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Massimo Tonacchera

Researcher at University of Pisa

Publications -  171
Citations -  5632

Massimo Tonacchera is an academic researcher from University of Pisa. The author has contributed to research in topics: Thyroid & Receptor. The author has an hindex of 42, co-authored 160 publications receiving 5230 citations. Previous affiliations of Massimo Tonacchera include Université libre de Bruxelles & University of Calabria.

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Relative potencies and additivity of perchlorate, thiocyanate, nitrate, and iodide on the inhibition of radioactive iodide uptake by the human sodium iodide symporter.

TL;DR: Results are consistent with a common mode of action by these anions of simple competitive interaction, in which a concentration of any one of ClO(4) (-) SCN(-), and NO(3) (-), occurring either individually or as part of a mixture of the three anions, is indistinguishable from a concentration or dilution of either of the remaining two ions in inhibiting iodine uptake at the NIS.
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Somatic mutations causing constitutive activity of the thyrotropin receptor are the major cause of hyperfunctioning thyroid adenomas: identification of additional mutations activating both the cyclic adenosine 3',5'-monophosphate and inositol phosphate-Ca2+ cascades.

TL;DR: The results demonstrate that 1) the first and second extracellular loops contribute to the silencing of the unliganded TSH receptor; 2) the two regulatory cascades normally under TSH control can be constitutively activated by somatic mutations of the receptor.
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Somatic and germline mutations of the TSH receptor gene in thyroid diseases.

TL;DR: The present review will summarize recent findings identifying mutations of the TSH receptor gene as a cause for thyroid diseases.
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Expression of IP-10/CXCL10 and MIG/CXCL9 in the thyroid and increased levels of IP-10/CXCL10 in the serum of patients with recent-onset Graves' disease.

TL;DR: The results of this study demonstrate that the CXCR3-binding chemokines IP-10/CXCL10 and Mig/CxCL9 play an important role in the recruitment of cells and in the amplification of inflammation in Graves' disease, and suggest that the production of these chemokine by resident follicular epithelial cells may contribute to the recruited CX CR3-expressing type 1 T-helper cells in the initial phases of GD.
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Functional characteristics of three new germline mutations of the thyrotropin receptor gene causing autosomal dominant toxic thyroid hyperplasia.

TL;DR: The differential effects of individual mutations on stimulation by bTSH of cAMP or IP accumulation suggest that individual mutant receptors may achieve different active conformations with selective abilities to couple to Gs alpha and to Gq alpha.