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1 versity Medical Center with the diagnosis of polymyositis.
2 vels lower than those in other patients with polymyositis.
3 high muscles seen on initial MRI represented polymyositis.
4 t be distinguished histologically early from polymyositis.
5 for inclusion body myositis and unresponsive polymyositis.
6 the determining factor, and in persons with polymyositis.
7 ewly identified in a subset of patients with polymyositis.
8 n only 1/28 patients with dermatomyositis or polymyositis.
9 d necrotizing myopathy with many features of polymyositis.
10 tients are frequently misdiagnosed as having polymyositis.
11 autoimmunity in inclusion body myositis and polymyositis.
12 ermatomyositis, inclusion body myositis, and polymyositis.
13 ed therapeutic trials of dermatomyositis and polymyositis.
14 ypes in individuals with dermatomyositis and polymyositis.
15 tomyositis and, to a lesser degree, juvenile polymyositis.
16 (n = 71), systemic sclerosis 36.0% (n = 22), polymyositis 6.2% (n = 16), and adult Still's disease 0%
17 patients with dermatomyositis and some with polymyositis, a blood type 1 interferon-signature correl
18 10 children (9 with dermatomyositis, 1 with polymyositis; ages 4-15 years) twice in one day (morning
19 ponse may not be antigen driven, there is in polymyositis an overexpression of certain T-cell recepto
22 (RA) (n = 80), Sjogren's syndrome (n = 30), polymyositis and dermatomyositis (n = 30), and progressi
23 omodulatory drugs are certainly effective in polymyositis and dermatomyositis despite the lack of ran
25 re is increasing evidence that patients with polymyositis and dermatomyositis have specific clinico-s
27 lieved that muscle weakness in patients with polymyositis and dermatomyositis is due to autoimmune an
29 itiation of therapy is essential, since both polymyositis and dermatomyositis respond to immunotherap
38 nflammatory muscle diseases dermatomyositis, polymyositis and inclusion body myositis are of unknown
43 s mycophenolate mofetil is effective in both polymyositis and refractory dermatomyosits (including re
45 igen(s) responsible for T-cell activation in polymyositis and sporadic inclusion-body myositis and th
46 -driven inflammatory cells that characterize polymyositis and sporadic inclusion-body myositis from t
49 ess with antigen-driven T cells identical to polymyositis, and a degenerative process in which beta-a
51 olated from samples of IBM, dermatomyositis, polymyositis, and control muscles were treated with reco
53 ecent therapeutic trials in dermatomyositis, polymyositis, and inclusion body myositis and suggests a
54 he inflammatory myopathies (dermatomyositis, polymyositis, and inclusion body myositis) remains obscu
57 whereas their prevalence in dermatomyositis, polymyositis, and other neuromuscular disorders appeared
59 Classification systems of dermatomyositis, polymyositis, and the other idiopathic inflammatory myop
60 Chronic graft-versus-host disease-related polymyositis appears to be very similar to idiopathic my
63 Although types of malignancy seen in DM and polymyositis are similar to those in the general populat
65 similar mechanisms appear to be involved in polymyositis associated with HTLV-I (human T cell lympho
66 transthyretin amyloidosis) can mimic that of polymyositis, but also shows that unique findings on MRI
67 rior chamber uveitis, and steroid-responsive polymyositis confirmed by electrophysiologic studies.
68 n the past 2 years, with particular focus on polymyositis, dermatomyositis and inclusion body myositi
69 eterogeneous group of diseases that includes polymyositis, dermatomyositis, and inclusion body myosit
70 yositis syndromes (the most common forms are polymyositis, dermatomyositis, and inclusion body myosit
71 and 2B, Miyoshi myopathy, nemaline myopathy, polymyositis, dermatomyositis, and inclusion body myosit
72 the most common inflammatory myopathies are polymyositis, dermatomyositis, and inclusion body myosit
73 ed in patients with inclusion-body myositis, polymyositis, dermatomyositis, and neurogenic muscle atr
74 pus erythematosus, Wegener's granulomatosis, polymyositis, dermatomyositis, polyarteritis nodosa, or
75 ly associated with a subset of patients with polymyositis/dermatomyositis (PM/DM) complicated by inte
76 to determine whether sera from patients with polymyositis/dermatomyositis (PM/DM) with or without int
77 se who had 45-55-kd bands, all patients with polymyositis/dermatomyositis (PM/DM), and a random selec
78 erythematosus, 121 with scleroderma, 86 with polymyositis/dermatomyositis [PM/DM]) and 248 Italian pa
79 cytoplasmic antibody-associated vasculitis, polymyositis/dermatomyositis, and primary Sjogren's synd
80 I, 1.10-1.27) and specific prior autoimmune (polymyositis/dermatomyositis, systemic sclerosis, autoim
81 nti-RHA was not observed in any patient with polymyositis/dermatomyositis, systemic sclerosis, rheuma
82 tingly, similar to what is observed in human polymyositis/dermatomyositis, the mice developed a stron
83 ated 10 patients with histologically typical polymyositis except for an excess of muscle fibres with
84 ermatomyositis, inclusion body myositis, and polymyositis gained from large-scale microarray gene exp
85 cle biopsy in 2 patients in the unresponsive polymyositis group demonstrated histological features of
86 All patients with dermatomyositis and polymyositis (> or =15 years old) were identified by dis
87 patients with adult-onset dermatomyositis or polymyositis had a baseline assessment a median of 30 mo
89 patients with IIM, in particular those with polymyositis, had no strong disease associations with HL
92 bellar degeneration (PCD) in HL and dermato/ polymyositis in both HL and NHL, other PNSs are uncommon
94 ) infection, studies into a primate model of polymyositis induced by HTLV-I may be particularly infor
98 rt here the first known case of inflammatory polymyositis leading to rhabdomyolysis in a male patient
101 c inflammatory myopathy (dermatomyositis and polymyositis) may have in certain instances extramuscula
102 y, certain intractable childhood epilepsies, polymyositis, multiple sclerosis, optic neuritis, and th
104 farction (n = 10), myonecrosis due either to polymyositis or crush injuries (n = 12), and septic shoc
106 milies with other siblings or relatives with polymyositis or dermatomyositis, and 2 families with inc
109 d systemic lupus erythematosus (SLE); 17 had polymyositis or dermatomyositis; 16 had scleroderma; eig
112 ) age-matched patients with dermatomyositis, polymyositis, or necrotizing myopathy, and 0/20 (0%) age
113 itis, Sjogren's syndrome, dermatomyositis or polymyositis, or scleroderma were of borderline statisti
114 e of onset was 9 years older than a group of polymyositis patients with normal COX staining of muscle
115 lt or juvenile IIM, comprising patients with polymyositis (PM) (n=114), dermatomyositis (DM) (n=102),
117 of UK Caucasian patients have confirmed that polymyositis (PM) and dermatomyositis (DM) are not genet
118 markers in IBM compared with normal control, polymyositis (PM) and non-inflammatory dystrophy sample
119 vo in patients with dermatomyositis (DM) and polymyositis (PM) in order to evaluate the role of mitoc
122 c controls, two dermatomyositis (DM) and two polymyositis (PM) patients was reverse transcribed and r
123 es, but occurred more often in patients with polymyositis (PM) than in those with dermatomyositis (DM
124 e episodes (MELAS), dermatomyositis (DM) and polymyositis (PM) using pairwise statistical comparison
125 the pathogenesis of the diverse entities of polymyositis (PM), dermatomyositis (DM), and inclusion b
126 echanisms were analysed in biopsies of sIBM, polymyositis (PM), dermatomyositis (DM), dystrophic and
127 from 44 patients with dermatomyositis (DM), polymyositis (PM), inclusion body myositis (IBM), myasth
128 scle disorders include Dermatomyositis (DM), Polymyositis (PM), Necrotizing Myositis (NM), and sporad
129 52), in the muscle biopsies of patients with polymyositis (PM), PM associated with human immunodefici
130 e dermatomyositis (DM), compared to juvenile polymyositis (PM), was assessed in 298 juvenile IIM pati
131 ctively from consecutive adult patients with polymyositis (PM; n = 134), dermatomyositis (n = 129), o
133 patients with established dermatomyositis or polymyositis receiving chronic medical therapies who are
136 the 100 kDa antigenic component of the human polymyositis scleroderma (PMSCL) autoantigen, is a 3'-->
137 100, an autoantibody target in patients with polymyositis, scleroderma, or polymyositis-scleroderma o
139 lated the rat (r) homologue of the human (h) polymyositis-scleroderma autoantigen (PM-Scl), which has
141 te domain that is found also in Homo sapiens polymyositis-scleroderma overlap syndrome 100 kDa autoan
146 ividual cancer sites for dermatomyositis and polymyositis separately, using national cancer rates by
148 in inclusion body myositis and unresponsive polymyositis than in responsive polymyositis and dermato
149 leroderma; Sjogren Syndrome; dermatomyositis/polymyositis; unspecified/mixed CTD; other inflammatory
150 ted, the association of Crohn's disease with polymyositis varies in its complexity and severity.
152 markers led to the suspicion of inflammatory polymyositis, which was confirmed by electromyography an
154 dence of autoimmunity in dermatomyositis and polymyositis, with strong correlations between particula
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