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1 thyroiditis) and autoimmune thyrotoxicosis (Graves' disease).
2 and provide new insight into the etiology of Graves disease.
3 e receptor (TSHR), is the primary antigen of Graves disease.
4 to localized overproduction of hyaluronan in Graves disease.
5 an, hyaluronan, which accumulates in orbital Graves disease.
6 lating variety are the cause of hyperthyroid Graves disease.
7 with HLA-DR3 in conferring susceptibility to Graves' disease.
8 loci for schizophrenia, type 1 diabetes, and Graves' disease.
9 of molecular mimicry in the pathogenesis of Graves' disease.
10 understanding the molecular pathogenesis of Graves' disease.
11 ic lymphocytic (Hashimoto's) thyroiditis and Graves' disease.
12 iagnosis, pathogenesis, and immunotherapy of Graves' disease.
13 ion and the hyperthyroidism was secondary to Graves' disease.
14 tes (T2D), coronary artery disease (CAD) and Graves' disease.
15 manifestation most commonly associated with Graves' disease.
16 diseases, including rheumatoid arthritis and Graves' disease.
17 r immune responses localized to the orbit in Graves' disease.
18 contributing to the relative T3 toxicosis of Graves' disease.
19 iated with both type 1 diabetes mellitus and Graves' disease.
20 roduced from lymphocytes from a patient with Graves' disease.
21 tions for new studies on the pathogenesis of Graves' disease.
22 exon 33 SNP, giving an odds ratio of 6.1 for Graves' disease.
23 man tropomodulin and a 64-kDa autoantigen in Graves disease (1D) are related: tropomodulin has 42 and
24 otoxicosis Therapy Follow-up Study; 91 % had Graves disease, 79% were female, and 65% were treated wi
28 patients who have a history of treatment of Graves disease, a subgroup that is not a target of scree
29 ave relevance to the pathogenesis of orbital Graves disease, an inflammatory autoimmune condition tha
32 les are more distal than those identified in Graves' disease and are in LD with Graves' disease prote
34 the common causes of thyrotoxicosis, such as Graves' disease and functioning nodular goiters, there a
35 ld of autoimmune thyroiditis (represented by Graves' disease and Hashimoto's thyroiditis) since Janua
36 genes is homologous to a gene implicated in Graves' disease and it, ANT2 and two others are confirme
39 hat manifest during the acute phase, such as Graves' disease and systemic lupus erythematosus, are di
42 e link between the orbital manifestations of Graves' disease and those in the pretibial skin, localiz
43 In 3 of the 14 regions, TCF7L2 (T2D), CTLA4 (Graves' disease) and CDKN2A-CDKN2B (T2D), much of the po
44 schizophrenia risk (rheumatoid arthritis and Graves' disease), and DICER1 is pivotal in miRNA process
45 uding type 1 diabetes, rheumatoid arthritis, Graves disease, and systemic lupus erythematosus, are as
46 ion has been found in the thyroid condition, Graves' disease, as well as in mothers of homosexual men
48 fibroblasts orchestrate tissue remodeling in Graves disease, at least in part, because they exhibit e
50 s of risk of the common autoimmune disorders Graves' disease, autoimmune hypothyroidism and type 1 di
51 cells to human serum from two patients with Graves' disease, but not control sera, led to secretion
52 is produces a novel truncated version of the Graves' disease carrier protein-like protein that lacks
54 (in total 42 agranulocytosis cases and 1,208 Graves' disease controls), using direct human leukocyte
55 unction (10 cases of hypothyroidism and 1 of Graves disease) developed in 11 of 19 (57.9%) of the DS
58 The most common cause of this syndrome is Graves' disease, followed by toxic multinodular goitre,
60 actors present in the serum of patients with Graves disease, forms the basis for the immunologic atta
61 e thyroid gland can be used to differentiate Graves' disease from painless thyroiditis in patients wi
62 sed as a threshold value for differentiating Graves' disease from painless thyroiditis, the best resu
63 oimmune thyroid diseases (AITDs), comprising Graves disease (GD) and Hashimoto thyroiditis (HT), deve
64 eases (AITDs) include two related disorders, Graves disease (GD) and Hashimoto thyroiditis, in which
70 Autoimmune thyroid disease (AITD), including Graves' disease (GD) and Hashimoto's thyroiditis (HT), i
71 eported recently that IgG from patients with Graves' disease (GD) can induce the expression of the CD
72 II-encoded HLA-DRB1-DQA1-DQB1 haplotype with Graves' disease (GD) has been known for several years.
80 rbital fibroblasts (GOFB) from patients with Graves' disease (GD), as well as fibrocyte abundance, we
85 s mellitus, psoriasis, rheumatoid arthritis, Graves disease, Hashimoto thyroiditis, Crohn disease, ul
86 e 1 diabetes mellitus, rheumatoid arthritis, Graves' disease, Hashimoto thyroiditis, autoimmune thyro
87 ta, ankylosing spondylitis, dermatomyositis, Graves' disease, Hashimoto thyroiditis, insulin-dependen
88 immune response to the TSHR, thereby causing Graves disease in genetically susceptible individuals.
91 une disease, autoimmune thyroid disease (and Graves' disease in particular) contributes disproportion
92 f Trp(620) with another autoimmune disorder, Graves' disease, in 1,734 case and control subjects (P =
95 mulating autoantibodies (TSAb), the cause of Graves' disease, interact with this region of the TSHR i
103 halmopathy (TAO), an autoimmune component of Graves' disease, is associated with profound connective
104 in receptor (TSHR), the major autoantigen in Graves' disease, is posttranslationally modified by intr
105 rst identified as a potential autoantigen in Graves' disease, is similar to the tropomodulin (Tmod) f
106 ne thyroid disease (Hashimoto thyroiditis or Graves disease), juvenile RA, inflammatory bowel disease
108 ically to treat autoimmune diseases, such as Graves' disease, may also diminish pathological inflamma
109 ssues (thyroiditis, n = 3; psoriasis, n = 2; Graves disease, n 1; membranous glomerulonephritis, n =
110 t from PGP, predictions of Gilbert syndrome, Graves' disease, non-Hodgkin lymphoma, and various blood
112 are the primary therapy, but some women with Graves disease opt to receive definitive therapy with RA
115 revious thyroid disease, particularly either Graves' disease or Hashimoto thyroiditis, suggesting the
116 umber in cohorts of patients with autoimmune Graves' disease or hepatitis B infection, whereas G138G
117 ulation iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of iod
119 imulating TSHR autoantibodies (TSHR-Ab's) in Graves disease patients may provide a functional explana
122 tified in Graves' disease and are in LD with Graves' disease protective alleles identified in both of
123 other patients with thyroiditis and two with Graves' disease recognized only the whole 589-633 fragme
127 his gene with type 1 diabetes mellitus (DM), Graves' disease, rheumatoid arthritis (RA), and multiple
128 ither of the 2 SNPs recently associated with Graves' disease showed evidence for association in the u
131 TSH receptor antibody-ELISA used to diagnose Graves disease ("third-generation assay") and also detec
132 se a new adenovirus-mediated animal model of Graves disease to show that goiter and hyperthyroidism o
133 ue in both normal patients and patients with Graves disease), together with the humoral factors prese
134 in thyroidal T3 production in patients with Graves' disease, toxic adenomas, and, perhaps, iodine de
135 The mean ADC value of the thyroid gland in Graves' disease was 2.03+/-0.28x10(-3) mm(2)/sec, and in
136 sues involved in Hashimoto's thyroiditis and Graves' disease, we performed ex vivo analysis of lympho
137 chanistic framework for molecular mimicry in Graves' disease, where early precursor B cells are expan
139 from a single experimental mouse undergoing Graves' disease, which shared the same H and L chain ger
141 ween induced and spontaneous mouse models of Graves' disease with implications for potential immunoth
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