ライフサイエンスコーパス: myositis

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

2 elicit a peripheral neuritis (with secondary myositis).

3 nterstitial lymphocytic and nongranulomatous myositis.

4 first report of cell cycle reentry in human myositis.

5 tic model for comparative studies with human myositis.

6 may facilitate the diagnosis of this type of myositis.

7 s the highest disease risk in inclusion body myositis.

8 linical and serologic expression of juvenile myositis.

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

10 myositis, dermatomyositis and inclusion body myositis.

11 lularly in some patients with inclusion body myositis.

12 antibody-in individuals with inclusion body myositis.

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

14 T cell and antibody responses in autoimmune myositis.

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

16 yositis, dermatomyositis, and inclusion body myositis.

17 therefore a potential therapeutic target in myositis.

18 tomyositis, polymyositis, and inclusion body myositis.

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

20 events in the pathogenesis of inclusion body myositis.

21 disease activity sensors for inclusion body myositis.

22 genic mouse model of autoimmune inflammatory myositis.

23 humans with myositis and in mouse models of myositis.

24 keletal muscle cell death and dysfunction in myositis.

25 time points for histopathologic evidence of myositis.

26 ctive target for therapeutic intervention in myositis.

27 hould help to define therapeutic targets for myositis.

28 innate immune responses in a murine model of myositis.

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

30 atomyositis, polymyositis and inclusion body myositis.

31 a were collected from children with juvenile myositis.

32 onal drug development for some patients with myositis.

33 nvolved in the initiation and propagation of myositis.

34 ignal recognition particle antibody-positive myositis.

35 ase of aging humans, sporadic inclusion body myositis.

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

37 nd predictive validity in juvenile and adult myositis.

38 and validity of a disease activity index in myositis.

39 re possibly important in the pathogenesis of myositis.

40 lementary miRNAs and therefore did not cause myositis.

41 Research Council criteria for inclusion body myositis.

42 been found, especially in masticatory muscle myositis.

43 el disorders and provide insights into human myositis.

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

45 levels and various disease manifestations of myositis.

46 developing similar systems in other forms of myositis.

47 the pathogenesis of sporadic inclusion-body myositis.

48 yositis, dermatomyositis, and inclusion body myositis.

49 autoantibodies in canine masticatory muscle myositis.

50 ss advantage in a mouse model of necrotizing myositis.

51 lly impaired in ability to cause necrotizing myositis.

52 lupus erythematosus, systemic sclerosis, and myositis.

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

54 ar degeneration, and sporadic inclusion body myositis.

55 able approach to treatment of inclusion body myositis.

56 9, p=0.0007) in patients with inclusion body myositis.

57 MRC criteria was required for inclusion body myositis.

58 mune pathways affecting murine virus-induced myositis.

59 plasma samples from patients diagnosed with myositis.

60 yopathy was recognized as a distinct form of myositis.

61 statins can induce an autoimmune necrotizing myositis.

62 yositis, dermatomyositis, and inclusion body myositis].

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

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

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

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

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

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

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

70 s of antibiotic treatment in E. coli-induced myositis and a clinically relevant S. aureus wound infec

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 -induced mouse muscle regeneration, in human myositis and DMD biopsies, and the tubb6 level correlate

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

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

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

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

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

83 genetic analyses to sporadic inclusion body myositis and sarcoidosis.

84 infection but succumb to chronic paralyzing myositis and skeletal muscle vasculitis, not cardiomyopa

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

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

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

88 to induce crippling chronic skeletal muscle myositis and vasculitis in the model.

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

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

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

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

93 led trial done in people with inclusion body myositis, and it provides important natural history data

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

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

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

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

98 Two myositis antibody-negative patients showed clinical impr

99 Necrotizing fasciitis and myositis are devastating infections characterized by hig

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 Myositis autoantibodies were detected by validated immun

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

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

120 n KLRG1 expressing T cells in inclusion body myositis blood.

121 placebo, in individuals with inclusion body myositis but did not improve 6MWD.

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

123 Myositis can be considered to be a rare extraintestinal

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

125 Necrotizing fasciitis and myositis caused by group A streptococci (GAS) are among

126 750 patients presenting to the Johns Hopkins Myositis Center (6%).

127 viable parasites were no longer detectable, myositis completely resolved, vasculitis was ~80% reduce

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

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

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

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

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

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

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

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

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

137 5% of the GAS genes required for necrotizing myositis encode known or putative transporters.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 Inclusion body myositis (IBM) is often viewed as an enigmatic disease w

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

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

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

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

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

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

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

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

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

168 sis and treatment of sporadic 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 e sono-immunotherapeutic eradication of MRSA myositis in mice.

174 y (P < 0.05) impaired in causing necrotizing myositis in NHPs.

175 tified GAS genes contributing to necrotizing myositis in nonhuman primates (NHP), a clinically releva

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

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

178 ted to both M1 and M28 strain fitness in NHP myositis, including putative importers for amino acids,

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

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

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

182 Inclusion body myositis is a late onset treatment-refractory autoimmune

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

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

185 Inclusion body myositis is an idiopathic inflammatory myopathy and the

186 Myositis is characterised by muscle inflammation and wea

187 sidered whenever the presentation of orbital myositis is not typical or when significant underlying c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 ure of T-cell cytotoxicity in inclusion body myositis muscle coupled with a signature of highly diffe

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

208 esence of KLRG1 on pathogenic inclusion body myositis muscle invading T cells and an increase in KLRG

209 We examined inclusion body myositis muscle T-cell proliferation by Ki67 immunohisto

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

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

212 abundant in polymyositis and inclusion body myositis muscle.

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

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

215 (2 nonmyositic IOIs), and idiopathic orbital myositis (myositic IOI).

216 le samples from patients with inclusion body myositis (n = 40), other muscle diseases (n = 265), and

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

218 116 genes of M28 strains of GAS required for myositis, of which 25% encode transporters, which could

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

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

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

222 Myositis ossificans is localized inflammatory process af

223 The term myositis ossificans refers to the formation of ossificat

224 ponses that resemble sporadic inclusion body myositis pathology.

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

226 t on translational studies of inclusion body myositis patient muscle compared with a diverse set of o

227 Two myositis patient registries have been developed for rese

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

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

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

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

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

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

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

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

236 Knowledge of myositis phenotypes should enhance clinicians' ability t

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

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

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

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

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

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

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

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

245 Investigator-initiated myositis research registries and biorepositories have pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

260 was correlated with AMPD1 expression and was myositis specific.

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

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

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

264 Myositis-specific autoantibodies (MSAs) are directed aga

265 Myositis-specific autoantibodies define clinical phenoty

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

267 The identification of myositis-specific autoantibodies provides both diagnosti

268 Myositis-specific autoantibodies target intracellular pr

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

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

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

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

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

274 entify additional disease subsets within the myositis spectrum.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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