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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
25       This single autoantigenic target makes Graves' disease a prime candidate for Ag-specific immuno
26                                           In Graves' disease a specific combination of polymorphisms
27                                              Graves disease, a common organ-specific autoimmune disea
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
30 tions causing endocrine dysfunctions such as Graves disease and hypo- and hyperthyroidism.
31 elopment of specific ligands useful to treat Graves disease and other dysfunctions of GPHRs.
32 les are more distal than those identified in Graves' disease and are in LD with Graves' disease prote
33      The autoimmune thyroid diseases (AITD), Graves' disease and chronic lymphocytic thyroiditis (CLT
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
37 ificant difference in the ADC values between Graves' disease and painless thyroiditis (P=0.001).
38 ighted MR imaging in differentiation between Graves' disease and painless thyroiditis.
39 hat manifest during the acute phase, such as Graves' disease and systemic lupus erythematosus, are di
40          New therapeutic modalities for both Graves' disease and the associated orbitopathy have hast
41         Because of the low remission rate in Graves' disease and the inability to cure toxic nodular
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
47 thogenic TSHR Abs as detected using clinical Graves' disease assays.
48 fibroblasts orchestrate tissue remodeling in Graves disease, at least in part, because they exhibit e
49                   The most frequent cause is Graves' disease (autoimmune hyperthyroidism).
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
53 ode a protein with homology to the mammalian Graves' disease carrier proteins.
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
56 ely 3% of women and 0.5% of men will develop Graves disease during their lifetime.
57 e the preferred therapy for the treatment of Graves' disease during pregnancy.
58    The most common cause of this syndrome is Graves' disease, followed by toxic multinodular goitre,
59  The most common cause of hyperthyroidism is Graves' disease, followed by toxic nodular 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
65                      The major AITDs include Graves disease (GD) and Hashimoto's thyroiditis (HT); al
66                                              Graves disease (GD) is a common autoimmune thyroid disor
67                                              Graves disease (GD) is an autoimmune condition caused by
68 s a common and debilitating manifestation of Graves disease (GD).
69 tibody generation in the autoimmune disorder Graves disease (GD).
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.
73                                              Graves' disease (GD) is a common autoimmune disease (AID
74                                              Graves' disease (GD) is a common thyroid disease, and Gr
75                                              Graves' disease (GD) is an autoimmune process involving
76                                              Graves' disease (GD) is an autoimmune thyroid disease de
77                                              Graves' disease (GD) is an autoimmune thyroid disorder t
78                                              Graves' disease (GD) is associated with T cell infiltrat
79                                              Graves' disease (GD), an autoimmune process involving th
80 rbital fibroblasts (GOFB) from patients with Graves' disease (GD), as well as fibrocyte abundance, we
81                                In autoimmune Graves' disease (GD), autoantibodies bind to the thyrotr
82 athy are connective tissue manifestations of Graves' disease (GD).
83 n's disease, and thyroid follicular cells in Graves' disease (GD).
84  thyroid function and is targeted by IgGs in Graves' disease (GD-IgG).
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.
89 ance pathogenic Ab production and exacerbate Graves' disease in humans.
90  Ag-specific immunotherapies aimed at curing Graves' disease in humans.
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 =
93                        Treatment options for Graves' disease include antithyroid drugs, radioactive i
94                                Management of Graves disease includes treatment with antithyroid drugs
95 mulating autoantibodies (TSAb), the cause of Graves' disease, interact with this region of the TSHR i
96                                              Graves disease is an autoimmune disorder that affects th
97                                              Graves disease is directly caused by thyroid-stimulating
98                              The etiology of Graves disease is multifactorial, with nongenetic factor
99                                              Graves disease is the most common cause of persistent hy
100                                              Graves' disease is an autoimmune disorder that causes hy
101                The classic clinical triad of Graves' disease is hyperthyroidism, diffuse goiter, and
102                                              Graves' disease is the leading cause of hyperthyroidism
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
107                                Patients with Graves disease may be treated with antithyroid drugs, ra
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
111        Propylthiouracil (PTU), used to treat Graves' disease, occasionally induces a lupus-like syndr
112 are the primary therapy, but some women with Graves disease opt to receive definitive therapy with RA
113 serve this association in the organ-specific Graves' disease or Addison's disease.
114 at least 1 member who had both SLE and AITD (Graves' disease or Hashimoto thyroiditis).
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
118 cosis (OR = 0.76, p = 1.5 x 10(-3)), but not Graves disease (OR = 1.03, p = 0.82).
119 imulating TSHR autoantibodies (TSHR-Ab's) in Graves disease patients may provide a functional explana
120                   Similarly, the majority of Graves' disease patients develop improved function over
121 eactivity in sera from 45 Hashimoto's and 47 Graves' disease patients.
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
124 opathy, a condition commonly associated with Graves' disease, remains inadequately treated.
125                                              Graves' Disease results from the production of autoantib
126                                              Graves' disease results from thyroid-stimulating Abs (TS
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
129 tis are more common than hyperthyroidism and Graves' disease (strong evidence).
130                                           In Graves' disease, the orbit of the eye can become severel
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
138                                              Graves' disease, which is autoimmune in nature, is the u
139  from a single experimental mouse undergoing Graves' disease, which shared the same H and L chain ger
140                                     Treating Graves disease with RAI and surgery result in gland dest
141 ween induced and spontaneous mouse models of Graves' disease with implications for potential immunoth

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