ライフサイエンスコーパス: Graves

1 Graves disease (GD) is a common autoimmune thyroid disor

2 Graves disease (GD) is an autoimmune condition caused by

3 Graves disease is an autoimmune disorder that affects th

4 Graves disease is directly caused by thyroid-stimulating

5 Graves disease is the most common cause of persistent hy

6 Graves disease, a common organ-specific autoimmune disea

7 Graves ophthalmopathy (GO) is an autoimmune disease that

8 Graves' disease (GD) is a common autoimmune disease (AID

9 Graves' disease (GD) is a common thyroid disease, and Gr

10 Graves' disease (GD) is an autoimmune process involving

11 Graves' disease (GD) is an autoimmune thyroid disease de

12 Graves' disease (GD) is an autoimmune thyroid disorder t

13 Graves' disease (GD) is associated with T cell infiltrat

14 Graves' disease (GD), an autoimmune process involving th

15 Graves' disease is an autoimmune disorder that causes hy

16 Graves' disease is the leading cause of hyperthyroidism

17 Graves' Disease results from the production of autoantib

18 Graves' disease results from thyroid-stimulating Abs (TS

19 Graves' disease, which is autoimmune in nature, is the u

20 Graves' hyperthyroidism, a common autoimmune disease cau

21 Graves' ophthalmopathy (GO) affects 50% to 60% of patien

22 100% of TSHR autoantibody activity in all 18 Graves' sera studied.

23 ssues (thyroiditis, n = 3; psoriasis, n = 2; Graves disease, n 1; membranous glomerulonephritis, n =

24 (in total 42 agranulocytosis cases and 1,208 Graves' disease controls), using direct human leukocyte

25 A total of 32 Graves patients and 37 eyelids underwent lower eyelid re

26 eactivity in sera from 45 Hashimoto's and 47 Graves' disease patients.

27 at least 1 member who had both SLE and AITD (Graves' disease or Hashimoto thyroiditis).

28 The autoimmune thyroid diseases (AITD), Graves' disease and chronic lymphocytic thyroiditis (CLT

29 ested repatriation under the Native American Graves Protection and Repatriation Act (NAGPRA).

30 schizophrenia risk (rheumatoid arthritis and Graves' disease), and DICER1 is pivotal in miRNA process

31 diseases, including rheumatoid arthritis and Graves' disease.

32 tes (T2D), coronary artery disease (CAD) and Graves' disease.

33 loci for schizophrenia, type 1 diabetes, and Graves' disease.

34 une disease, autoimmune thyroid disease (and Graves' disease in particular) contributes disproportion

35 isease (GD) is a common thyroid disease, and Graves ophthalmopathy(GO) is the most common extra-thyro

36 tis are more common than hyperthyroidism and Graves' disease (strong evidence).

37 iated with both type 1 diabetes mellitus and Graves' disease.

38 sues involved in Hashimoto's thyroiditis and Graves' disease, we performed ex vivo analysis of lympho

39 ic lymphocytic (Hashimoto's) thyroiditis and Graves' disease.

40 uding type 1 diabetes, rheumatoid arthritis, Graves disease, and systemic lupus erythematosus, are as

41 s mellitus, psoriasis, rheumatoid arthritis, Graves disease, Hashimoto thyroiditis, Crohn disease, ul

42 e 1 diabetes mellitus, rheumatoid arthritis, Graves' disease, Hashimoto thyroiditis, autoimmune thyro

43 tions causing endocrine dysfunctions such as Graves disease and hypo- and hyperthyroidism.

44 the common causes of thyrotoxicosis, such as Graves' disease and functioning nodular goiters, there a

45 hat manifest during the acute phase, such as Graves' disease and systemic lupus erythematosus, are di

46 ically to treat autoimmune diseases, such as Graves' disease, may also diminish pathological inflamma

47 In autoimmune Graves' disease (GD), autoantibodies bind to the thyrotr

48 copresence would facilitate AF in autoimmune Graves' hyperthyroidism.

49 umber in cohorts of patients with autoimmune Graves' disease or hepatitis B infection, whereas G138G

50 Because Graves' hyperthyroidism is preferentially induced in BAL

51 ighted MR imaging in differentiation between Graves' disease and painless thyroiditis.

52 ificant difference in the ADC values between Graves' disease and painless thyroiditis (P=0.001).

53 New therapeutic modalities for both Graves' disease and the associated orbitopathy have hast

54 ld of autoimmune thyroiditis (represented by Graves' disease and Hashimoto's thyroiditis) since Janua

55 immune response to the TSHR, thereby causing Graves disease in genetically susceptible individuals.

56 thogenic TSHR Abs as detected using clinical Graves' disease assays.

57 oimmune thyroid diseases (AITDs), comprising Graves disease (GD) and Hashimoto thyroiditis (HT), deve

58 ion has been found in the thyroid condition, Graves' disease, as well as in mothers of homosexual men

59 In 3 of the 14 regions, TCF7L2 (T2D), CTLA4 (Graves' disease) and CDKN2A-CDKN2B (T2D), much of the po

60 Ag-specific immunotherapies aimed at curing Graves' disease in humans.

61 ta, ankylosing spondylitis, dermatomyositis, Graves' disease, Hashimoto thyroiditis, insulin-dependen

62 ely 3% of women and 0.5% of men will develop Graves disease during their lifetime.

63 TSH receptor antibody-ELISA used to diagnose Graves disease ("third-generation assay") and also detec

64 e thyroid gland can be used to differentiate Graves' disease from painless thyroiditis in patients wi

65 sed as a threshold value for differentiating Graves' disease from painless thyroiditis, the best resu

66 tibody generation in the autoimmune disorder Graves disease (GD).

67 f Trp(620) with another autoimmune disorder, Graves' disease, in 1,734 case and control subjects (P =

68 s of risk of the common autoimmune disorders Graves' disease, autoimmune hypothyroidism and type 1 di

69 eases (AITDs) include two related disorders, Graves disease (GD) and Hashimoto thyroiditis, in which

70 his gene with type 1 diabetes mellitus (DM), Graves' disease, rheumatoid arthritis (RA), and multiple

71 revious thyroid disease, particularly either Graves' disease or Hashimoto thyroiditis, suggesting the

72 ance pathogenic Ab production and exacerbate Graves' disease in humans.

73 exon 33 SNP, giving an odds ratio of 6.1 for Graves' disease.

74 Treatment options for Graves' disease include antithyroid drugs, radioactive i

75 ulation iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of iod

76 lly available immunomodulatory therapies for Graves eye disease.

77 First, that activated T lymphocytes from Graves' patients drive the differentiation of PPAR-gamma

78 D2 mRNA was especially high in thyroids from Graves' patients and in follicular adenomas.

79 otoxicosis Therapy Follow-up Study; 91 % had Graves disease, 79% were female, and 65% were treated wi

80 lating variety are the cause of hyperthyroid Graves disease.

81 In Graves' disease a specific combination of polymorphisms

82 In Graves' disease, the orbit of the eye can become severel

83 n the genesis of atrial fibrillation (AF) in Graves' hyperthyroidism.

84 fficiently and neutralized autoantibodies in Graves' patients' sera.

85 bohydrate that neutralizes autoantibodies in Graves' patients' sera.

86 man tropomodulin and a 64-kDa autoantigen in Graves disease (1D) are related: tropomodulin has 42 and

87 in receptor (TSHR), the major autoantigen in Graves' disease, is posttranslationally modified by intr

88 rst identified as a potential autoantigen in Graves' disease, is similar to the tropomodulin (Tmod) f

89 n's disease, and thyroid follicular cells in Graves' disease (GD).

90 ment of dysthyroid optic neuropathy (DON) in Graves' orbitopathy (GO).

91 The mean ADC value of the thyroid gland in Graves' disease was 2.03+/-0.28x10(-3) mm(2)/sec, and in

92 to localized overproduction of hyaluronan in Graves disease.

93 les are more distal than those identified in Graves' disease and are in LD with Graves' disease prote

94 thyroid function and is targeted by IgGs in Graves' disease (GD-IgG).

95 genes is homologous to a gene implicated in Graves' disease and it, ANT2 and two others are confirme

96 Appearances of and increases in Graves' ophthalmopathy (GO) have been reported after tre

97 chanistic framework for molecular mimicry in Graves' disease, where early precursor B cells are expan

98 ve involvement of the extraocular muscles in Graves' ophthalmopathy, the absence of N-CAM expression

99 lasts or fat accumulation, such as occurs in Graves' ophthalmopathy, tissue fibrosis, abnormal wound

100 r immune responses localized to the orbit in Graves' disease.

101 Because of the low remission rate in Graves' disease and the inability to cure toxic nodular

102 fibroblasts orchestrate tissue remodeling in Graves disease, at least in part, because they exhibit e

103 imulating TSHR autoantibodies (TSHR-Ab's) in Graves disease patients may provide a functional explana

104 the basis for the immunologic attack seen in Graves ophthalmopathy.

105 e TSHR on the functional response to TSAb in Graves' patients' sera.

106 The major AITDs include Graves disease (GD) and Hashimoto's thyroiditis (HT); al

107 Autoimmune thyroid disease (AITD), including Graves' disease (GD) and Hashimoto's thyroiditis (HT), i

108 The most frequent cause is Graves' disease (autoimmune hyperthyroidism).

109 The most common cause of hyperthyroidism is Graves' disease, followed by toxic nodular goitre.

110 The most common cause of this syndrome is Graves' disease, followed by toxic multinodular goitre,

111 ype 1 diabetes, rheumatoid arthritis, lupus, Graves thyroiditis, Addison disease and other autoimmune

112 This single autoantigenic target makes Graves' disease a prime candidate for Ag-specific immuno

113 ode a protein with homology to the mammalian Graves' disease carrier proteins.

114 overed, paired and differentiated meteorites Graves Nunatak (GRA) 06128 and GRA 06129.

115 Microsomes from normal, Graves', and TSH-stimulated thyroids contained low Km D2

116 cosis (OR = 0.76, p = 1.5 x 10(-3)), but not Graves disease (OR = 1.03, p = 0.82).

117 unction (10 cases of hypothyroidism and 1 of Graves disease) developed in 11 of 19 (57.9%) of the DS

118 e receptor (TSHR), is the primary antigen of Graves disease.

119 mulating autoantibodies (TSAb), the cause of Graves' disease, interact with this region of the TSHR i

120 he thyrotropin receptor (TSHR), the cause of Graves' hyperthyroidism, only develop in humans.

121 for those undergoing the orbital changes of Graves' ophthalmopathy is often challenging, even as our

122 halmopathy (TAO), an autoimmune component of Graves' disease, is associated with profound connective

123 The etiology of Graves disease is multifactorial, with nongenetic factor

124 and provide new insight into the etiology of Graves disease.

125 iagnosis, pathogenesis, and immunotherapy of Graves' disease.

126 Similarly, the majority of Graves' disease patients develop improved function over

127 Management of Graves disease includes treatment with antithyroid drugs

128 The surgical management of Graves ophthalmopathy includes treatment of globe malpos

129 s a common and debilitating manifestation of Graves disease (GD).

130 athy are connective tissue manifestations of Graves' disease (GD).

131 e link between the orbital manifestations of Graves' disease and those in the pretibial skin, localiz

132 se a new adenovirus-mediated animal model of Graves disease to show that goiter and hyperthyroidism o

133 ween induced and spontaneous mouse models of Graves' disease with implications for potential immunoth

134 y a role in the etiology and pathobiology of Graves' ophthalmopathy and/or other ocular myopathies.

135 tions for new studies on the pathogenesis of Graves' disease.

136 of molecular mimicry in the pathogenesis of Graves' disease.

137 understanding the molecular pathogenesis of Graves' disease.

138 A prolonged course leads to remission of Graves' hyperthyroidism in about a third of cases.

139 In an important study of Graves hyperthyroidism, treatment with radioactive iodin

140 contributing to the relative T3 toxicosis of Graves' disease.

141 patients who have a history of treatment of Graves disease, a subgroup that is not a target of scree

142 e the preferred therapy for the treatment of Graves' disease during pregnancy.

143 The classic clinical triad of Graves' disease is hyperthyroidism, diffuse goiter, and

144 leading to the clinical findings typical of Graves ophthalmopathy.

145 The presence of bifoveal fusion and/or Graves orbitopathy were risk factors for these adverse o

146 ne thyroid disease (Hashimoto thyroiditis or Graves disease), juvenile RA, inflammatory bowel disease

147 an, hyaluronan, which accumulates in orbital Graves disease.

148 ave relevance to the pathogenesis of orbital Graves disease, an inflammatory autoimmune condition tha

149 py, and is the preferred choice for relapsed Graves' hyperthyroidism.

150 serve this association in the organ-specific Graves' disease or Addison's disease.

151 fic situations, for example, Duane syndrome, Graves' ophthalmopathy, may be particularly problematic.

152 t from PGP, predictions of Gilbert syndrome, Graves' disease, non-Hodgkin lymphoma, and various blood

153 The Graves' Ophthalmopathy Quality of Life (GO-QOL) scale wa

154 ts for the differences in length between the Graves protein (572 residues) and tropomodulin (359 resi

155 homologous repeats in the midsection of the Graves protein, together with the extension of a proline

156 is produces a novel truncated version of the Graves' disease carrier protein-like protein that lacks

157 pared between groups, the mean values of the Graves' patients differed from control at all angles (F

158 Clinical Activity Score, and results on the Graves' ophthalmopathy-specific quality-of-life question

159 ropomodulin has 42 and 41% identity with the Graves protein in the N-terminal (69 residue) and C-term

160 thyroiditis) and autoimmune thyrotoxicosis (Graves' disease).

161 ion and the hyperthyroidism was secondary to Graves' disease.

162 with HLA-DR3 in conferring susceptibility to Graves' disease.

163 elopment of specific ligands useful to treat Graves disease and other dysfunctions of GPHRs.

164 Propylthiouracil (PTU), used to treat Graves' disease, occasionally induces a lupus-like syndr

165 Treating Graves disease with RAI and surgery result in gland dest

166 from a single experimental mouse undergoing Graves' disease, which shared the same H and L chain ger

167 ither of the 2 SNPs recently associated with Graves' disease showed evidence for association in the u

168 opathy, a condition commonly associated with Graves' disease, remains inadequately treated.

169 manifestation most commonly associated with Graves' disease.

170 to the intense inflammation associated with Graves' ophthalmopathy.

171 II-encoded HLA-DRB1-DQA1-DQB1 haplotype with Graves' disease (GD) has been known for several years.

172 tified in Graves' disease and are in LD with Graves' disease protective alleles identified in both of

173 roduced from lymphocytes from a patient with Graves' disease.

174 Patients with Graves disease may be treated with antithyroid drugs, ra

175 ue in both normal patients and patients with Graves disease), together with the humoral factors prese

176 actors present in the serum of patients with Graves disease, forms the basis for the immunologic atta

177 was a retrospective review of patients with Graves ophthalmopathy undergoing lower eyelid retraction

178 ent of lower lid retraction in patients with Graves ophthalmopathy.

179 eported recently that IgG from patients with Graves' disease (GD) can induce the expression of the CD

180 rbital fibroblasts (GOFB) from patients with Graves' disease (GD), as well as fibrocyte abundance, we

181 cells to human serum from two patients with Graves' disease, but not control sera, led to secretion

182 in thyroidal T3 production in patients with Graves' disease, toxic adenomas, and, perhaps, iodine de

183 unoglobulin G purified from 38 patients with Graves' hyperthyroidism with AF (n=17) or sinus rhythm (

184 When present in patients with Graves' hyperthyroidism, AAbeta1AR and AAM2R facilitate

185 thy (GO) affects 50% to 60% of patients with Graves' hyperthyroidism, resulting in exophthalmos, peri

186 In patients with Graves' upper eyelid retraction, the method demonstrated

187 other patients with thyroiditis and two with Graves' disease recognized only the whole 589-633 fragme

188 are the primary therapy, but some women with Graves disease opt to receive definitive therapy with RA