337 resultados para Campos de Carvalho
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Pós-graduação em Odontologia Restauradora - ICT
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Pós-graduação em Odontologia Restauradora - ICT
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Human salivary gland tumors originated from intercalated ducts present a broad range of histologic and cytologic patterns, mainly due to the presence of myoepithelial cells. The aim of this study is to verify the differentiation grade of neoplastic cells and a possible relation between myoepithelial cell differentiation and the presence of luminal secretory contents. The expression of vimentin and cytokeratin (CK) intermediate filaments, actin myofilament and epithelial membrane antigen (EMA) was investigated by double labeling immunocytochemical technique, in thirty salivary gland neoplasms: 5 pleomorphic adenomas, 5 myoepitheliomas, 3 basal cell adenomas, 7 adenoid cystic carcinomas (ACC) and 10 polimorphous low grade adenocarcinomas (PLGA). Tumors with intercalated duct differentiation (pleomorphic adenomas, basal cell adenomas and ACC) express CKs 7, 8, 18 and 19 in the luminal cells and coexpress eventually CK14 with these CKs. Some luminal cells stained with anti-EMA antibody, mainly where a secretory content in the lumen was observed. Outer ductal cells and other myoepithelial-like cells express vimentin, sometimes coexpressing actin and/or CK14 with vimentin. Plasmacytoid cells in myoepitheliomas and pleomorphic adenomas express vimentin and rarely CKs 7, 8, 18 and 19, sometimes coexpressing these CKs with CK14 but they are negative for the remaining antigens. Tumors without intercalated duct differentiation (solid basal cell adenoma and PLGA) express vimentin and CKs 7, 8, 14 and 18, sometimes coexpressing CKs 8 and 18 with CK14. In conclusion, in tumors with intercalated duct differentiation, myoepithelial cells express vimentin and sometimes coexpress actin and/or CK14 with vimentin, never coexpressing other CKs with vimentin. CK14 and actin are independently expressed by myoepithelial cells, so their expression is probably induced by different stimulus. However, the secretory function of luminal cells, visualized by EMA staining, ....
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Pós-graduação em Ciência e Tecnologia de Materiais - FC
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Pós-graduação em Física - FEG
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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trans,trans-2,4-Decadienal (DDE) is an important breakdown product of lipid peroxidation. This aldehyde is cytotoxic to mammalian cells and is known to be implicated in DNA damage. Therefore, attempts were made in this work to assess the reactivity of DDE with 2'-deoxyadenosine (dAdo). It was shown that DDE is able to bind to 2'-deoxyadenosine, yielding highly fluorescent products. Besides 1,N-6-etheno-2'-deoxyadenosine (epsilon dAdo), two other related adducts, 1-[3-(2-deoxy-beta-D-erythro-pentofuranosyl)3H-imidazo[2,1-i]purin-7-yl]-1,2,3-octanetriol and 1-[3-(2-deoxy-beta-D-erythro-pentofuranosyl)-3H-imidazo[2,1-i]purin-7-yl]-1,2-heptanediol, were isolated by reverse phase high-performance liquid chromatography and characterized on the basis of their UV, fluorescence, nuclear magnetic resonance, and mass spectrometry features. The reaction mechanism for the formation of the DDE-2'-deoxyadenosine adducts involves 2,4-decadienal epoxidation and subsequent addition to the N-2 amino group of 2'-deoxyadenosine, followed by cyclization at the N-1 site. Adducts differ by the length of carbon side chain and the number of hydroxyl groups. The present data indicate that DDE can be epoxidized by peroxides, and the resulting products are able to form several adducts with 2'-deoxyadenosine and/or DNA. Endogenous DNA adduct formation can contribute to the already reported high cytotoxicity of DDE to mammalian cells.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Hepatic encephalopathy (HE) is a cognitive disturbance characterized by neuropsychiatric alterations. It occurs in acute and chronic hepatic disease and also in patients with portosystemic shunts. The presence of these portosystemic shunts allows the passage of nitrogenous substances from the intestines through systemic veins without liver depuration. Therefore, the embolization of these shunts has been performed to control HE manifestations, but the presence of portal vein thrombosis is considered a contraindication. In this presentation we show a cirrhotic patient with severe HE and portal vein thrombosis who was submitted to embolization of a large portosystemic shunt. Case report: a 57 years-old cirrhotic patient who had been hospitalized many times for persistent HE and hepatic coma, even without precipitant factors. She had a wide portosystemic shunt and also portal vein thrombosis. The abdominal angiography confirmed the splenorenal shunt and showed other shunts. The larger shunt was embolized through placement of microcoils, and the patient had no recurrence of overt HE. There was a little increase of esophageal and gastric varices, but no endoscopic treatment was needed. Since portosystemic shunts are frequent causes of recurrent HE in cirrhotic patients, portal vein thrombosis should be considered a relative contraindication to perform a shunt embolization. However, in particular cases with many shunts and severe HE, we found that one of these shunts can be safely embolized and this procedure can be sufficient to obtain a good HE recovery. In conclusion, we reported a case of persistent HE due to a wide portosystemic shunt associated with portal vein thrombosis. As the patient had other shunts, she was successfully treated by embolization of the larger shunt. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)