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Division of Nuclear Medicine, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Saint Louis, Missouri, USA
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consisted of physical examination and laboratory studies, including thyroid-stimulating hormone (TSH), triiodothyronine and free thyroxine for all patients, with the addition of thyroglobulin levels in the latter years of the study. Table 1 Patient
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of the presence of circulating autoantibodies such as thyrotropin receptor autoantibodies (TRAb), thyroid peroxidase autoantibodies (TPOAb) and thyroglobulin autoantibodies (TGAb). TRAb occurs predominantly in GD and plays a key role in Graves
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark
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Department of Medicine, Holbæk Hospital, Holbæk, Denmark
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Institute of Clinical Research, University of Southern Denmark, Odense, Denmark
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of thyroiditis. Some authors suggested that higher LH levels in PCOS could stimulate thyroid growth and increase the risk of goiter ( 11 ), but data from small clinical studies were conflicting ( 12 , 13 ). In our recent register-based study, Danish
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increased levels of free thyroid hormones and reduced levels of thyroid-stimulating hormone (TSH), GD is characterized by elevated serum thyrotropin receptor antibodies (TRAb) and anti-thyroid peroxidase antibodies (TPOAb). In the 1990s, multiple studies
School of Medicine, Ningbo University, Ningbo, China
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School of Medicine, Ningbo University, Ningbo, China
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School of Medicine, Ningbo University, Ningbo, China
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between THs and MetS in the euthyroid population is still controversial. A survey of 20,053 euthyroid Korean adults found that neither serum thyroid stimulating hormone (TSH) nor free thyroxine (FT4) was significantly associated with MetS ( 6 ). Mehran et
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surface of stimulated T cells (in the thymus, lymph nodes and spleen), B cells (spleen) and myeloid cells ( 2 ). In 1998, Nishimura et al . found that PD-1 is involved in the negative regulation of particular aspects of B cell proliferation and
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National and Kapodistrian University of Athens Medical School, ‘Aghia Sophia’ Children’s Hospital, Athens, Greece
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genetic causes of dyshormonogenesis include mutations in thyroglobulin (TG), thyroperoxidase (TPO), dual oxidase 2 (DUOX2) and its accessory protein (DUOXA2), the sodium-iodide symporter (SLC5A5), pendrin (SLC26A4), and iodotyrosine deiodinase ( 22
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in female mice ( 136 ). In vitro assays have confirmed TCS to act as an estrogen agonist using ERα and ERβ reporter gene assays ( 137 , 138 , 139 ) stimulate breast and ovarian cancer cell growth in vitro ( 140 , 141 ) and magnifying the