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1  of blocking gene repression correlated with muscle pathology.
2 ely lead to animal weakness and the observed muscle pathology.
3 sease model, does not improve all aspects of muscle pathology.
4 y, reproduce well and do not show any smooth muscle pathology.
5 ed to produce any significant differences in muscle pathology.
6 xpense of fat formation, and does not reduce muscle pathology.
7 traction mediated damage, and a reduction of muscle pathology.
8  complex and substantial changes in skeletal muscle pathology.
9 ficant inhibition of degenerative dystrophic muscle pathology.
10 et set of bands in many patients with active muscle pathology.
11 from mislocalized nNOS may contribute to mdx muscle pathology.
12 r physically normal despite their underlying muscle pathology.
13 f the early embryonic program and subsequent muscle pathology.
14 eratrol may mitigate against obesity-induced muscle pathology.
15 ub gene deletion did not augment Duchenne MD muscle pathology.
16 efficacy in addressing high-fat diet-induced muscle pathology.
17  enriching our understanding of DUX4-induced muscle pathology.
18 ockout (Mtm1KO) mice prevents development of muscle pathology.
19  fibers, which could in turn plays a role in muscle pathology.
20 hancing muscle regeneration and ameliorating muscle pathology.
21 been demonstrated and may also contribute to muscle pathology.
22 umulation and prominent cardiac and skeletal muscle pathology.
23 t its expression correlates with severity of muscle pathology.
24 the loss of nNOS impacts dystrophic skeletal muscle pathology.
25 ir clinical records, muscle MRI findings and muscle pathology.
26 mouse model, overexpression of ML1 decreased muscle pathology.
27 elta4 mice improved contractile function and muscle pathology.
28 ailure, even in the presence of non-specific muscle pathology.
29 be involved in the improvement of dystrophic muscle pathology.
30 tering the levels of these factors modulated muscle pathology.
31 l muscle innervation and are associated with muscle pathologies.
32 uscle differentiation and is dysregulated in muscle pathologies.
33                                     Skeletal muscle pathology also involves massive autophagic buildu
34 ver, an experimental model representing both muscle pathologies and displaying most of the distinctiv
35          Defective lamin A expression causes muscle pathologies and premature ageing syndromes, but t
36  genetic deletion of Fn14 results in reduced muscle pathology and better function.
37 ed ANO5 mutations contribute to the observed muscle pathology and broaden the genetic spectrum of LGM
38 urrence of myopathic and neurogenic skeletal muscle pathology and by the late development of neuronal
39         With increasing age, kyphoscoliosis, muscle pathology and cardiac conduction defects develop.
40 athy, we identified genetic loci that modify muscle pathology and cardiac fibrosis.
41 zation of NeflE397K motor function deficits, muscle pathology and changes in breathing.
42 st that GSLs may play a critical role in ALS muscle pathology and could lead to the identification of
43  and utrophin (mdx/utr(-/-)), exhibit severe muscle pathology and die prematurely.
44 the correlation between MRI characteristics, muscle pathology and expression of DUX4 target genes.
45 f these mice, considerably reducing skeletal muscle pathology and extending lifespan.
46 owed a synergistic improvement in temporalis muscle pathology and function coincident with increased
47                                              Muscle pathology and function continue to improve during
48 ed macrophage (MP) infiltration and improved muscle pathology and function in mdx diaphragm muscle at
49 e knockout (DKO) mice, and compared the limb muscle pathology and function of wild-type B10, muscle-s
50 rease in life expectancy and improvements in muscle pathology and function.
51      We show that nNOS-null mice do not have muscle pathology and have no loss of muscle-specific for
52 tion by greater than 20% is needed to reduce muscle pathology and improve muscle force.
53 Laminin-111 (msLam-111) protein could reduce muscle pathology and improve muscle function in the mdx
54 esents with fibrosis would result in reduced muscle pathology and improved muscle function.
55 n genes effectively ameliorated histological muscle pathology and improved muscle strength as well as
56  was associated with reduced spinal cord and muscle pathology and improved neuromuscular junction siz
57 t by pde10a morpholino-mediated reduction in muscle pathology and improvement in locomotion, muscle,
58  markedly reduces SLN expression, attenuates muscle pathology and improves diaphragm, skeletal muscle
59 cal inhibition of PTEN similarly ameliorates muscle pathology and improves muscle integrity and funct
60 expression per se is not sufficient for FSHD muscle pathology and indicate that quantitative modifier
61 -) mdx mice had increased heart and skeletal muscle pathology and inflammation, and also worsened car
62 latory factors and to improve the dystrophic muscle pathology and microenvironment is through parabio
63 lar dystrophy (mdx-Mss51 KO) counteracts the muscle pathology and mitochondrial irregularities observ
64 e therapies exist to improve lower extremity muscle pathology and mobility loss due to peripheral art
65 g of the relationship between DUX4 activity, muscle pathology and muscle magnetic resonance imaging (
66 antagonistic anti-Tweak antibody ameliorates muscle pathology and notably, decreases microglial activ
67 ation of autophagy result in improvements of muscle pathology and of functional performance in the PD
68 ted the effects of TFEB systemic delivery on muscle pathology and on functional performance, a primar
69 regulation that is characterized by profound muscle pathology and weakness and that is caused by muta
70 t associated with hearing loss rather than a muscle pathology, and because there are no homologous mu
71 ion prevented weight loss, motor phenotypes, muscle pathology, and motor neuronopathy and dramaticall
72  the precise molecular mechanisms leading to muscle pathology are poorly understood.
73 rospective studies to test which features of muscle pathology are prognostic of disease course or out
74  loss of dystrophin leads to severe skeletal muscle pathologies as well as cardiomyopathy, which mani
75  those observed in human DM1, aggravated the muscle pathology as evidenced by increased central nucle
76 ned immunodeficient animals have evidence of muscle pathology as long as 5 weeks p.i., suggesting tha
77 onucleated cell types that contribute to the muscle pathology associated with DMD, we performed singl
78 cles and has no effect on the development of muscle pathology associated with muscular dystrophy.
79  providing a mechanistic explanation for the muscle pathology associated with mutations in caveolae p
80 ndicate that treatment efficacy and state of muscle pathology at the time of intervention are linked,
81                         Clenbuterol improved muscle pathology, attenuated the glycolytic-to-oxidative
82 We hypothesized that differences in skeletal muscle pathology between men and women with HFrEF may ex
83 ibers and caveolin and cavin mutations cause muscle pathology, but the underlying mechanism is unknow
84  Galgt2 in the DMD mdx murine model prevents muscle pathology by increasing CT2 modified alpha-dystro
85 e injury represents a collection of skeletal muscle pathologies caused by trauma to the muscle tissue
86 anti-cN1A), an HLA autoimmune haplotype, and muscle pathology characterized by cytotoxic CD8+ T cell
87 l/Col6a2Deltaex5 mice indeed exhibit reduced muscle pathology compared with gamma-sarcoglycan-null mi
88                             Documentation of muscle pathology compatible with targeting of sarcolemma
89 came weak, had early lethality and developed muscle pathology consistent with myopathy after 2 months
90 ly similar to previously reported cases, and muscle pathology demonstrated diagnostic features of MFM
91 lso demonstrate that a reduction in skeletal muscle pathology does not necessarily lead to an improve
92 e relationship between NKX2-5 expression and muscle pathology due to RNA toxicity.
93 nction and help guide research into striated muscle pathology, especially that which arises due to dy
94 luation was based on recent discussions with muscle pathology experts to develop criteria for assessi
95 her extraocular muscles, suggesting that the muscle pathology extends beyond the muscles innervated b
96 ting regeneration in skeletal muscle, but in muscle pathologies FAPs the are main source of excess ex
97                         Despite clinical and muscle pathology features highly suggestive of collagen
98                                              Muscle pathology findings were highly variable and inclu
99                           Analyzing skeletal muscle pathology from histological images is labor inten
100  muscular dystrophy mice improved dystrophic muscle pathologies; however, complete loss of Dock3 wors
101 ectation, this results in a worsening of the muscle pathology implying that any future strategies bas
102 es of laminin-alpha2-deficient mice prevents muscle pathology, improves muscle strength, and dramatic
103  signaling, decreased fibrosis, and improved muscle pathology in a mouse model of muscular dystrophy.
104  suggest that loss of nNOS may contribute to muscle pathology in AR-LGMD with primary mutations in th
105 t with previous reports, we found dystrophic muscle pathology in both mouse strains.
106 ortant implications for our understanding of muscle pathology in dermatomyositis of both adults and c
107 onuclear inclusions are a key feature of the muscle pathology in DM and that sequestration of muscleb
108 delivery of MBNL1 partially rescues skeletal muscle pathology in DM mice, there is strong interest in
109 inopril and spironolactone improves skeletal muscle pathology in Duchenne muscular dystrophy (DMD) mo
110 -associated virus both reduced the extent of muscle pathology in dy(W)/dy(W) skeletal muscle.
111 nt (C3) of the complement system ameliorated muscle pathology in dysferlin-deficient mice but had no
112 complement system plays an important role in muscle pathology in dysferlinopathy.
113 ression of Galgt2 failed to inhibit skeletal muscle pathology in dystroglycan-deficient muscles, in c
114  contrast, verapamil did not prevent cardiac muscle pathology in dystrophin-deficient mdx mice, which
115 ntified seven small molecules that influence muscle pathology in dystrophin-null zebrafish without re
116                                 We show that muscle pathology in embryos lacking Fukutin or FKRP is d
117 LGT2 overexpression can reduce the extent of muscle pathology in FKRP mutant muscles, but that it may
118 at GALGT2 gene therapy significantly reduces muscle pathology in FKRP P448Lneo(-) mice, a model for l
119 VI-mediated fibrosis contributes to skeletal muscle pathology in gamma-sarcoglycan-null mice.
120                           Sex differences in muscle pathology in HFrEF exist, with men showing greate
121 ceutical proteasome inhibitor MG-132 reduces muscle pathology in laminin alpha2 chain-deficient dy(3K
122 ibrosis and inflammation, and it ameliorates muscle pathology in mdx mice.
123 of expression that mirror the progression of muscle pathology in mdx mice.
124 2 and dystrophin surrogates known to inhibit muscle pathology in mouse models of congenital muscular
125 eviously GALGT2) inhibits the development of muscle pathology in mouse models of Duchenne muscular dy
126               Here, we investigated skeletal muscle pathology in myofibers and myofibrils isolated fr
127  loss of PABPN1 function could contribute to muscle pathology in OPMD.
128       CKD significantly exacerbates ischemic muscle pathology in PAD, as evidenced by diminished musc
129 critical role in the development of skeletal muscle pathology in patients with Myotonic Dystrophy 1 (
130 or EB (TFEB) gene was effective in improving muscle pathology in PD mice injected intramuscularly wit
131 ion, the two major hallmarks of the skeletal muscle pathology in sporadic inclusion body myositis (sI
132 s effective in inhibiting the development of muscle pathology in the dy(W) mouse model of MDC1A, much
133 cytotoxic T lymphocytes (CTLs) contribute to muscle pathology in the dystrophin-null mutant mouse (md
134  effects of transgenes on the development of muscle pathology in the mdx mouse model for Duchenne mus
135 lates utrophin at the sarcolemma and reduces muscle pathology in the mdx mouse model of DMD.
136  class I protein is a common feature of many muscle pathologies including idiopathic myositis and can
137 e observed significantly improved dystrophic muscle pathology, including decreased inflammation, necr
138 gene expression can ameliorate the extent of muscle pathology, inflammation, and dysfunction in mdx m
139      These preliminary data question whether muscle pathology is a primary mechanism contributing to
140                                     Skeletal muscle pathology is characterized by changes in myofiber
141 ve diagnosis of cardiac injury when skeletal muscle pathology is present.
142  we have investigated whether DM1-associated muscle pathology is related to deregulation of central m
143                        Despite the fact that muscle pathology is reported in up to one-third of indiv
144 al muscles, but their application to monitor muscle pathology is sparse.
145                            Lung, kidney, and muscle pathologies, lung proteostasis, endoplasmic retic
146  disorders with often difficult to interpret muscle pathology, making them challenging to diagnose.
147  Surprisingly, in spite of this reduction in muscle pathology, muscle function is not significantly i
148 del recapitulates the progressive congenital muscle pathology observed in patients.
149     Reduced voluntary locomotor activity and muscle pathology occurred without significant denervatio
150                         We hypothesized that muscle pathologies of different etiologies have distinct
151 racranial and orbital pathology of 1 and the muscle pathology of 2 other affected members of a family
152                               We studied the muscle pathology of SINV infection ex vivo by examining
153                                              Muscle pathology on MRI correlated positively with disea
154  effectively ameliorate cardiac and skeletal muscle pathology, profoundly improve cardiac and whole-b
155 f 111In-antimyosin in the detection of heart muscle pathology, radiation dose estimates were made for
156 term treatment had a positive effect on limb muscle pathology, reduced fibrosis, increased sarcolemma
157                             This progressive muscle pathology resembles the muscular dystrophy phenot
158 muscle disease as evidenced by an absence of muscle pathology, restored contractile function and a re
159 mportantly, restoring SMN after the onset of muscle pathology reversed disease.
160 y score, disease duration, D4Z4 repeat size, muscle pathology scorings and functional outcome measure
161 ice had partial embryonic lethality and mild muscle pathology, similar to alpha7 integrin-deficient m
162 nal perspective on the treatment of skeletal muscle pathologies such as catastrophic wounds, wasting,
163 es provide a high-fidelity platform to study muscle pathology, such as emergence of dysmorphic nuclei
164 f inflammatory macrophages and NK cells, and muscle pathology, suggesting that the adaptive immune re
165              Although surviving mice exhibit muscle pathology, these results suggest that either isof
166 ntribute significantly to the progression of muscle pathology through a variety of mechanisms.
167  the role of overexpression of CUGBP1 in DM1 muscle pathology using transgenic mice that overexpress
168 d demonstrated that the skeletal and cardiac muscle pathology was completely reversible if the treatm
169 tological progression of the D2.mdx skeletal muscle pathology was evaluated to determine the distingu
170                                          The muscle pathology was preceded by mitochondrial enlargeme
171  dystrophin expression levels and effects on muscle pathology were greater with the use of micro-dyst
172 ion, variants in other genes associated with muscle pathology were identified, possibly affecting the
173 oved spinal cord, neuromuscular junction and muscle pathology when ML372 and the ASO were administere
174 nifests as a chaperonopathy with progressive muscle pathology, which discovers the previously unknown
175                                     Abnormal muscle pathology, which included coarse internal archite
176           In addition, evidence for skeletal muscle pathology, which might have implications for huma
177 suggest stabilization or less progression of muscle pathology with delandistrogene moxeparvovec-addin
178 age significantly contribute to CTX-mediated muscle pathology with implications for human muscle dise
179 and alendronate provided best improvement in muscle pathology with normalized fiber size distribution
180                        Prednisolone improved muscle pathology with significant reduction in muscle de
181  severely affected mice leads to reversal of muscle pathology within 2 weeks.
182 dies have been performed to correct skeletal muscle pathology, yet little is known about cardiomyopat

 
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