891 resultados para colorectal mucosa


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Um experimento foi conduzido para verificar a influência da glutamina no turnover do carbono na mucosa intestinal de leitões desmamados. Nove matrizes receberam dietas compostas basicamente de plantas do ciclo fotossintético C4 durante toda a gestação (d‰13C = 17,12) e lactação (d‰13C = -19,26). Os leitões foram desmamados aos 21 dias de idade e 68 deles foram alimentados com ração composta de plantas do ciclo fotossintético C3 (d‰13C = -25,12). Os leitões foram aleatoriamente distribuídos em duas dietas: uma sem suplementação de glutamina; e outra suplementada com 1% de glutamina. Aos 0; 1; 1,5; 2; 2,5; 3; 3,5; 4; 4,5; 5; 5,5; 8; 11; 15, 20; 29 e 46 dias pós-desmame, dois leitões de cada dieta foram abatidos para coleta de amostras da mucosa intestinal, que foram analisadas quanto à composição isotópica de d‰13C e mensurada a velocidade de substituição do carbono no tempo. Os valores da meia-vida do carbono para a mucosa intestinal foram de 6,0 e 3,5 dias para as dietas controle e com glutamina, respectivamente. A glutamina acelerou a velocidade de substituição do carbono na mucosa intestinal, evidenciando sua ação benéfica na recuperação da estrutura do intestino após o desmame.

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Lipomas are benign mesenchymal neoplasms of soft tissue that can be found in any part of the human body. Conversely, their presence in the oral mucosa is rather uncommon, with approximately 4% of the cases occurring in the oral cavity. In such cases, they are likely to have originated from mature adipose tissue and to be among several described histological variants of lipomas, which are identified according to the predominant type of tissue. There is a rare lipoma, known as an osteolipoma or an ossifying lipoma; however, little has been written this type of lipoma characterized by a classical lipoma with areas of osseous metaplasia. Considering the few cases of oral osteolipomas previously described in the English-related literature and the consequent risk of misdiagnosis and overtreatment, this paper describes an extreme case of an osteolipoma affecting the buccal mucosa of an adult patient. This paper focuses particularly on the pathogenesis of this lesion and the discussion of a correct diagnosis.

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Aims: To investigate the prevalence of oral mucosa alterations in patients with type 2 diabetes and to identify possible risk factors related to oral mucosa alterations.Methods: 146 patients with type 2 diabetes and 111 age-and gender-matched healthy controls subjects were consecutively recruited from Araraquara School of Dentistry to answer a structured questionnaire designed to collect demographic data as well as current and former history of diabetes. Clinical examination of the oral mucosa was carried out by a stomatologist.Results: A higher prevalence of oral mucosa alterations was found in patients with diabetes than in patients without diabetes (p < 0.001), with significant difference to development conditions (p < 0.0001), potentially malignant disorders (p < 0.0001) and fungal infections (p < 0.05). In the multiple logistic regression, diabetes (odds ratio 9.9 IC 5.11-19.16) and smoking habit (odds ratio 3.17 IC 1.42-7.12) increased the odds of oral mucosa alterations significantly.Conclusions: Patients with diabetes mellitus not only showed an increased prevalence of oral mucosa alterations but also a significant percentage of potentially malignant disorders. These findings elucidate the necessity of regular clinical examination to ensure early diagnosis and prompt management of oral mucosa lesions in patients with diabetes. (C) 2011 Elsevier B.V. All rights reserved.

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O objetivo deste estudo foi investigar a prevalência do papilomavírus humano 6/11 e 16/18 em pacientes, com lesões orais clínicamente diagnosticadas como leucoplasias, atendidas na Faculdade de Odontologia de Araraquara, UNESP, Brasil. Após a inclusão em parafina, os cortes corados com H&E, foram selecionadas 30 biópsias e separadas em 3 grupos: lesões sem displasia (n=10), lesões com diferentes graus de displasia (n=10) e carcinoma espinocelular invasivo(n=10). As lesões que apresentaram displasia epitelial foram classificadas de acordo com os critérios histopatológicos propostos por Van Der Waal. As lesões foram investigadas para a presença de HPV por hibridização in situ com sondas biotiniladas de amplo espectro, 6/11 e 16/18. HPV 16/18 foi detectado em 20% (n=2) das biópsias com displasia severa. A presença de HPV 16/18 em lesões malignas sugere sua importância como fator de risco na carcinogênese oral.

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O objetivo desse trabalho foi determinar a freqüência da infecção por Candida sp. em biópsias de lesões da mucosa bucal, assim como associar a presença de Candida sp. com lesões malignas e lesões com vários graus de displasia. Foram utilizadas 832 biópsias da mucosa bucal, previamente incluídas em parafinas, cujos blocos foram obtidos dos arquivos da Disciplina de Patologia da Faculdade de Odontologia de Araraquara da UNESP, no período entre 1990-2001. Três cortes seqüenciais foram corados pelo ácido periódico de Schiff (PAS). do total de biópsias 27,2% foram PAS positivas, dessas 83,25% eram provenientes de pacientes do sexo masculino. Houve associação positiva entre infecção com displasia epitelial leve, moderada, severa, carcinoma espinocelular e hiperqueratose (p < 0,05). Não houve associação entre hiperplasia fibrosa inflamatória, líquen plano, granuloma piogênico (p < 0,05) com infecções fúngicas. A língua foi o sítio mais acometido por infecções em relação a outros sítios (p < 0,05). A partir dos dados quantitativos, concluiu-se que houve correlação positiva de infecção por fungos, lesões displásicas e carcinoma, sendo mais freqüente no sexo masculino. Estes dados não permitem inferir se o fungo causa displasia epitelial e carcinoma, mas confirmam a maior presença de Candida nessas lesões.

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In order to examine the effects of alcohol on the hard palatine mucosa of rats, sixty adult female rats (Rattus norvegicus albinus) were divided into two experimental groups. The control group received solid diet (Purina rat chow) and tap water ad libitum. The alcoholic group received the same solid diet and was allowed to drink only sugar cane brandy dissolved in 30% Gay Lussac (v/v). At the end of periods of 90, 180 and 270 days of treatment, the animals at estro were sacrificed and the hard palatine mucosa were prepared for TEM and SEM methods. The basal cells of the alcoholic groups (90, 180 and 270 days of treatment) demonstrated some alterations: the intercellular spaces between these cells were higher, presented cytoplasmatic lipid droplets and autolysis. Also, the connective tissue showed intense lipid droplets accumulation in the alcoholic groups. These modifications suggested that chronic alcohol ingestion was able to modify the integrity of the cells in the rat hard palatine mucosa.

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Smoking is considered to be the most albeit preventable cause of diseases and premature deaths in the history of mankind. The local action of tobacco on the oral mucosa can cause precancerous and cancerous lesions. However, there is not enough evidence to establish all the systemic effects caused by nicotine on the organism. Thus, the aim of the present study was to characterize the cellular changes of the cheek mucosa of rats submitted to long-term systemic nicotine treatment. Twenty male rats were divided into two experimental groups: a nicotine group and a control group, each consisting of 10 animals. The nicotine group was injected daily with 0.250 mg of nicotine per 100 g of body weight. All animals received a solid diet and water ad libitum. After 90 days of treatment, all animals were weighed and sacrificed. Samples of cheek mucosa were collected for light and transmission electron microscopy. The results revealed oral epithelium containing atypical cells that were characterized by atrophy, cell membrane disorganization and tissue damage. It was concluded that systemic administration of nicotine damaged the cellular integrity of the oral mucosa, impairing tissue function and predisposing the tissue to the action of different pathogenic agents and also to that of other carcinogenic substances present in tobacco. (c) 2006 Elsevier Ltd. All rights reserved.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Ethanol-induced oxidative damage is commonly associated with the generation of reactive oxygen molecules, leading to oxidative stress. Considering that antioxidant activity is an important mechanism of action involved in cytoprotection, the aim of this work was to evaluate the antioxidant properties of the alkaloid indigo (1) (2 mg/kg, p. o.), obtained from the leaves of Indigofera truxillensis Kunth (Fabaceae), on rat gastric mucosa submitted to ethanol-induced (100%, 1 mL, p.o.) gastric ulcer. Enzymatic assays and DNA fragmentation analysis were performed. When ethanol was administered to the control group, the sulfhydryl content (SH) and the glutathione peroxidase (GPx) activity decreased by 41% and 50%, respectively; in contrast, superoxide dismutase (SOD) and glutathione reductase (GR) activities increased by 56% and 67%, respectively. Additionally, myeloperoxidase (MPO) activity, a marker for free radical generation caused by polymorphonuclear neutrophil (PMN) tissue infiltration, also increased 4.5-fold after ethanol treatment. Rat gastric mucosa exposed to ethanol showed DNA fragmentation. Indigo alkaloid pretreatment protected rats from ethanol-induced gastric lesions. This effect was determined by the ulcerative lesion area (ULA), indicating an inhibition of around 80% at 2 mg/kg. This alkaloid also diminished GPx activity, which was higher than that observed with ethanol alone. However, this effect was counterbalanced by increased GR activity. Indigo was unable to restore alterations in SOD activity promoted by ethanol. After indigo pretreatment, SH levels and MPO activity remained normal and gastric mucosa DNA damage caused by ethanol was also partially prevented by indigo. These results suggest that the gastroprotective mechanisms of indigo include non-enzymatic antioxidant effects and the inhibition of PMN infiltration which, in combination, partially protect the gastric mucosa against ethanol-induced DNA damage.

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