ライフサイエンスコーパス: muscle injury

1 ling in a mouse model of cardiotoxin induced muscle injury.

2 receptor (TLR) signaling may be involved in muscle injury.

3 in a model of sterile toxin-induced skeletal muscle injury.

4 flammatory response to repair acute skeletal muscle injury.

5 assessed the ability of these mice to repair muscle injury.

6 compared with wild-type mice after skeletal muscle injury.

7 the apparent absence of hepatic or skeletal muscle injury.

8 uscle regeneration after cardiotoxin-induced muscle injury.

9 ly elevated as a result of liver or skeletal muscle injury.

10 ell differentiation and down-regulated after muscle injury.

11 with atrophy and fibrosis following skeletal muscle injury.

12 Akt phosphorylation in satellite cells after muscle injury.

13 g Sca-1 display increased fibrosis following muscle injury.

14 regulated in a subset of myogenic cells upon muscle injury.

15 h increasing pain at sites of nonpenetrating muscle injury.

16 brafish embryos prevented lovastatin-induced muscle injury.

17 injury but not protective against histologic muscle injury.

18 lactate dehydrogenase levels consistent with muscle injury.

19 nflammatory drugs are often prescribed after muscle injury.

20 AST and ALT levels in our cases with chronic muscle injury.

21 n to resolution and regeneration in skeletal muscle injury.

22 t neutrophils exacerbate contraction-induced muscle injury.

23 d with the resolution of contraction-induced muscle injury.

24 ls aid the resolution of contraction-induced muscle injury.

25 ression of markers of regeneration following muscle injury.

26 ophil accumulation after contraction-induced muscle injury.

27 ized antigen-presenting cells to the site of muscle injury.

28 differentiation of myogenic stem cells after muscle injury.

29 e will induce oxidative damage and result in muscle injury.

30 hase; this in vivo effect was potentiated by muscle injury.

31 ic progression following contractile-induced muscle injury.

32 fferentiation of AAMs and tissue repair upon muscle injury.

33 in cultures and in other models of skeletal muscle injury.

34 trates the regenerative response to skeletal muscle injury.

35 ro-adipogenic progenitors) evident following muscle injury.

36 rative potential following acute and chronic muscle injury.

37 CWI in improving muscle regeneration after a muscle injury.

38 ing heat therapy to facilitate recovery from muscle injury.

39 d with Duchenne muscular dystrophy and acute muscle injury.

40 206 exhibit increased adipogenesis following muscle injury.

41 ss is lost, for example, following traumatic muscle injury.

42 ression of which is activated in response to muscle injury.

43 y sustained immunological reaction following muscle injury.

44 polymer polycaprolactone (PCL) into a distal muscle injury.

45 ammatory environment encountered in an acute muscle injury.

46 rapy attenuates stroke-induced limb skeletal muscle injury.

47 henotypic transition following acute sterile muscle injury.

48 d IRE1 are increased in satellite cells upon muscle injury.

49 es regeneration after experimentally induced muscle injury.

50 e being widely investigated for treatment of muscle injury.

51 elicited in mSCs early after acute skeletal muscle injury.

52 skeletal muscle growth in response to acute muscle injury.

53 d during satellite cell activation following muscle injury.

54 ration and blunts the epicardial response to muscle injury.

55 fibre size in selected muscles, or following muscle injury.

56 hen designing therapies for the treatment of muscle injury.

57 d impaired satellite cell self-renewal after muscle injury.

58 liferation of satellite cells in response to muscle injury.

59 that vitamin D improves muscle healing after muscle injury.

60 beta mediated action in response to skeletal muscle injury.

61 pular strategy for the treatment of skeletal muscle injuries.

62 he most commonly used methods for evaluating muscle injuries.

63 mprove recovery outcomes following traumatic muscle injuries.

64 s who exhibited clinical signs of lower limb muscle injuries.

65 s commonly used in the treatment of skeletal muscle injuries.

66 he clinical relevance of imaging features of muscle injuries.

67 ficial to promote repair in various types of muscle injuries.

68 ve a detrimental effect and certain types of muscle injury a positive effect.

69 Skeletal muscle injury activates adult myogenic stem cells, known

70 that myoblasts can differentiate and repair muscle injury after an ischemic insult.

71 ymptoms does not exacerbate exercise-induced muscle injury after moderate exercise.

72 n potential of SASCs in alleviating skeletal muscle injuries and diseases.

73 nical applications in patients with skeletal muscle injuries and diseases.

74 firm and assess the extent of sports-related muscle injuries and may help to guide management, which

75 Deviations due to direct muscle injury and "sensory" deviations due to poor visio

76 exerts a protective effect against skeletal muscle injury and associated lung injury following limb

77 eviously identified as a genetic modifier of muscle injury and disease.

78 beneficial in preventing muscle mass loss in muscle injury and disease.

79 ha signaling in pre-clinical models of acute muscle injury and DMD.

80 we captured early cell activation following muscle injury and found that an essential ERK1/2 primary

81 Immune cells are critical responders to muscle injury and guide tissue resident stem cell- and p

82 In contrast, the skeletal muscle injury and hemorrhage group had lower systemic me

83 hermore, neutrophils appear to contribute to muscle injury and impair some of the events associated w

84 The dnTGFbetaRII transgene also reduced muscle injury and improved muscle regeneration after car

85 y steroid treatment in mouse models of acute muscle injury and in muscular dystrophy and determined t

86 Intriguingly, ablation of TRAF6 exacerbates muscle injury and increases fibrosis in 9-month-old mdx

87 .0001), whereas correlations with markers of muscle injury and inflammation were weak.

88 d in satellite cells in response to skeletal muscle injury and muscular dystrophy.

89 eneration consecutive to cardiotoxin-induced muscle injury and observed a significant hypotrophy and

90 integrin CD18, (2) neutrophils contribute to muscle injury and oxidative damage after contraction-ind

91 how that complement is activated in skeletal muscle injury and plays a key role during regeneration.

92 n culture, were more susceptible to skeletal muscle injury and reduced maximum load tolerated by isol

93 Skeletal muscle injury and regeneration are closely associated wi

94 The mechanisms linking muscle injury and regeneration are not fully understood.

95 ed following experimentally-induced skeletal muscle injury and regeneration in non-dystrophic mice.

96 ular damage and time course of repair during muscle injury and regeneration induced by the myotoxin B

97 We show that, in a mouse model of skeletal muscle injury and regeneration, the accumulation of leuk

98 nt system may produce therapeutic benefit in muscle injury and regeneration.

99 Skeletal muscle injury and repair have been a major research focu

100 mouse model, cardiotoxin was used to induce muscle injury and repair, and expression of Mi-2 during

101 Using a model of skeletal muscle injury and repair, herein we identified annexin A

102 To evaluate the impact of HIF-1 in skeletal muscle injury and repair, we examined mice with a condit

103 ring muscle regeneration in a mouse model of muscle injury and repair.

104 reased accumulation of macrophages following muscle injury and severely impaired muscle regeneration.

105 Muscle injury and subsequent activation of myogenic prog

106 unctional (isometric force deficit) signs of muscle injury and total carbonyl content, a marker of ox

107 tography, consistent with the development of muscle injury and weakness.

108 IL-33(+) cells were more frequent after muscle injury and were reduced in old mice.

109 in non-liver injury conditions (for example, muscle injury) and in apparently healthy people.

110 f the features of muscle degeneration due to muscle injuries, and its presence interferes with muscle

111 d oxidative damage after contraction-induced muscle injury, and (3) neutrophils aid the resolution of

112 iferation and survival in culture, decreased muscle injury, and accelerated recovery of maximum load

113 e with induced arthritis, C57BL/6J mice with muscle injury, and BALB/C mice with both FR-alpha tumor

114 lytic 2B levels to >= 40% frequency, reduces muscle injury, and improves fiber hypertrophy relative t

115 S) often develops at sites of nonpenetrating muscle injury, and nonsteroidal anti-inflammatory drugs

116 ent but are rapidly activated in response to muscle injury, and the derived myogenic cells then fuse

117 anscripts are prominent in cardiogenesis and muscle injury, and they are under complex regulation by

118 recovery of muscle function after traumatic muscle injury, and this effect might be associated with

119 Severe skeletal muscle injuries are common and can lead to extensive fib

120 Muscle injuries are common in competitive sports.

121 Muscle injuries are defined by their cause and anatomica

122 current therapeutic approaches for treating muscle injuries are dependent on the clinical severity b

123 mechanical weakness and contraction-induced muscle injury are not required for muscle degeneration a

124 symptoms of premature fatigue and potential muscle injury are unmasked.

125 known, confusion exists concerning skeletal muscle injury as the cause of this rise.

126 rnesol treatment accelerated the recovery of muscle injury associated with enhanced muscle stem cell

127 tive brachial nerve stimulation nor skeletal muscle injury attenuated the increase in plasma volume,

128 ich ICAM-1 expressed by myogenic cells after muscle injury augments their adhesive and fusogenic prop

129 mpared to nonpregnant control mice following muscle injury based on improved muscle histology, superi

130 In a murine model of acute muscle injury, BE2012 upregulated myogenic transcription

131 re quiescent myogenic precursors that, after muscle injury, become mitotically active, proliferate, a

132 HO-1 is strongly induced after muscle injury, being expressed mostly in the infiltratin

133 ogs, EDG-5506 reversibly reduced circulating muscle injury biomarkers and increased habitual activity

134 In barium chloride-induced muscle injury, both lipin1(Myf5cKO) and DKO showed prolo

135 is upregulated in satellite cells following muscle injury, but its role in muscle regeneration has n

136 ng little scarring or fibrosis after skin or muscle injury, but the Acomys response to spinal cord in

137 In adult mCherry-titin mice, treatment of muscle injury by implantation of titin-eGFP myoblasts re

138 fiber breakdown; however, the mechanisms of muscle injury by statins are poorly understood.

139 Traumatic muscle injury can affect people across the lifespan and

140 use may exacerbate exercise-induced skeletal muscle injury caused by reduced coenzyme Q10 (CoQ10) lev

141 Muscle injury caused early localization of lymphocytes t

142 ermine whether eccentric contraction-induced muscle injury causes impaired plasmalemmal action potent

143 y and retained the proliferative response to muscle injury characteristic of younger animals.

144 score (e.g. as one method, British Athletics Muscle Injury Classification - BAMIC) to describe edema

145 raded by a clinician using a semiqualitative muscle injury classification score (e.g. as one method,

146 he inflammatory and regenerative response to muscle injury, compromising functional recovery.

147 or from external impact, resulting in direct muscle injuries (contusion or laceration).

148 those muscle nuclei immediately adjacent to muscle injury demonstrate high-level TGFbeta signaling.

149 The degeneration/regeneration response to muscle injury/disease is modulated by the proinflammator

150 Skeletal muscle injury disrupts its capillary supply secondary to

151 Current rodent models of skeletal muscle injury do not accurately mimic the complex physio

152 ocyte growth factor, which is produced after muscle injury, down-regulates caveolin-1.

153 d to monitor the dynamic recovery process of muscle injuries during physiotherapies.

154 functional muscle ischemia and exacerbating muscle injury during exercise.

155 Disruption of the dystrophin complex causes muscle injury, dysfunction, cell death and fibrosis.

156 kinase, suggesting that statins produce mild muscle injury even among asymptomatic subjects.

157 Lack of HO-1 augments skeletal muscle injury, evidenced by increased creatinine kinase

158 cells in their niche are quiescent and upon muscle injury, exit quiescence, proliferate to repair mu

159 animals and analyzed cellular response after muscle injury, focusing on muscle satellite cells (SCs),

160 The management of muscle injury has changed within the past 5 years from i

161 erstanding of ventilator-induced respiratory muscle injury has not reached the stage where meaningful

162 Several classification systems for muscle injuries have been published.

163 step for satellite cell activation following muscle injury, have not been defined.

164 standard charges before hemorrhage (skeletal muscle injury + hemorrhage, n = 6).

165 ular strategies in the treatment of skeletal muscle injury; however, existing literature is equivocal

166 cal to the development of fibrosis following muscle injury; however, the mechanism of their role in f

167 o increasing satellite cell number following muscle injury, improve myoblast proliferation and surviv

168 ail of small molecules and transplanted into muscle injuries in adult, aged or dystrophic mice-led to

169 , play essential roles in regeneration after muscle injury in adult skeletal muscle.

170 Skeletal muscle injury in Ebola virus disease (EVD) has been repo

171 rt on the action of antithrombin on skeletal muscle injury in experimental endotoxemia.

172 entric contraction-induced acute and chronic muscle injury in mice.

173 uscle regeneration after cardiotoxin-induced muscle injury in mice.

174 Studies examining recovery from muscle injury in models of older animals principally use

175 creased skeletal muscle mass and ameliorated muscle injury in myopathic mouse models.

176 n exacerbate rather than rejuvenate skeletal muscle injury in old animals.

177 improves recovery from metabolic disease and muscle injury in older wild-type mice.

178 Regenerative response to skeletal muscle injury in Speg-KO mice was compared with that of

179 ed moderate-intensity exercise on markers of muscle injury in statin users with and without statin-as

180 1 macrophages play a major role in worsening muscle injury in the mdx mouse model of Duchenne muscula

181 onsible for amplification and propagation of muscle injury in these diseases.

182 combinant annexin A6 protected against acute muscle injury in vitro and in vivo.

183 letal muscle after cardiotoxin (CTX)-induced muscle injury in vivo and differentiating myoblasts in v

184 and active-Notch) after cardiotoxin-induced muscle injury in vivo and in SCs cultured in vitro.

185 the HGF receptor c-met were increased after muscle injury in wild-type mice.

186 alities for the assessment of sports-related muscle injuries, including advanced imaging techniques,

187 y formed myofibers after cardiotoxin-induced muscle injury, increased glycolysis, partially impaired

188 Peak stress was the best predictor of muscle injury, independent of contraction mode (i.e. ecc

189 Here we show that macrophages at sites of muscle injury induce activation of satellite cells via e

190 regenerative SEA (rSEA) applied to a murine muscle injury induced accumulation of IL-4-expressing T

191 rophages at multiple stages before and after muscle injury induced by cardiotoxin.

192 of animals had bilateral hindlimbs skeletal muscle injury induced by firing a captive-bolt handgun w

193 cachexia to study inflammatory and oxidative muscle injury induced by tumor-derived signals.

194 We uncovered a novel mechanism by which muscle injury induces a macrophage-dependent sequestrati

195 Skeletal muscle injury induces retrograde axonal transport of pol

196 l muscle structure and functions and reduced muscle injury, inflammation and fiber necrosis.

197 ered levels overlapped with known markers of muscle injury, inflammation, regeneration, and extracell

198 Following muscle injury, integrin-beta3 was initially expressed, m

199 st common explanation for the cause of toxic muscle injury invokes the deficiency of one of three mai

200 find that a notable early phase response to muscle injury is an increased association of mitochondri

201 The diagnosis of muscle injury is based on patient history and physical e

202 results demonstrate that complement-mediated muscle injury is central to the pathogenesis of dysferli

203 ophil accumulation after contraction-induced muscle injury is dependent on CD18.

204 ophil accumulation after contraction-induced muscle injury is dependent on the beta(2) integrin CD18,

205 Acute skeletal muscle injury is followed by an inflammatory response, r

206 Hamstring muscle injury is highly prevalent in sports involving re

207 Research on ventilator-induced respiratory muscle injury is in its infancy and portends to be an ex

208 Skeletal muscle injury is known to predispose its sufferers to ne

209 Recovery from skeletal muscle injury is often incomplete because of the formati

210 motor nerve regeneration following skeletal muscle injury is undefined.

211 Myofibre regeneration after skeletal muscle injury is well-studied, although little is known

212 injuries, as well as for cardiac and smooth muscle injuries, is currently being explored.

213 d eight adverse events of grade 3 (fracture, muscle injury, laceration, paralytic ileus, pain, presyn

214 n of activin A with a monoclonal antibody in muscle injury leads to the early onset of tissue degrada

215 Here the authors show that in response to muscle injury, macrophages secrete Adamts1, which induce

216 One challenge of muscle injury management is that numerous medical treatm

217 ell expansion and differentiation upon acute muscle injury, markedly delaying regeneration.

218 Muscle injury markers (lactate dehydrogenase, creatine k

219 All muscle injury markers were comparable at baseline (P > 0

220 Muscle injury markers were not related to leukocyte CoQ1

221 2.3 nmol/U; P = 0.20), and did not relate to muscle injury markers, fatigue resistance, or reported m

222 rotected against CS-induced lung, renal, and muscle injury; mitochondrial dysfunction; and unfolded p

223 Following muscle injury, MNF is present transiently in proliferati

224 Here, using an acute sterile skeletal muscle injury model combined with irradiation, bone marr

225 with a specific monoclonal antibody in this muscle injury model decreased the muscle protein levels

226 epair and regeneration in this mouse induced muscle injury model independent of its effect on erythro

227 In this study, we used a murine acute muscle injury model to assess global chromatin accessibi

228 In a cardiotoxin-induced muscle injury model, lack of MKP-1 impaired muscle regen

229 ibrotic ischemia reperfusion and cardiotoxin muscle injury model.

230 generation differences between two different muscle injury models, cardiotoxin and glycerol.

231 hy, and 2 myotoxin (cardiotoxin and notexin) muscle injury models.

232 n-DM1 mouse models of muscular dystrophy and muscle injury, most likely due to recapitulation of neon

233 Following muscle injury, muscle stiffness remained elevated after

234 In the adult, after a muscle injury, newly generated fibers transition through

235 increase fibroid risk through uterine smooth muscle injury, not unlike atherosclerosis.

236 g grading to reflect the diverse spectrum of muscle injuries observed in athletes.

237 However, muscle injury often leads to an ischemic hypoxia environ

238 In skeletal muscle, injury often associates with plasma membrane dis

239 ociated with two different types of skeletal muscle injury, one induced by direct destruction of musc

240 d control animals, nor was there evidence of muscle injury or apoptosis.

241 Upon muscle injury or degeneration, members of this self-rene

242 oteases to muscle wasting in any instance of muscle injury or disease has remained unknown because of

243 skeletal muscle pathogenesis associated with muscle injury or disease-related muscle degeneration.

244 ion and proteolytic activity following acute muscle injury or in muscle from mdx mice, a model of DMD

245 the microcirculation is affected by skeletal muscle injury or its recovery during regeneration.

246 d in peripheral blood of WT mice after acute muscle injury or mdx(5cv) mice.

247 Muscle injury or modified muscle use can stimulate muscl

248 ct subpopulations of macrophages can promote muscle injury or repair in muscular dystrophy, and that

249 ls of atherosclerosis, rheumatoid arthritis, muscle injury, or ulcerative colitis.

250 Another challenge is the prevention of muscle injury owing to the multifactorial and complex na

251 ling ( P = 0.0004), and reduced histological muscle injury ( P = 0.012).

252 ed vesicles, in mitigating radiation-induced muscle injury, particularly in the context of military m

253 Muscle injury precipitates a complex inflammatory respon

254 Skeletal muscle injury produced early systemic arterial hypotensi

255 MPK axis as an important pathway in skeletal muscle injury regeneration.

256 s or the effectiveness of cardiovascular and muscle injury rehabilitation programmes.

257 s or the effectiveness of cardiovascular and muscle injury rehabilitation programmes.

258 They likely contribute to the normal muscle injury repair by producing growth factors.

259 e that CX3CR1 is important to acute skeletal muscle injury repair by regulating macrophage phagocytos

260 ude that CCR2 is essential to acute skeletal muscle injury repair primarily by recruiting Ly-6C(+) MO

261 Muscle injury repair was delayed in CX3CR1(GFP/GFP) mice

262 scular macrophages to promote acute skeletal muscle injury repair.

263 ptor 2 (CCR2) is essential to acute skeletal muscle injury repair.

264 infiltration is essential to acute skeletal muscle injury repair.

265 tion, we examined the role of macrophages in muscle injury, repair and regeneration during modified m

266 Traumatic muscle injury represents a collection of skeletal muscle

267 ferrogel scaffolds implanted at the site of muscle injury resulted in uniform cyclic compressions th

268 Muscle injury resulting from aortic clamping was measure

269 Muscle injury (rhabdomyolysis) and subsequent deposition

270 Severe muscle injury (rhabdomyolysis) is accompanied by the rel

271 In response to muscle injury, satellite cells activate the p38alpha/bet

272 In response to skeletal muscle injury, satellite cells, which function as a myog

273 tellite cell activity and regeneration after muscle injury.Satellite cells are crucial for growth and

274 diseases, genetic syndromes, traumatic nerve/muscle injuries, seizure disorders, decreased cognitive

275 Upon muscle injury, stem cells that lie between the muscle fi

276 ening, resulting in indirect and non-contact muscle injuries (strains or ruptures), or from external

277 ent increase in Septin7 expression following muscle injury suggest that it may be involved in muscle

278 ssess the impact of respiratory and skeletal muscle injury sustained during ICU stay on physical perf

279 Rhabdomyolysis is defined as skeletal muscle injury that leads to the lysis of muscle cells an

280 bed a novel rat model of compression-induced muscle injury that results in multicomponent injury to t

281 In sports-related muscle injuries, the main goal of the sports medicine ph

282 ociated with dysfunction of smell and taste, muscle injury, the Guillain-Barre syndrome, and its vari

283 Notably, upon muscle injury, the loss-of-function of Rev-erbalpha in v

284 Toxin-induced muscle injury to tibialis anterior muscles of wild-type

285 release of local environmental stimuli after muscle injury triggers the differentiation of myogenic c

286 nase-2-specific inhibitors to treat skeletal muscle injuries warrants caution because they may interf

287 Muscle injury was also accompanied by increased expressi

288 In contrast, muscle injury was significantly attenuated in mMCP-5-nul

289 andard experimental method of acute skeletal muscle injury, was used to investigate the response of t

290 n hippocampus, in the presence or absence of muscle injury, we find that, in many cases, the inhibito

291 By studying a model of cardiotoxin-induced muscle injury, we identify a population of monocyte-deri

292 mine the validity of using these drugs after muscle injury, we investigated the working mechanism of

293 , in which only limited MC degranulation and muscle injury were apparent.

294 ablished murine model of compression-induced muscle injury, where we collected resistance, reactance,

295 pathway is rapidly activated in response to muscle injury, which activates AMPK and induces a Warbur

296 to a lengthening protocol to produce maximal muscle injury, which produced rapid accumulation of nucl

297 ity was addressed in the context of ischemic muscle injury, which typically leads to necrosis and los

298 xpression after cardiotoxin-induced skeletal muscle injury, while single MSulf knockouts regenerate n

299 malities, ataxia, dysautonomia, and skeletal muscle injury with normal orientation and arousal signs)

300 /beta MAPK signaling to link the response to muscle injury with satellite cell self-renewal.