9 research outputs found

    An Examination of the Oxygen Reduction Reaction on RuO2-based Oxide Coatings Formed on Titanium Substrates

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    The RuO2-based electrocatalysts were prepared by using a dip-coating method on Ti plate substrates at 400 degrees C. The catalytic activity of the oxide-coated electrodes for the oxygen reduction reaction (ORR) was evaluated by cyclic voltammetry in 0.5 M H2SO4 at 60 degrees C in a stationary state. The examination was focused on the enhancement of the catalytic activity in the reaction by the enlargement of the surface area of the RuO2 coating with the help of lanthunum. The onset potential for the ORR, EORR-0, of the RuO2/Ti electrode showed that the highest value was 0.84 V vs. RHE.ArticleCatalysis Today. 146(1-2):248-252. (2009)journal articl

    Erythromycin derivatives inhibit HIV-1 replication in macrophages through modulation of MAPK activity to induce small isoforms of C/EBPĪ²

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    Macrophages (MĪ¦s) are a major source of HIV-1 especially in patients with tuberculosis. There are MĪ¦s that are permissive and those that restrict HIV-1. Regulation of hematopoietic cell kinase (Hck) activity and selective expression of CCAAT enhancer binding protein Ī² (C/EBPĪ²) isoforms greatly contribute to determine distinct susceptibility of MĪ¦s to HIV-1. Resistance is attributable to reduced expression of Hck and augmented expression of an inhibitory small isoform of C/EBPĪ². Derivatives of erythromycin A (EMA) EM201 and EM703 inhibit the replication of HIV-1 in tissue MĪ¦s, at posttranscriptional and translational levels. We demonstrate that EM201 and EM703 convert tissue MĪ¦s from HIV-1 susceptible to HIV-1 resistant through down-regulation of Hck and induction of small isoforms of C/EBPĪ². These drugs inhibit p38MAPK activation which is expressed only in susceptible tissue MĪ¦s. Activated CD4+T cells stimulate the viral replication in HIV-1 resistant MĪ¦s through down-regulation of small isoforms of C/EBPĪ² via activation of ERK1/2. EM201 and EM703 can inhibit the MAPK activation and inhibit the burst of viral replication produced when CD4+T cells and MĪ¦s interact. These EM derivatives may be highly beneficial for repression of residual HIV-1 in the lymphoreticular system of HIV-1-infected patients and offer great promise for the creation of new anti-HIV drugs for the future treatment of AIDS patients

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