ライフサイエンスコーパス: Graves' disease

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