

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

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

235 f motoneurons that successfully reinnervated muscle fibres recovered to normal despite the absence of

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

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

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

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

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

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

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

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

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

245 geing mice did not increase muscle weight or muscle fibre size, but significantly increased single fi

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

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

248 cord motor neurones of ageing mice prevents muscle fibre specific force decline, a hallmark of agein

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

250 the ventricular myocardium and slow skeletal muscle fibres such as the masseter and is an important s

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

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

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

254 ing satellite cells) and prevented growth of muscle fibres that normally occurred in control animals

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

256 of satellite cells within their niche on the muscle fibre, the contribution of satellite cell-derived

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

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

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

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

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

262 simultaneously increased by exposing resting muscle fibres to extracellular solutions that contained

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

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

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

266 None of the injections changed muscle fibre type composition, but neuromuscular junctio

267 2 week aerobic training protocol on skeletal muscle fibre type distribution and satellite cell conten

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

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

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

271 ed on the similar findings in soleus and EDL muscles, fibre type does not appear to determine the inn

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

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

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

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

276 Both muscle fibre types expressed a cytosolic GCR.

277 vascular control mechanisms among different muscle fibre types, we tested the hypothesis that, in re

278 e differentiation of several early zebrafish muscle fibre types.

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

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

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

282 Contraction of skeletal muscle fibres via electrical field stimulation produced

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

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

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

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

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

288 Furthermore, muscle fibres went through extensive qualitative changes

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

290 By 12 h all muscle fibres were denervated.

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

292 Muscle fibres were isolated from the flexor digitorum br

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

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

295 our RU interactions, in contrast to skeletal muscle fibres where the effect was enhanced.

296 lation to the previous findings in isometric muscle fibres which showed that a T-jump promotes an ear

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

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

299 oss of myogenesis by specific populations of muscle fibres, with parallel up-regulation of Pax3/7.

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