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1 JDM and adult-onset dermatomyositis (DM) have similar cl
2 JDM patients can be monitored with noninvasive P-31 MRS
3 JDM patients displayed a high prevalence (72%) of abnorm
4 JDM patients with anti-p140 antibodies and tumour necros
5 JDM skin and muscle both showed evidence for type 1 inte
6 scle biopsies of four untreated DQA1*0501(+) JDM children with profiles from children with a known ne
9 with this, peripheral blood Tregs of active JDM patients were less capable of suppressing effector T
11 Free Mg(2+) levels were normal in DM and JDM myopathic muscles at rest, but were significantly lo
15 hallenges of studying a rare disease such as JDM have been overcome by several collaborative studies
19 seases, especially juvenile dermatomyositis (JDM) and systemic sclerosis; however, little is known ab
28 in high levels in juvenile dermatomyositis (JDM), which may account the frequency of autoantibodies
31 ich appear to be risk factors for developing JDM or for developing complications such as calcinosis,
35 henotype and function of Tregs in blood from JDM patients by flow cytometry and in vitro suppression
36 33.75 +/- 8.4 IFN-gamma-producing cells from JDM cells vs 5.0 +/- 1.25 from maternal cells), and that
40 ence of maternally derived chimeric cells in JDM patients and healthy controls, and assessed immunolo
41 nization for classifying inactive disease in JDM have practical applicability to the current clinical
42 are informative of molecular disruptions in JDM and provide transcriptional evidence of chronic infl
45 nal data solidify the role of type I IFNs in JDM disease pathogenesis, integration of clinical and mo
47 rtance of annual lipid profile monitoring in JDM patients, potentially followed by early intervention
48 eviews clinical and molecular phenotyping in JDM and translational insights into immune pathogenesis
49 rnational definition of disease remission in JDM has been agreed, which will aid disease assessment i
50 Falpha isolated from the calcific tissues in JDM have also been implicated in the pathologic process.
53 Surprisingly, PBMCs from clinically inactive JDM individuals had persistent immune activation that wa
56 ), juvenile-onset, type 1 diabetes mellitus (JDM), Down syndrome (DS)/trisomy 21, and the carrier sta
58 s, we developed a jaguar distribution model (JDM), livestock density model, and ecotourism lodge dens
59 all, Treg percentages in peripheral blood of JDM patients were similar compared to both control group
65 ta regarding extramuscular manifestations of JDM should allow researchers to continue elucidating the
66 ifferentially abundant in the microbiomes of JDM probands compared to their unaffected siblings, incl
68 or caretakers of children within 6 months of JDM diagnosis were interviewed by the registry study nur
70 Mean ATP and PCr levels in the muscles of JDM patients were 35-40% below the normal control values
72 to understand the molecular underpinnings of JDM, particularly when untreated, which would facilitate
74 t definite symptom (rash and/or weakness) of JDM are supported by immunologic data that suggest that
79 Diagnoses were as follows: definite/probable JDM (n = 234, 82%), possible JDM (n = 43, 15%), or rash
80 imeric T cells are responsive to the host's (JDM childs') lymphocytes (33.75 +/- 8.4 IFN-gamma-produc
83 hat chimeric cells play a direct role in the JDM disease process and that the mother's HLA genotype f
86 We studied the RNA-Seq data from untreated JDM peripheral blood mononuclear cells (PBMCs; n = 11),
90 rvational cohort study, we evaluated whether JDM is associated with discrete oral and gut microbiome
91 cal HLA allele most strongly associated with JDM [odds ratio (OR) 1.66; 95% confidence interval (CI)
92 d chimeric cells more often in children with JDM (60 of 72) than in their unaffected siblings (11 of