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1 h nodes might prevent missing a diagnosis of autoimmune thyroiditis.
2               Hashimoto disease is a chronic autoimmune thyroiditis.
3 two cases of hyperthyroidism consistent with autoimmune thyroiditis.
4 production, and amelioration of experimental autoimmune thyroiditis.
5 ier resolution of granulomatous experimental autoimmune thyroiditis.
6 e identification of susceptibility genes for autoimmune thyroiditis.
7 ical investigation that have been applied to autoimmune thyroiditis.
8 ptide binding and presentation to T-cells in autoimmune thyroiditis.
9 orts a disease-limiting role of IFN-gamma in autoimmune thyroiditis.
10  were highly correlated with the progress of autoimmune thyroiditis.
11 ma in the thyroid dysfunction that occurs in autoimmune thyroiditis.
12 also recognized by the sera of patients with autoimmune thyroiditis.
13 ted with type 1 diabetes: celiac disease and autoimmune thyroiditis.
14 79 cases of celiac disease and 1000 cases of autoimmune thyroiditis.
15 ased or decreased risk for celiac disease or autoimmune thyroiditis.
16 ndrome (1% vs. 1%), sarcoidosis (1% vs. 1%), autoimmune thyroiditis (1% vs. 0%), type 1 diabetes (1%
17 f patients showed autoimmune disorders, i.e. autoimmune thyroiditis (26.3%), dermatitis herpetiformis
18 of coexistence of rheumatoid arthritis (RA), autoimmune thyroiditis (AIT), multiple sclerosis (MS), a
19 analysis of hypothyroidism, hyperthyroidism, autoimmune thyroiditis (AIT), serum concentrations of th
20 e co-occurrence of type 1 diabetes (T1D) and autoimmune thyroiditis (AITD).
21 B1 polymorphism determines susceptibility to autoimmune thyroiditis and implicate Tg as an important
22 tive was to evaluate the association between autoimmune thyroiditis and the Delphian lymph node durin
23 t was found that SjD patients diagnosed with autoimmune thyroiditis and/or hypothyroidism were signif
24 ythematosus, 2 had multiple sclerosis, 2 had autoimmune thyroiditis, and 7 had other conditions.
25 ncluding chronic inducible urticaria (>10%), autoimmune thyroiditis (approximately 20%), metabolic sy
26 how that the regulatory T cells that prevent autoimmune thyroiditis are generated in vivo only when t
27 ease of the Tg-cleaving activity in IgG from autoimmune thyroiditis (ATh) and systemic lupus erythema
28          Further diagnostic work-up revealed autoimmune thyroiditis, but no signs of inflammatory bow
29             Previous studies have shown that autoimmune thyroiditis can be induced in normal laborato
30 hrenia (SCZ)) and seven autoimmune diseases (autoimmune thyroiditis, celiac disease, inflammatory bow
31 with the publication of a paper showing that autoimmune thyroiditis could be induced in animals.
32  dominant peptide when inducing experimental autoimmune thyroiditis (EAT) in NOD mice expressing huma
33 ence of anti-B7.2 had decreased experimental autoimmune thyroiditis (EAT) severity compared with reci
34 -transgenic model (A(-)E(+)) of experimental autoimmune thyroiditis (EAT) that permits disease induct
35  responses to rat neu and mTg with resultant autoimmune thyroiditis (EAT) were both enhanced.
36                                 Experimental autoimmune thyroiditis (EAT) with granulomatous histopat
37 logous to HLA-DR) predispose to experimental autoimmune thyroiditis (EAT), a classical mouse model of
38       On the other hand, murine experimental autoimmune thyroiditis (EAT), a model for HT, presents a
39 he development of granulomatous experimental autoimmune thyroiditis (EAT), DBA1 mice with a disrupted
40  can prevent the development of experimental autoimmune thyroiditis (EAT), experimental autoimmune my
41 in development of granulomatous experimental autoimmune thyroiditis (EAT), IL-4 gene-disrupted mice e
42 autoimmune diseases, as well as experimental autoimmune thyroiditis (EAT).
43  prevent, but also to suppress, experimental autoimmune thyroiditis (EAT).
44 ted resolution of granulomatous experimental autoimmune thyroiditis (G-EAT) at least in part through
45                   Granulomatous experimental autoimmune thyroiditis (G-EAT) is induced by mouse thyro
46                   Granulomatous experimental autoimmune thyroiditis (G-EAT) is induced by mouse thyro
47                   Granulomatous experimental autoimmune thyroiditis (G-EAT) is induced by mouse thyro
48              When granulomatous experimental autoimmune thyroiditis (G-EAT) was induced in CBA/J or D
49 es, resolution of granulomatous experimental autoimmune thyroiditis (G-EAT) was promoted when thyroid
50 a murine model of granulomatous experimental autoimmune thyroiditis (G-EAT) was used to determine the
51 cal studies have linked an increased risk of autoimmune thyroiditis, Graves disease and goitre to low
52 st common cause of hypothyroidism is chronic autoimmune thyroiditis (Hashimoto's thyroiditis), althou
53  of the humoral autoimmune response in human autoimmune thyroiditis (Hashimoto's thyroiditis).
54 ium supplementation in patients with chronic autoimmune thyroiditis have generally resulted in reduce
55 e investigated their effects on experimental autoimmune thyroiditis in CBA/J mice.
56 associated with a modestly increased risk of autoimmune thyroiditis in infancy analysis.
57 ncy but is more frequently caused by chronic autoimmune thyroiditis in iodine-replete areas.
58  of thyroid follicular cells in experimental autoimmune thyroiditis, in a manner similar to what is o
59                                 Experimental autoimmune thyroiditis, induced in mice after challenge
60 te the incidence and severity of spontaneous autoimmune thyroiditis [iodide-accelerated spontaneous a
61 rticularly prevalent in older women, in whom autoimmune thyroiditis is common.
62 usceptibility and resistance to experimental autoimmune thyroiditis is encoded by MHC H2A genes.
63         The results suggest that spontaneous autoimmune thyroiditis is inhibited in mice expressing t
64  of chickens, which suffers from spontaneous autoimmune thyroiditis, is an excellent animal model for
65 water develop iodine-accelerated spontaneous autoimmune thyroiditis (ISAT) with chronic inflammation
66  thyroiditis [iodide-accelerated spontaneous autoimmune thyroiditis (ISAT)] in NOD.H2(h4) mice.
67 s the development of lymphocytic spontaneous autoimmune thyroiditis (L-SAT) in NOD.H-2h4 mice and inh
68 mates, which develop lymphocytic spontaneous autoimmune thyroiditis (L-SAT), all TGF-beta transgenic
69 lin, to which tolerance is typically lost in autoimmune thyroiditis leading to hypothyroidism.
70                    One serious adverse event-autoimmune thyroiditis of grade 2 severity-was reported
71 ) had a prior diagnosis of hypothyroidism or autoimmune thyroiditis, of whom 56 were receiving thyrox
72                     Nineteen were found with autoimmune thyroiditis or hypothyroidism, and replacemen
73  treatable causes and comorbidities, such as autoimmune thyroiditis or infections.
74   WT lymphocytes could transfer experimental autoimmune thyroiditis or L-SAT to Tg mice, indicating t
75 combinatorial Ig-gene libraries derived from autoimmune thyroiditis patients and specific for the mai
76 -defective C3H/gld mice, lupus patients, and autoimmune thyroiditis patients.
77 uding age, family history of thyroid cancer, autoimmune thyroiditis, prior radiation exposure, cancer
78  studies have been published in the field of autoimmune thyroiditis (represented by Graves' disease a
79           NOD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) and anti-mouse thyroglobuli
80 y 100% of NOD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) and produce anti-mouse thyr
81  are required for development of spontaneous autoimmune thyroiditis (SAT) in NOD.H-2h4 mice where the
82                                  Spontaneous autoimmune thyroiditis (SAT) is an organ-specific autoim
83 type (WT) NOD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) when given 0.05% NaI in the
84  of B cells in a murine model of spontaneous autoimmune thyroiditis (SAT), B cells were depleted from
85 the thyroid gland during the early stages of autoimmune thyroiditis suggests a possible effector func
86 stations included atopy, granulomatous rash, autoimmune thyroiditis, the presence of antinuclear anti
87           Both peptides induced experimental autoimmune thyroiditis upon direct challenge of CBA/J mi
88          Importantly, treatment of mice with autoimmune thyroiditis using mouse thyroglobulin (mTg)-p
89                                      Risk of autoimmune thyroiditis was similar by vaccination status
90                      In a humanized model of autoimmune thyroiditis, we investigated the mechanism un