The Kinetics of the Silver(i)-induced Oxidation of Chromium(iii) by Peroxodisulphate

Chromium(III) and chromium(VI) compounds play an important role in natural oxidation processes in terrestrial and atmospheric water. During the oxidation of SO2, peroxodisulphate is formed as an intermediate. In acidic and neutral solutions, peroxodisulphate oxidizes chromium(III) very slowly. This reaction rate is markedly enhanced by silver ions, resulting in a reaction rate that allows the reaction to be studied conveniently under laboratory conditions. The kinetics of the Cr(III)/Ag(I)/S2O82– reaction system were studied as a function of different Cr(III), Ag(I) and S2O82– concentrations, temperature and pressure. The formation of Cr(VI) was observed as a first-order process at high [Cr(III)] and as a zero-order process at low [Cr(III)].Aninduction period was observed in both cases. For the first-order process, reaction rates were found to be independent of [Cr(III)], linearly dependent on [Ag+] and independent of [S2O82–]. The activation enthalpy (ΔH≠) was calculated as 56 ± 5 kJ mol–1, the activation entropy (ΔS≠) as –136 ± 16 J K–1 mol–1 and the activation volume as –5.8 ± 0.7 cm3 mol–1. At low [Cr(III)], the reaction rate was independent of [Cr(III)], linearly dependent on [S2O82–] and non-linearly dependent on [Ag+], reaching a limiting value at high [Ag+]. The activation enthalpy (ΔH≠) was calculated as 61±5kJmol–1, the activation entropy (ΔS≠) as –119±15 J K–1 mol–1 and the activation volume as –1.7±0.1 cm3 mol–1. A mechanism involving the reversible formation of a silver-peroxodisulphate complex that decomposes into oxidizing intermediates is proposed. The empirical observations can be adequately described by this mechanism.Keywords: Chromium(III), peroxodisulphate, oxidation, silver

Observations of the Crab Nebula with H.E.S.S. Phase II

The High Energy Stereoscopic System (H.E.S.S.) phase I instrument was an array of four $100\,\mathrm{m}^2$ mirror area Imaging Atmospheric Cherenkov Telescopes (IACTs) that has very successfully mapped the sky at photon energies above $\sim 100\,$GeV. Recently, a $600\,\mathrm{m}^2$ telescope was added to the centre of the existing array, which can be operated either in standalone mode or jointly with the four smaller telescopes. The large telescope lowers the energy threshold for gamma-ray observations to several tens of GeV, making the array sensitive at energies where the Fermi-LAT instrument runs out of statistics. At the same time, the new telescope makes the H.E.S.S. phase II instrument. This is the first hybrid IACT array, as it operates telescopes of different size (and hence different trigger rates) and different field of view. In this contribution we present results of H.E.S.S. phase II observations of the Crab Nebula, compare them to earlier observations, and evaluate the performance of the new instrument with Monte Carlo simulations.Comment: In Proceedings of the 34th International Cosmic Ray Conference (ICRC2015), The Hague, The Netherland

Microglial-Associated Responses to Comorbid Amyloid Pathology and Hyperhomocysteinemia in an Aged Knock-in Mouse Model of Alzheimer\u27s Disease

BACKGROUND: Elevated blood homocysteine levels, termed hyperhomocysteinemia (HHcy), is a prevalent risk factor for Alzheimer\u27s disease (AD) in elderly populations. While dietary supplementation of B-vitamins is a generally effective method to lower homocysteine levels, there is little if any benefit to cognition. In the context of amyloid pathology, dietary-induced HHcy is known to enhance amyloid deposition and certain inflammatory responses. Little is known, however, about whether there is a more specific effect on microglia resulting from combined amyloid and HHcy pathologies. METHODS: The present study used a knock-in mouse model of amyloidosis, aged to 12 months, given 8 weeks of B-vitamin deficiency-induced HHcy to better understand how microglia are affected in this comorbidity context. RESULTS: We found that HHcy-inducing diet increased amyloid plaque burden, altered the neuroinflammatory milieu, and upregulated the expression of multiple damage-associated and homeostatic microglial genes. CONCLUSIONS: Taken together, these data indicate complex effects of comorbid pathologies on microglial function that are not driven solely by increased amyloid burden. Given the highly dynamic nature of microglia, their central role in AD pathology, and the frequent occurrence of various comorbidities in AD patients, it is increasingly important to understand how microglia respond to mixed pathological processes

Personality, depressive symptoms, the interparental relationship and parenting: Prospective associations of an actor-partner interdependency model.

Grounded on Belsky's process model and family systems theories and using an actor-partner interdependency modeling (APIM) approach (Belsky & Jaffee, 2006; Cox & Paley, 2003), the current study was the first to examine whether Big Five personality characteristics and depressive symptoms of parents and their partners are related to adolescent-perceived parenting behavior directly and indirectly via interparental stress experienced by both parents. Longitudinal data (Time 1: 2001; Time 2: 2007; and Time 3: 2009) from a large community sample of Flemish families was used (N = 455; Time 1 children: Mage = 7.10 years). Results revealed that, for both parents, more agreeableness and autonomy predicted more parental warmth, and more depressive symptoms and lower agreeableness predicted more overreactive discipline (i.e., actor effects). Both parents' depressive symptoms predicted their own interparental stress (i.e., actor effects). Regarding partner-effects, paternal overreactive discipline was shaped by mother's extraversion and experienced interparental stress, and paternal warmth was affected by mother's experienced interparental stress in addition to fathers' own psychological resources. In contrast, maternal parenting was affected by their own psychological resources only. Although no consistent mediating role of interparental stress was found, one small dyadic indirect effect indicated that maternal depressive symptoms were related to more paternal overreactive discipline via heightened levels of interparental stress experienced by both parents. These results provide new support for the idea of interdependency between parents and specifically support the fathering vulnerability hypothesis. Tentatively, this study informs clinical practice by showing that family interventions aiming to improve parenting should pay attention to specific personality characteristics affecting parenting behavior and adopt a dyadic approach including both parents, especially when targeting paternal parenting. (PsycINFO Database Record (c) 2019 APA, all rights reserved)

Mechanism of tetrachloroplatinate(II) oxidation by hydrogen peroxide in hydrochloric acid solution

Oxidation of tetrachloroplatinate(II) by hydrogen peroxide in hydrochloric acid was studied by UV-Vis spectrophotometry. Oxidation takes place via two parallel reactions with hypochlorous acid and hydrogen peroxide, respectively, according to the overall rate law d[Pt(IV)]/dt = (k0 + kH2O2[Pt(II)])[H2O2]. For oxidation of [PtCl4]2− at relatively low concentrations, [PtCl4]2− ≪ 0.5 mM, hypochlorous acid formation is fast relative to the oxidation of [PtCl4]2− by hydrogen peroxide, as a result of the rate determining reaction H2O2 + H+ + Cl− → HOCl + H2O, resulting in a rate law d[Pt(IV)]/dt = k0[H2O2] with a value k0 = (8 ± 2) × 10−7 s−1 at 35 °C. For concentrations of [PtCl4]2− > 0.5 mM, oxidation by hydrogen peroxide becomes dominant, resulting in the pseudo-first order rate law d[Pt(IV)]/dt = kH2O2[Pt(II)][H2O2] with the value kH2O2 = (1.5 ± 0.1) × 10−2 M−1 s−1 at 35 °C. The final oxidation product is a mixture of [PtCl5(H2O)]− and [PtCl6]2−, with [PtCl6]2− formed as a result of [PtCl4]2− assisted chloride anation reactions

Spectroscopic and kinetic evidence for redox cycling, catalase and degradation activities of MnIII(TPPS) in a basic aqueous peroxide medium

MnIII(TPPS) was found to react rapidly with hydrogen peroxide in basic aqueous solution to form intermediate (TPPS)MnV[double bond, length as m-dash]O and (TPPS)MnIV[double bond, length as m-dash]O species which, in the presence of excess H2O2, are reduced fully back to MnIII(TPPS) with clear evidence for redox cycling of MnIII(TPPS). The system shows very strong catalase and degradation activities

Microglial p38α MAPK is a key regulator of proinflammatory cytokine up-regulation induced by toll-like receptor (TLR) ligands or beta-amyloid (Aβ)

<p>Abstract</p> <p>Background</p> <p>Overproduction of proinflammatory cytokines from activated microglia has been implicated as an important contributor to pathophysiology progression in both acute and chronic neurodegenerative diseases. Therefore, it is critical to elucidate intracellular signaling pathways that are significant contributors to cytokine overproduction in microglia exposed to specific stressors, especially pathways amenable to drug interventions. The serine/threonine protein kinase p38α MAPK is a key enzyme in the parallel and convergent intracellular signaling pathways involved in stressor-induced production of IL-1β and TNFα in peripheral tissues, and is a drug development target for peripheral inflammatory diseases. However, much less is known about the quantitative importance of microglial p38α MAPK in stressor-induced cytokine overproduction, or the potential of microglial p38α MAPK to be a druggable target for CNS disorders. Therefore, we examined the contribution of microglial p38αMAPK to cytokine up-regulation, with a focus on the potential to suppress the cytokine increase by inhibition of the kinase with pharmacological or genetic approaches.</p> <p>Methods</p> <p>The microglial cytokine response to TLR ligands 2/3/4/7/8/9 or to Aβ_1-42was tested in the presence of a CNS-penetrant p38α MAPK inhibitor, MW01-2-069A-SRM. Primary microglia from mice genetically deficient in p38α MAPK were used to further establish a linkage between microglia p38α MAPK and cytokine overproduction. The <it>in vivo </it>significance was determined by p38α MAPK inhibitor treatment in a LPS-induced model of acute neuroinflammation.</p> <p>Results</p> <p>Increased IL-1β and TNFα production by the BV-2 microglial cell line and by primary microglia cultures was inhibited in a concentration-dependent manner by the p38α MAPK-targeted inhibitor. Cellular target engagement was demonstrated by the accompanying decrease in the phosphorylation state of two p38α MAPK protein substrates, MK2 and MSK1. Consistent with the pharmacological findings, microglia from p38α-deficient mice showed a diminished cytokine response to LPS. Further, oral administration of the inhibitor blocked the increase of IL-1β in the cerebral cortex of mice stressed by intraperitoneal injection of LPS.</p> <p>Conclusion</p> <p>The p38α MAPK pathway is an important contributor to the increased microglial production of proinflammatory cytokines induced by diverse stressors. The results also indicate the feasibility of targeting p38α MAPK to modulate CNS proinflammatory cytokine overproduction.</p

Solvent, salt and high pressure effects on the rate and equilibrium constants for the formation of tri-n-butylphosphoniumdithiocarboxylate

Solvent, salt and high pressure effects on the rate and equilibrium constants for the formation of tri-n-butylphosphoniumdithiocarboxylate at 298.2 K are reported. This equilibrium is shifted to the phosphobetaine in polar solvents, salt solutions and under high external pressure. The reaction volume changes dramatically on going from less polar diethyl ether (-69 cm3 mol-1) and tetrahydrofurane (THF) (-66 cm3 mol -1), to more polar acetonitrile (-39 cm3 mol-1) and acetone (-38 cm3 mol-1). Copyright © 2010 John Wiley & Sons, Ltd

Brain Structure Changes over Time in Normal and Mildly Impaired Aged Persons

Structural brain changes in aging are known to occur even in the absence of dementia, but the magnitudes and regions involved vary between studies. To further characterize these changes, we analyzed paired MRI images acquired with identical protocols and scanner over a median 5.8-year interval. The normal study group comprised 78 elders (25M 53F, baseline age range 70-78 years) who underwent an annual standardized expert assessment of cognition and health and who maintained normal cognition for the duration of the study. We found a longitudinal grey matter (GM) loss rate of 2.56 ± 0.07 ml/year (0.20 ± 0.04%/year) and a cerebrospinal fluid (CSF) expansion rate of 2.97 ± 0.07 ml/year (0.22 ± 0.04%/year). Hippocampal volume loss rate was higher than the GM and CSF global rates, 0.0114 ± 0.0004 ml/year (0.49 ± 0.04%/year). Regions of greatest GM loss were posterior inferior frontal lobe, medial parietal lobe and dorsal cerebellum. Rates of GM loss and CSF expansion were on the low end of the range of other published values, perhaps due to the relatively good health of the elder volunteers in this study. An additional smaller group of 6 subjects diagnosed with MCI at baseline were followed as well, and comparisons were made with the normal group in terms of both global and regional GM loss and CSF expansion rates. An increased rate of GM loss was found in the hippocampus bilaterally for the MCI group