ライフサイエンスコーパス: muscle injury

1 trates the regenerative response to skeletal muscle injury.

2 uscle regeneration after cardiotoxin-induced muscle injury.

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

4 ell differentiation and down-regulated after muscle injury.

5 henotypic transition following acute sterile muscle injury.

6 Akt phosphorylation in satellite cells after muscle injury.

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

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

9 h increasing pain at sites of nonpenetrating muscle injury.

10 brafish embryos prevented lovastatin-induced muscle injury.

11 injury but not protective against histologic muscle injury.

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

13 lactate dehydrogenase levels consistent with muscle injury.

14 nflammatory drugs are often prescribed after muscle injury.

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

16 t neutrophils exacerbate contraction-induced muscle injury.

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

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

19 ression of markers of regeneration following muscle injury.

20 ophil accumulation after contraction-induced muscle injury.

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

22 differentiation of myogenic stem cells after muscle injury.

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

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

25 es regeneration after experimentally induced muscle injury.

26 e being widely investigated for treatment of muscle injury.

27 skeletal muscle growth in response to acute muscle injury.

28 d during satellite cell activation following muscle injury.

29 ration and blunts the epicardial response to muscle injury.

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

31 hen designing therapies for the treatment of muscle injury.

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

33 liferation of satellite cells in response to muscle injury.

34 that vitamin D improves muscle healing after muscle injury.

35 beta mediated action in response to skeletal muscle injury.

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

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

38 rapy attenuates stroke-induced limb skeletal muscle injury.

39 flammatory response to repair acute skeletal muscle injury.

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

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

42 the apparent absence of hepatic or skeletal muscle injury.

43 he clinical relevance of imaging features of muscle injuries.

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

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

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

47 Skeletal muscle injury activates adult myogenic stem cells, known

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Skeletal muscle injury and regeneration are closely associated wi

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

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

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

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

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

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

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

73 Muscle injury and subsequent activation of myogenic prog

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 Muscle injury caused early localization of lymphocytes t

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

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

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

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

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

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

101 functional muscle ischemia and exacerbating muscle injury during exercise.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 1 macrophages play a major role in worsening muscle injury in the mdx mouse model of Duchenne muscula

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

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

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

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

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

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

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

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

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

127 Skeletal muscle injury induces retrograde axonal transport of pol

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 Following muscle injury, MNF is present transiently in proliferati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 Muscle injury or modified muscle use can stimulate muscl

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

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

161 Muscle injury precipitates a complex inflammatory respon

162 Skeletal muscle injury produced early systemic arterial hypotensi

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

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

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

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

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

168 infiltration is essential to acute skeletal muscle injury repair.

169 scular macrophages to promote acute skeletal muscle injury repair.

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

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

172 Muscle injury resulting from aortic clamping was measure

173 Muscle injury (rhabdomyolysis) and subsequent deposition

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

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

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

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

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

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

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

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

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

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

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

185 Muscle injury was also accompanied by increased expressi

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

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

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

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

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

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

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

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

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