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Search Results: 1 - 10 of 184462 matches for " Dahir Ramos de;Andrade "
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The influence of the human genome on chronic viral hepatitis outcome
Andrade Júnior, Dahir Ramos de;Andrade, Dahir Ramos de;
Revista do Instituto de Medicina Tropical de S?o Paulo , 2004, DOI: 10.1590/S0036-46652004000300001
Abstract: the mechanisms that determine viral clearance or viral persistence in chronic viral hepatitis have yet to be identified. recent advances in molecular genetics have permitted the detection of variations in immune response, often associated with polymorphism in the human genome. differences in host susceptibility to infectious disease and disease severity cannot be attributed solely to the virulence of microbial agents. several recent advances concerning the influence of human genes in chronic viral hepatitis b and c are discussed in this article: a) the associations between human leukocyte antigen polymorphism and viral hepatic disease susceptibility or resistance; b) protective alleles influencing hepatitis b virus (hbv) and hepatitis c virus (hcv) evolution; c) prejudicial alleles influencing hbv and hcv; d) candidate genes associated with hbv and hcv evolution; d) other genetic factors that may contribute to chronic hepatitis c evolution (genes influencing hepatic stellate cells, tgf-b1 and tnf-alpha production, hepatic iron deposits and angiotensin ii production, among others). recent discoveries regarding genetic associations with chronic viral hepatitis may provide clues to understanding the development of end-stage complications such as cirrhosis or hepatocellular carcinoma. in the near future, analysis of the human genome will allow the elucidation of both the natural course of viral hepatitis and its response to therapy.
Typhoid fever as cellular microbiological model
Andrade, Dahir Ramos de;Andrade Júnior, Dahir Ramos de;
Revista do Instituto de Medicina Tropical de S?o Paulo , 2003, DOI: 10.1590/S0036-46652003000400002
Abstract: the knowledge about typhoid fever pathogenesis is growing in the last years, mainly about the cellular and molecular phenomena that are responsible by clinical manifestations of this disease. in this article are discussed several recent discoveries, as follows: a) bacterial type iii protein secretion system; b) the five virulence genes of salmonella spp. that encoding sips (salmonella invasion protein) a, b, c, d and e, which are capable of induce apoptosis in macrophages; c) the function of toll r2 and toll r4 receptors present in the macrophage surface (discovered in the drosophila). the toll family receptors are critical in the signalizing mediated by lps in macrophages in association with lbp and cd14; d) the lines of immune defense between intestinal lumen and internal organs; e) the fundamental role of the endothelial cells in the inflammatory deviation from bloodstream into infected tissues by bacteria. in addition to above subjects, the authors comment the correlation between the clinical features of typhoid fever and the cellular and molecular phenomena of this disease, as well as the therapeutic consequences of this knowledge.
Typhoid fever as cellular microbiological model
Andrade Dahir Ramos de,Andrade Júnior Dahir Ramos de
Revista do Instituto de Medicina Tropical de S?o Paulo , 2003,
Abstract: The knowledge about typhoid fever pathogenesis is growing in the last years, mainly about the cellular and molecular phenomena that are responsible by clinical manifestations of this disease. In this article are discussed several recent discoveries, as follows: a) Bacterial type III protein secretion system; b) The five virulence genes of Salmonella spp. that encoding Sips (Salmonella invasion protein) A, B, C, D and E, which are capable of induce apoptosis in macrophages; c) The function of Toll R2 and Toll R4 receptors present in the macrophage surface (discovered in the Drosophila). The Toll family receptors are critical in the signalizing mediated by LPS in macrophages in association with LBP and CD14; d) The lines of immune defense between intestinal lumen and internal organs; e) The fundamental role of the endothelial cells in the inflammatory deviation from bloodstream into infected tissues by bacteria. In addition to above subjects, the authors comment the correlation between the clinical features of typhoid fever and the cellular and molecular phenomena of this disease, as well as the therapeutic consequences of this knowledge.
Quantification of the Expression of HIF-1alpha by Real-Time PCR in Rat Hepatocytes Cultures Invaded by Shigella flexneri under Normoxic and Hypoxic Conditions  [PDF]
Camila Bárbara Cantalupo Lima, Sania Alves dos Santos, Dahir Ramos de Andrade Júnior
Advances in Microbiology (AiM) , 2015, DOI: 10.4236/aim.2015.57052
Abstract: Aim: Shigella flexneri (S. flexneri) is a gram-negative enterobacterium responsible for severe intestinal end systemic infection in humans. The bacteria can reach the liver due to degeneration of the colonic epithelium. Hypoxia is present in many human diseases and can induce the expression of the transcription factor HIF-1alpha that may have a cell protective role. The influence of hypoxia and HIF-1alpha on bacterial infection, studied in this work, is unclear. Hypoxia inducible factor-1alpha (HIF-1alpha) is a transcription factor that acts as a master regulator of gene expression induced by hypoxia. Methods: We compared the ability of S. flexneri to invade rat hepatocytes in primary culture both in normoxic and hypoxic conditions. We evaluated TNF-alpha released by hepatocytes, apoptosis rate and HIF-1alpha expression by confocal microscopy as well as real time PCR technique. Results: We showed that S. flexneri invaded less hepatocytes previously submitted to 24 h hypoxia (6.5% O2) than those cultivated in normoxia (21% O2). S. flexneri also induced HIF-1α expression in hepatocytes, TNF-α secretion and apoptosis. Conclusion: a) Hypoxia alone was not a stimulus to TNF-α secretion, but induced cell apoptosis and HIF-1α expression; b) S. flexneri was able to invade rat hepatocytes and hypoxia apparently influenced significantly bacterial cell invasiveness; c)
Study of rat hepatocytes in primary culture submitted to hypoxia and reoxygenation: action of the cytoprotectors prostaglandin E1, superoxide dismutase, allopurinol and verapamil
Andrade Jr., Dahir Ramos de;Andrade, Dahir Ramos de;Santos, Sania Alves dos;
Arquivos de Gastroenterologia , 2009, DOI: 10.1590/S0004-28032009000400016
Abstract: context: exposure of hepatocytes to pathological conditions in a microenvironment of hypoxia and reoxygenation is very frequent in hepatic diseases. several substances present perspectives for cytoprotective action on hepatocyte submitted to reoxygenation after hypoxia and simple hypoxia. objective: we research therapeutic options for hepatocytes submitted to hypoxia and hypoxia + reoxygenation injury. methods: primary culture of rat hepatocytes was submitted to hypoxia (2 hours) plus reoxygenation (2 hours) and simple hypoxia (4 hours) in the presence or the absence of cytoprotectors. the hepatocyte lesion was evaluated by functional criteria through percentage of lactate dehydrogenase released and cell viability. the effects of the cytoprotectors prostaglandin e1 3 ηg/ml, superoxide dismutase 80 μg/ml, allopurinol 20 μm and verapamil 10-4 m were studied in this model of injury. results: reoxygenation after hypoxia induced more significant lesion in cultured hepatocytes compared to simple hypoxia, detected by analysis of functional criteria. there was a significant reduction of percentage of lactate dehydrogenase released and a significant increase of percentage of cell viability in the hypoxia + reoxygenation + cytoprotectors groups compared to hypoxia + reoxygenation groups. prostaglandin e1, superoxide dismutase and verapamil also protected the group submitted to simple hypoxia, when evaluated by functional criteria. conclusions: we conclude that reoxygenation after hypoxia significantly increased the lesion of cultured rat hepatocytes when compared to simple hypoxia. prostaglandin e1, superoxide dismutase, allopurinol and verapamil acted as cytoprotectors to the rat cultured hepatocytes submitted to hypoxia + reoxygenation in vitro. the substances prostaglandin e1, superoxide dismutase and verapamil protected hepatocytes submitted to simple hypoxia on the basis of all the criteria studied in this experimental model.
Measurement of peripheral blood mononuclear cells producing IFN-Gamma in patients with tuberculosis
Andrade Júnior, Dahir Ramos de;Santos, Sania Alves dos;Andrade, Dahir Ramos de;
Brazilian Journal of Infectious Diseases , 2008, DOI: 10.1590/S1413-86702008000200005
Abstract: the type of immune response induced by tuberculosis (th1 or th2) and its correlation with the clinical outcome is unclear. we studied 13 patients with active tuberculosis (tbc). the peripheral blood mononuclear cells producing ifn-gamma (pbmc-ig) were measured by enzyme-linked immunospot (elispot) technique. the control group had ten healthy individuals vaccinated against tuberculosis. we collected blood samples of each patient in two moments: a) in the hospital admission without treatment (tbc1); b) after seven to 20 days of treatment (tbc2). the comparison of the spots forming units of pbmc-ig between tbc group and controls showed that there was a significant difference between tbc1 and control group (p < 0.001) and between tbc2 and control group (p < 0.005), but there was no difference between tbc1 and tbc2 (p > 0.05). a positive correlation was found between pbmc-ig and hemoglobin value, as well as between pbmc-ig and weight loss. there was no correlation between pbmc-ig and other variables [age, erythrocyte sedimentation rate (esr), c-reactive protein (crp)]. we conclude that tuberculosis activates th1 immune response due to increase of pbmc producing ifn-gamma. there was no difference between the first sample (tbc1) and the second sample (tbc2) of pbmc-ig. this result can have occurred due to treatment influence, or can indicate that the immune response reachs a plateau. the positive correlation among pbmc-ig and both hemoglobin level and weight loss indicates that may exist a link between patient's clinical status and the immune response intensity.
Tnf-a production and apoptosis in hepatocytes after listeria monocytogenes and salmonella typhimurium invasion
Santos, Sania Alves Dos;Andrade Júnior, Dahir Ramos De;Andrade, Dahir Ramos De;
Revista do Instituto de Medicina Tropical de S?o Paulo , 2011, DOI: 10.1590/S0036-46652011000200009
Abstract: invasion of hepatocytes by listeria monocytogenes (lm) and salmonella typhimurium (st) can stimulate tumor necrosis factor alpha (tnf-α) release and induce apoptosis. in this study, we compared the behavior of hepatocytes invaded by three l. monocytogenes serotypes (lm-4a, lm-4b and lm-1/2a) and by st to understand which bacterium is more effective in the infectious process. we quantified tnf-α release by elisa, apoptosis rates by annexin v (early apoptosis) and tunel (late apoptosis) techniques. the cell morphology was studied too. tnf-α release rate was highest in st-invaded hepatocytes. st and lm-1/2a induced the highest apoptosis production rates evaluated by tunel. lm-4b produced the highest apoptosis rate measured by annexin. invaded hepatocytes presented various morphological alterations. overall, lm-4b and lm-1/2a proved to be the most efficient at cell invasion, although st adapted faster to the environment and induced earlier hepatocyte tnf-α release.
Rat hepatocyte invasion by Listeria monocytogenes and analysis of TNF-alpha role in apoptosis
Santos, Sania Alves dos;Andrade, Dahir Ramos de;Andrade Júnior, Dahir Ramos de;
Revista do Instituto de Medicina Tropical de S?o Paulo , 2005, DOI: 10.1590/S0036-46652005000200003
Abstract: listeria monocytogenes, etiological agent of severe human foodborne infection, uses sophisticated mechanisms of entry into host cytoplasm and manipulation of the cellular cytoskeleton, resulting in cell death. the host cells and bacteria interaction may result in cytokine production as tumor necrosis factor (tnf) a. hepatocytes have potential to produce pro-inflammatory cytokines as tnf-a when invaded by bacteria. in the present work we showed the behavior of hepatocytes invaded by l. monocytogenes by microscopic analysis, determination of tnf-a production by bioassay and analysis of the apoptosis through tunel technique. the presence of bacterium, in ratios that ranged from 5 to 50,000 bacteria per cell, induced the rupture of cellular monolayers. we observed the presence of internalized bacteria in the first hour of incubation by electronic microscopy. the levels of tnf-a increased from first hour of incubation to sixth hour, ranging from 0 to 3749 pg/ml. after seven and eight hours of incubation non-significant tnf-a levels decrease occurred, indicating possible saturation of cellular receptors. thus, the quantity of tnf-a produced by hepatocytes was dependent of the incubation time, as well as of the proportion between bacteria and cells. the apoptosis rate increased in direct form with the incubation time (1 h to 8 + 24 h), ranging from 0 to 43%, as well as with the bacteria : cells ratio. these results show the ability of hepatocyte invasion by non-hemolytic l. monocytogenes, and the main consequences of this phenomenon were the release of tnf-a by hepatocytes and the induction of apoptosis. we speculate that hepatocytes use apoptosis induced by tnf-a for release bacteria to extracellular medium. this phenomenon may facilitate the bacteria destruction by the immune system.
Os radicais livres de oxigênio e as doen?as pulmonares
Andrade Júnior, Dahir Ramos de;Souza, Rodrigo Becco de;Santos, Sania Alves dos;Andrade, Dahir Ramos de;
Jornal Brasileiro de Pneumologia , 2005, DOI: 10.1590/S1806-37132005000100011
Abstract: oxygen free radicals are molecules that present unpaired electrons in their outer orbit and can transform other molecules such as proteins, carbohydrates, lipids and deoxyribonucleic acid. oxygen free radicals are produced in various clinical conditions in which hypoxic microenvironments are generated and reoxygenation follows. such situations include clinical shock, septicemia, systemic inflammatory response, fulminant hepatitis, organ transplant and respiratory failure. in this review, we discuss the main concepts related to oxygen free radicals: the principal types and their formation, as well as the way in which they affect cellular structures and cause significant tissue damage. we present also the main antioxidants that guard against oxidative stress, including glutathione, glutathione peroxidase, superoxide dismutase, catalase, and n-acetylcysteine. the influence of oxygen free radicals on the principal pulmonary diseases are also discussed, with special emphasis given to oxygen free radicals in cigarette smoke, chronic obstructive pulmonary disease, asthma, sleep apnea syndrome and acute respiratory distress syndrome.
Correlation between serum tumor necrosis factor alpha levels and clinical severity of tuberculosis
Andrade Júnior, Dahir Ramos de;Santos, Sania Alves dos;Castro, Isac de;Andrade, Dahir Ramos de;
Brazilian Journal of Infectious Diseases , 2008, DOI: 10.1590/S1413-86702008000300013
Abstract: this study verified the correlation between the serum levels of tnf alpha and different clinical forms of tuberculosis. we described a group of 24 patients presenting several clinical forms of tuberculosis and a control group of 13 healthy individuals. the levels of tnf alpha were measured by bioassay method. the levels of tnf-alpha had significant differences between the tuberculosis and control groups. the patients with abnormal chest x-ray findings had higher tnf alpha levels (15328.48 ± 4602.19 pg/ml) when compared to patients with normal x-rays (3353.18 ± 1495.29 pg/ml) (p<0.05). patients that lost weight had higher tnf alpha levels (15468.54 ± 4580.54 pg/ml) than those that didn't loose weight (2904.98 ± 1367.89) (p<0.05). the levels of tnf alpha were higher in patients with a positive ppd skin test than in those with a negative ppd test (p<0.05). there was a positive correlation between patients' clinical severity and the serum levels of tnf alpha. in patients with successive measurements of tnf alpha, we observed that there was a drop in cytokine levels, and also a clinical improvement concomitantly. we concluded that there was a correlation between serum tnf alpha levels and chest x-ray alterations, loss of weight, positive ppd skin test and clinical severity in patients with tuberculosis. there was evidence of a worse clinical outcome in patients with tuberculosis that presented higher tnf alpha serum levels.
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