429 resultados para adrenocortical adenoma
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The Ag-NOR staining technique and image analysis were used to evaluate morphological parameters (area, perimeter and axis ratio) in nucleoli from normal thyroids and from thyroids bearing proliferating lesions (carcinomas, adenomas and hyperplasias). Regions with normal appearance located close to adenomatous and carcinomatous regions, in the thyroid of every patient, were also analyzed for comparison with the respective pathological regions and with normal thyroids. Statistical analysis of data for the nucleolar area and perimeter allowed the separation of adenomas and carcinomas from hyperplasias and normal tissue but not the two components in each of these two groups. However, if we look at the numbers, a sequence of increasing nucleolar mean areas in the order: normal, hyperplasia, adenoma and carcinoma may be observed, indicating the sequence of increasing rRNA requirements in these different kinds of cells. The axis ratio that denotes the nucleolar shape (round or oblong) did not show significant differences among tissues, suggesting that shape is not important in the characterization of these pathologies. Differences in nucleolar areas and perimeter between normal and affected regions from each patient were statistically significant for adenomas and carcinomas. When these normal regions were compared with the normal thyroids, significant differences were not obtained in the three evaluated parameters. The observations and their importance for histopathological diagnosis are discussed.
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Purpose: to investigate if combining VT to DGR through the pylorus can modulate the biological behavior of PL induced by DGR and to verify if TV alone can induce morphologic lesions in the gastric mucosa. Methods: 62 male Wistar rats were assigned to four groups: 1 - Control (CT) gastrotomy; 2 - Troncular Vagotomy (TV) plus gastrotomy; 3 - Duodenogastric reflux through the pylorus (R) and 4 - Troncular vagotomy plus DGR (RTV). The animals were killed at the 54 week of the experiment. DGR was obtained by anastomosing a proximal jejunal loop to the anterior gastric wall. TV was performed through isolation and division of the vagal trunks. Gastrotomy consisted of 1 cm incision at the anterior gastric wall. PL were analyzed gross and histologically in the antral mucosa, at the gastrojejunal stoma and at the squamous portion of the gastric mucosa. Results: Groups R and RTV developed exophytic lesions in the antral mucosa (R=90.9%; RTV=100%) and at the gastrojejunal stoma (R=54.54%; RTV=63.63%). Histologically they consisted of proliferative benign lesions, without cellular atypias, diagnosed as adenomatous hyperplasia. Both groups exposed to DGR presented squamous hyperplasia at the squamous portion of the gastric mucosa (R= 54.5%; RTV= 45.4%). TV, alone, did not induce gross or histological alterations in the gastric mucosa. TV did note change the morphologic pattern of the proliferative lesions induced by DGR. Conclusions: DGR induces the development of PL in the pyloric mucosa and at the gastrojejunal stoma. TV does not change the morphologic pattern of the proliferative lesions induced by DGR. TV alone is not able to induce morphologic lesions in the gastric mucosa.
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Chronic and excessive alcohol consumption has been related to an increased risk of several cancers, including that of the liver; however, studies in animal models have yet to conclusively determine whether ethanol acts as a tumor promoter in hepatic tumorigenesis. We examined whether prolonged alcohol consumption could act as a hepatic tumor promoter after initiation by diethylnitrosamine (DEN) in a rat model. Male Sprague-Dawley rats were injected with 20 mg DEN/kg body weight 1 wk before introduction of either an ethanol liquid diet or an isoenergic control liquid diet. Hepatic pathological lesions, hepatocyte proliferation, apoptosis, PPARα and PPARγ, and plasma insulin-like growth factor 1 (IGF-1) levels were assessed after 6 and 10 mo. Mean body and liver weights, plasma IGF-1 concentration, hepatic expressions of proliferating cellular nuclear antigen and Ki-67, and cyclin D1 in ethanol-fed rats were all significantly lower after 10 mo of treatment compared with control rats. In addition, levels of hepatic PPARγ protein, not PPARα, were significantly higher in the ethanol-fed rats after prolonged treatment. Although ethanol feeding also resulted in significantly fewer altered hepatic foci, hepatocellular adenoma was detected in ethanol-fed rats at 10 mo, but not in control rats given the same dose of DEN. Together, these results indicate that chronic, excessive ethanol consumption impairs normal hepatocyte proliferation, which is associated with reduced IGF-1 levels, but promotes hepatic carcinogenesis. © 2011 American Society for Nutrition.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Pós-graduação em Genética - IBILCE
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Pós-graduação em Medicina Veterinária - FCAV
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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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, ....