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1 itis or dermatomyositis, and 2 families with inclusion body myositis.
2 A alterations may be accelerated in sporadic inclusion body myositis.
3 group demonstrated histological features of inclusion body myositis.
4 proposed criteria for definite and possible inclusion body myositis.
5 stological confirmation may nonetheless have inclusion body myositis.
6 scles, quadriceps, and ankle dorsiflexors in inclusion body myositis.
7 ly definite by MRC criteria was required for inclusion body myositis.
8 genotype confers the highest disease risk in inclusion body myositis.
9 r focus on polymyositis, dermatomyositis and inclusion body myositis.
10 mulate intracellularly in some patients with inclusion body myositis.
11 includes polymyositis, dermatomyositis, and inclusion body myositis.
12 omprising dermatomyositis, polymyositis, and inclusion body myositis.
13 sent key early events in the pathogenesis of inclusion body myositis.
14 ntotemporal lobar degeneration, and sporadic inclusion body myositis.
15 s are potential disease activity sensors for inclusion body myositis.
16 vided into dermatomyositis, polymyositis and inclusion body myositis.
17 ive muscle disease of aging humans, sporadic inclusion body myositis.
18 ulates early in Alzheimer's disease (AD) and inclusion body myositis.
19 l (3.3%, 1.8-4.9, p=0.0007) in patients with inclusion body myositis.
20 thies are polymyositis, dermatomyositis, and inclusion body myositis.
21 otoxic T lymphocyte-mediated autoimmunity in inclusion body myositis.
22 muscle fibers that are specific to sporadic inclusion-body myositis.
23 e new avenues toward the therapy of sporadic inclusion-body myositis.
24 slightly to muscle fiber damage in sporadic inclusion-body myositis.
25 subsets: dermatomyositis, polymyositis, and inclusion-body myositis.
26 ortant clues to the pathogenesis of sporadic inclusion-body myositis.
27 ent concepts of the pathogenesis of sporadic inclusion-body myositis.
28 myopathy, polymyositis, dermatomyositis, and inclusion body myositis].
30 tal muscle biopsies taken from patients with inclusion body myositis, a degenerative disorder in whic
31 individual cells from patients with sporadic inclusion body myositis, a late-onset inflammatory myopa
32 Muscle biopsies from patients with sporadic inclusion body myositis, a well defined myopathy with ch
33 likely that genetic muscular dystrophies and inclusion body myositis account for some cases of appare
36 in scattered muscle fibers occur in sporadic inclusion body myositis and clinically similar disorders
37 of mtDNA deletions in patients with sporadic inclusion body myositis and control subjects, mtDNA alte
38 predicted the presence of dendritic cells in inclusion body myositis and of an IFN-alpha/beta respons
39 tically significant benefit in patients with inclusion body myositis and paraproteinemic anti-myelin-
44 trials in dermatomyositis, polymyositis, and inclusion body myositis and suggests an approach to trea
45 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Inclusion body myositis and T cell large granular lympho
47 ripheral neuropathy were also more common in inclusion body myositis and unresponsive polymyositis th
48 d knee extensor involvement was specific for inclusion body myositis and unresponsive polymyositis.
49 y provides insights into the pathogenesis of inclusion-body myositis and concludes that in sIBM one s
50 cell activation in polymyositis and sporadic inclusion-body myositis and the cause of vacuolar degene
51 cot-Marie-Tooth disease 1A, 20 patients with inclusion body myositis, and 29 healthy controls (alloca
52 fibers are common in patients with sporadic inclusion body myositis, and multiple [correction of mut
53 o the disease mechanisms of dermatomyositis, inclusion body myositis, and polymyositis gained from la
55 quences of genes that predispose to sporadic inclusion-body myositis, and of human muscle fiber aging
57 e diseases dermatomyositis, polymyositis and inclusion body myositis are of unknown cause, but immune
59 forms are polymyositis, dermatomyositis, and inclusion body myositis) are systemic autoimmune disease
60 itochondrial pathology (IM-VAMP), which have inclusion body myositis as a pathologic subtype and are
61 pect that patients with clinical features of inclusion body myositis but lacking histological confirm
64 of the vacuolated muscle fibers of sporadic inclusion body myositis contained well-defined, strongly
66 inclusion-body myositis muscle biopsies with inclusion-body myositis experimental models in tissue cu
67 , we prospectively screened 38 patients with inclusion body myositis for the presence of expanded lar
69 The most important feature distinguishing inclusion body myositis from the other two inflammatory
70 that characterize polymyositis and sporadic inclusion-body myositis from the non-specific, secondary
72 elated with the lower limb components of the inclusion body myositis functional rating score (rho=-0.
76 tained muscle biopsy specimens from sporadic inclusion body myositis, hereditary inclusion body myopa
78 histologically distinct patient populations, inclusion body myositis (IBM) and anti-Jo-1-associated m
79 inst a 43 kDa muscle autoantigen in sporadic inclusion body myositis (IBM) and demonstrated the feasi
87 ted muscle cells or markers of cell death in inclusion body myositis (IBM) is in distinction to the s
92 New candidate genes have been examined in inclusion body myositis (IBM), and a novel gene transfer
93 polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM), diseases that result from
95 ith dermatomyositis (DM), polymyositis (PM), inclusion body myositis (IBM), myasthenia gravis, or gen
106 ease (AD) brain, vacuolated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumul
108 are an important diagnostic criterion of the inclusion-body myositis (IBM) muscle biopsy; but, until
109 egulated kinase (ERK) in the pathogenesis of inclusion-body myositis (IBM) was investigated by immuno
110 e describe the occurrence of an inflammatory inclusion body myositis in siblings of a single generati
111 , s-IBM can also occur in families (familial inclusion body myositis), in a pattern analogous to the
115 structs coding for the Alzheimer disease and inclusion body myositis-linked beta-amyloid precursor pr
119 equences, and correlate findings in sporadic inclusion-body myositis muscle biopsies with inclusion-b
120 he recent identification within the sporadic inclusion-body myositis muscle fibers of several abnorma
124 nsubstantiated benefit in some patients with inclusion-body myositis, paraproteinemic IgM demyelinati
126 ge granular lymphocytes into muscle in 15/15 inclusion body myositis patients but in only 1/28 patien
129 s of 46 patients newly diagnosed with either inclusion body myositis, polymyositis, or dermatomyositi
130 een reported to be elevated in patients with inclusion-body myositis, polymyositis, dermatomyositis,
135 , are the characteristic feature of sporadic inclusion body myositis (s-IBM) muscle biopsies, we stud
136 eficiency virus infection (HIV-PM), sporadic inclusion body myositis (s-IBM), dermatomyositis (DM), a
139 seeking the pathogenic mechanism of sporadic inclusion-body myositis (s-IBM) and hereditary inclusion
144 ause in the muscle of patients with sporadic inclusion body myositis (sIBM) clonally expanded CD8+ T
150 TAR DNA binding protein TDP-43, in sporadic inclusion body myositis (sIBM) sarcoplasm are important
151 myositis (DM) who improved and patients with inclusion body myositis (sIBM) who did not improve after
153 of the skeletal muscle pathology in sporadic inclusion body myositis (sIBM), have remained elusive.
157 eta-analysis of the apolipoprotein E gene in inclusion body myositis suggests that this gene does not
161 ciated with aging and is related to sporadic inclusion body myositis, the most common acquired muscle
163 In conceptualizing a treatment for sporadic inclusion-body myositis, the accumulations of amyloid-be
166 .3]) and MTR reduced compared with controls (inclusion body myositis thigh -1.5 percentage units [pu;
167 ared with controls (regression coefficients: inclusion body myositis thigh 4.0 ms [SE 0.5], calf 3.5
171 ith either Charcot-Marie-Tooth disease 1A or inclusion body myositis who were attending the inherited
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