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524 results on '"FENZI G"'

54. Endemic goiter and iodine deficiency diffusion in province of Avellino

Author

Pagliara S., Spagnuolo E., D'Avanzo A., Vitale M., Macchia P. E., Salvatore D., Ramundo V., Ciasullo M., Macchia V., Fenzi G., Pagliara, S., Spagnuolo, E., D'Avanzo, A., Vitale, M., Macchia, P. E., Salvatore, D., Ramundo, V., Ciasullo, M., Macchia, V., and Fenzi, G.

Subjects
Thyroid, Urinary iodine excretion, Endemic goiter, Thyroid echography, Iodine deficiency
Abstract

1352 schoolchildren between 6-14 years old (699 males and 653 females) and 943 adults (176 males and 767 females) from eight villages of the province of Avellino were studied. All subjects were examined for thyroid size by at least two expert examiners. In most of them urine samples were collected for iodine determinations. 387 schoolchildren and 161 adults from Flumeri and Villanova were evaluated by thyroid echography. The prevalence of goiter was from 23.5 to 52.2% and the median urinary iodine excretion was from 42.3 to 66.2 μg/l in schoolchildren. In adults the prevalence of goiter was from 41.2 to 86.7% and the median urinary iodine excretion was from 37.1 to 53.7 μg/l. Our data showed a degree of iodine deficiency from low to moderate. The echography permitted to point out a greater prevalence of nodules than the thyroid palpation.

Published
1998

61. TSH-receptor antibodies

Author

Vitti, P., primary, Fenzi, G. F., additional, Chiovato, L., additional, Marcocci, C., additional, and Pinchera, A., additional

Published
1987
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82. APPROCCIO CLINICO AL PAZIENTE CON GOZZO

Author

FENZI G., VITALE M., BASSI V., DE RIU S., SALVATORE, DOMENICO, ILLARIO, MADDALENA, MACCHIA, PAOLO EMIDIO, Fenzi, G., Salvatore, Domenico, Illario, Maddalena, Vitale, M., Bassi, V., Macchia, PAOLO EMIDIO, and DE RIU, S.

Published
1991

83. Increased in vivo phosphorylation of ret tyrosine 1062 is a potential pathogenic mechanism of multiple endocrine neoplasia type 2B

Author

Salvatore D, Melillo RM, Monaco C, Visconti R, Fenzi G, Vecchio G, Fusco A, and Santoro M

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, endocrine system, endocrine system diseases, neoplasms
Abstract

Mutations of the Ret receptor tyrosine kinase are responsible for inheritance of multiple endocrine neoplasia (MEN2A and MEN2B) and familial medullary thyroid carcinoma syndromes. Although several familial medullary thyroid carcinoma and most MEN2A mutations involve substitutions of extracellular cysteine residues, in most MEN2B cases there is a methionine-to-threonine substitution at position 918 (M918T) of the Ret kinase domain. The mechanism by which the MEN2B mutation converts Ret into a potent oncogene is poorly understood. Both MEN2A and MEN2B oncoproteins exert constitutive activation of the kinase. However, the highly aggressive MEN2B phenotype is not supported by higher levels of Ret-MEN2B kinase activity compared with Ret-MEN2A. It has been proposed that Ret-MEN2B is more than just an activated Ret kinase and that the M918T mutation, by targeting the kinase domain of Ret, might alter Ret substrate specificity, thus affecting Ret autophosphorylation sites and the ability of Ret to phosphorylate intracellular substrates. We show that the Ret-MEN2B mutation causes specific potentiated phosphorylation of tyrosine 1062 (Y1062) compared with Ret-MEN2A. Phosphorylated Y1062 is part of a Ret multiple effector docking site that mediates recruitment of the Shc adapter and of phosphatidylinositol-3 kinase (PI3K). Accordingly, we show that Ret-MEN2B is more active than Ret-MEN2A in associating with She and in causing constitutive activation of the Ras/mitogen-activated protein kinase and PI3K/Akt cascades. We conclude that the MEN2B mutation specifically potentiates the ability of Ret to autophosphorylate Y1062 and consequently to couple to the Ras/mitogen-activated protein kinase and the PI3K/Akt pathways. The more efficient triggering of these pathways may account for the difference between MEN2A and MEN2B syndromes.

Published
2001

90. Laminin receptors in differentiated thyroid tumors: restricted expression of the 67-kilodalton laminin receptor in follicular carcinoma cells

Author

Nunzia Montuori, Müller, F., Riu, S., Fenzi, G., Sobel, M. E., Rossi, G., Vitale, M., Montuori, Nunzia, Müeller, F, DE RIU, S, Fenzi, Gianfranco, Sobel, Me, Rossi, Guido, and Vitale, Mario

Subjects
INVASION, Blotting, Western, Thyroid Gland, Biotin, BINDING PROTEIN, Flow Cytometry, Precipitin Tests, PLATELETS, ACYLATION, ATTACHMENT, Receptors, Laminin, ALPHA-6-BETA-1, METASTASIS, Adenocarcinoma, Follicular, Cell Adhesion, Tumor Cells, Cultured, Humans, Laminin, Thyroid Neoplasms, CANCER-CELLS, Protein Precursors, INTEGRIN EXPRESSION, PRECURSOR
Abstract

The expression of integrin laminin receptors was investigated in normal thyroid primary cultures; immortalized normal thyroid cells (TAD-2); papillary (NPA), follicular (WRO), and anaplastic (ARO) thyroid tumor cell lines; seven thyroid tumors (four papillary and three follicular carcinomas); and normal thyroid glands. The expression of alpha1beta1, alpha2beta1, alpha3beta1, alpha6beta1, and alpha6beta4 was found in all tumor specimens and in tumor cell lines, whereas normal thyroid cells and TAD-2 cells lacked the expression of alpha6beta4. Despite the presence of several integrin laminin receptors, adhesion of TAD-2, NPA, and ARO cells to immobilized laminin-1 was poor, whereas WRO cells and follicular carcinoma-derived cells displayed a strong adhesion. Indeed, WRO and follicular carcinoma-derived cells showed expression of a nonintegrin laminin receptor, the 67-kDa high affinity laminin receptor (67LR). TAD-2, NPA, and ARO cells as well as nodular goiter, toxic adenoma, follicular adenoma, and papillary carcinoma-derived cells did not express the 67LR. Adhesion of WRO and follicular carcinoma-derived cells to laminin-1 was specifically inhibited by a recombinant polypeptide containing laminin-binding domains of 67LR, demonstrating that this receptor confers to follicular carcinoma cells attachment capacity to laminin. Moreover, tissue specimens from follicular carcinomas expressed the 67LR, whereas follicular adenomas and normal thyroid tissues were negative. In thyroid tumors, integrin receptors, although abundant, participate weakly in adhesion to laminin. The expression in follicular carcinoma cells of a functional, high affinity 67LR together with nonfunctional integrin LM receptors could be responsible for the tendency of follicular carcinoma cells to metastasize by mediating stable contacts with basal membranes.

Published
1999

94. Sediment features, macrozoobenthic assemblages and trophic relationships (d13C and d15N analysis) following a dystrophic event with anoxia and sulphide development in the Santa Giusta lagoon (western Sardinia, Italy)

Author

Magni, P., Rajagopal, S., Velde, G. van der, Fenzi, G., Kassenberg, J., Vizzini, S., Mazzola, A., Giordani, G., Magni, P., Rajagopal, S., Velde, G. van der, Fenzi, G., Kassenberg, J., Vizzini, S., Mazzola, A., and Giordani, G.

Abstract

Contains fulltext : 72606.pdf (publisher's version ) (Closed access)

Published
2008

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