ライフサイエンスコーパス: muscle damage

1 mbining tibia fracture and pin fixation with muscle damage.

2 te in Pompe myofibers and may cause profound muscle damage.

3 ty infiltration of the liver and evidence of muscle damage.

4 prolonged endplate currents, and consequent muscle damage.

5 been found to be upregulated by exercise or muscle damage.

6 or satellite cell activation following local muscle damage.

7 in early events in the myogenic response to muscle damage.

8 of the vasoconstrictor response and eventual muscle damage.

9 exercise that causes an increase in skeletal muscle damage.

10 retained at 85% of the synaptic sites after muscle damage.

11 nd possibly protection from exercise-induced muscle damage.

12 mechanism to resist statin-induced skeletal muscle damage.

13 uscle pain nor reduce circulating markers of muscle damage.

14 ficult interpretation due to co-existence of muscle damage.

15 d ECM degradation as an important pathway of muscle damage.

16 velop better therapies for snakebite-induced muscle damage.

17 y and to facilitate regeneration after major muscle damage.

18 g in sarcolemmal instability and progressive muscle damage.

19 to mechanically induced skeletal and cardiac muscle damage.

20 F1alpha), which is induced in the setting of muscle damage.

21 generation and serves as a general marker of muscle damage.

22 ength loss was associated with indicators of muscle damage.

23 ngth at the same time it prevents subsequent muscle damage.

24 te cell activation and delayed recovery from muscle damage.

25 cial outcome, tempering oxidative stress and muscle damage.

26 ytokines, including IL-6, to repair skeletal muscle damage.

27 howing that Tregs can directly contribute to muscle damage.

28 -SRP and anti-HMGCR Abs could be involved in muscle damage.

29 s associate with impaired liver function and muscle damage.

30 ells enter muscles in response to repetitive muscle damage.

31 iotoxin (CTX)-induced tibialis anterior (TA) muscle damage.

32 invasive method of detecting and quantifying muscle damage.

33 direct link between anti-FHL1 responses and muscle damage.

34 e removal of those with potential iatrogenic muscle damage.

35 ng that RARgamma agonist may oppose skeletal muscle damage.

36 iltration, indicating exacerbated dystrophic muscle damage.

37 on partners) in myofibril assembly and after muscle damage.

38 e immunoreactivity for Xin was indicative of muscle damage.

39 ally after dialysis, thyroid malfunction and muscle damage.

40 al integrity and increased susceptibility to muscle damage.

41 lopment of muscle atrophy, in statin-induced muscle damage.

42 educed HGF levels and c-met activation after muscle damage.

43 ays responsible for atrogin-1 expression and muscle damage.

44 onnects the immune and nonimmune pathways of muscle damage.

45 The mechanism of relentless muscle damage (a classic manifestation of the disease) h

46 Our findings indicate that muscle damage affects the lineage choices of muscle SP c

47 controls, Akita mice demonstrated increased muscle damage after eccentric exercise along with a decl

48 Repeated muscle damage also elicited key aspects of muscular dyst

49 y, dramatically prevented lovastatin-induced muscle damage and abrogated atrogin-1 induction both in

50 of genetic muscle disorders, trauma-induced muscle damage and age-related muscle weakness.

51 estoring muscle ERRgamma pathway ameliorated muscle damage and also prevented DMD hallmarks of postex

52 oprene units to protein targets cause statin muscle damage and atrogin-1 induction in cultured cells

53 s, are rare diseases marked by immune-driven muscle damage and complications like skin lesions and in

54 ), occurs as a result of contraction-induced muscle damage and deficient muscular repair.

55 nonimmune mechanism responsible for skeletal muscle damage and dysfunction in autoimmune myositis.

56 D 2B and 2C, daily prednisone dosing reduced muscle damage and fibroinflammatory infiltration.

57 deficiency reduced quadriceps and diaphragm muscle damage and fibrosis at 14 wk but not at 6 mo, and

58 890F)/mdx showed a significant resistance to muscle damage and force loss following repeated eccentri

59 conclusion, voluntary running did not induce muscle damage and had no drastic detrimental effect on t

60 transcriptome and mRNA isoforms that govern muscle damage and homeostasis with age.

61 amma signaling in muscular dystrophy reduces muscle damage and improves motor performance by promotin

62 marked and significant reduction in cardiac muscle damage and infarct size.

63 significant alterations in plasma markers of muscle damage and metabolism in DMD(mdx) rats compared t

64 hed protein biomarkers associated with heart muscle damage and point-of-care monitoring of both these

65 d its forced activation reverts the enhanced muscle damage and poorer regeneration.

66 romosome that result in skeletal and cardiac muscle damage and premature death.

67 agic buildup may be responsible for skeletal muscle damage and prevent efficient trafficking of repla

68 can to the cytoplasm is sufficient to induce muscle damage and provides a new model of muscular dystr

69 ion-reambulation model was used for inducing muscle damage and recovery in the lower hindlimbs in mic

70 that can be used for imaging and quantifying muscle damage and recovery in vivo.

71 ins in response to cardiotoxin (CTX) induced muscle damage and regeneration at unique sequential stag

72 actile function, SC myogenic progression and muscle damage and repair following eccentric contractile

73 sing creatine kinase (CK-MM), a biomarker of muscle damage and several disorders for which rapid clin

74 ury, SC-Bmal1(iKO) animals displayed reduced muscle damage and subsequent repair post-injury (Dystrop

75 ntion of the onset of skeletal and diaphragm muscle damage and the blocking of stress-induced cardiac

76 a hospital setting and effective in reducing muscle damage and the local inflammatory process caused

77 All morphant fish showed muscle damage and vascular abnormalities at day 1 post-f

78 The strong correlation between the degree of muscle damage and Xin immunoreactivity suggests that Xin

79 their varied etiologies, are associated with muscle damage and, often, other organ system involvement

80 channels leads to defective Ca2+ signaling, muscle damage, and impaired exercise capacity.

81 line diet develop hepatosteatosis, liver and muscle damage, and lymphocyte apoptosis.

82 This treatment also reduced muscle damage, as evidenced by decreases in serum creati

83 nd oxidative remodeling, alleviated baseline muscle damage, boosted regeneration in dystrophic muscle

84 indicating that MTR may be more sensitive to muscle damaged by denervation than conventional MRI.

85 es and transiently increases in regenerating muscles damaged by bupivacaine.

86 ral treatment with UDCA prevents gallbladder muscle damage caused by BDL, whereas oral treatment with

87 ndlimb was found to have a greater amount of muscle damage compared to that in the contralateral noni

88 ceptibility to eccentric contraction-induced muscle damage compared with mdx controls.

89 Both paralysis and muscle damage could be rescued with collagen IV overexpr

90 inflammation (C-reactive protein [CRP]), and muscle damage (creatine kinase [CK]) by turbidimetry.

91 ted the elevation of inflammatory markers of muscle damage (creatine kinase activity, C-reactive prot

92 rential effects on macrophage dispersion and muscle damage depending on the stage of dystrophic patho

93 eripheral nerve injury and statin-associated muscle damage diminished grip strength and force profile

94 ewing the ECT complication, it appeared that muscle damage due to catatonic immobility led to acute h

95 Muscle damage elicits a sterile immune response that fac

96 Two cohorts of young adults-the Eccentric Muscle Damage (EMD; n = 156) cohort and the Functional S

97 control mice (Acsl1(flox/flox) ), indicating muscle damage, even without exercise, in the Acsl1(M) (-

98 Taken together, we hypothesised that muscle damaging exercise could be harnessed to enhance m

99 muscular repair, hence we hypothesised that muscle damaging exercise may increase C1q 'spill-over' i

100 e-induced microtrauma. kg(-1) . d(-1)) after muscle-damaging exercise (300 eccentric contractions).

101 prior to and at 3, 24, and 72 h following a muscle-damaging exercise in young and old individuals.

102 s is accompanied by transient improvement of muscle damage, fibrosis, and regeneration.

103 but differentiate to generate myocytes upon muscle damage, forming new myofibers along with self-ren

104 ed inflammation is regarded as a response to muscle damage from mechanical stress, but controlled imm

105 fibers, implicating mild direct or indirect muscle damage from the WNV infection.

106 Muscle damage has been shown to enhance the contribution

107 roles of ER stress and autophagy in skeletal muscle damage have been explored in multiple muscle dise

108 lemmal nNOS leads to functional ischemia and muscle damage; however, the mechanism of nNOS subcellula

109 also prevented DMD hallmarks of postexercise muscle damage, hypoxia, and fatigue in mdx mice.

110 ced biochemical and histological evidence of muscle damage, improved muscle function and increased ex

111 vities diminished or enhanced (respectively) muscle damage in a dystrophy model.

112 markably, loss of Fnip1 profoundly mitigated muscle damage in a murine model of Duchenne muscular dys

113 Ca(2+) overload and ECM degradation-mediated muscle damage in C. elegans.

114 lovastatin-induced atrogin-1 expression and muscle damage in cultured mouse myotubes and zebrafish c

115 c muscles, leading to transient increases in muscle damage in foci where macrophages were highly conc

116 ata demonstrate Xin as a useful biomarker of muscle damage in healthy individuals and in patients wit

117 ured by the chronic inflammation elicited by muscle damage in humans.

118 muscle regeneration give rise that ischemic muscle damage in limb transplantation might be reversibl

119 nsight into the molecular pathophysiology of muscle damage in LOPD and identified potential avenues f

120 st muscle susceptible to contraction-induced muscle damage in mdx mice.

121 AC4 in muscle fibers is sufficient to induce muscle damage in mice.

122 plasma in response to acute notexin-induced muscle damage in rats.

123 are robust and promising biomarkers of acute muscle damage in rats.

124 evated myoplasmic[Ca(2+)](rest), and present muscle damage in soleus with a strong sex bias.

125 (Exercise-induced Muscle Damage in Statin Users; NCT05011643).

126 ltration is not a driving force behind acute muscle damage in the mdx mouse strain.

127 on of IL-10 expression in mdx mice increased muscle damage in vivo and reduced mouse strength.

128 In contrast, ablation of IFN-gamma reduced muscle damage in vivo during the regenerative stage of t

129 Recurrent muscle damages in DMD patients and DMD mouse model, mdx,

130 ve of severe inflammation, coagulopathy, and muscle damage including less bacterial clearance, hypogl

131 in some Dysf(-/-) mice, indicating possible muscle damage induced by hypertrophy.

132 atrogin-1 may be a critical mediator of the muscle damage induced by statins.

133 following electrically stimulated eccentric muscle damage inducing regenerative mechanisms.

134 Skeletal muscle damage is an often-occurring event.

135 Muscle damage is currently assessed through methods such

136 y of inflammatory cells and thereby increase muscle damage is unknown.

137 Significant muscle damage is very rare when statin therapy is used i

138 In skeletal muscle, DAMAGE is at the postsynaptic membrane and is as

139 Conversely, muscle damage leading to regeneration may promote some i

140 Two hours after cardiotoxin-induced muscle damage, local activin A protein expression increa

141 trength, and increased circulating levels of muscle damage marker LDH.

142 ry, microcirculatory/cardiac dysfunction and muscle damage may also facilitate kidney damage.

143 ggest that myalgias and relatively low-level muscle damage may occur in a substantial number of patie

144 Other muscle damage measures also showed a correlation with se

145 otassium homeostasis mechanisms may minimize muscle damage of myopathies due to certain RyR1 mutation

146 ts have a lower susceptibility to structural muscle damage of the cytoskeleton and sarcolemma with ac

147 Muscle damage or disease leads to progressive weakness a

148 exercise lead to protection against striated muscle damage, oxidative stress and injury.

149 muscle pain or reduce circulating markers of muscle damage (P >= 0.207).

150 to muscle size) and histological markers of muscle damage (percentage of regenerating fibers and fib

151 Macrophages recruited at the site of sterile muscle damage play an essential role in the regeneration

152 ic perceived pain and circulating markers of muscle damage, potentially influenced inflammatory mecha

153 Thirty-four participants underwent a muscle damage protocol induced by electrically stimulate

154 low-choline diet, some people presented with muscle damage rather than liver damage; several effect a

155 h Pompe disease are associated with skeletal muscle damage, rather than acute myocardial injury.

156 = 0.6175, P = <0.0001) with the severity of muscle damage, regardless of myopathy type.

157 Although the mechanism of muscle damage remains to be fully elucidated, a number o

158 rce production, influencing the magnitude of muscle damage/repair, with an altered SC myogenic progre

159 that cachexia was associated with a type of muscle damage resulting in activation of both satellite

160 multiparous rabbits suffer pelvic nerve and muscle damage, resulting in alterations in pelvic floor

161 Muscle damage results in rapid recruitment of eosinophil

162 GTP-binding proteins lead to statin-induced muscle damage since these molecules require modification

163 d worms, and its down-regulation rescued the muscle damage, suggesting that calcium overload acts as

164 scle wasting diseases underscored by chronic muscle damage that is continually repaired by satellite

165 t of HSPs may provide protection against the muscle damage that occurs by a pathological increase in

166 inophils promote characteristic inflammatory muscle damage, this has not been fully examined.

167 d by phagocytes upon recruitment to sites of muscle damage to facilitate muscular repair, hence we hy

168 e kinase activity, an established measure of muscle damage, to near-normal levels.

169 regenerative pathways, along with increased muscle damage upon mechanical overload.

170 CK), CK-myocardial band levels, and skeletal muscle damage was assessed.

171 Renal and organ muscle damage was enhanced in PC(+/-) mice, as shown by

172 Confirmation of muscle damage was obtained using in vivo indocyanine gre

173 71%) and CRP (+ 66%) suggests some degree of muscle damage was present.

174 Using notexin-induced muscle damage, we have shown that regeneration is attenu

175 e diagnostic importance of CK in determining muscle damage, we tested the association of the variant

176 muscle force/endurance as well as increased muscle damage when compared to regular mdx mice.

177 ere observed in the quantitative measures of muscle damage when comparing mdx versus mdx.PHIL versus

178 ostmenopausal women developed fatty liver or muscle damage, whereas only 44% of premenopausal women d

179 e regeneration and a meaningful indicator of muscle damage, which correlates with the clinical severi

180 rly indicator of altered kidney function and muscle damage, which could be added into NCAA guidelines

181 d signs of organ dysfunction (fatty liver or muscle damage), while less than half of premenopausal wo

182 ife-threatening condition caused by skeletal muscle damage with acute kidney injury being the main co

183 glycogen accumulation in skeletal muscle and muscle damage with exertion.

184 FER animals displayed progressive muscle damage with myofiber necrosis, internalized nucle