102,611 research outputs found

    Anaerobic digestion as a means of energy regeneration in sewage purification plant "Città di Verona"

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    In the article we report the results achieved in energy recovery at Verona wastewater treatmont plant. Such recovery is obtained through sludge anaerobic digestion and use of biogas in a cogeneration station (two groups, 500 kW of electric power and 700 kw of thermic power each). In 1985 20 million cubic meters of sewage were processed, 10,000 tons of dewatered sludge 23% were obtained, producing 4,200-4,500 m^3/day of biogas with an average methane concentration of 70%, 7,200-7,500 kwh/day of electric energy were produced. Average specific biogas production was 17-22 l/people x day. These values allowed a saving of 45% in electric energy used by utilities of wastewater treatment plant in 1985. Each kwh produced costed L 18. Owing to the good results obtained in sludge processing, we are now considering the possibility to dispose of organic fraction of MSW through the same biologica process. Therefore it follows that reutilization of power within municipal service permits the best economic exploitation and a high profitability of investments

    Endemic goiter: clinical picture and evolution

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    The 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

    The different cardiac expression of the type 2 iodothyronine deiodinase gene between human and rat is related to the differential response of the Dio2 genes to Nkx-2.5 and GATA-4 transcription factors.

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    By producing T3 from T4, type 2 iodothyronine deiodinase (D2) catalyzes the first step in the cascade underlying the effect exerted by thyroid hormone. Type 2 iodothyronine deiodinase mRNA is expressed at high levels in human heart but is barely detectable in the corresponding rodent tissue. Although the heart is a major target of thyroid hormone, the role of cardiac D2 and the factors that regulate its expression are unknown. Here we report that the human Dio2 promoter is very sensitive to the cardiac transcription factors Nkx-2.5 and GATA-4. Nkx-2.5 transactivates a 6.5-kb human (h)Dio2-chloramphenicol acetyltransferase construct, with maximal induction reached with a 633-bp proximal promoter region. Interestingly, despite 73% identity with the corresponding human region, the rat Dio2 promoter is much less responsive to Nkx-2.5 induction. Using EMSA, we found that two sites in the human promoter (C and D) specifically bind Nkx-2.5. In coexpression studies, GATA-4 alone was a poor inducer of the hDio2 promoter; however in synergy with Nkx-2.5, it activated D2 reporter gene expression in the human, but not the rat promoter. Functional analysis showed that both C and D sites are required for the complete Nkx-2.5 response and for the Nkx-2.5/GATA-4 synergistic effect. In neonatal rat primary myocardiocytes, most of the hDio2-chloramphenicol acetyltransferase activity was suppressed by mutation of the Nkx-2.5 binding sites. Finally, a mutant Nkx-2.5 protein (N188K), which causes, in heterozygosity, congenital heart diseases, did not transactivate the Dio2 promoter and interfered with its activity in cardiomyocytes, possibly by titrating endogenous Nkx-2.5 protein away from the promoter. In conclusion, this study shows that Nkx-2.5 and GATA-4 play prime roles in Dio2 gene regulation in the human heart and suggests that it is their synergistic action in humans that causes the differential expression of the cardiac Dio2 gene between humans and rats

    Cell-to-cell contact modulates the expression of the beta 1 family of integrins in primary cultures of thyroid cells.

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    The 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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