1,721,154 research outputs found
Endemic goiter: clinical picture and evolution
No full textThe goiter is the most frequent clinical manifestation of the nutritional deficiency of iodine. If present in more than 5% of the general population or more than 10% of the children in school of a defined geographic area, goiter is defined endemic. Endemic goiter is an adaptive disease produced by the persistent stimulation of the thyroid gland as consequence of the thyrotropin increased secretion due to the iodine deficiency. If iodine deficiency is severe or persistent, other manifestations can be observed in the clinical picture of the iodine deficiency disorders (IDD), such as cretinism. In general goiter is not associated to other manifestations during the initial state of the disease, but nodular and toxic evolution are frequent complication of long standing disease
Loss of polarity and de novo expression of the beta 1 family of integrins in thyroid tumors.
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Novel motations of thyrotropin receptor gene in thyroid hyperfunctioning adenomas. Rapid identification by fine needle aspiration biopsy.
No full textRapporto tra variabili antropometriche, androgeni e complicanze dell’obesità nel sesso femminile
No full textRole of the adenylate cyclase-cAMP system on TSH-stimulated thyroid cell growth
No full text: TSH is a trophic factor for cultured rat thyroid cells (FRTL-5). In the present study we have investigated the mechanism by which TSH promotes cell growth and evaluated the possible role of the adenylate cyclase (AC)-cAMP system in this process. The mitogenic activity of several agents was evaluated by measuring their effect on cell number or 3H-thymidine incorporation into DNA. Forskolin and cholera toxin, two potent and specific activators of the AC, induced a dose dependent increase of 3H-thymidine incorporation. The maximal stimulation, observed at concentrations of 10 microM and 10 ng/ml, respectively, was beta 80% of that obtained with optimal concentrations of TSH. A similar effect was obtained with a Graves' IgG preparation (0.2 mg/ml) able to stimulate the thyroid AC or with 3-isobutyl-1-methyl-xanthine (IBMX, 0.5 mM), a phosphodiesterase inhibitor. 8-bromo cAMP (0.5 mM), a cAMP analog, also stimulated 3H-thymidine incorporation, and its potency was approximately 60% of that of TSH. Similar results were obtained when the mitogenic activity of these compounds was evaluated by cell number. Norepinephrine (NE, 10 microM), although devoid of AC stimulatory activity in these cells, also stimulated 3H-thymidine incorporation, but its potency was only 20-30% of that of TSH. Indomethacin (100 microM), an inhibitor of phospholipid and arachidonic acid metabolism, was able to inhibit the stimulatory effect of NE (84%), and to a lesser extent of TSH (63%) and cholera toxin, had minor effect on forskolin (24%), IBMX (16%) and Graves' IgG (8%), and no effect on 8-bromo cAMP.(ABSTRACT TRUNCATED AT 250 WORDS
Cell-to-cell contact modulates the expression of the beta 1 family of integrins in primary cultures of thyroid cells.
No full textThe expression of the beta(1) family of integrins was studied in normal thyroid tissue cultures and monolayer cell cultures. The expression of the various subunits was measured by how cytofluorometry with specific monoclonal antibodies and by Northern analysis. In monolayer cell cultures but not in tissue cultures, the expression of the alpha(3) subunit on the cell membrane progressively increased soon after plating, reaching a 30-fold higher intensity. The alpha(2) subunit, not detectable in native follicular cells, was expressed de novo and reached a remarkable high level. Up-regulation of alpha(2) and alpha(3) in monolayer cell cultures was serum-independent and preceded the expression of proliferating cell nuclear antigen, [H-3]thymidine incorporation, and cell replication, Northern analysis demonstrated an increased level of beta(1) integrin mRNA. The increase of alpha(2) and alpha(3) was readily reversible since the expression of these molecules returned to a lower level when cultures reached a high cell density. Down-regulation did not occur until cell cultures were confluent. When cells from high cell density and low integrin expression were harvested and sparsely seeded in culture, up-regulation of integrins was observed again, while rapid reaggregation of isolated cells inhibited this phenomenon. Altogether these data suggest that cell-to-cell contact may regulate the expression of beta(1) integrins in thyroid primary cultures
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