Browsing by Author "Ramirez, G."

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    Electro-reduction of Oxygen to Water Mediated by Stable Glassy Carbon Electrodes Modified by Co(II)-porphyrins with Voluminous Meso-Substituent
    (2015) Marin, A., V; Aguirre, M. J.; Muena, J. P.; Dehaen, W.; Maes, W.; Ngo, Thien H.; Ramirez, G.; Arevalo, M. C.
    Glassy carbon electrodes were modified by physisorption of two different Co(II)-porphyrins, specifically designed and synthesized to study the effect of the substitution pattern (and the resulting steric hindrance) on the electrocatalytic behavior for a characteristic inner-sphere reaction such as the reduction of oxygen. In spite of the change in morphology caused by a change in the relative positions of the meso substituents, they showed practically the same behavior toward the electro-reduction of O-2. In both cases, water was obtained as the main product. The modified electrodes were also active toward the electro-reduction of hydrogen peroxide. Both electrodes were found stable for more than a month upon exposure to air and the current for the electro-reduction remained practically the same.
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    Improved photoelectrocatalytic effect of Co(ii) and Fe(iii) mixed porphyrins on graphite paste electrodes towards hydrogen evolution reaction
    (2019) Gidi Chomalí, Leyla Denisse; Honores Sotelo, Jessica Scarlet; Ibarra, J.; Arce, R.; Aguirre, M.J.; Ramirez, G.
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    REDUCTION OF beta-AMYLOID-INDUCED NEUROTOXICITY ON HIPPOCAMPAL CELL CULTURES BY MODERATE ACIDOSIS IS MEDIATED BY TRANSFORMING GROWTH FACTOR beta
    (PERGAMON-ELSEVIER SCIENCE LTD, 2009) Martin, R. Uribe San; Herrera Molina, R.; Olavarria, L.; Ramirez, G.; von Bernhardi, R.
    Progression of Alzheimer's disease (AD) is associated with chronic inflammation and microvascular alterations, which can induce impairment of brain perfusion because of vascular pathology and local acidosis. Acidosis can promote amyloidogenesis, which could further contribute to neurodegenerative changes. Nevertheless, there is also evidence that acidosis has neuroprotective effects in hypoxia models. Here we studied the effect of moderate acidosis on beta-amyloid (A beta)-mediated neurotoxicity. We evaluated morphological changes, cell death, nitrite production and reductive metabolism of hippocampal cultures from Sprague-Dawley rats exposed to A beta under physiological (pH 7.4) or moderate acidosis (pH 7.15-7.05). In addition, because transforming growth factor beta (TGF beta) 1 is neuroprotective and is induced by several pathophysiological conditions, we assessed its presence at the different pHs. The exposure of hippocampal cells to A beta induced a conspicuous reduction of neurites' arborization, as well as increased neuronal death and nitric oxide production. However, A beta neurotoxicity was significantly attenuated when hippocampal cultures were kept at pH 7.15-7.05, showing a 68% reduction on lactate dehydrogenase release compared with cultures exposed to A beta at pH 7.4 (P<0.01). Similarly, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide reduction increased 3.5-fold (P<0.05), and A beta-induced nitrite production was reduced by 65% when exposed to moderate acidosis compared with basal pH media (P<0.05). At the same time, moderate acidosis decreased intracellular TGF beta 1 precursor (latency associated protein-TGF beta 1) and increased up to fourfold TGF beta 1 bioactivity, detecting a 43% increase in the active TGF beta levels in cultures exposed to A beta and moderate acidosis. Inhibition of TGF beta signaling abolished the neuroprotective effect of moderate acidosis. Our results show that moderate acidosis protected hippocampal cells from A beta-mediated neurotoxicity through the increased activation and signaling potentiation of TGF beta. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.