ライフサイエンスコーパス: IBM

1 IBM blood samples were screened using mass spectrometry

2 IBM has joined a growing list of diseases known as TDP-4

3 IBM is a rare disease and international multicentre coll

4 IBM is a slowly progressive disease, leading to wheelcha

5 IBM mesoangioblasts, different from mesoangioblasts in o

6 IBM remains a poorly understood muscle disease, although

7 IBM remains an enigmatic and often misdiagnosed disease.

8 IBM SPSS statistical software (version 22) was used to p

9 IBM vacuolated fibers also contain accumulations of seve

10 IBMs are utilized by a number of proapoptotic proteins t

11 Inclusion body myopathy 3 (IBM-3) is an autosomal dominant disease associated with

12 nity and muscle degeneration, and develop an IBM blood test with high diagnostic accuracy.

13 The division models are integrated into an IBM framework (iAlgae), which combines a lumped system r

14 (IBM) and demonstrated the feasibility of an IBM diagnostic blood test.

15 ent run within less than 3 min of time on an IBM RX 6000 computer.

16 of 168 200 Arabidopsis ESTs in 15 min on an IBM xSeries cluster with 30 dual-processor nodes.

17 .1, SigmaPlot(R) 12, BioDataFit(R) 1.02, and IBM SPSS Statistics(R) Desktop 19.0.

18 ribute to the phenotypic changes in Jo-1 and IBM myositis.

19 tially expressed in the muscle from Jo-1 and IBM patients, respectively.

20 d the top canonical pathway in both Jo-1 and IBM was oxidative phosphorylation and mitochondrial dysf

21 ts that the cytopathogenesis in AD brain and IBM muscle may share similarities.

22 Across NAM and IBM families, 18 family-nested QTL and 141 significant G

23 In PM and IBM cytotoxic CD8-positive T-cells clonally expand in si

24 Although PM and IBM have been modeled as having similar immunologic proc

25 7-derived mapping populations (F2, Syn5, and IBM) demonstrate that allele frequencies were significan

26 lines (IRILs) from the intermated B73xMo17 (IBM) population.

27 cle diseases, and may provide a link between IBM's dual processes of autoimmunity and myodegeneration

28 ntibody, understand the relationship between IBM autoimmunity and muscle degeneration, and develop an

29 Other similarities between IBM muscle and AD brain phenotypes include paired helica

30 ncRNAs were differentially expressed in both IBM and Jo-1 myositis and included upregulated H19, lncM

31 pendent manner, and this can be regulated by IBM-containing proteins.

32 such as Smac and caspase-9 via the conserved IBM-binding groove.

33 The deterministic cell cycle IBM model fails the batch culture test, because it has a

34 cally diagnosed IBM and clinically diagnosed IBM seen within a single UK specialist muscle centre.

35 patients with histopathologically diagnosed IBM and clinically diagnosed IBM seen within a single UK

36 uential muscle biopsies from three different IBM patients over a 19-22 month period using immunohisto

37 w insights into the pathogenesis of familial IBM are opening novel therapeutic pathways for these dis

38 An intermated B73xMo17 family (IBM) of 196 RILs and a panel of 2,453 diverse inbreds fr

39 rganism with homogeneous populations of fast IBM-3 myosin and muscle fibers.

40 iable effective therapy currently exists for IBM.

41 iomarker has high diagnostic performance for IBM, and through identification of its target links, IBM

42 bodies is of high diagnostic performance for IBM.

43 antigen appears to have high specificity for IBM among muscle diseases.

44 AK were found in differentiation medium from IBM mesoangioblasts.

45 lize to amyloid-like fibrils in muscles from IBM patients.

46 A functional IBM is required for the association of cleaved IMD with

47 ve inclusions characteristic of the s- and h-IBM abnormal muscle fibers.

48 M) and hereditary inclusion-body myopathy (h-IBM).

49 A classification of the various h-IBM syndromes is also presented.

50 term hereditary inclusion-body myopathies (h-IBMs) designates autosomal-recessive or autosomal-domina

51 In neither s-IBM nor the h-IBMs are the sequential steps of the pathogenic cascade

52 olated muscle fibers of both s-IBM and the h-IBMs contain accumulations of several "Alzheimer-charact

53 Because s-IBM and the h-IBMs have a number of characteristic pathologic features

54 The several forms of the h-IBMs have different genetic transmissions and probably d

55 In HIV-IBM, a subset of CD8(+) T cells surrounding muscle fiber

56 However, IBMs are often computationally expensive and difficult t

57 Human IBM skeletal muscle biopsies were investigated to determ

58 In human IBM muscle, GSK-3beta and phospho-tau were colocalized,

59 enic role for betaAPP mismetabolism in human IBM.

60 These features are similar to those of human IBM.

61 In IBM muscle, we found increased TWEAK-Fn14 expression.

62 The pathogenesis of these abnormalities in IBM muscle and AD brain is not known.

63 e for mitochondrial and COX abnormalities in IBM muscle and perhaps AD brain.

64 cal event in Alzheimer's disease and also in IBM, where in the latter, it predominantly occurs intrac

65 idence regarding the role of autoimmunity in IBM.

66 Dysregulation of the TWEAK-Fn14 axis in IBM muscle may induce progressive muscle atrophy and red

67 a is one of the key pathogenic components in IBM pathology and subsequent skeletal muscle degeneratio

68 ed levels of Ki-67, PCNA and cyclins E/D1 in IBM compared with normals and non-inflammatory condition

69 46 lncRNAs were differentially expressed in IBM and Jo-1 myositis, respectively.

70 was to investigate TWEAK-Fn14 expression in IBM and other inflammatory myopathies and explore whethe

71 id precursor protein (betaAPP) expression in IBM.

72 c 5'-nucleotidase 1A have been identified in IBM showing moderate diagnostic performance.

73 nd an avenue for therapeutic intervention in IBM.

74 cy favoring fast twitch fiber involvement in IBM, reminiscent of the tissue specific patterns of misf

75 e have observed an explosion of knowledge in IBM in the recent past, which challenges traditional dog

76 We examined cell cycle markers in IBM compared with normal control, polymyositis (PM) and

77 The role of MRI in IBM is expanding and knowledge about pathological biomar

78 ether TWEAK modulation affects myogenesis in IBM mesoangioblasts.

79 Recent important advances have occurred in IBM.

80 r aberrant cell cycle reentry also occurs in IBM.

81 TWEAK-RNA interference was performed in IBM and dermatomyositis mesoangioblasts.

82 of the PHFs and accumulations of proteins in IBM muscle are not known.

83 K, a signal transducer, might play a role in IBM pathogenesis, including participation in the patholo

84 w therapeutic strategies are being tested in IBM patients, namely the upregulation of the heat shock

85 The results indicate that in IBM there is a restricted expression of the TCR gene fam

86 indings support previous suggestions that in IBM, the muscle fibres have the capacity for antigen pre

87 s may not be present in all muscle tissue in IBM patients.

88 or diagnosis and future studies or trials in IBM as adherence to histopathologically focused diagnost

89 n perinuclear regions and rimmed vacuoles in IBM muscle, localizing to areas of myonuclear degenerati

90 MRI may also be of monitoring value in IBM.

91 A new genetic map of maize, ISU-IBM Map4, that integrates 2029 existing markers with 132

92 idase 1A (cN1A; NT5C1A) as the likely 43 kDa IBM autoantigen, which was then confirmed in dot blot an

93 Despite improved knowledge, IBM continues to be a puzzling disease and the pathogene

94 mean-field approximation of the off-lattice IBM leads to a single partial integro-differential equat

95 address this problem by using an off-lattice IBM to derive a continuum approximation which does take

96 through identification of its target links, IBM autoimmunity and degeneration together, supporting t

97 house cluster at Baylor College of Medicine, IBM power PC Blue BioU at Rice and Rhea at Oak Ridge Nat

98 mbrane (CM) and the inner boundary membrane (IBM)--under different physiological conditions.

99 on mapping (NAM) and intermated B73 by Mo17 (IBM) populations of maize recombinant inbreds, indicatin

100 e inbreds and in the inter-mated B73 x Mo17 (IBM) linkage population.

101 The intermated B73 x Mo17 (IBM) population, an advanced intercross recombinant inbr

102 ng population was the intermated B73 x Mo17 (IBM) population.

103 e demonstrate how an individual-based model (IBM) can be implemented to model mortality as explicit,

104 ess, we developed an individual-based model (IBM) of a freshwater amphipod detritivore, Gammarus pseu

105 An individual-based model (IBM), formulated as a system of stochastically determine

106 Individual-based (agent-based) modeling (IBM) does not make the assumption of average properties

107 ng a set of simple, individual-based models (IBM's) and their population-level iterative map counterp

108 at off-lattice individual cell based models (IBMs) can accurately capture the correlations observed e

109 culated trends in incidence-based mortality (IBM), annual hazard rates for breast cancer deaths after

110 posing a highly conserved IAP-binding motif (IBM) at its neo-N terminus.

111 We have identified an IAP-binding motif (IBM) at the amino terminus of NIK.

112 f XIAP interact with the IAP-binding-motifs (IBM) in several apoptosis proteins such as Smac and casp

113 By validating this 'multitrait IBM' against three independent lines of empirical data,

114 Multitrait IBMs also allow trait-based mortality to be modelled eit

115 protein (VCP) cause inclusion body myopathy (IBM) associated with Paget's disease of the bone, fronto

116 protein (VCP) cause inclusion body myopathy (IBM), Paget's disease of the bone, and frontotemporal de

117 atient populations, inclusion body myositis (IBM) and anti-Jo-1-associated myositis (Jo-1).

118 antigen in sporadic inclusion body myositis (IBM) and demonstrated the feasibility of an IBM diagnost

119 res are shared with inclusion body myositis (IBM) and this entity cannot be entirely excluded as vacu

120 ed muscle fibers of inclusion-body myositis (IBM) contain abnormally accumulated beta-amyloid precurs

121 agnosis of sporadic inclusion body myositis (IBM) has required the demonstration of the presence of a

122 Inclusion body myositis (IBM) is a poorly understood autoimmune and degenerative

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

124 Inclusion body myositis (IBM) is an inflammatory muscle disease, although the rol

125 Inclusion body myositis (IBM) is an inflammatory myopathy characterized immunohis

126 Inclusion body myositis (IBM) is an inflammatory myopathy with distinctive clinic

127 rs of cell death in inclusion body myositis (IBM) is in distinction to the specific and early intrace

128 Inclusion body myositis (IBM) is the most common muscle disease in the elderly.

129 Sporadic inclusion-body myositis (IBM) is the most common muscle disease of the elderly po

130 ic criterion of the inclusion-body myositis (IBM) muscle biopsy; but, until now, their presence could

131 or individuals with inclusion body myositis (IBM) remains uncertain.

132 the pathogenesis of inclusion-body myositis (IBM) was investigated by immunostaining the active phosp

133 ients with sporadic inclusion body myositis (IBM) was subjected to agarose gel immunofixation electro

134 Inclusion body myositis (IBM), a degenerative and inflammatory disorder of skelet

135 ve been examined in inclusion body myositis (IBM), and a novel gene transfer experiment has been cond

136 omyositis (DM), and inclusion body myositis (IBM), diseases that result from interactions between env

137 opments in sporadic inclusion body myositis (IBM), including updated clinical and prognostic factors,

138 polymyositis (PM), inclusion body myositis (IBM), myasthenia gravis, or genetically determined myopa

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

140 pathogenic basis of inclusion body myositis (IBM), the leading muscle degenerative disease afflicting

141 Inclusion body myositis (IBM), the most common age-related muscle disease in the

142 Inclusion body myositis (IBM), the most common muscle disease to afflict the elde

143 s, polymyositis and inclusion body myositis (IBM).

144 cusing primarily on inclusion body myositis (IBM).

145 eatment of sporadic inclusion body myositis (IBM).

146 indings in sporadic inclusion body myositis (IBM).

147 from patients with inclusion body myositis (IBM).

148 aging biomarkers of inclusion body myositis (IBM).

149 d in the presence of c-IAP1, whereas the NIK IBM mutant is stable.

150 Furthermore, in the presence of the NIK IBM mutant, we observed an elevated processing of p100 t

151 novel identification and function of the NIK IBM, which promotes c-IAP1-dependent ubiquitylation of N

152 Between 80% and 90% of IBM vacuolated muscle fibers contained well-defined ERK-

153 theories regarding the aetiopathogenesis of IBM are being explored and new therapeutic approaches ar

154 The mean age of IBM patients with gammopathy was 60.6 years (range, 35-7

155 hophysiological and diagnostic biomarkers of IBM are reviewed.

156 es in 31 electron microscopy proven cases of IBM (20 untreated and 11 immunosuppressed).

157 velopment of some features characteristic of IBM, including abnormal tau histochemistry.

158 ical and clinical features characteristic of IBM, including centric nuclei, inflammation, and deficie

159 muscular Centre (ENMC) 2011), a diagnosis of IBM was made in 88% of patients whereas 76% fulfilled th

160 s procedure greatly facilitates diagnosis of IBM.

161 ould improve early and reliable diagnosis of IBM.

162 sitive and 98% specific for the diagnosis of IBM.

163 ring RNA induced myogenic differentiation of IBM mesoangioblasts.

164 The etiology of IBM remains elusive.

165 The expression of IBM-like lesions was age dependent.

166 ave further defined the clinical features of IBM, including natural history, pattern of muscle involv

167 We report that the abnormal muscle fibers of IBM contained (i) acridine-orange-positive RNA inclusion

168 A transgenic mouse model of IBM was utilized in which acute and chronic inflammation

169 e tool for understanding the pathogenesis of IBM and the role of the UPS in skeletal muscle.

170 Various hypothesis about the pathogenesis of IBM continue to be investigated, including autoimmune fa

171 betaAPP mismetabolism in the pathogenesis of IBM, transgenic mice were derived in which we selectivel

172 arallels between the pathologic phenotype of IBM muscle fibers and Alzheimer's disease brain are summ

173 ation in the pathological phosphorylation of IBM tau; and 2) that signal transduction abnormalities m

174 he ERK localized in nonjunctional regions of IBM fibers may underlie the known pathological up-regula

175 Mesoangioblasts isolated from samples of IBM, dermatomyositis, polymyositis, and control muscles

176 ent which are available on the web server of IBM's Bioinformatics and Pattern Discovery group.

177 ent which are available on the web server of IBM's Bioinformatics and Pattern Discovery group.

178 sgenic mice provide a model for the study of IBM and for the peripheral expression of a key element i

179 been successful in stimulating the study of IBM pathophysiology for over three decades.

180 nt issues in the pathogenesis and therapy of IBM.

181 The treatment of IBM with conventional immunosuppressive agents has been

182 is as well as to deepen our understanding of IBM pathophysiology.

183 able progress toward better understanding of IBM, with relatively few developments toward understandi

184 ftware for analysis of the databases runs on IBM- compatible computers.

185 ftware for analysis of the databases runs on IBM-compatible computers with Microsoft Windows.

186 ftware for analysis of the databases runs on IBM-compatible computers.

187 Other IBM-like pathological features, such as inclusion bodies

188 ation of cells in simulations using both our IBM and our continuum model, but not in the continuum mo

189 table analyses using the statistical package IBM SPSS Statistics software (SPSS).

190 ote detector system, consisting of a palmtop IBM-compatible personal computer, specialized software,

191 During the study period, IBM and annual hazard rates for breast cancer deaths dec

192 de linkage analyses identified the recessive IBM locus on chromosome 9 band p1-q1 (maximum lod score

193 autophagosomal-lysosomal pathway using 14 s-IBM and 30 disease control and normal control muscle bio

194 In all s-IBM muscle biopsies, all five of the ER chaperones were

195 tudies and suggest that in PM, HIV-PM, and s-IBM the muscle fibers are not only targets of CD8+ cytot

196 CTLA-4 was up-regulated in PM, HIV-PM, and s-IBM, but not the controls.

197 In PM, HIV-PM, and s-IBM, but not the disease controls, the nonnecrotic, MHC-

198 asive CD8+ T cells only in PM, HIV-PM, and s-IBM, the BB-1 molecule in these diseases should have a f

199 Because s-IBM and the h-IBMs have a number of characteristic patho

200 remarkable pathologic similarities between s-IBM muscle and Alzheimer disease brain are discussed.

201 nt of the vacuolated muscle fibers of both s-IBM and autosomal-recessive inclusion-body myopathy had

202 Vacuolated muscle fibers of both s-IBM and the h-IBMs contain accumulations of several "Alz

203 calf muscles of 12 patients with definite s-IBM.

204 oprecipitation/immunoblotting technique in s-IBM and control muscle biopsies, and in AbetaPP-overexpr

205 reticulin, GRP94, BiP/GRP78, and ERp72, in s-IBM and control muscle biopsies.

206 Our studies provide evidence of the UPR in s-IBM muscle and demonstrate for the first time that the E

207 We report that in s-IBM muscle biopsies 26S proteasome subunits were immunod

208 Thus, unblocking protein degradation in s-IBM muscle fibers may be a desirable therapeutic strateg

209 Accordingly, proteasome dysfunction in s-IBM muscle fibers may play a role in accumulation of mis

210 We conclude that in s-IBM muscle, decreased lysosomal proteolytic activity mig

211 ERp72 physically associate with AbetaPP in s-IBM muscle, suggesting their playing a role in AbetaPP f

212 We report for the first time that in s-IBM, lysosomal enzyme activities of cathepsin D and B we

213 e conclude that the classic, inflammatory, s-IBM can also occur in families (familial inclusion body

214 Sporadic inclusion-body myositis (s-IBM) and hereditary inclusion body myopathies are progre

215 anism of sporadic inclusion-body myositis (s-IBM) and hereditary inclusion-body myopathy (h-IBM).

216 Sporadic inclusion body myositis (s-IBM) is a chronic inflammatory myopathy of unknown patho

217 Sporadic inclusion-body myositis (s-IBM) is the most common progressive muscle disease of ol

218 Sporadic inclusion-body myositis (s-IBM) is the most common progressive muscle disease of ol

219 ature of sporadic inclusion body myositis (s-IBM) muscle biopsies, we studied expression and immunolo

220 ogies of sporadic inclusion-body myositis (s-IBM) muscle fibers are autophagic vacuoles and accumulat

221 istic of sporadic inclusion-body myositis (s-IBM) muscle fibers.

222 HIV-PM), sporadic inclusion body myositis (s-IBM), dermatomyositis (DM), and normal or disease contro

223 tical to sporadic inclusion body myositis (s-IBM).

224 In neither s-IBM nor the h-IBMs are the sequential steps of the patho

225 nvironment modified to resemble aspects of s-IBM pathology.

226 somes, and that ERS is a possible cause of s-IBM-impaired lysosomal function.

227 a significant role in the pathogenesis of s-IBM.

228 hese observations strengthen the view that s-IBM behaves like other autoimmune diseases and has disea

229 are important factors contributing to the s-IBM-specific muscle fiber destruction.

230 cle biopsies cytopathologically similar to s-IBM but without inflammation.

231 lities of the 26S proteasome contribute to s-IBM pathogenesis and whether the multiprotein aggregates

232 A deletions in the muscle of patients with s-IBM have suggested that a deficit of energy metabolism m

233 ostain muscle biopsies of 12 patients with s-IBM, 5 patients with autosomal-recessive inclusion-body

234 from exercise was normal in patients with s-IBM, as maximum rates of mitochondrial ATP production an

235 roteasome inhibition, also associated with s-IBM, putatively aggrandize the accumulation of misfolded

236 of the various pathogenetic aspects of the s-IBMs and hereditary inclusion body myopathies may lead t

237 of the transgenic mice with the most severe IBM-like lesions.

238 ylated form of ERK in muscle biopsies of six IBM and 14 control patients.

239 The deterministic cell size IBM model reproduces the data and PLM results for all ex

240 Sporadic IBM has an unknown etiology, although affected muscle fi

241 Data were analyzed with SPSS IBM statistical software (version 22) using 1-way analys

242 nalysis was performed using SPSS Statistics (IBM, Armonk, NY).

243 The stochastic IBM model fails the steady chemostat culture test, becau

244 of the mutant grim lacking either N-terminal IBM or internal GH3 domain indicated that both domains a

245 We conclude that IBM, regardless of age, is frequently associated with mo

246 Muscle biomarkers have suggested that IBM pathophysiology is linked to myonuclear degeneration

247 eneration together, supporting the view that IBM pathophysiology includes abnormal nucleic acid metab

248 The IBM models are evaluated against a conventional PLM (bec

249 ive muscle strength of knee extensor and the IBM functional rating scale seem to be sensitive disease

250 ral systems leads to differences between the IBM and PLM models.

251 ly derived from the same parental cross: the IBM advanced intercross population and a conventional re

252 close agreement with those obtained from the IBM for a wide range of mechanical interaction strengths

253 The predominant localization in the IBM under fermentable growth conditions is prevented by

254 e growth conditions, Oxa1 is enriched in the IBM, whereas under nonfermentable (respiratory) growth c

255 By crossing the Rp1-D21 gene into the IBM mapping population, it was possible to map and ident

256 ffected skeletal muscle fibers mitigates the IBM-like myopathological features as well as motor impai

257 cantly altered during the development of the IBM IRILs.

258 which describes the average behavior of the IBM over a large number of simulations.

259 udy demonstrates two novel components of the IBM paired helical filaments, which may lead to better u

260 tion abnormalities may be a component of the IBM pathogenic cascade.

261 with 66.1 years (range, 42-80 years) of the IBM patients without gammopathy.

262 to significant changes in expression of the IBM phenotype.

263 reveals the unambiguous consequences of the IBM-3 lesion on fast muscle myosin and fibers.

264 imer through the region corresponding to the IBM-binding groove.

265 1 shifts the distribution of Oxa1 toward the IBM.

266 Mapping was performed using the IBM (B73 x Mo17) recombinant inbred line population.

267 s IAP repeat (BIR2) domain of c-IAP1 via the IBM, and this interaction, in turn, provides substrate r

268 were detected in both populations, with the IBM providing between 5 and, in one case, 50 times great

269 In this IBM, life history emerges from the individuals' energy b

270 ght to identify the molecular target of this IBM autoantibody, understand the relationship between IB

271 domain of XIAP, which does not possess this IBM-binding groove and cannot interact with Smac or casp

272 ltiple muscle biopsies from two of the three IBM patients.

273 st cN1A are common in and highly specific to IBM among muscle diseases, and may provide a link betwee

274 ies of many patients with clinically typical IBM do not show all of these histopathological findings,

275 e absent in patients with clinically typical IBM.

276 Statistics analyses were performed using IBM SPSS 20.0.

277 ned weakness, atrophy and vacuolation in VCP-IBM mice.

278 activity and increased the fiber size in VCP-IBM mouse skeletal muscle.

279 nderstand the regulation of autophagy in VCP-IBM muscle, we examined the AKT/FOXO3 and mammalian targ

280 extent by amino acid (AA) stimulation in VCP-IBM muscle.

281 utophagosome biogenesis was increased in VCP-IBM muscle.

282 ytosolic 5' nucleotidase 1A in patients with IBM is a potentially important advance that may aid earl

283 l studies in four HIV-infected patients with IBM were performed.

284 Sixteen of 70 (22.8%) patients with IBM, compared with 2% of age-matched controls, had a mon

285 with active DM or PM, but not patients with IBM, had significant and high up-regulation of the type

286 is prominent in the muscle of patients with IBM.

287 will exclude large numbers of patients with IBM.

288 siologic response to exercise in people with IBM.

289 nical implications for those who suffer with IBM.