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1 uld be a favourable approach to treatment of inclusion body myositis.
2 otoxic T lymphocyte-mediated autoimmunity in inclusion body myositis.
3 d 2010 Medical Research Council criteria for inclusion body myositis.
4 itis or dermatomyositis, and 2 families with inclusion body myositis.
5 A alterations may be accelerated in sporadic inclusion body myositis.
6 group demonstrated histological features of inclusion body myositis.
7 proposed criteria for definite and possible inclusion body myositis.
8 stological confirmation may nonetheless have inclusion body myositis.
9 ntotemporal lobar degeneration, and sporadic inclusion body myositis.
10 scles, quadriceps, and ankle dorsiflexors in inclusion body myositis.
11 cceptable safety profile in individuals with inclusion body myositis.
12 , and efficacy of arimoclomol in people with inclusion body myositis.
13 l (3.3%, 1.8-4.9, p=0.0007) in patients with inclusion body myositis.
14 ly definite by MRC criteria was required for inclusion body myositis.
15 genotype confers the highest disease risk in inclusion body myositis.
16 r focus on polymyositis, dermatomyositis and inclusion body myositis.
17 mulate intracellularly in some patients with inclusion body myositis.
18 includes polymyositis, dermatomyositis, and inclusion body myositis.
19 omprising dermatomyositis, polymyositis, and inclusion body myositis.
20 sent key early events in the pathogenesis of inclusion body myositis.
21 s are potential disease activity sensors for inclusion body myositis.
22 uman monoclonal antibody-in individuals with inclusion body myositis.
23 vided into dermatomyositis, polymyositis and inclusion body myositis.
24 ive muscle disease of aging humans, sporadic inclusion body myositis.
25 ulates early in Alzheimer's disease (AD) and inclusion body myositis.
26 thies are polymyositis, dermatomyositis, and inclusion body myositis.
27 muscle fibers that are specific to sporadic inclusion-body myositis.
28 e new avenues toward the therapy of sporadic inclusion-body myositis.
29 slightly to muscle fiber damage in sporadic inclusion-body myositis.
30 subsets: dermatomyositis, polymyositis, and inclusion-body myositis.
31 ortant clues to the pathogenesis of sporadic inclusion-body myositis.
32 ent concepts of the pathogenesis of sporadic inclusion-body myositis.
33 myopathy, polymyositis, dermatomyositis, and inclusion body myositis].
35 tal muscle biopsies taken from patients with inclusion body myositis, a degenerative disorder in whic
36 individual cells from patients with sporadic inclusion body myositis, a late-onset inflammatory myopa
37 Muscle biopsies from patients with sporadic inclusion body myositis, a well defined myopathy with ch
38 likely that genetic muscular dystrophies and inclusion body myositis account for some cases of appare
41 in scattered muscle fibers occur in sporadic inclusion body myositis and clinically similar disorders
42 of mtDNA deletions in patients with sporadic inclusion body myositis and control subjects, mtDNA alte
43 predicted the presence of dendritic cells in inclusion body myositis and of an IFN-alpha/beta respons
44 tically significant benefit in patients with inclusion body myositis and paraproteinemic anti-myelin-
49 trials in dermatomyositis, polymyositis, and inclusion body myositis and suggests an approach to trea
50 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Inclusion body myositis and T cell large granular lympho
52 ripheral neuropathy were also more common in inclusion body myositis and unresponsive polymyositis th
53 d knee extensor involvement was specific for inclusion body myositis and unresponsive polymyositis.
54 y provides insights into the pathogenesis of inclusion-body myositis and concludes that in sIBM one s
55 cell activation in polymyositis and sporadic inclusion-body myositis and the cause of vacuolar degene
56 cot-Marie-Tooth disease 1A, 20 patients with inclusion body myositis, and 29 healthy controls (alloca
57 domised controlled trial done in people with inclusion body myositis, and it provides important natur
58 fibers are common in patients with sporadic inclusion body myositis, and multiple [correction of mut
59 o the disease mechanisms of dermatomyositis, inclusion body myositis, and polymyositis gained from la
61 quences of genes that predispose to sporadic inclusion-body myositis, and of human muscle fiber aging
63 e diseases dermatomyositis, polymyositis and inclusion body myositis are of unknown cause, but immune
65 forms are polymyositis, dermatomyositis, and inclusion body myositis) are systemic autoimmune disease
66 itochondrial pathology (IM-VAMP), which have inclusion body myositis as a pathologic subtype and are
69 pect that patients with clinical features of inclusion body myositis but lacking histological confirm
70 arison to other mimicking diagnoses, such as inclusion body myositis, cervical or lumbar radiculopath
71 odel performance on cohorts of patients with inclusion body myositis, cervical radiculopathy, lumbar
74 of the vacuolated muscle fibers of sporadic inclusion body myositis contained well-defined, strongly
76 inclusion-body myositis muscle biopsies with inclusion-body myositis experimental models in tissue cu
77 , we prospectively screened 38 patients with inclusion body myositis for the presence of expanded lar
79 The most important feature distinguishing inclusion body myositis from the other two inflammatory
80 that characterize polymyositis and sporadic inclusion-body myositis from the non-specific, secondary
82 Eligible participants had a diagnosis of inclusion body myositis fulfilling the European Neuromus
83 the change from baseline to month 20 in the Inclusion Body Myositis Functional Rating Scale (IBMFRS)
84 elated with the lower limb components of the inclusion body myositis functional rating score (rho=-0.
88 tained muscle biopsy specimens from sporadic inclusion body myositis, hereditary inclusion body myopa
90 histologically distinct patient populations, inclusion body myositis (IBM) and anti-Jo-1-associated m
91 inst a 43 kDa muscle autoantigen in sporadic inclusion body myositis (IBM) and demonstrated the feasi
99 ted muscle cells or markers of cell death in inclusion body myositis (IBM) is in distinction to the s
106 New candidate genes have been examined in inclusion body myositis (IBM), and a novel gene transfer
107 polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM), diseases that result from
108 om muscle biopsies of patients with sporadic inclusion body myositis (IBM), immune-mediated necrotizi
109 To examine new developments in sporadic inclusion body myositis (IBM), including updated clinica
110 ith dermatomyositis (DM), polymyositis (PM), inclusion body myositis (IBM), myasthenia gravis, or gen
112 t molecular similarities between PM-Mito and inclusion body myositis (IBM), suggesting a trajectory f
116 nosis and treatment persist, particularly in inclusion body myositis (IBM), where no effective therap
124 ease (AD) brain, vacuolated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumul
126 are an important diagnostic criterion of the inclusion-body myositis (IBM) muscle biopsy; but, until
127 egulated kinase (ERK) in the pathogenesis of inclusion-body myositis (IBM) was investigated by immuno
128 e describe the occurrence of an inflammatory inclusion body myositis in siblings of a single generati
129 yositis, reduced key pathological markers of inclusion body myositis in two in-vitro models represent
130 , s-IBM can also occur in families (familial inclusion body myositis), in a pattern analogous to the
137 structs coding for the Alzheimer disease and inclusion body myositis-linked beta-amyloid precursor pr
140 tified a signature of T-cell cytotoxicity in inclusion body myositis muscle coupled with a signature
141 entified the presence of KLRG1 on pathogenic inclusion body myositis muscle invading T cells and an i
144 equences, and correlate findings in sporadic inclusion-body myositis muscle biopsies with inclusion-b
145 he recent identification within the sporadic inclusion-body myositis muscle fibers of several abnorma
148 ata on 411 muscle samples from patients with inclusion body myositis (n = 40), other muscle diseases
150 nsubstantiated benefit in some patients with inclusion-body myositis, paraproteinemic IgM demyelinati
152 Here, we report on translational studies of inclusion body myositis patient muscle compared with a d
153 ge granular lymphocytes into muscle in 15/15 inclusion body myositis patients but in only 1/28 patien
155 drome, immune-mediated necrotizing myopathy, inclusion body myositis, polymyositis and overlap myosit
156 drome, immune-mediated necrotizing myopathy, inclusion body myositis, polymyositis and overlap myosit
158 s of 46 patients newly diagnosed with either inclusion body myositis, polymyositis, or dermatomyositi
159 een reported to be elevated in patients with inclusion-body myositis, polymyositis, dermatomyositis,
160 ne of the largest trials done in people with inclusion body myositis, providing data on disease progr
161 safe and well-tolerated in a pilot study of inclusion body myositis, reduced key pathological marker
166 , are the characteristic feature of sporadic inclusion body myositis (s-IBM) muscle biopsies, we stud
167 eficiency virus infection (HIV-PM), sporadic inclusion body myositis (s-IBM), dermatomyositis (DM), a
170 seeking the pathogenic mechanism of sporadic inclusion-body myositis (s-IBM) and hereditary inclusion
174 ause in the muscle of patients with sporadic inclusion body myositis (sIBM) clonally expanded CD8+ T
181 TAR DNA binding protein TDP-43, in sporadic inclusion body myositis (sIBM) sarcoplasm are important
182 myositis (DM) who improved and patients with inclusion body myositis (sIBM) who did not improve after
184 of the skeletal muscle pathology in sporadic inclusion body myositis (sIBM), have remained elusive.
188 ions, including muscular dystrophy, sporadic inclusion body myositis, spinal muscular atrophy, cachex
189 eta-analysis of the apolipoprotein E gene in inclusion body myositis suggests that this gene does not
193 ciated with aging and is related to sporadic inclusion body myositis, the most common acquired muscle
195 In conceptualizing a treatment for sporadic inclusion-body myositis, the accumulations of amyloid-be
198 .3]) and MTR reduced compared with controls (inclusion body myositis thigh -1.5 percentage units [pu;
199 ared with controls (regression coefficients: inclusion body myositis thigh 4.0 ms [SE 0.5], calf 3.5
202 2017 and May 22, 2019, 152 participants with inclusion body myositis were randomly assigned to arimoc
204 ith either Charcot-Marie-Tooth disease 1A or inclusion body myositis who were attending the inherited