Thyrotropin Tsh
Mostrando 13-24 de 139 artigos, teses e dissertações.
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13. Biphasic modulation of insulin receptor substrate-1 during goitrogenesis
Insulin receptor substrate-1 (IRS-1) is the main intracellular substrate for both insulin and insulin-like growth factor I (IGF-I) receptors and is critical for cell mitogenesis. Thyrotropin is able to induce thyroid cell proliferation through the cyclic AMP intracellular cascade; however, the presence of either insulin or IGF-I is required for the mitogenic
Brazilian Journal of Medical and Biological Research. Publicado em: 22/03/2007
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14. PAX8 and rTSH genes involvement in congenital hypothyrodism in patients with thyroid dysgenesis / "Avaliação do envolvimento dos genes PAX8 e rTSH no hipotireoidismo congênito em pacientes com disgenesia tireoidiana"
Estudamos 32 crianças com HC devido à agenesia ou ectopia tireoideana para mutações no PAX8 e 30 crianças com hipoplasia da tireóide para mutações no rTSH. Todos os exons de ambos os genes foram amplificados a partir do DNA genômico, seguido por seqüenciamento direto. Encontramos, em dois pacientes com ectopia, duas alterações no gene PAX8, uma n
Publicado em: 2005
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15. Tratamento do hipertireoidismo na infância e adolescência
A Doença de Graves (DG) é responsável por mais de 90% dos casos de hipertireoidismo em crianças. Na DG, o hipertireoidismo é causado por anticorpos estimuladores dirigidos contra o receptor do TSH, conhecidos como TRAb (TRAb, Thyrotropin Receptor Antibody), que mimetizam os efeitos do TSH. O hipertireoidismo pode, ainda, ser devido a mutações nos gene
Arquivos Brasileiros de Endocrinologia & Metabologia. Publicado em: 2001-02
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16. Effect of medroxyprogesterone acetate on thyrotropin secretion in adult and old female rats
Steroid hormones have been implicated in the modulation of TSH secretion; however, there are few and controversial data regarding the effect of progesterone (Pg) on TSH secretion. Medroxyprogesterone acetate (MPA) is a synthetic alpha-hydroxyprogesterone analog that has been extensively employed in therapeutics for its Pg-like actions, but that also has some
Brazilian Journal of Medical and Biological Research. Publicado em: 2000-09
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17. The human thyrotropin receptor: a heptahelical receptor capable of stimulating members of all four G protein families.
Thyrotropin is the primary hormone that, via one heptahelical receptor, regulates thyroid cell functions such as secretion, specific gene expression, and growth. In human thyroid, thyrotropin receptor activation leads to stimulation of the adenylyl cyclase and phospholipase C cascades. However, the G proteins involved in thyrotropin receptor action have been
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18. Assessment of Thyrotropin-Releasing Hormone and Thyrotropin Reserve in Man
Endogenous thyrotropin-releasing hormone (TRH) reserve and pituitary thyrotropin (TSH) reserve were assessed in four normal subjects, three patients post-cryohypophysectomy, one patient with a hypothalamic lesion secondary to trauma, and four patients with Sheehan's syndrome. TSH reserve was determined by the immunoassayable TSH response to 500 μg TRH given
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19. Inhibition of thyrotropin response to thyrotropin-releasing hormone by small quantities of thyroid hormones
Inhibition of thyrotropin (TSH) release by chronic treatment with small quantities of triiodothyronine (T3) and thyroxine (T4) was evaluated by determining the serum TSH response to thyrotropin-releasing hormone (TRH) in normal subjects and hypothyroid patients. Response to TRH was determined before treatment and after each dosage of a synthetic combination
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20. Thyrotropin-luteinizing hormone/chorionic gonadotropin receptor extracellular domain chimeras as probes for thyrotropin receptor function.
To define the sites in the extracellular domain of the human thyrotropin (TSH) receptor that are involved in TSH binding and signal transduction we constructed chimeric thyrotropin-luteinizing hormone/chorionic gonadotropin (TSH-LH/CG) receptors. The extracellular domain of the human TSH receptor was divided into five regions that were replaced, either singl
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21. A circulating, biologically inactive thyrotropin caused by a mutation in the beta subunit gene.
Mutation of a critical carboxy-terminal cysteine residue (C105V) in the thyrotropin-beta (TSH-beta) subunit gene was found in two related families with central hypothyroidism. Affected patients had low thyroid hormone levels and radioactive iodine uptake in the thyroid gland associated with measurable serum TSH. Thyrotropin-releasing hormone-stimulated TSH s
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22. Thyrotropin-induced hyperthyroidism caused by selective pituitary resistance to thyroid hormone. A new syndrome of "inappropriate secretion of TSH".
An 18-yr-old woman with clinical and laboratory features of hyperthyroidism had persistently elevated serum levels of immunoreative thyrotropin (TSH). During 11 yr of follow-up there had been no evidence of a pituitary tumor. After thyrotropin-releasing hormone (TRH), there was a marked increase in TSH and secondarily in triiodothyronine (T3), the latter obs
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23. Cloning, chromosomal assignment, and regulation of the rat thyrotropin receptor: expression of the gene is regulated by thyrotropin, agents that increase cAMP levels, and thyroid autoantibodies.
A rat thyrotropin (thyroid-stimulating hormone, TSH) receptor cDNA was isolated that encoded a protein of 764 amino acids, Mr 86,528. Transfection of the cDNA caused COS-7 cells to develop a TSH-sensitive adenylate cyclase response and the ability to bind 125I-labeled TSH; both activities were similar to those of rat FRTL-5 thyroid cells and not duplicated b
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24. Use of thyrotropin and cholera toxin to probe the mechanism by which interferon initiates its antiviral activity.
Thyrotropin (10 muM) inhibited the antiviral activity of interferon. When added after interferon, thyrotropin (TSH) had no effect on antiviral activity. There was also no inhibition of interferon action in cells washed with medium between incubations with TSH and interferon. 125I-Labeled TSH and 125I-labeled cholera toxin could bind to preparations of mouse