ライフサイエンスコーパス: muscle pathology

1 y, reproduce well and do not show any smooth muscle pathology.

2 ed to produce any significant differences in muscle pathology.

3 xpense of fat formation, and does not reduce muscle pathology.

4 traction mediated damage, and a reduction of muscle pathology.

5 complex and substantial changes in skeletal muscle pathology.

6 ficant inhibition of degenerative dystrophic muscle pathology.

7 et set of bands in many patients with active muscle pathology.

8 from mislocalized nNOS may contribute to mdx muscle pathology.

9 r physically normal despite their underlying muscle pathology.

10 fibers, which could in turn plays a role in muscle pathology.

11 hancing muscle regeneration and ameliorating muscle pathology.

12 been demonstrated and may also contribute to muscle pathology.

13 umulation and prominent cardiac and skeletal muscle pathology.

14 t its expression correlates with severity of muscle pathology.

15 the loss of nNOS impacts dystrophic skeletal muscle pathology.

16 ir clinical records, muscle MRI findings and muscle pathology.

17 mouse model, overexpression of ML1 decreased muscle pathology.

18 elta4 mice improved contractile function and muscle pathology.

19 ailure, even in the presence of non-specific muscle pathology.

20 ockout (Mtm1KO) mice prevents development of muscle pathology.

21 of blocking gene repression correlated with muscle pathology.

22 ely lead to animal weakness and the observed muscle pathology.

23 sease model, does not improve all aspects of muscle pathology.

24 uscle differentiation and is dysregulated in muscle pathologies.

25 Skeletal muscle pathology also involves massive autophagic buildu

26 ver, an experimental model representing both muscle pathologies and displaying most of the distinctiv

27 genetic deletion of Fn14 results in reduced muscle pathology and better function.

28 urrence of myopathic and neurogenic skeletal muscle pathology and by the late development of neuronal

29 With increasing age, kyphoscoliosis, muscle pathology and cardiac conduction defects develop.

30 athy, we identified genetic loci that modify muscle pathology and cardiac fibrosis.

31 st that GSLs may play a critical role in ALS muscle pathology and could lead to the identification of

32 and utrophin (mdx/utr(-/-)), exhibit severe muscle pathology and die prematurely.

33 f these mice, considerably reducing skeletal muscle pathology and extending lifespan.

34 Muscle pathology and function continue to improve during

35 ed macrophage (MP) infiltration and improved muscle pathology and function in mdx diaphragm muscle at

36 We show that nNOS-null mice do not have muscle pathology and have no loss of muscle-specific for

37 tion by greater than 20% is needed to reduce muscle pathology and improve muscle force.

38 esents with fibrosis would result in reduced muscle pathology and improved muscle function.

39 n genes effectively ameliorated histological muscle pathology and improved muscle strength as well as

40 was associated with reduced spinal cord and muscle pathology and improved neuromuscular junction siz

41 markedly reduces SLN expression, attenuates muscle pathology and improves diaphragm, skeletal muscle

42 expression per se is not sufficient for FSHD muscle pathology and indicate that quantitative modifier

43 -) mdx mice had increased heart and skeletal muscle pathology and inflammation, and also worsened car

44 antagonistic anti-Tweak antibody ameliorates muscle pathology and notably, decreases microglial activ

45 ation of autophagy result in improvements of muscle pathology and of functional performance in the PD

46 ted the effects of TFEB systemic delivery on muscle pathology and on functional performance, a primar

47 regulation that is characterized by profound muscle pathology and weakness and that is caused by muta

48 ion prevented weight loss, motor phenotypes, muscle pathology, and motor neuronopathy and dramaticall

49 the precise molecular mechanisms leading to muscle pathology are poorly understood.

50 rospective studies to test which features of muscle pathology are prognostic of disease course or out

51 loss of dystrophin leads to severe skeletal muscle pathologies as well as cardiomyopathy, which mani

52 those observed in human DM1, aggravated the muscle pathology as evidenced by increased central nucle

53 ned immunodeficient animals have evidence of muscle pathology as long as 5 weeks p.i., suggesting tha

54 cles and has no effect on the development of muscle pathology associated with muscular dystrophy.

55 providing a mechanistic explanation for the muscle pathology associated with mutations in caveolae p

56 Clenbuterol improved muscle pathology, attenuated the glycolytic-to-oxidative

57 ibers and caveolin and cavin mutations cause muscle pathology, but the underlying mechanism is unknow

58 l/Col6a2Deltaex5 mice indeed exhibit reduced muscle pathology compared with gamma-sarcoglycan-null mi

59 Documentation of muscle pathology compatible with targeting of sarcolemma

60 came weak, had early lethality and developed muscle pathology consistent with myopathy after 2 months

61 ly similar to previously reported cases, and muscle pathology demonstrated diagnostic features of MFM

62 lso demonstrate that a reduction in skeletal muscle pathology does not necessarily lead to an improve

63 e relationship between NKX2-5 expression and muscle pathology due to RNA toxicity.

64 luation was based on recent discussions with muscle pathology experts to develop criteria for assessi

65 her extraocular muscles, suggesting that the muscle pathology extends beyond the muscles innervated b

66 Muscle pathology findings were highly variable and inclu

67 ectation, this results in a worsening of the muscle pathology implying that any future strategies bas

68 es of laminin-alpha2-deficient mice prevents muscle pathology, improves muscle strength, and dramatic

69 signaling, decreased fibrosis, and improved muscle pathology in a mouse model of muscular dystrophy.

70 suggest that loss of nNOS may contribute to muscle pathology in AR-LGMD with primary mutations in th

71 t with previous reports, we found dystrophic muscle pathology in both mouse strains.

72 ortant implications for our understanding of muscle pathology in dermatomyositis of both adults and c

73 onuclear inclusions are a key feature of the muscle pathology in DM and that sequestration of muscleb

74 delivery of MBNL1 partially rescues skeletal muscle pathology in DM mice, there is strong interest in

75 inopril and spironolactone improves skeletal muscle pathology in Duchenne muscular dystrophy (DMD) mo

76 -associated virus both reduced the extent of muscle pathology in dy(W)/dy(W) skeletal muscle.

77 nt (C3) of the complement system ameliorated muscle pathology in dysferlin-deficient mice but had no

78 complement system plays an important role in muscle pathology in dysferlinopathy.

79 ression of Galgt2 failed to inhibit skeletal muscle pathology in dystroglycan-deficient muscles, in c

80 contrast, verapamil did not prevent cardiac muscle pathology in dystrophin-deficient mdx mice, which

81 ntified seven small molecules that influence muscle pathology in dystrophin-null zebrafish without re

82 We show that muscle pathology in embryos lacking Fukutin or FKRP is d

83 LGT2 overexpression can reduce the extent of muscle pathology in FKRP mutant muscles, but that it may

84 at GALGT2 gene therapy significantly reduces muscle pathology in FKRP P448Lneo(-) mice, a model for l

85 VI-mediated fibrosis contributes to skeletal muscle pathology in gamma-sarcoglycan-null mice.

86 ceutical proteasome inhibitor MG-132 reduces muscle pathology in laminin alpha2 chain-deficient dy(3K

87 of expression that mirror the progression of muscle pathology in mdx mice.

88 2 and dystrophin surrogates known to inhibit muscle pathology in mouse models of congenital muscular

89 eviously GALGT2) inhibits the development of muscle pathology in mouse models of Duchenne muscular dy

90 Here, we investigated skeletal muscle pathology in myofibers and myofibrils isolated fr

91 loss of PABPN1 function could contribute to muscle pathology in OPMD.

92 critical role in the development of skeletal muscle pathology in patients with Myotonic Dystrophy 1 (

93 or EB (TFEB) gene was effective in improving muscle pathology in PD mice injected intramuscularly wit

94 ion, the two major hallmarks of the skeletal muscle pathology in sporadic inclusion body myositis (sI

95 s effective in inhibiting the development of muscle pathology in the dy(W) mouse model of MDC1A, much

96 cytotoxic T lymphocytes (CTLs) contribute to muscle pathology in the dystrophin-null mutant mouse (md

97 effects of transgenes on the development of muscle pathology in the mdx mouse model for Duchenne mus

98 lates utrophin at the sarcolemma and reduces muscle pathology in the mdx mouse model of DMD.

99 class I protein is a common feature of many muscle pathologies including idiopathic myositis and can

100 gene expression can ameliorate the extent of muscle pathology, inflammation, and dysfunction in mdx m

101 ve diagnosis of cardiac injury when skeletal muscle pathology is present.

102 we have investigated whether DM1-associated muscle pathology is related to deregulation of central m

103 al muscles, but their application to monitor muscle pathology is sparse.

104 disorders with often difficult to interpret muscle pathology, making them challenging to diagnose.

105 Surprisingly, in spite of this reduction in muscle pathology, muscle function is not significantly i

106 del recapitulates the progressive congenital muscle pathology observed in patients.

107 Reduced voluntary locomotor activity and muscle pathology occurred without significant denervatio

108 racranial and orbital pathology of 1 and the muscle pathology of 2 other affected members of a family

109 We studied the muscle pathology of SINV infection ex vivo by examining

110 effectively ameliorate cardiac and skeletal muscle pathology, profoundly improve cardiac and whole-b

111 f 111In-antimyosin in the detection of heart muscle pathology, radiation dose estimates were made for

112 term treatment had a positive effect on limb muscle pathology, reduced fibrosis, increased sarcolemma

113 This progressive muscle pathology resembles the muscular dystrophy phenot

114 muscle disease as evidenced by an absence of muscle pathology, restored contractile function and a re

115 ice had partial embryonic lethality and mild muscle pathology, similar to alpha7 integrin-deficient m

116 f inflammatory macrophages and NK cells, and muscle pathology, suggesting that the adaptive immune re

117 Although surviving mice exhibit muscle pathology, these results suggest that either isof

118 ntribute significantly to the progression of muscle pathology through a variety of mechanisms.

119 the role of overexpression of CUGBP1 in DM1 muscle pathology using transgenic mice that overexpress

120 d demonstrated that the skeletal and cardiac muscle pathology was completely reversible if the treatm

121 The muscle pathology was preceded by mitochondrial enlargeme

122 Abnormal muscle pathology, which included coarse internal archite

123 In addition, evidence for skeletal muscle pathology, which might have implications for huma

124 age significantly contribute to CTX-mediated muscle pathology with implications for human muscle dise

125 and alendronate provided best improvement in muscle pathology with normalized fiber size distribution

126 Prednisolone improved muscle pathology with significant reduction in muscle de

127 severely affected mice leads to reversal of muscle pathology within 2 weeks.

128 dies have been performed to correct skeletal muscle pathology, yet little is known about cardiomyopat