961 resultados para defense mechanisms


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Macrófagos são conhecidos por exercerem uma importante função de mecanismo de defesa quando estas células são estimuladas com produtos naturais e produtos bacterianos (dentre outros). Uma variedade de citocinas e compostos químicos são liberados para induzir sistema de defesa fundamental. Entre outros peróxido de hidrogênio (H2O2) tem sido identificado como moléculas tendo multifunções. Entretanto está bem estabelecido que (H2O2) está envolvido em inúmeros processos fisiológicos, como por exemplo, neurotransmissão, relaxamento da musculatura lisa ou regulação imune. Para a determinação de peróxido de hidrogênio (H2O2) em macrófago peritoneal em camundongos, determinou-se a ação imunomodulatória de extratos (etanólico e etanólico 70%) obtidos de quatro espécies do gênero Paepalanthus (Eriocaulaceae) na concentração de 10 mg/mL. Os estratos etanólicos 70 % de capítulos de P. Hilairei, P. robustus, P. vellozioides e P. speciocus apresentaram maior liberação de (H2O2) do que os outros extratos etanólicos.

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Este estudo visou investigar as vivências emocionais e mecanismos de defesa de pais de crianças com deficiência auditiva. Foram entrevistados 12 genitores masculinos, de 25 a 38 anos, com escolaridade de primeiro grau incompleto a superior incompleto. Dos entrevistados, sete eram pais de filhos únicos, três, pais pela segunda vez e um pai pela terceira vez da criança com necessidade específica. As respostas foram categorizadas e analisadas com base no referencial psicodinâmico e apresentam vivências de choque, ansiedade e angústia e o uso de mecanismos de defesa frente ao diagnóstico e implicações da deficiência. As defesas constatadas foram analisadas como reações situacionalmente esperadas, podendo favorecer formas mais realistas de enfrentamento posterior. Sugere-se que, assim como mães, pais vivenciam impacto e dificuldades emocionais frente ao diagnóstico de seus filhos. Diferenças de papéis familiares facilitam ao pai um menor envolvimento na educação da criança, devendo-se valorizar a sua importância no processo de reabilitação.

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Fatores de virulência em fungos de micoses sistêmicaFungos patogênicos causadores de micoses sistêmicas possuem vários fatores que permitem seu crescimento nas condições adversas oferecidas pelo hospedeiro, propiciando o estabelecimento da relação parasitária e contribuindo no processo de doença. Esses fatores são conhecidos como fatores de virulência auxiliando no desenvolvimento da infecção e interferindo com a patogênese das micoses. O presente trabalho avalia os fatores de virulência em fungos patogênicos como Blastomyces dermatitidis, Coccidioides immitis, Cryptococcus neoformans, Histoplasma capsulatum e Paracoccidioides brasiliensis, em relação à termotolerância, dimorfismo, componentes da parede celular ou cápsula, bem como a produção de enzimas. Os fatores de virulência auxiliam na aderência, colonização, disseminação e habilidade do fungo para resistir a ambientes hostis e escapar dos mecanismos da resposta imune do hospedeiro.Tanto os fatores de virulência apresentados por diferentes fungos, como os mecanismos de defesa oferecidos pelo hospedeiro requerem ação e interação de processos complexos, cujo conhecimento permitirá a melhor compreensão da patogenia das micoses sistêmicas.

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Background: Lectins are mainly described as simple carbohydrate- binding proteins. Previous studies have tried to identify other binding sites, which possible recognize plant hormones, secondary metabolites, and isolated amino acid residues. We report the crystal structure of a lectin isolated from Canavalia gladiata seeds ( CGL), describing a new binding pocket, which may be related to pathogen resistance activity in ConA- like lectins; a site where a non- protein amino- acid, aaminobutyric acid ( Abu), is bound.Results: the overall structure of native CGL and complexed with alpha- methyl- mannoside and Abu have been refined at 2.3 angstrom and 2.31 angstrom resolution, respectively. Analysis of the electron density maps of the CGL structure shows clearly the presence of Abu, which was confirmed by mass spectrometry.Conclusion: the presence of Abu in a plant lectin structure strongly indicates the ability of lectins on carrying secondary metabolites. Comparison of the amino acids composing the site with other legume lectins revealed that this site is conserved, providing an evidence of the biological relevance of this site. This new action of lectins strengthens their role in defense mechanisms in plants.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Risk assessments suggest that intermediate and long-term exposure to triazine herbicides and its metabolites through water can cause severe damage to human health. The objective of this study was to investigate the possible effects of atrazine on Wistar rats submitted to subacute treatment. For this purpose, the activity of catalase and alanine aminotransferase was quantified, and the effect of the herbicide on cell membranes was examined based on the measurement of lipid peroxidation and consequent formation of malondialdehyde and on the mRNA expression of antioxidant enzymes (Mn-superoxide dismutase [SOD] and GSTM1) and connexins. In addition, we evaluated histopathological alterations in the liver, cellular expression of SOD and glutathione (GST), activation of heat shock proteins (HSPs) by immunohistochemistry, and the induction of apoptosis. The genotoxic potential of the herbicide was investigated by the micronucleus test in bone marrow smears. Adult male Wistar rats were treated with an aqueous solution of atrazine at a concentration of 400 mg/kg/day, by gavage, for 14 consecutive days. Control groups were also included. The results showed an increase of catalase levels and maintenance of the expression of antioxidant enzymes (SOD and GST). In addition, lipid peroxidation, hepatic tissue degeneration, activation of HSP90, increased levels of connexin mRNA, and genotoxicity were observed. In conclusion, atrazine induced early hepatic oxidative stress that triggered defense mechanisms to maintain the morphophysiological integrity of the liver. Further studies are needed to better understand the effects of this herbicide on human health. (C) 2011 Elsevier B.V. All rights reserved.

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The alcoholic liver cirrhosis usually causes overall immunological changes which might be attributed to either the hepatic disease itself, to ethanol action and/or to malnourishment of the patient. These immune abnormalities comprise both cellular and humoral immunity, consisting of increased immunoglobulin levels, depressed late-skin response to antigens, lowered proliferative response of lymphocytes to mitogens, lower plasma levels of complement proteins (C3 and C4) and by either lower (IL2 and gamma IF) or increased (IL1, TNF, IL6 and IL8) cytokine levels. Parallel to the systemic immune suppression found in most patients, there is also a concomitant local, genetically based, immune stimulation at the liver level which leads to hepatic self-aggression. The systemic immune-suppression could be responsible for periodical infections or neoplasia found in these patients. The possible factors for the immune exhaustion are: a) lower hepatic clearance of toxins and/or bacteria; b) lower hepatic synthesis of complement components; c) cytokines (IL2 and gamma IF) deficiencies, and d) deficiencies of nutrients related to the antioxidant and/or immune defense mechanisms. The immune stimulation of the liver self aggression is characterized by the preferential migration of cytotoxic T cell and neutrophils to the liver, following stimulatory factors such as Mallory bodies, acetaldehyde and/or antibodies. Moreover, the local increase of cytokines (IL1, TNF, IL6 and IL8) levels would be liable for the local phagocyte chemotaxy (IL8) or part of liver injury (TNF) eased by the lower antioxidant defense of the cirrhotic liver.(ABSTRACT TRUNCATED AT 250 WORDS)

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The chronic kidney disease (CKD) it is characterized by irreversible structural lesions that can develop progressively for uremia and chronic renal failure (CRF). In the CRF it happens the incapacity of executing the functions of maintenance of the electrolyte balance and acid-base, catabolitos excretion and hormonal regulation appropriately. When the mechanism basic physiopathology of the renal upset is analyzed, it is observed that present factors, predispose to the unbalance oxidative. Most of the time, the renal patient comes badly nurtured, with lack in reservations of vitamins and minerals, what reduces the antioxidant defense mechanisms, what favors the installation of the renal oxidative stress, with the formation of species you reactivate of reactive oxygen species (ROS), substances these potentially harmful to the organism. The reduction of the glomerular filtration rate (GFR) in the evolution of CKD in dogs and cats is a component for the installation of the renal oxidative stress. The ROS possesses important action in the kidneys, and these substances are highly reactivate, and when presents in excess damage lipids, proteins, DNA and carbohydrate, driving functional and structural abnormalities taking the cellular apoptosis and necrosis. Against the harmful potential action of these substances you reactivate, she becomes fundamental a delicate control of his production and consumption in the half intracellular, in other words, a balance of his concentration intra and extracellular. That is possible due to the activity of the antioxidants. Like this, to present literature revision had as objective describes the participation of the oxidative stress in CRF, as well as the mechanisms defenses against the harmful action of those substances.