ライフサイエンスコーパス: myositis

1 e gammadelta-TCR (gammadelta-T cell-mediated myositis).

2 lly impaired in ability to cause necrotizing myositis.

3 tissue lesion of gammadelta-T cell-mediated myositis.

4 T cell and antibody responses in autoimmune myositis.

5 e weakness that occurs in the mouse model of myositis.

6 yositis, dermatomyositis, and inclusion body myositis.

7 therefore a potential therapeutic target in myositis.

8 tomyositis, polymyositis, and inclusion body myositis.

9 1) may be responsible for muscle weakness in myositis.

10 events in the pathogenesis of inclusion body myositis.

11 disease activity sensors for inclusion body myositis.

12 genic mouse model of autoimmune inflammatory myositis.

13 humans with myositis and in mouse models of myositis.

14 keletal muscle cell death and dysfunction in myositis.

15 time points for histopathologic evidence of myositis.

16 ctive target for therapeutic intervention in myositis.

17 hould help to define therapeutic targets for myositis.

18 innate immune responses in a murine model of myositis.

19 on of NF-kappaB and autophagic cell death in myositis.

20 ar degeneration, and sporadic inclusion body myositis.

21 atomyositis, polymyositis and inclusion body myositis.

22 a were collected from children with juvenile myositis.

23 onal drug development for some patients with myositis.

24 nvolved in the initiation and propagation of myositis.

25 ignal recognition particle antibody-positive myositis.

26 ase of aging humans, sporadic inclusion body myositis.

27 Alzheimer's disease (AD) and inclusion body myositis.

28 nd predictive validity in juvenile and adult myositis.

29 and validity of a disease activity index in myositis.

30 re possibly important in the pathogenesis of myositis.

31 lementary miRNAs and therefore did not cause myositis.

32 9, p=0.0007) in patients with inclusion body myositis.

33 been found, especially in masticatory muscle myositis.

34 el disorders and provide insights into human myositis.

35 nductive phase, of RRV-induced arthritis and myositis.

36 levels and various disease manifestations of myositis.

37 developing similar systems in other forms of myositis.

38 the pathogenesis of sporadic inclusion-body myositis.

39 yositis, dermatomyositis, and inclusion body myositis.

40 autoantibodies in canine masticatory muscle myositis.

41 ammatory autoimmune diseases sarcoidosis and myositis.

42 between cancer tissues and muscle tissue in myositis.

43 ency in this group of Japanese patients with myositis.

44 nd was subsequently diagnosed as having Lyme myositis.

45 del for the development of cancer-associated myositis.

46 , LPS was injected intramuscularly to induce myositis.

47 ntribute to alphavirus-induced arthritis and myositis.

48 MRC criteria was required for inclusion body myositis.

49 mune pathways affecting murine virus-induced myositis.

50 plasma samples from patients diagnosed with myositis.

51 yopathy was recognized as a distinct form of myositis.

52 statins can induce an autoimmune necrotizing myositis.

53 nterstitial lymphocytic and nongranulomatous myositis.

54 first report of cell cycle reentry in human myositis.

55 tic model for comparative studies with human myositis.

56 may facilitate the diagnosis of this type of myositis.

57 s the highest disease risk in inclusion body myositis.

58 te to the phenotypic changes in Jo-1 and IBM myositis.

59 linical and serologic expression of juvenile myositis.

60 nts contributing to our model of HRS-induced myositis.

61 myositis, dermatomyositis and inclusion body myositis.

62 lularly in some patients with inclusion body myositis.

63 yositis, dermatomyositis, and inclusion body myositis].

64 with cutaneous disease, followed by proximal myositis 6 months later.

65 sies taken from patients with inclusion body myositis, a degenerative disorder in which intramyofiber

66 s from patients with sporadic inclusion body myositis, a late-onset inflammatory myopathy with promin

67 s from patients with sporadic inclusion body myositis, a well defined myopathy with chronic inflammat

68 ssion of MHC-I induces a poorly inflammatory myositis accompanied by the unfolded protein response (U

69 Damage is common in myositis after a median duration of 5 years in patients

70 cases of Crohn's disease associated orbital myositis and 3 cases of ulcerative colitis associated or

71 nuated in both a zebrafish model of necrotic myositis and a murine subcutaneous ulcer model, highligh

72 end upon recognizing these distinct forms of myositis and analyzing them as separate entities.

73 many muscle pathologies including idiopathic myositis and can induce ER stress.

74 scle fibers occur in sporadic inclusion body myositis and clinically similar disorders.

75 ghts into the pathogenesis of inclusion-body myositis and concludes that in sIBM one series of Alemtu

76 olyomavirus in endothelial cells at sites of myositis and cutaneous necrosis.

77 agy markers were up-regulated in humans with myositis and in mouse models of myositis.

78 ifferentially expressed in both IBM and Jo-1 myositis and included upregulated H19, lncMyoD and MALAT

79 resulted in rapid resolution of the orbital myositis and ocular symptoms with no recurrences on foll

80 Dendritic cells present in inclusion body myositis and polymyositis are primarily myeloid dendriti

81 Although inclusion body myositis and polymyositis have been characterized as cyt

82 r Ag-specific autoimmunity in inclusion body myositis and polymyositis.

83 genetic analyses to sporadic inclusion body myositis and sarcoidosis.

84 C COMMENTARY ON THIS ARTICLE: Inclusion body myositis and T cell large granular lymphocytic leukaemia

85 al lung disease associated with inflammatory myositis and the antisynthetase syndrome.

86 interstitial lung disease in the setting of myositis and the antisynthetase syndrome.

87 To help clinicians to distinguish between myositis (and other immune-mediated and immunosuppressan

88 disease 1A, 20 patients with inclusion body myositis, and 29 healthy controls (allocated to one or b

89 -related complications (respiratory failure, myositis, and an acute coronary event), which could have

90 is an autoantigen in the autoimmune disorder myositis, and borrelidin, a potent inhibitor of TARS, in

91 al manifestation of Crohn's disease, orbital myositis, and its temporal relationship to the discontin

92 ilia (>5%), clinical or laboratory-supported myositis, and negative trichinellosis serology.

93 echanisms of dermatomyositis, inclusion body myositis, and polymyositis gained from large-scale micro

94 atients with dermatomyositis, inclusion body myositis, and polymyositis.

95 ic presentations of synovitis, bone disease, myositis, and vasculitis.

96 Two myositis antibody-negative patients showed clinical impr

97 s) and their roles in the various subsets of myositis are discussed.

98 factors initiating cell death and damage in myositis are not well defined.

99 yositis, dermatomyositis, and inclusion body myositis) are systemic autoimmune diseases defined by ch

100 Using a mouse model of RRV-induced myositis/arthritis, we found that myeloid differentiatio

101 thology (IM-VAMP), which have inclusion body myositis as a pathologic subtype and are poorly treatabl

102 tions of anti-Mup44 antibodies were found in myositis as well as other neuromuscular disorders, but n

103 muscular Centre (ENMC) and The International Myositis Assessment and Clinical Studies Group (IMACS).

104 mpared the time to achieve the International Myositis Assessment and Clinical Studies Group prelimina

105 (PM) (n=114), dermatomyositis (DM) (n=102), myositis associated with another connective tissue disea

106 Serotyping for myositis-specific/myositis-associated autoantibodies (MSAs/MAAs) was perfo

107 olecules contributing to the pathogenesis of myositis-associated ILD.

108 randomized clinical trials in patients with myositis-associated interstitial lung disease have not o

109 n, Istituto Giannina Gaslini (Genoa, Italy), Myositis Association (USA).

110 severely affected, and were associated with myositis, atrophy, paresis/paralysis, and death.

111 All patients were tested for myositis autoantibodies and received weekly rituximab in

112 e relative prevalence of dermatomyositis and myositis autoantibodies in 380 patients with myositis fr

113 ciation between UVR exposure and presence of myositis autoantibodies was assessed.

114 Myositis autoantibodies were detected by validated immun

115 nce of anti-MJ autoantibodies or lack of any myositis autoantibodies.

116 Myositis autoantigen expression is also markedly increas

117 to virulence in mouse models of necrotizing myositis, bacteremia, and skin and soft tissue infection

118 Investigations of autoantigen expression in myositis biopsies have revealed that regenerating muscle

119 and abrogated osteoclastogenic bone loss and myositis, but did not affect in vivo viral replication.

120 own to be associated with the development of myositis, but not in corresponding normal tissue.

121 ncers known to be associated with autoimmune myositis, but not in their related normal tissues, demon

122 rare manifestation of Lyme disease, and Lyme myositis can be an important consideration in the differ

123 Myositis can be considered to be a rare extraintestinal

124 s and site of reactivation - encephalitis or myositis can develop.

125 750 patients presenting to the Johns Hopkins Myositis Center (6%).

126 hies have been enabled by recent progress in myositis classification, differential diagnosis, basic s

127 ated with another connective tissue disease (myositis-CTD overlap syndrome) (n=64), or juvenile DM (n

128 We undertook this study to validate the Myositis Damage Index (MDI) in juvenile and adult myosit

129 accumulated in the University of Pittsburgh Myositis Database from 1982 to 2007.

130 ctivity was retrospectively graded using the Myositis Disease Activity Assessment Tool, which measure

131 ctivity in 7 different organ systems via the Myositis Disease Activity Assessment Visual Analog Scale

132 onship between anti-Jo-1 antibody levels and myositis disease activity, demonstrating equivocal resul

133 orbent assays (ELISAs) and novel measures of myositis disease activity, the current study was underta

134 be a reliable and valid instrument to assess myositis disease activity.

135 type, serotype and clinical phenotype in the myositis disease spectrum.

136 myositis muscle biopsies with inclusion-body myositis experimental models in tissue culture and in tr

137 m the largest randomized controlled trial in myositis failed to meet the primary endpoint.

138 eneration and to slow muscle degeneration in myositis, focusing primarily on inclusion body myositis

139 include eosinophilic pneumonitis, localized myositis, folliculitis, erythema multiforme, or ophthalm

140 ely screened 38 patients with inclusion body myositis for the presence of expanded large granular lym

141 the ability to differentiate inclusion body myositis from other myopathies.

142 myositis autoantibodies in 380 patients with myositis from referral centers in the US.

143 lower limb components of the inclusion body myositis functional rating score (rho=-0.64, p=0.002) an

144 st (22/38; 58%) patients with inclusion body myositis had aberrant populations of large granular lymp

145 Myositis has been reported as a rare manifestation of Ly

146 ogenesis of alphavirus-induced arthritis and myositis has not been extensively studied.

147 Novel animal models of myositis have been recently developed using Leishmania i

148 ses of ulcerative colitis associated orbital myositis have been reported in the published literature

149 Similar data in inflammatory myositis have illustrated that disease-specific autoanti

150 Patients with this form of myositis have unique clinical, pathologic and pathophysi

151 distinct patient populations, inclusion body myositis (IBM) and anti-Jo-1-associated myositis (Jo-1).

152 uscle autoantigen in sporadic inclusion body myositis (IBM) and demonstrated the feasibility of an IB

153 ly, the diagnosis of sporadic inclusion body myositis (IBM) has required the demonstration of the pre

154 Inclusion body myositis (IBM) is a poorly understood autoimmune and deg

155 PURPOSE OF REVIEW: Inclusion body myositis (IBM) is a poorly understood progressive muscle

156 Inclusion body myositis (IBM) is an inflammatory muscle disease, althou

157 Sporadic inclusion-body myositis (IBM) is the most common muscle disease of the

158 Inclusion body myositis (IBM), a degenerative and inflammatory disorder

159 new developments in sporadic inclusion body myositis (IBM), including updated clinical and prognosti

160 itis (DM), polymyositis (PM), inclusion body myositis (IBM), myasthenia gravis, or genetically determ

161 Alzheimer's disease (AD) and inclusion body myositis (IBM), respectively.

162 The pathogenic basis of inclusion body myositis (IBM), the leading muscle degenerative disease

163 Inclusion body myositis (IBM), the most common muscle disease to afflic

164 atomyositis, polymyositis and inclusion body myositis (IBM).

165 ositis, focusing primarily on inclusion body myositis (IBM).

166 sis and treatment of sporadic inclusion body myositis (IBM).

167 antibodies from patients with inclusion body myositis (IBM).

168 rum and imaging biomarkers of inclusion body myositis (IBM).

169 dalimumab (Abbott, Canada, Inc.) for orbital myositis in a patient with Crohn's disease who discontin

170 died from treatment-related adverse events (myositis in addition to grade 3 thyroiditis, grade 3 hep

171 neutrophils and significantly reduced lethal myositis in adult zebrafish.

172 that is known to cause severe arthritis and myositis in affected patients.

173 an oncolytic picornavirus that causes lethal myositis in tumor-bearing mice.

174 sporine or tacrolimus have shown efficacy in myositis including those patients with interstitial lung

175 This biopsy finding occurs in various forms myositis, including the antisynthetase syndrome, sclerod

176 We have adapted a transgenic model of myositis induced by overexpression of MHC class I protei

177 Assessment Visual Analog Scale (VAS) and the Myositis Intention-to-Treat Index (MITAX) components.

178 Orbital myositis is a rare extra-intestinal manifestation of inf

179 Virus-induced myositis is an emerging global affliction that remains p

180 Myositis is characterised by muscle inflammation and wea

181 onship between the development of cancer and myositis is reminiscent of that seen in neurological par

182 lthough the cause of sporadic inclusion body myositis is unknown, GNE myopathy is associated with mut

183 n body myositis (sIBM), a common adult-onset myositis, is characterized by an antigen-driven inflamma

184 body myositis (IBM) and anti-Jo-1-associated myositis (Jo-1).

185 h interstitial lung disease in patients with myositis led us to study HisRS expression and conformati

186 ere also induced in an experimental allergic myositis-like model of PM in mice.

187 for the Alzheimer disease and inclusion body myositis-linked beta-amyloid precursor protein and for i

188 T FINDINGS: There are few clinical trials in myositis, making it difficult to provide clear recommend

189 ole of the innate immune system in childhood myositis may lead to novel treatment strategies.

190 ry myoblasts of mdm (muscular dystrophy with myositis) mice (pMB(mdm)) overexpress ANKRD2 and ID3 (in

191 MD using diaphragm muscles from mdm (MD with myositis) mice, an animal model of human tibial MD (titi

192 nd limb sections revealed severe necrotizing myositis, mixed inflammatory cell arthritis, chronic act

193 k is required to produce disease in a murine myositis model of infection.

194 In a rodent myositis model, [(18)F]FPTMP identified live bacterial i

195 In the LPS-induced myositis model, a smaller visible difference was seen (1

196 In a murine myositis model, fluorine-labeled analogs of all 3 molecu

197 In an in vivo myositis model, Rho-FF-Van results in a significant incr

198 imaging tracers, were evaluated in a murine myositis model.

199 data demonstrate that TRAIL is expressed in myositis muscle and may mediate both activation of NF-ka

200 orrelate findings in sporadic inclusion-body myositis muscle biopsies with inclusion-body myositis ex

201 nt of CD8+ and CD57+ cells in inclusion body myositis muscle correlated with the size of blood large

202 TRAIL was expressed predominantly in myositis muscle fibers, but not in biopsy specimens from

203 and pathogenesis in vitro and in vivo, using myositis muscle tissues from humans and mice.

204 tly been observed that regenerating cells in myositis muscle, but not its normal counterpart, express

205 ightly contribute to sporadic inclusion-body myositis muscle-fiber damage.

206 abundant in polymyositis and inclusion body myositis muscle.

207 In a rare variant of myositis, muscle fibers are similarly attacked by CD8-ne

208 In polymyositis and inclusion body myositis, muscle fibers are surrounded and invaded by CD

209 (2 nonmyositic IOIs), and idiopathic orbital myositis (myositic IOI).

210 yositis (DM), Polymyositis (PM), Necrotizing Myositis (NM), and sporadic Inclusion Body Myositis (sIB

211 f a 43-year-old man who presented with focal myositis of the proximal lower extremity and was subsequ

212 er (one [5%]), increased amylase (one [5%]), myositis (one [5%]), and dysphonia (one [5%]) in three p

213 No clinically recognized cases of myositis or myopathy were observed.

214 t uncommonly presents as uveitis, arthritis, myositis or neurologic disease.

215 Myositis ossificans is localized inflammatory process af

216 The term myositis ossificans refers to the formation of ossificat

217 sk factors in African American patients with myositis overlap (DRB1*08) and in African American patie

218 ponses that resemble sporadic inclusion body myositis pathology.

219 Gene expression profiling was performed in myositis patient and control muscle specimens.

220 Two myositis patient registries have been developed for rese

221 stries have been developed for research, and myositis patient support groups maintain demographic reg

222 ositories, in addition to those developed by myositis patient support groups, deserve continued suppo

223 ficant seasonal patterns of disease onset in myositis patients as a whole or in the total PM or DM po

224 phocytes into muscle in 15/15 inclusion body myositis patients but in only 1/28 patients with dermato

225 st phase of the reliability study, 123 adult myositis patients were evaluated in 7 centers, and in th

226 ondary end points, 83% of adult and juvenile myositis patients with refractory disease met the DOI.

227 tophagy are active in the skeletal muscle of myositis patients, and the proinflammatory nuclear facto

228 hat ultraviolet (UV) radiation modulates the myositis phenotype and Mi-2 autoantigen expression, we c

229 This first study of the distribution of myositis phenotypes and UV radiation exposure in the US

230 Knowledge of myositis phenotypes should enhance clinicians' ability t

231 be elevated in patients with inclusion-body myositis, polymyositis, dermatomyositis, and neurogenic

232 les were converted to slow-twitch muscles as myositis progressed, and microarray results indicated th

233 Moreover, immunization of myositis-prone mice with FHL1 aggravated muscle weakness

234 mucous after recovery from an acute phase of myositis proved a diagnostic challenge.

235 rombocytopenia, hypothyroidism, inflammatory myositis, Raynaud's disease and vitiligo.

236 luded haemorrhage related to clopidogrel and myositis related to simvastatin.

237 ociated with the antisynthetase syndrome and myositis-related interstitial lung disease.

238 Treatment of sporadic inclusion-body myositis remains a challenge.

239 Investigator-initiated myositis research registries and biorepositories have pr

240 We have identified 46 myositis research registries, including many with biorep

241 ere differentially expressed in IBM and Jo-1 myositis, respectively.

242 lmark pathologies of sporadic inclusion-body myositis (s-IBM) muscle fibers are autophagic vacuoles a

243 Sporadic inclusion body myositis (sIBM) is a poorly understood immune and degene

244 Sporadic inclusion body myositis (sIBM) is an inflammatory myopathy characterize

245 Sporadic Inclusion Body Myositis (sIBM) is the most common acquired muscle disea

246 Sporadic inclusion-body myositis (sIBM) is the most common disabling, adult-onse

247 ers of patients with sporadic inclusion body myositis (sIBM) is unknown.

248 Sporadic inclusion body myositis (sIBM) pathogenesis is unknown; however, rimmed

249 g protein TDP-43, in sporadic inclusion body myositis (sIBM) sarcoplasm are important recent observat

250 Sporadic inclusion body myositis (sIBM), a common adult-onset myositis, is chara

251 muscle pathology in sporadic inclusion body myositis (sIBM), have remained elusive.

252 g Myositis (NM), and sporadic Inclusion Body Myositis (sIBM).

253 esis of familial and sporadic inclusion body myositis (sIBM).

254 was correlated with AMPD1 expression and was myositis specific.

255 iagnostic use, it is likely that testing for myositis-specific antibodies will soon become readily av

256 One patient was positive for a myositis-specific antibody, anti-Mi-2, and demonstrated

257 with strong correlations between particular myositis-specific autoantibodies (MSAs) and clinical sub

258 Myositis-specific autoantibodies (MSAs) are directed aga

259 Myositis-specific autoantibodies define clinical phenoty

260 n contrast to other inflammatory myopathies, myositis-specific autoantibodies had not been found in s

261 The identification of myositis-specific autoantibodies provides both diagnosti

262 Myositis-specific autoantibodies target intracellular pr

263 s review highlights the recent work on novel myositis-specific autoantibodies, their autoantigen targ

264 pies in the treatment of juvenile DM in both myositis-specific autoantibody-positive and -negative pa

265 to ultraviolet (UV) damage and expression of myositis-specific autoantigens in rat newborn skeletal m

266 s normal counterpart, express high levels of myositis-specific autoantigens.

267 k and may participate in the initiation of a myositis-specific autoimmune response.

268 Serotyping for myositis-specific/myositis-associated autoantibodies (MS

269 c and clinical phenotype within the juvenile myositis spectrum that includes an association with calc

270 entify additional disease subsets within the myositis spectrum.

271 the apolipoprotein E gene in inclusion body myositis suggests that this gene does not confer risk of

272 The idiopathic inflammatory myopathies or myositis syndromes (the most common forms are polymyosit

273 dditional support to the hypothesis that the myositis syndromes comprise multiple, distinct disease e

274 rch suggests that categorizing heterogeneous myositis syndromes into mutually exclusive and stable ph

275 , the idiopathic inflammatory myopathies, or myositis syndromes, have benefited from individual resea

276 upus and 13 (23.2%) were associated with the myositis syndromes.

277 In many patients with inclusion body myositis, the autoimmune T cell expansion has evolved in

278 In inclusion body myositis, the HLA 8.1 ancestral haplotype may not only i

279 ng and is related to sporadic inclusion body myositis, the most common acquired muscle disease of agi

280 Sporadic inclusion-body myositis, the most common muscle disease of older person

281 Inclusion body myositis, the most common muscle disorder in the elderly

282 ogenesis of alphavirus-induced arthritis and myositis, the role that Toll-like receptors (TLRs), whic

283 duced compared with controls (inclusion body myositis thigh -1.5 percentage units [pu; 0.2], calf -1.

284 ols (regression coefficients: inclusion body myositis thigh 4.0 ms [SE 0.5], calf 3.5 ms [0.6]; Charc

285 tis Damage Index (MDI) in juvenile and adult myositis, to describe the degree and types of damage and

286 ades contribute to this model of HRS-induced myositis, underscoring the antigenic versatility of HRS

287 ly with CK levels (R(2) = 0.65, P = 0.0002), myositis VAS (R(2) = 0.53, P = 0.0008), arthritis VAS (R

288 ilar for CK levels (r(s) = 0.38, P = 0.002), myositis VAS (r(s) = 0.36, P = 0.002), and arthritis VAS

289 Autoimmune myositis, vasculitis and primary Sjogren's syndrome are

290 The role of B cell-depleting therapies in myositis warrants further study, with consideration for

291 Myositis was confirmed by magnetic resonance imaging and

292 onous involvement and a diagnosis of orbital myositis was made.

293 Myositis was seen occasionally.

294 Myositis was seen occasionally.

295 DNA samples from 100 Caucasian children with myositis were genotyped for HLA class II haplotype assoc

296 from 37 (23%) of 162 patients with juvenile myositis were positive for anti-p140 autoantibodies, whi

297 cot-Marie-Tooth disease 1A or inclusion body myositis who were attending the inherited neuropathy or

298 association of interstitial lung disease and myositis with anti-tRNA synthetase autoantibodies.

299 Toxoplasma gondii causes a nonresolving Th1 myositis with prolonged tissue damage associated with pe

300 In both patients, there was development of myositis with rhabdomyolysis, early progressive and refr