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 as performed using SPSS software version 22 (IBM, Armonk, NY).

12 erformed using IBM SPSS software version 23 (IBM Corp, Armonk, NY) and R package software version 3.4

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

14 Although IBM T cell autoimmunity has long been recognized, enormo

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

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

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

18 Using this algorithm on an IBM quantum computer enables us to experimentally demons

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

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

21 .1, SigmaPlot(R) 12, BioDataFit(R) 1.02, and IBM SPSS Statistics(R) Desktop 19.0.

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

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

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

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

26 t DeltaPsi(m) , corresponding to cristae and IBM.

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

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

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

30 7-derived mapping populations (F2, Syn5, and IBM) demonstrate that allele frequencies were significan

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

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

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

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

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

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

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

38 disease of bone and frontotemporal dementia (IBM-PFD)-together with its adaptor nuclear protein local

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

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

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

42 When assuming EPIONCHO-IBM exposure patterns, children aged <10 years are the m

43 resholds largely explains differing EPIONCHO-IBM and ONCHOSIM elimination predictions.

44 parasite establishment (included in EPIONCHO-IBM but not ONCHOSIM) on positive predictive values for

45 onchocerciasis transmission model (EPIONCHO-IBM) that projects trial outcomes of a hypothetical macr

46 ndividual-based transmission model, EPIONCHO-IBM, was used to assess (1) the most informative age gro

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

48 mutations, the most common cause of familial IBM.

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

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

51 iable effective therapy currently exists for IBM.

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

53 bodies is of high diagnostic performance for IBM.

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

55 em with a general mathematical framework for IBMs containing interactions of an unlimited level of co

56 sey and Pennsylvania, and national data from IBM MarketScan Research Database.

57 AK were found in differentiation medium from IBM mesoangioblasts.

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

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

60 systems-developed by Amazon, Apple, Google, IBM, and Microsoft-to transcribe structured interviews c

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

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

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

64 However, IBMs are often computationally expensive and difficult t

65 Human IBM skeletal muscle biopsies were investigated to determ

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

67 enic role for betaAPP mismetabolism in human IBM.

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

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

70 e past decade that implicate autoimmunity in IBM include the identification of a circulating autoanti

71 idence regarding the role of autoimmunity in IBM.

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

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

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

75 46 lncRNAs were differentially expressed in IBM and Jo-1 myositis, respectively.

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

77 id precursor protein (betaAPP) expression in IBM.

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

79 nd an avenue for therapeutic intervention in IBM.

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

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

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

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

84 ether TWEAK modulation affects myogenesis in IBM mesoangioblasts.

85 Recent important advances have occurred in IBM.

86 r aberrant cell cycle reentry also occurs in IBM.

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

88 Yet the roles of core autophagy proteins in IBM and stress granule dynamics remain poorly characteri

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

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

91 lectronic health record AF (EHR-AF) score in IBM Explorys Life Sciences, a multi-institutional datase

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

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

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

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

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

97 MRI may also be of monitoring value in IBM.

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

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

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

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

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

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

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

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

106 e distinct from the inner boundary membrane (IBM).

107 ing of cristae and inner boundary membranes (IBM), is considered to carry a uniform DeltaPsi(m) .

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

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

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

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

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

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

114 try, we developed an individual-based model (IBM) reproducing the population's sociodemography, expli

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

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

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

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

119 Individual-based models, 'IBMs', describe naturally the dynamics of interacting or

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

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

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

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

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

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

126 chanisms underlying inclusion body myopathy (IBM) and related disorders.

127 ke syndrome-such as inclusion body myopathy (IBM) associated with Paget's disease of bone and frontot

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

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

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

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

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

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

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

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

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

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

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

139 Inclusion body myositis (IBM) is often viewed as an enigmatic disease with uncert

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

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

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

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

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

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

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

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

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

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

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

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

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

153 aging biomarkers of inclusion body myositis (IBM).

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

155 cusing primarily on inclusion body myositis (IBM).

156 eatment of sporadic inclusion body myositis (IBM).

157 from patients with inclusion body myositis (IBM).

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

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

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

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

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

163 hophysiological and diagnostic biomarkers of IBM are reviewed.

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

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

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

167 ould improve early and reliable diagnosis of IBM.

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

169 ring RNA induced myogenic differentiation of IBM mesoangioblasts.

170 The etiology of IBM remains elusive.

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

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

173 ess granules for therapeutic intervention of IBM and related disorders.

174 n the matrix, in addition to invagination of IBM.

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

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

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

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

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

180 ith the relative treatment refractoriness of IBM, to a competing view that IBM is not an autoimmune d

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

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

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

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

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

186 nt issues in the pathogenesis and therapy of IBM.

187 The treatment of IBM with conventional immunosuppressive agents has been

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

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

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

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

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

193 al and simulation results for any particular IBM without algebraic manipulation.

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

195 cial Sciences version 20.0 software program (IBM Corp., Armonk, NY, USA).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 ding sample t test was performed using SPSS (IBM SPSS version 22).

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

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

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

238 Mounting evidence that IBM is an autoimmune T cell-mediated disease provides ho

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

240 ractoriness of IBM, to a competing view that IBM is not an autoimmune disease.

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

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

243 The IBM(R) Marketscan(R) database provide health care utiliz

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

245 ing the IBM Qiskit quantum simulator and the IBM Q 5 Tenerife quantum device.

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

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

248 tes national commercial claims database, the IBM MarketScan, to identify patients aged 18-64 years wi

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

250 ysis of commercially insured patients in the IBM MarketScan claims database from 2011 to 2018.

251 erimentally examined with four qubits in the IBM Quantum Experience setups, and the experimental resu

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

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

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

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

256 cantly altered during the development of the IBM IRILs.

257 f 73,002 commercially insured members of the IBM MarketScan commercial claims database who underwent

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 to significant changes in expression of the IBM phenotype.

262 ation-based, cross-sectional analysis of the IBM Watson Health MarketScan insurance claim dataset, wh

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

264 res isolated in the matrix additional to the IBM, suggesting that it may participate in the formation

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

266 1 shifts the distribution of Oxa1 toward the IBM.

267 We used the IBM MarketScan database to select 59,016,145 commerciall

268 We used the IBM MarketScan Research Databases to identify patients w

269 We used the IBM(R) MarketScan(R) Research Databases to identify adul

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

271 hm on an amplitude damping channel using the IBM Qiskit quantum simulator and the IBM Q 5 Tenerife qu

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

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

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

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

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

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

278 eltaPsi(m) was higher at cristae compared to IBM.

279 itive lamellar cristae were not connected to IBM.

280 ive stress granule disassembly contribute to IBM-like disease in Ulk1/2-deficient mice.

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

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

283 e absent in patients with clinically typical IBM.

284 We used IBM MarketScan Research Database (2010-2017) to examine

285 This study uses IBM MarketScan database data to describe trends in zolpi

286 Statistics analyses were performed using IBM SPSS 20.0.

287 and regression analysis were performed using IBM SPSS software version 23 (IBM Corp, Armonk, NY) and

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

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

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

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

292 utophagosome biogenesis was increased in VCP-IBM muscle.

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

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

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

296 will exclude large numbers of patients with IBM.

297 is prominent in the muscle of patients with IBM.

298 present in <1% of myofibres in patients with IBM.

299 siologic response to exercise in people with IBM.

300 nical implications for those who suffer with IBM.