Blood TSH Level in Idjwi Island: Modifications related to regional prevalence of goitre and not to individual thyroidal size and function

info:eu-repo/semantics/publishe

Relationship between the serum thyrotropin level, the prevalence of goiter and the pattern of iodine metabolism in Idjwi Island.

Radioimmunoassay of serum thyrotropin was performed in 185 patients, 4-30 yr old, living in Brussels (control group), in the nongoitrous (southwest) and in the goitrous (north) areas of Idjwi Island (Dem. Rep. of the Congo). Both these regions in Idjwi Island have a severe and quite similar iodine deficiency. The serum TSH level was higher in the inhabitants of Idjwi Island than in the Belgian controls; it was still higher in the goitrous area (in both goitrous and nongoitrous subjects) than in the nongoitrous area. No difference was observed in the 3 areas as a function of age, size of the thyroid, or its nodularity. There was a significant correlation between the TSH level and the plasma [l27I]PBI in the goitrous area. There was no correlation between the TSH level, the 6-hr thyroidal radioiodine uptake, the [125I]PBI estimated at the time of equilibrium in isotopic distribution and the organic exchangeable iodine pool of the thyroid in all 3 areas. The results observed in southwest Idjwi show that the human thyroid is capable of adapting itself adequately to a very severe iodine deficiency under the influence of an increased thyrotropic stimulation without clinical evidence of thyroidal hyperplasia. The higher serum TSH level observed in north Idjwi suggests that thyrotropic hyperstimulation is responsible for endemic goiter in Idjwi Island. In this island, the serum TSH level seems to be more closely related to the geographic environment than to the age of the subjects or the individual size of the thyroid. © 1971 by The Endocrine Society.SCOPUS: ar.jSCOPUS: ar.jinfo:eu-repo/semantics/publishe

Regulation of p27Kip1 protein levels contributes to mitogenic effects of the RET/PTC kinase in thyroid carcinoma cells.

We show that treatment of a panel of thyroid carcinoma cell lines naturally harboring the RET/PTC1 oncogene, with the RET kinase inhibitors PP1 and ZD6474, results in reversible G(1) arrest. This is accompanied by interruption of Shc and mitogen-activated protein kinase (MAPK) phosphorylation, reduced levels of G(1) cyclins, and increased levels of the cyclin-dependent kinase inhibitor p27Kip1 because of a reduced protein turnover. MAP/extracellular signal-regulated kinase 1/2 inhibition by U0126 caused G(1) cyclins down-regulation and p27Kip1 up-regulation as well. Forced expression of RET/PTC in normal thyroid follicular cells caused a MAPK- and proteasome-dependent down-regulation of p27Kip1. Reduction of p27Kip1 protein levels by antisense oligonucleotides abrogated the G(1) arrest induced by RET/PTC blockade. Therefore, in thyroid cancer, RET/PTC-mediated MAPK activation contributes to p27Kip1 deregulation. This pathway is implicated in cell cycle progression and in response to small molecule kinase inhibitors