Adsorption of O2, SO2, and SO3 on nickel oxide. Mechanism for sulfate formation

Calculations based on the atom superposition and electron delocalization molecular orbital (ASED-MO) technique suggest that O2 will adsorb perferentially end-on at an angle 45 deg from normal on a nickel cation site on the (100) surface of NiO. SO2 adsorption is also stronger on the nickel site; SO2 bonds through the sulfur atom is a plane perpendicular to the surface. Adsorption energies for SO3 on the nickel and oxygen sites are comparable in the perferred orientation in which the SO3 plane is parallel to the surface. On activation, SO3 adsorbed to an O2(-) site forms a trigonal pyramidal SO4 species which yields, with a low barrier, a tetrahedral sulfate anion. Subsequently the anion reorients on the surface. Possibilities for alternative mechanisms which require the formation of Ni3(+) or O2(-) are discussed. NiSO4 thus formed leads to the corrosion of Ni at high temperatures in the SO2+O2/SO3 The SO2+O2/SO3 atmosphere, as discussed in the experimental literature

CO adsorption on (111) and (100) surfaces of the Pt sub 3 Ti alloy. Evidence for parallel binding and strong activation of CO

The CO adsorption on a 40 atom cluster model of the (111) surface and a 36 atom cluster model of the (100) surface of the Pt3Ti alloy was studied. Parallel binding to high coordinate sites associated with Ti and low CO bond scission barriers are predicted for both surfaces. The binding of CO to Pt sites occurs in an upright orientation. These orientations are a consequence of the nature of the CO pi donation interactions with the surface. On the Ti sites the orbitals donate to the nearly empty Ti 3d band and the antibonding counterpart orbitals are empty. On the Pt sites, however, they are in the filled Pt 5d region of the alloy band, which causes CO to bond in a vertical orientation by 5 delta donation from the carbon end

Impact of Antiretroviral Therapy on Intestinal Lymphoid Tissues in HIV Infection

Veazey and Lackner discuss a new study which found that most patients who start antiretroviral drugs as early as possible after HIV infection still do not experience complete restoration of intestinal CD4+ T cells to baseline levels

Floating Spherical Gaussian Orbital (FSGO) Studies with a Model Potential: Methane, Silane & Germane

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Effect of divalent cation ionophore (A 23187) on renal handling of phosphorus

Effect of divalent cation ionophore (A 23187) on renal handling of phosphorus. To evaluate the effect of an increase in intracellular calcium on renal handling of phosphorus, calcium ionophore, which facilitates passive entry of calcium into cytosol, was given i.v. to four groups of rats: group 1, animals with intact parathyroid glands; group 2, parathyroidectomized (PTX) rats; group 3, PTX animals receiving i.v. parathyroid hormone (PTH); and group 4, PTX animals pretreated with i.v. ionophore, then given i.v. PTH. During the administration of ionophore in group 1, serum calcium (Sca) decreased from 8.7 ± 0.2 (mean ±SEM) to 7.5 ± 0.2mg/100 ml (P < 0.001), fractional excretion of phosphorus (CP/CIn) decreased from 0.110 ± 0.020 to 0.019 ± 0.006 (P < 0.001), and urinary cyclic 3′, 5′-adenosine monophosphate (UcAMP) decreased from 131 ± 23 to 46 ± 16 pmoles/min (P < 0.0125). In group 2, during the administration of ionophore, Sca decreased from 6.5 ± 0.2 to 5.7 ± 0.2mg/100 ml (P < 0.001), but neither CP/CIn nor UcAMP were altered. In group 2, during the administration of ionophore, CP/Cm decreased from 0.43 ± 0.05 to 0.19 ± 0.04 (P < 0.005), UcAMP decreased from 254 ± 20 to 159 ± 11 (P < 0.001). In group 4, during combined i.v. administration of ionophore and PTH, CP/CIn was reduced from 0.19 ± 0.009 to 0.044 ± 0.012 (P < 0.005), and serum calcium was reduced from 6.5 ± 0.3 to 5.1 ± 0.3mg/100 ml (P < 0.01). These findings indicate that i.v. ionophore suppresses urinary excretion of phosphorus, only in the presence of either endogenous or exogenous PTH. The associated decrease in UcAMP suggests that this effect could be mediated through inhibition of PTH-dependent formation of cAMP, possibly resulting from the ionophore-induced increase in intracellular calcium in renal tubular cells.Effet d'un ionophore des cations divalents (A 23187) sur le comportement renal vis a vis du phosphate. Afin d'évaluer l'effet de l'augmentation du calcium intracellulaire sur le comportement rénal vis à vis du phosphore, on a donné à quatre groupes de rats un ionophore de calcium qui facilite l'entrée passive de ce cation dans le cytosol. Le groupe 1 est composé d'animaux dont les parathyroïdes sont intactes, le groupe 2 d'animaux parathyroïdectomisés (PTX), le groupe 3 d'animaux PTX recevant de l'hormone parathyroïdienne (PTH) par voie intra-veineuse et le groupe 4 d'animaux pré-traités par l'ionophore qui reçoivent de la PTH. Au cours de l'administration de l'ionophore au groupe 1, le calcium séreique (SCa) diminue de 8,7 ± 0,2 (m ±SEM) à 7,5 ± 0,2mg/100 ml (P < 0,001), l'excrétion fractionnelle du phosphore (CP/CIn) diminue de 0,110 ± 0,020 à 0,019 ± 0,006 (P < 0,001) et l'AMP cyclique urinaire (UcAMP) diminue de 131 ± 23 à 46 ± 16 pmoles/min (P < 0,0125).Dans le groupe 2, au cours de l'administration de l'ionophore, Sca diminue de 6,5 ± 0,2 a 5,7 ± 0,2 mg/100 ml (P < 0,001), mais ni CP/CIn ni UcAMP ne sont modifiés. Dans le groupe 3, au cours de l'administration de l'ionophore, CP/CIn diminue de 254 ± 20 à 159 ± 11 (P < 0,001). Dans le groupe 4, au cours de l'administration combinée d'ionophore et de PTH, CP/CIn diminue de 0,19 ± 0,009 à 0,004 ± 0,012 (P < 0,005) et Sca de 6,5 ± 0,3 à 5,1 ± 0,3 mg/100 ml (P < 0,01). Ces constatations indiquent que l'ionophore ne diminue l'excrétion urinaire de phosphate qu'en présence de PTH endogène ou exogène. La baisse associée de UcAMP suggère que cet effet peut avoir pour médiateur l'inhibition de la formation d'AMP cyclique dépendante de la PTH, conséquence de l'augmentation du calcium intracellulaire dans les cellules tubulaires rénales, induite par l'ionophore

The BG News November 28, 2012

The BGSU campus student newspaper November 28, 2012. Volume 103 - Issue 43https://scholarworks.bgsu.edu/bg-news/9579/thumbnail.jp

Planning for pre-exposure prophylaxis to prevent HIV transmission: challenges and opportunities

There are currently several ongoing or planned trials evaluating the efficacy of pre-exposure prophylaxis (PrEP) as a preventative approach to reducing the transmission of HIV. PrEP may prove ineffective, demonstrate partial efficacy, or show high efficacy and have the potential to reduce HIV infection in a significant way. However, in addition to the trial results, it is important that issues related to delivery, implementation and further research are also discussed. As a part of the ongoing discussion, in June 2009, the Bill & Melinda Gates Foundation sponsored a Planning for PrEP conference with stakeholders to review expected trial results, outline responsible educational approaches, and develop potential delivery and implementation strategies. The conference reinforced the need for continued and sustained dialogue to identify where PrEP implementation may fit best within an integrated HIV prevention package. This paper identifies the key action points that emerged from the Planning for PrEP meeting

Strong mucosal immune responses in SIV infected macaques contribute to viral control and preserved CD4+ T-cell levels in blood and mucosal tissues

<p>Abstract</p> <p>Background</p> <p>Since there is still no protective HIV vaccine available, better insights into immune mechanism of persons effectively controlling HIV replication in the absence of any therapy should contribute to improve further vaccine designs. However, little is known about the mucosal immune response of this small unique group of patients. Using the SIV-macaque-model for AIDS, we had the rare opportunity to analyze 14 SIV-infected rhesus macaques durably controlling viral replication (controllers). We investigated the virological and immunological profile of blood and three different mucosal tissues and compared their data to those of uninfected and animals progressing to AIDS-like disease (progressors).</p> <p>Results</p> <p>Lymphocytes from blood, bronchoalveolar lavage (BAL), and duodenal and colonic biopsies were phenotypically characterized by polychromatic flow cytometry. In controllers, we observed higher levels of CD4+, CD4+CCR5+ and Gag-specific CD8+ T-cells as well as lower immune activation in blood and all mucosal sites compared to progressors. However, we could also demonstrate that immunological changes are distinct between these three mucosal sites.</p> <p>Intracellular cytokine staining demonstrated a significantly higher systemic and mucosal CD8+ Gag-specific cellular immune response in controllers than in progressors. Most remarkable was the polyfunctional cytokine profile of CD8+ lymphocytes in BAL of controllers, which significantly dominated over their blood response. The overall suppression of viral replication in the controllers was confirmed by almost no detectable viral RNA in blood and all mucosal tissues investigated.</p> <p>Conclusion</p> <p>A strong and complex virus-specific CD8+ T-cell response in blood and especially in mucosal tissue of SIV-infected macaques was associated with low immune activation and an efficient suppression of viral replication. This likely afforded a repopulation of CD4+ T-cells in different mucosal compartments to almost normal levels. We conclude, that a robust SIV-specific mucosal immune response seems to be essential for establishing and maintaining the controller status and consequently for long-term survival.</p

Treatment with IL-7 Prevents the Decline of Circulating CD4+ T Cells during the Acute Phase of SIV Infection in Rhesus Macaques

Although treatment with interleukin-7 (IL-7) was shown to transiently expand the naïve and memory T-cell pools in patients with chronic HIV-1 infection receiving antiretroviral therapy (ART), it is uncertain whether a full immunologic reconstitution can be achieved. Moreover, the effects of IL-7 have never been evaluated during acute HIV-1 (or SIV) infection, a critical phase of the disease in which the most dramatic depletion of CD4+ T cells is believed to occur. In the present study, recombinant, fully glycosylated simian IL-7 (50 µg/kg, s.c., once weekly for 7 weeks) was administered to 6 rhesus macaques throughout the acute phase of infection with a pathogenic SIV strain (mac251); 6 animals were infected at the same time and served as untreated controls. Treatment with IL-7 did not cause clinically detectable side effects and, despite the absence of concomitant ART, did not induce significant increases in the levels of SIV replication except at the earliest time point tested (day 4 post-infection). Strikingly, animals treated with IL-7 were protected from the dramatic decline of circulating naïve and memory CD4+ T cells that occurred in untreated animals. Treatment with IL-7 induced only transient T-cell proliferation, but it was associated with sustained increase in the expression of the anti-apoptotic protein Bcl-2 on both CD4+ and CD8+ T cells, persistent expansion of all circulating CD8+ T-cell subsets, and development of earlier and stronger SIV Tat-specific T-cell responses. However, the beneficial effects of IL-7 were not sustained after treatment interruption. These data demonstrate that IL-7 administration is effective in protecting the CD4+ T-cell pool during the acute phase of SIV infection in macaques, providing a rationale for the clinical evaluation of this cytokine in patients with acute HIV-1 infection