82 resultados para Solid oxide fuel cells (SOFC)


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We have used a pharmacological approach to study the mechanisms underlying the rat lung injury and the airway reactivity changes induced by inhalation of formaldehyde (FA) (1% formalin solution, 90 min once a day, 4 days). The reactivity of isolated tracheae and intrapulmonary bronchi were assessed in dose-response curves to methacholine (MCh). Local and systemic inflammatory phenomena were evaluated in terms of leukocyte countings in bronchoalveolar lavage (BAL) fluid, blood, bone marrow lavage and spleen. Whereas the tracheal reactivity to MCh did not change, a significant bronchial hyporesponsiveness (BHR) was found after FA inhalation as compared with naive rats. Also, FA exposure significantly increased the total cell numbers in BAL, in peripheral blood and in the spleen, but did not modify the counts in bone marrow. Capsaicin hindered the increase of leukocyte number recovered in BAL fluid after FA exposure. Both compound 48/80 and indomethacin were able to prevent the lung neutrophil influx after FA, but indomethacin had no effect on that of mononuclear cells. Following FA inhalation, the treatment with sodium cromoglycate (SCG), but not with the nitric oxide (NO) synthase inhibitor L-NAME, significantly reduced the total cell number in BAL. Compound 48/80, L-NAME and SCG significantly prevented BHR to MCh after FA inhalation, whereas capsaicin was inactive in this regard. on the other hand, indomethacin exacerbated BHR. These data suggest that after FA inhalation, the resulting lung leukocyte influx and BHR may involve nitric oxide, airway sensory fibers and mast cell-derived mediators. The effect of NO seemed to be largely restricted to the bronchial tonus, whereas neuropeptides appeared to be linked to the inflammatory response, therefore indicating that the mechanisms responsible for the changes of airway responsiveness caused by FA may be separate from those underlying its inflammatory lung effects. (c) 2005 Elsevier B.V. All rights reserved.

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Interleukin-1 (IL-1) may be a mediator of β-cell damage in insulin-dependent diabetes mellitus (IDDM). The IL-1 mechanism of action on insulin-producing cells probably includes activation of the transcription nuclear factor κB (NF-κB), increased transcription of the inducible form of nitric oxide synthase (iNOS) and the subsequent production of nitric oxide (NO). Reactive oxygen intermediates, particularly H2O2, have been proposed as second messengers for NF-κB activation. In the present study, we tested whether ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one), a glutathione peroxidase mimicking compound, could counteract the effects of IL-1β, H2O2 and alloxan in rat pancreatic islets and in the rat insulinoma cell line RINm5F (RIN cells). Some of these experiments were also reproduced in human pancreatic islets. Ebselen (20 μM) prevented the increase in nitrite production by rat islets exposed to IL-1β for 6 hr and induced significant protection against the acute inhibitory effects of alloxan or H2O2 exposure, as judged by the preserved glucose oxidation rates. However, ebselen failed to prevent the increase in nitrite production and the decrease in glucose oxidation and insulin release by rat islets exposed to IL-1β for 24 hr. Ebselen prevented the increase in nitrite production by human islets exposed for 14 hr to a combination of cytokines (IL-1β, tumor necrosis factor-α and interferon-γ). In RIN cells, ebselen counteracted both the expression of iNOS mRNA and the increase in nitrite production induced by 6 hr exposure to IL-β but failed to block IL-1β-induced iNOS expression following 24 hr exposure to the cytokine. Moreover, ebselen did not prevent IL-1β-induced NF-κB activation. As a whole, these data indicate that ebselen partially counteracts cytokine-induced NOS activation in pancreatic β-cells, an effect not associated with inhibition of NF-κB activation.

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This work reports on the changes of performance of solid-state cells dye-sensitized solar cells with the variation of concentration of spiro-OMeTAD between 5% and 25% in the fabrication of the cell. Variations of charge recombination and capacitance correlate with the improvement of current-potential characteristics at increasing spiro-OMeTAD content, which is explained by reduction of transport resistance for hole transport, the increase of charge separation in the dye molecules, and importantly, with the increase of the β-factor in the recombination resistance, that causes a reduction of the diode ideality factor. © 2010 Materials Research Society.

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This work describes the synthesis and characterization of a new octakis[3-(2,2'-dipyridylamine)propyl]octasilsesquioxane (T8-Pr-DPA), and a study of the metal ion preconcentration in fuel ethanol. Batch and column experiments were conducted to investigate for the removal of heavy metal ions from fuel ethanol. The results showed that the Langmuir allowed to describe the sorption equilibrium data of the metal ions on T8-Pr-DPA in a satisfactory way. The following maximum adsorption capacities (in mmolg-1) were determined: 3.62 for Fe (III), 3.32 for Cr (III), 2.15 for Cu (II), 1.80 for Co (II), 1.62 for Pb (II), 1.32 for Ni (II) and 0.88 for Zn (II). The thermodynamic parameters for the adsorption process such as free energy of adsorption (δG), enthalpy of adsorption (δH) and entropy of adsorption (δS) were calculated. Thermodynamic parameters showed that the system has favorable enthalpic, Gibbs free energy, and entropic values. The sorption-desorption of the metal ions has made possible the development of a preconcentration and determination method of metal ions at trace level in fuel ethanol. The method of quantitative analysis for Fe, Cu, Ni and Zn in fuel ethanol by Flame AAS was validated. Several parameters have been taken into account and evaluated for the validation of method, namely: linearity, limit of detection, limit of quantification, and the relative standard deviation and accuracy. The accuracy of the method was assessed by testing analyte recovery in the fuel ethanol samples. © 2013 Elsevier B.V.

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