戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 of the dystrophy in the dystrophin-deficient mdx mouse.
2 on is elevated in muscle from the dystrophic mdx mouse.
3 strophin-deficient muscular dystrophy in the mdx mouse.
4 e at high levels in the dystrophin-deficient mdx mouse.
5 e disease that is commonly studied using the mdx mouse.
6 e observed in DMD patients compared with the mdx mouse.
7 hways in muscles of the dystrophin-deficient mdx mouse.
8 le growth and improve muscle function in the mdx mouse.
9 e cardiac and skeletal muscles in dystrophic mdx mouse.
10 n and therapeutic interventions has been the mdx mouse.
11 iculum to release Ca2+ may be altered in the mdx mouse.
12 MS) ion channels in skeletal muscle from the mdx mouse, a deletion mutant that lacks the cytoskeletal
13  exposure altered the muscle function of the mdx mouse, a genetic model of DMD.
14  in several muscle tissues of the dystrophic mdx mouse, a model for continuous muscle degeneration an
15 tively mild dystrophic phenotype) and in the mdx mouse, a model for DMD.
16 liorate aspects of muscular dystrophy in the mdx mouse, a model for Duchenne muscular dystrophy.
17                     Using this technique the mdx mouse, a model of Duchenne muscular dystrophy (DMD)
18 pathways in skeletal muscles from normal and mdx mouse, a model of Duchenne muscular dystrophy (DMD),
19                                       In the mdx mouse, a model of Duchenne muscular dystrophy (DMD),
20                                       In the mdx mouse, a model of Duchenne muscular dystrophy in whi
21 trophin expression in skeletal muscle in the mdx mouse, a model of Duchenne muscular dystrophy.
22 on coupling in skeletal muscle fibres of the mdx mouse, a model of the human disease Duchenne muscula
23                                          The mdx mouse, a model of the human disease Duchenne muscula
24 gentamicin on cultured muscle cells from the mdx mouse - an animal model for DMD that possesses a pre
25  and function have benefited from use of the mdx mouse, an animal model for DMD/BMD.
26 cation of muscle-derived stem cells from the mdx mouse, an animal model for Duchenne muscular dystrop
27 f bone marrow transplantation studies in the mdx mouse, an animal model of Duchenne's muscular dystro
28 are also present in the dystrophin-deficient mdx mouse and are believed to result from alternative sp
29 med exon-skipping, has been reported for the mdx mouse and in four DMD patients by local intramuscula
30 xercise-induced cardiac injury models in the mdx mouse and rigorous testing of AAV-muUtro for efficac
31 in the muscle of the mouse model of DMD, the mdx mouse, and that pharmacological inhibition of the BE
32                         Using cells from the mdx mouse as a model system, we show that chimeraplast-m
33                 The results substantiate the mdx mouse as an important model system for studies of th
34 ophy (DMD) and in mouse models including the mdx mouse but with inconsistent findings.
35 orrecting the morphological pathology of the mdx mouse, but still functioned to assemble the DGC at t
36             AAV was delivered to the newborn mdx mouse cardiac cavity.
37 as upregulated in DMD-iCMs, DMD exosomes and mdx mouse cardiac tissue.
38               Spontaneous Ca2+ transients in mdx mouse cells are sensitive to depolarization and are
39                                           In mdx mouse cells the intrinsic gating property of fast vo
40 netic downregulation of Nox2 activity in the mdx mouse decreases reactive oxygen species (ROS) produc
41                         These studies in the mdx mouse demonstrate that oral administration of SMT022
42                               Data show that mdx mouse EOM contains dystrophin-glycoprotein complex (
43                                      The mdx/mdx mouse has been widely used to study DMD; this model
44                                       The D2-mdx mouse has genetic modifiers, including latent transf
45                 As a result, research in the mdx mouse has largely focused on early adulthood.
46                                    AIMS: The mdx mouse has proven to be useful in understanding the c
47 ough the increase in MLP and utrophin in the mdx mouse heart was able to compensate for the loss of d
48 efficient and persistent transduction of the mdx mouse heart.
49 mediated microdystrophin gene therapy in the mdx mouse heart.
50  models accumulated desmin and beta-tubulin, mdx mouse hearts accumulated utrophin and MLP, and MLP-n
51                                           In mdx mouse hearts, LV-to-body weight ratio, cavity volume
52 rmalize blood flow regulation in contracting mdx mouse hindlimb muscles suggests a putative novel tre
53     Analysis of gephyrin -/-, agrin -/-, and mdx mouse hippocampal neurons in culture indicated that
54                                    Using the mdx mouse homologue, we have shown previously that the a
55                                          The mdx mouse is a valuable animal model of DMD as it bears
56                                          The mdx mouse is a widely used animal model of DMD.
57                            Heart function of mdx mouse is normal in the absence of external stress.
58  which is unable to prevent dystrophy in the mdx mouse, is able to ameliorate these abnormalities in
59                               A mouse model (mdx mouse) lacks Dp427 in muscle and CNS and exhibits ex
60 l model for Duchenne muscular dystrophy, the mdx mouse, loss of dystrophin causes more severe abnorma
61 chronic elevation of tubb6, as occurs in the mdx mouse, may contribute to the repeated cycles of rege
62 study is to improve the understanding of the mdx mouse model by tracking pathological features of the
63  skeletal muscle pathological lesions in the mdx mouse model for DMD.
64 he symptoms associated with dystrophy in the mdx mouse model for DMD.
65 pathology and improve muscle function in the mdx mouse model for DMD.
66 phin expression into skeletal muscles of the mdx mouse model for Duchenne muscular dystrophy (DMD).
67 n the development of muscle pathology in the mdx mouse model for Duchenne muscular dystrophy, but non
68 exercise, moderate and low intensity, in the mdx mouse model in the DBA2J background.
69  responsible for the death of muscles in the mdx mouse model of DMD and human DMD lymphoblasts.
70                            Here, we used the mdx mouse model of DMD and non-invasive spectroscopy to
71 is a highly potent therapeutic agent for the mdx mouse model of DMD and represents a paradigm for the
72 c silencing of the klotho gene occurs in the mdx mouse model of DMD and whether klotho silencing is a
73 gative muscle cell line established from the mdx mouse model of DMD but not in normal myoblasts, expo
74    Injection of laminin-111 protein into the mdx mouse model of DMD increased expression of alpha(7)-
75 indromic repeats (CRISPR)-Cas9 system to the mdx mouse model of DMD to remove the mutated exon 23 fro
76                                          The mdx mouse model of DMD was used to test whether the path
77                       In the mildly affected mdx mouse model of DMD, brief scruff stress causes inact
78 ne muscular dystrophy (DMD) and the standard mdx mouse model of DMD, dystrophin deficiency causes los
79               Studies in mice, including the mdx mouse model of DMD, have demonstrated that circulati
80 l muscle mass and functional strength in the mdx mouse model of DMD, providing a therapeutic rational
81                                       In the mdx mouse model of DMD, the pharmacological reduction of
82 eurogenesis in the dentate gyrus (DG) in the mdx mouse model of DMD, using bromodeoxyuridine incorpor
83 cles, we genetically ablated miR-133b in the mdx mouse model of DMD.
84 on to IgG-Fc improved pathophysiology of the mdx mouse model of DMD.
85 n to improve the dystrophic phenotype in the mdx mouse model of DMD.
86 y have been identified in myoblasts from the mdx mouse model of DMD.
87 ion and recover dystrophin expression in the mdx mouse model of DMD.
88 mediates salutary therapeutic effects in the mdx mouse model of DMD.
89 A expression in the tibialis anterior of the mdx mouse model of DMD.
90 n binding and amelioration of disease in the mdx mouse model of DMD.
91 itophagy pathway, would be beneficial in the mdx mouse model of DMD.
92 regulation and functional improvement in the mdx mouse model of DMD.
93 rcolemma and reduces muscle pathology in the mdx mouse model of DMD.
94 of Duchenne muscular dystrophy (DMD) and the mdx mouse model of DMD.
95 rtant role in promoting the pathology in the mdx mouse model of DMD.
96 o ameliorate the dystrophic phenotype in the mdx mouse model of Duchenne muscular dystrophy (DMD).
97 damage, and hypotension-induced death in the mdx mouse model of Duchenne muscular dystrophy (DMD).
98 ic streptomycin from onset of disease in the mdx mouse model of Duchenne muscular dystrophy (DMD).
99 in the development of cardiac disease in the mdx mouse model of Duchenne muscular dystrophy (DMD); ho
100 expression is also normally increased in the mdx mouse model of Duchenne muscular dystrophy compared
101                      Deletion of MSTN in the mdx mouse model of Duchenne muscular dystrophy enhances
102 phin protein restoration is sustained in the mdx mouse model of Duchenne muscular dystrophy for 1 yea
103 portantly, genetically deleting S1PR3 in the mdx mouse model of Duchenne muscular dystrophy produced
104 diac function and mouse survival, and in the mdx mouse model of Duchenne muscular dystrophy, exosomes
105 tegy to target LIF to sites of damage in the mdx mouse model of Duchenne muscular dystrophy, leading
106                  In the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy, limb mus
107 major role in worsening muscle injury in the mdx mouse model of Duchenne muscular dystrophy.
108 iomyopathy by reducing SR Ca(2+) leak in the mdx mouse model of Duchenne muscular dystrophy.
109 bit regeneration in the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy.
110                                       In the mdx mouse model of dystrophinopathy, this protective mec
111                      Previous studies in the mdx mouse model of muscular dystrophy demonstrate that i
112 asmic reticulum Ca2+ release channel, in the mdx mouse model of muscular dystrophy that contributes t
113 reatment of dystrophic DMD muscles using the mdx mouse model, and found that Wnt7a treatment efficien
114  been identified in the Dystrophin-deficient mdx mouse model, in vivo evidence of pathology based on
115                            In the dystrophic mdx mouse model, overexpression of ML1 decreased muscle
116       Here, using the severely dystrophic D2-mdx mouse model, we generated a high-resolution cellular
117                                    Using the mdx mouse model, we performed a large-scale metabolomic
118 rophic pathology in the dystrophin-deficient mdx mouse model.
119 d in skeletal muscle of DMD patients and the mdx mouse model.
120 ates both in cell culture and in vivo in the mdx mouse model.
121 phic environment has been established in the mdx mouse model.
122 e skeletal muscle of DMD patients and in the mdx mouse model.
123 elta-sarcoglycan (Sgcd(-/-)), Dysf(-/-), and mdx mouse models of muscular dystrophy.
124 ned these agents in vivo using wild-type and mdx mouse models.
125 tribute to regeneration upon reinjury and in mdx mouse models.
126  the more severe D2.B10-Dmd(mdx)/J mouse (D2-mdx) mouse models.
127  muscle size and absolute muscle strength in mdx mouse muscle along with a significant decrease in mu
128 arcolemma isolated from dystrophin-deficient mdx mouse muscle even though it was localized to costame
129  long-term OVL are detrimental for hind limb mdx mouse muscle, a murine model of Duchene muscular dys
130 ndogenously corrected myogenic precursors in mdx mouse muscle.
131 ed to confer protection on Dag1(Y890F/Y890F)/mdx mouse muscle.
132  dystrophin promoters results in a series of mdx mouse mutants that differ in their repertoire of iso
133  canine myocytes than in the mildly affected mdx mouse myocytes, and this was associated with a lack
134 ds also demonstrated readthrough activity in mdx mouse myotube cells carrying a nonsense mutation and
135                         MSCs in patches from mdx mouse myotubes have higher levels of resting activit
136 ong exon-skipping activity in differentiated mdx mouse myotubes in culture in the absence of an added
137  in individual resting normal and dystrophic mdx mouse myotubes in culture.
138 lar dystrophy (DMD) in vitro model using H2K mdx mouse myotubes.
139               While the dystrophin-deficient mdx mouse on the C57BL/10 genetic background (B10.mdx) i
140  microtubule defects have been linked to the mdx mouse pathology.
141 1beta and tumor necrosis factor alpha in the mdx mouse precede the onset of muscular dystrophy.
142                   The dystrophin gene in the mdx mouse provides a favored system for study of exon sk
143 y in healthy (wild-type, WT) and dystrophic (mdx) mouse quadriceps muscles and evaluated transcript l
144                     Genetic crosses with the mdx mouse showed that neither transgenic syntrophin coul
145 rophin transgene in the dystrophin-deficient mdx mouse significantly improves the dystrophic muscle p
146                                          The mdx mouse strain has a point mutation in the dystrophin
147 ving force behind acute muscle damage in the mdx mouse strain.
148     We have recently shown in the dystrophic mdx mouse that exon 23, bearing a nonsense mutation, can
149 rcolemmal membrane of skeletal muscle of the mdx mouse that lacks dystrophin.
150 c mouse models to identify phenotypes of the mdx mouse that remain despite transgenic utrophin overex
151 roximately 20 years of investigations of the mdx mouse, the impact of the disease on the life span of
152 Our results suggest that in myofibers of the mdx mouse, the membrane- associated cytoskeleton, but no
153                                          The mdx mouse, the most widely used animal model of DMD, has
154 rove aspects of the disease phenotype in the mdx mouse; therefore, utrophin up-regulation is under in
155  regeneration of dystrophin in the muscle of mdx mouse through a 2'O-methyl phosphorothioate-mediated
156 mprovement, we used in situ protocols in the mdx mouse to measure muscle strength and resistance to e
157 of stop codons, successfully achieved in the mdx mouse using gentamicin, represents an important evol
158       Consequently, a life span study of the mdx mouse was designed that included cohorts of male and
159 , but muscle fibre degeneration found in the mdx mouse was reduced almost to wild-type levels.
160  for Duchenne muscular dystrophy, the mutant mdx mouse, was used to determine whether disruption of t
161  Obviation of such a blockage is seen in the mdx mouse, where despite a nonsense mutation in exon 23
162                                       In the mdx mouse, where muscular dystrophy is due to a nonsense
163                              In a transgenic mdx mouse, where utrophin was over expressed in the skel
164 ed in the dystrophin-deficient model of DMD (mdx mouse), which may explain the relatively mild dystro
165 nditioned startle responses to threat to the mdx mouse, which in the mouse respond to brain dystrophi
166 e studied the expression of myoferlin in the mdx mouse, which lacks dystrophin and whose muscles unde
167 nsive protein biomarkers in the serum of the mdx mouse with potential utility in DMD patients.
168 lecular signature of dystrophinopathy in the mdx mouse, with evidence that secondary mechanisms are k
169 body-wide skeletal muscles of the dystrophic mdx mouse, with resulting improvement in muscle function

 
Page Top