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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].
34                                              Inclusion body myositis, a chronic inflammatory disorder
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
39           There are candidate treatments for inclusion body myositis and a need for additional double
40 retin Val122Ile allele who has both sporadic inclusion body myositis and cardiac amyloidosis.
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-
45                   Dendritic cells present in inclusion body myositis and polymyositis are primarily m
46                                     Although inclusion body myositis and polymyositis have been chara
47 ed intramuscular Ag-specific autoimmunity in inclusion body myositis and polymyositis.
48 ociated through genetic analyses to sporadic inclusion body myositis and sarcoidosis.
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
51                                     Sporadic inclusion body myositis and the hereditary inclusion bod
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
60  in muscle in patients with dermatomyositis, inclusion body myositis, and polymyositis.
61 quences of genes that predispose to sporadic inclusion-body myositis, and of human muscle fiber aging
62                 In polymyositis and sporadic inclusion-body myositis, antigen-specific and clonally e
63 e diseases dermatomyositis, polymyositis and inclusion body myositis are of unknown cause, but immune
64                                The causes of inclusion body myositis are still unknown.
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
67 d an increase in KLRG1 expressing T cells in inclusion body myositis blood.
68 le, relative to placebo, in individuals with inclusion body myositis but did not improve 6MWD.
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
72                 In polymyositis and sporadic inclusion body myositis, clonal expansion of CD8+ cells
73                          In polymyositis and inclusion-body myositis, clonally expanded CD8-positive
74  of the vacuolated muscle fibers of sporadic inclusion body myositis contained well-defined, strongly
75 nd eight studies using various treatments in inclusion body myositis did not show benefit.
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
78  Ultrasound has the ability to differentiate inclusion body myositis from other myopathies.
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
81                                              Inclusion body myositis, from its origins 30 years ago,
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.
85              Most (22/38; 58%) patients with inclusion body myositis had aberrant populations of larg
86                         Interest in sporadic inclusion-body myositis has been enhanced by the recent
87                  Although most patients with inclusion body myositis have characteristic muscle biops
88 tained muscle biopsy specimens from sporadic inclusion body myositis, hereditary inclusion body myopa
89                       Compared with sporadic inclusion body myositis, however, in which the T-cell re
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
92       Some of these features are shared with inclusion body myositis (IBM) and this entity cannot be
93      Historically, the diagnosis of sporadic inclusion body myositis (IBM) has required the demonstra
94                                              Inclusion body myositis (IBM) is a poorly understood aut
95                           PURPOSE OF REVIEW: Inclusion body myositis (IBM) is a poorly understood pro
96                                              Inclusion body myositis (IBM) is an inflammatory muscle
97                                              Inclusion body myositis (IBM) is an inflammatory myopath
98                                              Inclusion body myositis (IBM) is an inflammatory myopath
99 ted muscle cells or markers of cell death in inclusion body myositis (IBM) is in distinction to the s
100                                              Inclusion body myositis (IBM) is often viewed as an enig
101                                     Sporadic inclusion body myositis (IBM) is the most common acquire
102                                              Inclusion body myositis (IBM) is the most common muscle
103 IM, their effectiveness for individuals with inclusion body myositis (IBM) remains uncertain.
104         Serum from 70 patients with sporadic inclusion body myositis (IBM) was subjected to agarose g
105                                              Inclusion body myositis (IBM), a degenerative and inflam
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
111 scle wasting in Alzheimer's disease (AD) and inclusion body myositis (IBM), respectively.
112 t molecular similarities between PM-Mito and inclusion body myositis (IBM), suggesting a trajectory f
113                      The pathogenic basis of inclusion body myositis (IBM), the leading muscle degene
114                                              Inclusion body myositis (IBM), the most common age-relat
115                                              Inclusion body myositis (IBM), the most common muscle di
116 nosis and treatment persist, particularly in inclusion body myositis (IBM), where no effective therap
117 e consistent histologic findings in sporadic inclusion body myositis (IBM).
118 aimed to elucidate the molecular features of inclusion body myositis (IBM).
119 genesis, diagnosis and treatment of sporadic inclusion body myositis (IBM).
120 arget of serum antibodies from patients with inclusion body myositis (IBM).
121 reatment and serum and imaging biomarkers of inclusion body myositis (IBM).
122 fications: dermatomyositis, polymyositis and inclusion body myositis (IBM).
123 eneration in myositis, focusing primarily on inclusion body myositis (IBM).
124 ease (AD) brain, vacuolated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumul
125                                     Sporadic inclusion-body myositis (IBM) is the most common muscle
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
131                                     Sporadic inclusion body myositis is a frequent, acquired, adult-o
132                                              Inclusion body myositis is a late onset treatment-refrac
133                                              Inclusion body myositis is an idiopathic inflammatory my
134                                              Inclusion body myositis is much less responsive to immun
135                                              Inclusion body myositis is the most common progressive m
136               Although the cause of sporadic inclusion body myositis is unknown, GNE myopathy is asso
137 structs coding for the Alzheimer disease and inclusion body myositis-linked beta-amyloid precursor pr
138                          Typical of sporadic inclusion body myositis muscle biopsies are vacuolated m
139        The extent of CD8+ and CD57+ cells in inclusion body myositis muscle correlated with the size
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
142                                  We examined inclusion body myositis muscle T-cell proliferation by K
143 ritic cells are abundant in polymyositis and inclusion body myositis muscle.
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
146 ent may only slightly contribute to sporadic inclusion-body myositis muscle-fiber damage.
147                          In polymyositis and inclusion body myositis, muscle fibers are surrounded an
148 ata on 411 muscle samples from patients with inclusion body myositis (n = 40), other muscle diseases
149                           In all control and inclusion body myositis or myopathy biopsy specimens, Ap
150 nsubstantiated benefit in some patients with inclusion-body myositis, paraproteinemic IgM demyelinati
151 nflammatory responses that resemble sporadic inclusion body myositis pathology.
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
154 s that accumulate in the myocyte vacuoles of inclusion body myositis patients.
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
157                                              Inclusion body myositis, polymyositis, and dermatomyosit
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
162 e cause of vacuolar degeneration in sporadic inclusion-body myositis remain unclear.
163                        Treatment of sporadic inclusion-body myositis remains a challenge.
164 opathies (dermatomyositis, polymyositis, and inclusion body myositis) remains obscure.
165                                     Sporadic inclusion body myositis (s-IBM) is a chronic inflammator
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
168 atients have a disease identical to sporadic inclusion body myositis (s-IBM).
169                                     Sporadic inclusion-body myositis (s-IBM) and hereditary inclusion
170 seeking the pathogenic mechanism of sporadic inclusion-body myositis (s-IBM) and hereditary inclusion
171                                     Sporadic inclusion-body myositis (s-IBM) is the most common progr
172         The hallmark pathologies of sporadic inclusion-body myositis (s-IBM) muscle fibers are autoph
173 in-aggregates are characteristic of sporadic inclusion-body myositis (s-IBM) muscle fibers.
174 ause in the muscle of patients with sporadic inclusion body myositis (sIBM) clonally expanded CD8+ T
175                                     Sporadic inclusion body myositis (sIBM) is a poorly understood im
176                                     Sporadic inclusion body myositis (sIBM) is an idiopathic inflamma
177                                     Sporadic inclusion body myositis (sIBM) is an inflammatory myopat
178                                     Sporadic Inclusion Body Myositis (sIBM) is the most common acquir
179  the muscle fibers of patients with sporadic inclusion body myositis (sIBM) is unknown.
180                                     Sporadic inclusion body myositis (sIBM) pathogenesis is unknown;
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
183                                     Sporadic inclusion body myositis (sIBM), a common adult-onset myo
184 of the skeletal muscle pathology in sporadic inclusion body myositis (sIBM), have remained elusive.
185 PM), Necrotizing Myositis (NM), and sporadic Inclusion Body Myositis (sIBM).
186 in the pathogenesis of familial and sporadic inclusion body myositis (sIBM).
187                                     Sporadic inclusion-body myositis (sIBM) is the most common disabl
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
190                                  In sporadic inclusion-body myositis the inflammatory cells invade no
191                        In many patients with inclusion body myositis, the autoimmune T cell expansion
192                                           In inclusion body myositis, the HLA 8.1 ancestral haplotype
193 ciated with aging and is related to sporadic inclusion body myositis, the most common acquired muscle
194                                              Inclusion body myositis, the most common muscle disorder
195  In conceptualizing a treatment for sporadic inclusion-body myositis, the accumulations of amyloid-be
196                                     Sporadic inclusion-body myositis, the most common muscle disease
197                                     Sporadic inclusion-body myositis, the most common muscle disease
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
200         We studied 56 patients with sporadic inclusion body myositis, using a combination of clinical
201                                           In inclusion-body myositis, vacuolar formation with amyloid
202 2017 and May 22, 2019, 152 participants with inclusion body myositis were randomly assigned to arimoc
203                                              Inclusion body myositis, which now appears to be the mos
204 ith either Charcot-Marie-Tooth disease 1A or inclusion body myositis who were attending the inherited

 
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