428 resultados para Imunidade mucosa
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Avaliou-se o efeito da substituição parcial do farelo de soja (FS) por hidrolisado protéico do conteúdo celular de levedura (HPCCL), proteína isolada de soja (PIS) ou hidrolisado protéico de mucosa intestinal de suínos (HPMIS) em dietas com leite em pó integral (LPI) sobre o desempenho, os níveis séricos de uréia e a incidência de diarréia em leitões desmamados. Foram utilizados 40 leitões desmamados aos 21 dias de idade (20 machos castrados e 20 fêmeas), distribuídos em delineamento em blocos ao acaso, com cinco tratamentos (dietas) e oito repetições. As dietas foram fornecidas em três fases, de acordo com a idade dos animais: fase pré-inicial 1 (21 aos 35 dias de idade): dieta à base de milho e farelo de soja (FS); dieta com 15,0% LPI; dieta com 15,0% LPI + 3,5% HPMIS; dieta com 15,0% LPI + 5,0% de PIS; dieta com 15,0% LPI + 5,0% HPCCL. Na fase pré-inicial 2 (36 aos 49 dias de idade), foi mantida a dieta à base de milho e farelo de soja e o LPI foi reduzido para 7,5% em todas as dietas, o HPMIS para 1,5%, a PIS para 4% e o HPCCL foi mantido em 5%. Na fase inicial (50 aos 70 dias de idade), foi mantida a dieta à base de milho e farelo de soja, o LPI foi retirado de todas as dietas e os animais que nas fases pré-inicial 1 e 2 foram alimentados com as dietas contendo LPI e LPI + HPMIS passaram a ser alimentados com a dieta à base de milho e farelo de soja; a PIS foi reduzida para 3% e o HPCCL para 2,5%. No período de 21 a 35 dias, a dieta LPI + PIS proporcionou maior ganho diário de peso e melhor conversão alimentar. Nas fases seguintes, não houve diferença no desempenho entre as dietas. Até cinco dias após o desmame, os animais alimentados com as rações FS e LPI + PIS apresentaram menor índice de diarréia. Os níveis séricos de uréia não foram influenciados pelas dietas. A utilização de PIS, HPMIS e HPCCL em dietas complexas contendo leite em pó pode consistir em alternativa biologicamente viável em dietas para leitões.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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JUSTIFICATIVA E OBJETIVOS: As lesões da mucosa traqueal em contato com o balonete do tubo traqueal são proporcionais à pressão exercida pelo balonete e ao tempo de exposição. O objetivo foi estudar as eventuais lesões da mucosa do segmento traqueal em contato com o balonete do tubo traqueal insuflado com volume de ar suficiente para se obter pressão de "selo" ou com a pressão limite de 25 cmH2O, abaixo da pressão crítica de 30 cm de água para produção de lesão da mucosa traqueal. MÉTODO: Dezesseis cães foram submetidos à anestesia venosa e ventilação artificial. Os cães foram distribuídos aleatoriamente em dois grupos de acordo com a pressão no balonete do tubo traqueal (Portex Blue-Line, Inglaterra): Gselo (n = 8) balonete com pressão mínima de "selo" para impedir vazamento de ar durante a respiração artificial; G25 (n = 8) balonete insuflado até obtenção da pressão de 25 cmH2O. A medida da pressão do balonete foi realizada por meio de manômetro digital no início (controle) e após 60, 120 e 180 minutos. Após o sacrifício dos cães, foram feitas biópsias nas áreas da mucosa traqueal adjacentes ao balonete e ao tubo traqueal para análise à microscopia eletrônica de varredura (MEV). RESULTADOS: A pressão média do balonete em G25 manteve-se entre 24,8 e 25 cmH2O e em Gselo entre 11,9 e 12,5 cmH2O durante o experimento. As alterações à MEV foram pequenas e não significantemente diferentes nos grupos (p > 0,30), mas ocorreram lesões mais intensas nas áreas de contato da mucosa traqueal com o balonete do tubo traqueal, nos dois grupos, em relação às áreas da mucosa adjacentes ou não ao tubo traqueal (p < 0,05). CONCLUSÕES: No cão, nas condições experimentais empregadas, a insuflação do balonete de tubo traqueal em volume de ar suficiente para determinar pressão limite de 25 cmH2O ou de "selo" para impedir vazamento de ar determina lesões mínimas da mucosa traqueal em contato com o balonete e sem diferença significante entre elas.
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OBJETIVO: Avaliar as alterações histológicas e biomecânicas do diclofenaco de sódio na mucosa intestinal do rato e a associação com o uso de Imipenem. MÉTODOS: Foram estudados 240 ratos Wistar distribuídos aleatoriamente em quatro grupos experimentais: GI: 60 ratos tratados com injeção IM de soro fisiológico 0,9%; GII: 60 ratos tratados com injeção IM de diclofenaco de sódio na dose de 6mg/kg de peso por 4 dias; GIII: 60 ratos tratados com injeção IM de Imipenem na dose de 30 mg/kg de peso por 4 dias; GIV: 60 ratos tratados com injeção IM de soro fisiológico e diclofenaco de sódio nas doses acima. em cada grupo os animais foram posteriormente divididos em 4 momentos de 15 animais em cada um para sacrifício, respectivamente, no 4º, 7º, 14º e 21º dias após o início do tratamento. As alterações da cavidade abdominal, assim como as características histológicas e de força de ruptura do intestino delgado foram analisadas em cada momento, em cada grupo. RESULTADOS: Não foram encontradas alterações histológicas e biomecânicas nos animais do Grupo I nesse estudo. Lesões ulceradas na mucosa do intestino delgado foram observadas nos animais tratados com diclofenaco de sódio, assim como diminuição da força de ruptura. As lesões ulceradas encontradas foram prevenidas pelo uso de Imipenem. CONCLUSÃO: O diclofenaco de sódio induz lesões ulceradas na mucosa intestinal do rato que podem ser prevenidas pelo uso de Imipenem.
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Helicobacter pylori (H. pylori) is believed to dispose carriers to gastric cancer by inducing chronic inflammation. The inflammatory processes may result in the generation of reactive oxygen and nitrogen species that damage DNA. In this study, we investigated the relationships between DNA damage in the gastric mucosa and cogA, vocA, and iceA genotypes of H. pylori. The study was conducted with biopsies from the gastric antrum and corpus of 98 H. pylori-infected and 26 uninfected control patients. H. pylori genotypes were determined by PCR and DNA damage was measured in gastric mucosal cells by the Comet assay (single cell gel electrophoresis). All patients were nonsmokers, not abusing alcohol, and not using prescription or recreational drugs. Levels of DNA damage were significantly higher (P < 0.0001) in the H. pylori-infected patients than in uninfected patients. In comparison with the level of DNA damage in the uninfected controls, the extent of DNA damage in both the antrum (OR = 8.45; 95% Cl 2.33-37.72) and the corpus (OR 6.55; 95% Cl 2.52-17.72) was related to infection by cagA(+)/vocAs1m1 and iceA1 strains. The results indicate that the genotype of H. pylori is related to the amount of DNA damage in the gastric mucosa. These genotypes could serve as biomarkers for the risk of extensive DNA damage and possibly gastric cancer. (C) 2004 Wiley-Liss, Inc.
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Objetivo: Apresentar um portador de leishmaniose com lesão palpebral e dilatação de via lacrimal excretora. Relato de caso: O paciente em questão foi portador de leishmaniose do tipo cutâneo-mucosa, tendo apresentado múltiplas lesões de pele, ectrópio da pálpebra inferior, lesões na mucosa nasal e alterações na drenagem lacrimal. Discussão: O acometimento da pálpebra e da via lacrimal raramente ocorre em portadores de leishmaniose. Os autores chamam atenção para o diagnóstico e para a necessidade de se adotar medidas preventivas contra os vetores e a rápida instituição do tratamento.
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Introduction: Head and neck cancers are linked to smoking. The most affected sites are the oral cavity, pharynx and larynx. Experimental studies show epithelial lesions caused by cigarette smoke. Objectives: To investigate in rats the effects of acute cigarette smoke exposure on the mucosa of the tongue, pharynx and larynx.Material and method: Wistar rats were allocated into two groups of 20 animals: CG (control) receiving food and water ad libitum and TG (Tobacco) exposed to the smoke of 40 cigarettes/day for 60 days. Biopsy of their tongues, pharynxes and larynxes were subjected to histopathological, histomorphometric and immunohistochemical studies of protein p53 and ki-67.Result: The histological analysis of tongue from the Tobacco group revealed epithelial hyperplasia (90%), basal cell hyperplasia (95%) and mild to moderate dysplasia (85%). In pharynx showed basal cell hyperplasia (85%), dysplasia (25%) and vascular congestion (95%). In larynx showed basal cell hyperplasia (70%), epithelial hyperplasia (55%), congestion (100%) and inflammatory infiltrate (25%). Morphometric analysis revealed that keratin layer thickness was greater in the tobacco group. P53 immunoexpression was negative in both groups. Ki-67 immunoexpression was positive in basal cell nuclei but in parabasal cell nuclei it was positive only in the Tobacco group.Conclusions: The exposure of animals to cigarette smoke for 60 days resulted in benign lesions. The duration of exposure was not enough to cause the development cancer, as confirmed by the negative expression of p53 protein in all slides examined. Analysis of ki-67 expression showed intense epithelial proliferation in response to damage.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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The different potential of initiated and non-initiated urinary bladder mucosa (UBM) to develop neoplasia was quantitatively evaluated in the male Wistar rat. Initiation of carcinogenesis was accomplished with N-butyl-N- (4-hydroxybutyl) -nitrosamine (BBN). Stimuli for cell proliferation and apoptosis were obtained by exposure followed by withdrawal of 3% Uracil in the diet. The proliferation index (PI) was estimated in UBM immunostained for the proliferating nuclear cell antigen (PCNA). The apoptotic index (AI) and the density of papillary/nodular hyperplasia (PNH) were estimated in hematoxilin-eosin stained sections. PNH was the main proliferative response to the mechanical irritation by uracil, irrespective of previous initiation with BBN. Uracil exposure induced higher PI and PNH density in the initiated rats. After uracil withdrawal, there was a significant increase of the AI in both uracil-treated groups, which correlated well to the respective PNH density. However, at the end of the experiment, PNH incidence and density were significantly higher in the BBN-initiated mucosa, which also presented 18% incidence of papillomas and 27% of carcinomas. Therefore, under prolonged uracil calculi trauma, the UBM of BBN-initiated Wistar rats gives rise to epithelial proliferative lesions that progress to neoplasia through acquired resistance to apoptosis. (C) 1999 Wiley-Liss, Inc.
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Buccal mucosa (BM) cells have been used in human biomonitoring studies for detecting DNA adducts and chromosomal damage in an epithelial cell population. In the present study, we have investigated if human BM cells are suitable for use in the single-cell gel electrophoresis (SCGE)/Comet assay as an approach for estimating the exposure of epithelial cells to DNA-damaging agents. Our results indicate that only a few cells from BM cell samples yield comets that can be analyzed by current methods, and that the yield of cells with comets is independent of the percentage of viable BM cells in the sample. Data generated after enzymatic enrichment of viable cells and immunomagnetic separation of epithelial cells suggest that most of the BM cells that do form comets are probably leukocytes. Moreover, by reevaluating specific cells after running the Comet assay, we found that viable epithelial BM cells give rise to atypical comets that are not included in the analysis. Comparing DNA migration patterns between small groups of smokers and nonsmokers indicated that long-term smoking had no effect on the subpopulation of cells that yield typical comets. Our results indicate that the SCGE assay, as it is commonly performed, may not be useful for genotoxicity monitoring in human epithelial BM cells.
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This study evaluated cytogenetic damage by measuring the frequency of micronucleated cells (MNC) in peripheral blood and buccal mucosa of head-and-neck cancer patients undergoing radiotherapy.MNC frequencies were assessed in 31 patients before, during, and after radiotherapy, and in 17 C, healthy controls matched for gender, age, and smoking habits. Results showed no statistically significant difference between patients and controls prior to radiotherapy in cytokinesis-blocked lymphocytes or buccal mucosa cells. During treatment, increased MNC frequencies were observed in both cell types. Micronucleated lymphocyte levels remained high in samples collected 30 to 140 days after the end of treatment, while MNC frequency in buccal mucosa decreased to values statistically similar to baseline values. There is controversy over the effects of age, smoking habit, tumor stage, and/or metastasis on MNC frequency. However, increased frequency of micronucleated buccal mucosa cells was seen in patients under 60 years old and in those with tumors >4cm.In conclusion, the data show that radiotherapy has a potent clastogenic effect in Circulating lymphocytes and buccal mucosa cells of head-and-neck cancer patients, and that the baseline MNC frequency in these two tissues is not a sensitive marker for head-and neck neoplasm.
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4-Nitroquinotine 1-oxide (4NQO)-induced rat tongue carcinogenesis is a useful model for studying oral squamous cell carcinoma. The aim of this study was to investigate the level of DNA damage induced by 4NQO in oral mucosa cells by the single cell get (comet) assay. Mate Wistar rats were distributed into three groups of 10 animals each and treated with 50 ppm 4NQO solution by drinking water for 4, 12 or 20 weeks. Ten animals were used as negative control. Statistically significant increase of DNA damage was observed in non-neoplastic oral cells at four weeks of 4NQO administration when compared with control (P < 0.05). The level of DNA damage was directly associated with the severity of histological changes. The results suggest that histologically normal tissue is able to harbor genetically unstable cells contributing to the initiation of oral carcinogenesis. Genomic instability appears to be associated with the risk and progression of oral cancer. (C) 2004 Elsevier Ltd. All rights reserved.
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While it has been clearly demonstrated that smoking is the most significant exogenous factor involved in oral carcinogenesis, little is known about the global molecular and cellular changes that occur prior to the appearance of clinically detectable symptoms. Thus, the aim of this study was to investigate the expressivity of bcl-2, bax and PCNA in the rat tongue mucosa exposed to cigarette smoke by means of immunohistochemistry. A total of twelve male Wistar rats were distributed into 2 groups: negative control and experimental group exposed to cigarette smoke during 75 days. After experimental period, no histopathological changes in the tongue mucosa were detected in the negative control and the experimental group. on the other hand, an overexpression of bcl-2 was detected (p < 0.01) throughout all layers of the epithelium, whereas bax did not show significant differences (p > 0.05). Also, the labeling index for bcl-2 and bax showed an increase 75 days after cigarette exposure (p < 0.01). PCNA-labeling index did not show remarkable changes between groups. Taken together, our results show that bcl-2 is overexpressed in the rat tongue keratinocytes after cigarette smoke exposure.