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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
7          A retrospective chart review of 142 JDM patients who had fasting lipid profiles was conducte
8                                 Therefore, a JDM-focused genetic analysis was performed using the lar
9  with this, peripheral blood Tregs of active JDM patients were less capable of suppressing effector T
10                                          All JDM samples were compared to non-inflammatory control ti
11     Free Mg(2+) levels were normal in DM and JDM myopathic muscles at rest, but were significantly lo
12                      Mg-ATP levels in DM and JDM myopathic muscles were at least 37% lower than those
13 with weakness and fatigue observed in DM and JDM patients.
14 recovery (P < 0.029 and P < 0.005 for DM and JDM, respectively).
15 hallenges of studying a rare disease such as JDM have been overcome by several collaborative studies
16 nt with the weakness and fatigue reported by JDM patients.
17                                    Caucasian JDM samples (n = 952) obtained via international collabo
18                               In conclusion, JDM patients have a high prevalence of dyslipidemia, esp
19 seases, especially juvenile dermatomyositis (JDM) and systemic sclerosis; however, little is known ab
20                    Juvenile dermatomyositis (JDM) is a multisystem autoimmune disease that at times r
21                    Juvenile dermatomyositis (JDM) is a rare immune-mediated disease of childhood with
22                    Juvenile dermatomyositis (JDM) is a rare, severe autoimmune disease and the most c
23                    Juvenile dermatomyositis (JDM) is an immune-mediated inflammatory disease affectin
24 e 1 month prior to juvenile dermatomyositis (JDM) may trigger the onset of disease.
25                    Juvenile dermatomyositis (JDM), the most common pediatric inflammatory myopathy, i
26                    Juvenile dermatomyositis (JDM), the most common pediatric inflammatory myopathy, i
27                 In juvenile dermatomyositis (JDM), the most common pediatric inflammatory myopathy, w
28  in high levels in juvenile dermatomyositis (JDM), which may account the frequency of autoantibodies
29 he many aspects of juvenile dermatomyositis (JDM).
30 y in children with Juvenile Dermatomyositis (JDM).
31 ich appear to be risk factors for developing JDM or for developing complications such as calcinosis,
32                  MRI is useful in diagnosing JDM and may be used as a disease assessment tool.
33 sphorylation in the mitochondria of diseased JDM muscles.
34 on 37 within HLA-DRB1, which may distinguish JDM from adult DM.
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
37 ingival, and subgingival plaque samples from JDM probands (n = 28).
38          These include new autoantibodies in JDM (p140, which appears to have an association with cal
39                                      Both in JDM and Duchenne's muscular dystrophy the proportion of
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
43 arly half (47%) of the dysregulated genes in JDM were associated with the immune response.
44        One of the latest to be identified in JDM targets the protein NXP-2 and is associated with an
45 nal data solidify the role of type I IFNs in JDM disease pathogenesis, integration of clinical and mo
46 o an infectious process may be implicated in JDM disease pathogenesis.
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.
51 , and suggest a regulatory role for Tregs in JDM inflammation.
52                          A role for Tregs in JDM pathogenesis has not yet been established.
53 Surprisingly, PBMCs from clinically inactive JDM individuals had persistent immune activation that wa
54                               Interestingly, JDM is not a self-remitting disease, suggesting that the
55 tegrate across judgment and decision making (JDM) phenomena.
56 ), juvenile-onset, type 1 diabetes mellitus (JDM), Down syndrome (DS)/trisomy 21, and the carrier sta
57                                    "Mindful" JDM research leverages our knowledge about psychological
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
60 ective in increasing the aerobic capacity of JDM patients in remission.
61 as performed using the largest collection of JDM samples to date.
62 iversity, more so than having a diagnosis of JDM.
63                 While microbiome features of JDM are often shared by unaffected family members, the l
64 er 16.8 years of symptom onset, over half of JDM patients still have active disease.
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
67              The oral and gut microbiomes of JDM probands were more similar to their own unaffected s
68 or caretakers of children within 6 months of JDM diagnosis were interviewed by the registry study nur
69 d function in peripheral blood and muscle of JDM patients.
70    Mean ATP and PCr levels in the muscles of JDM patients were 35-40% below the normal control values
71 ll activation in vitro, compared to Tregs of JDM in clinical remission.
72 to understand the molecular underpinnings of JDM, particularly when untreated, which would facilitate
73 ad no muscle weakness (amyopathic variant of JDM).
74 t definite symptom (rash and/or weakness) of JDM are supported by immunologic data that suggest that
75                 Muscle biopsies of new onset JDM patients showed increased infiltration of numbers of
76 s than they were to the microbiomes of other JDM probands.
77                                          Our JDM indicate that 64% of the Pantanal holds suitable hab
78 finite/probable JDM (n = 234, 82%), possible JDM (n = 43, 15%), or rash only (n = 9, 3%).
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
81            This study provides evidence that JDM affects young children.
82 edical records were reviewed, confirming the JDM diagnosis.
83 hat chimeric cells play a direct role in the JDM disease process and that the mother's HLA genotype f
84             The presence of chimerism in the JDM patients, their healthy siblings, and unaffected con
85  cells in muscles were increased compared to JDM peripheral blood.
86   We studied the RNA-Seq data from untreated JDM peripheral blood mononuclear cells (PBMCs; n = 11),
87 ich was significantly increased in untreated JDM PBMCs and correlated with all 3 DAS domains.
88 n = 8/11), and separate samples of untreated JDM skin and muscle (n = 4 each).
89                                The untreated JDM PBMCs showed a strong signature for type1 interferon
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
93  addition in the evaluation of children with JDM.
94                       Thirteen patients with JDM (ages 4-16 years) were studied.
95 eve its primary end point, but patients with JDM did show good improvement in disease activity.
96 ave been found in the serum of patients with JDM.
97 tients with DM and 10 juvenile patients with JDM.