480 research outputs found

    Does the Eco-Management and Audit Scheme Foster Innovation in European Firms?

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    This paper studies whether environmental management systems can spur eco-innovation, analyzing EMAS (Eco-Management and Audit Scheme) adoption and patented innovations (at the European Patent Office) at firm level. It uses an original panel database of 30 439 European firms belonging to all sectors from 2003 to 2012. An original instrumental variable is implemented to control for potential endogeneity. The analysis reveals that EMAS adoption is conducive to more innovation at the firm level. The results vary across countries and sectors. In particular, EMAS is positively related to green patents for medium and low technology manufacturing. Copyright \ua9 2017 John Wiley & Sons, Ltd and ERP Environment

    Oxidative stress and immunosenescence in spleen of obese mice can be reversed by 2-hydroxyoleic acid.

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    We aimed to investigate the effects of obesity on oxidative stress and leukocyte function in spleen of mice, and to assess whether supplementation with 2-hydroxyoleic acid (2-OHOA) or n-3 polyunsaturated fatty acids (PUFA) could reverse those effects. Female ICR/CD1 mice (8 weeks old, n = 24) received an obesogenic diet (22% fat for 4 weeks and 60% fat for 14 weeks). After 6 weeks, mice were split in three groups (n = 8/group): no supplementation, 2-OHOA supplementation (1500 mg kg(-1) ) and n-3 PUFA supplementation (EPA + DHA, 3000 mg kg(-1) diet). Eight mice were fed standard diet for the whole duration of the study (control group). At the end of the experiment, the following variables were assessed in spleens: levels of reduced (GSH) and oxidized (GSSG) glutathione, GSH/GSSG, xanthine oxidase (XO) activity, lipid peroxidation, lymphocyte chemotaxis, natural killer (NK) activity and mitogen (ConA and LPS)-induced lymphocyte proliferation. Obese animals presented higher GSSG levels (P = 0.003), GSSG/GSH ratio (P = 0.013), lipid peroxidation (P = 0.004), XO activity (P = 0.015) and lymphocyte chemotaxis (P < 0.001), and lower NK activity (P = 0.003) and proliferation in response to ConA (P < 0.001) than controls. 2-OHOA reversed totally or partially most of the changes (body weight, fat content, GSSG levels, GSH/GSSG, lipid peroxidation, chemotaxis and proliferation, all P < 0.05), while n-3 PUFA reversed the increase in XO activity (P = 0.032). In conclusion, 2-OHOA, and to a lesser extent n-3 PUFA, could ameliorate the oxidative stress and alteration of leukocyte function in spleen of obese mice. Our findings support a link between obesity and immunosenescence and suggest a potential therapeutic tool for obesity-related immune dysfunction. This article is protected by copyright. All rights reserved

    In Silico Analysis of the Apolipoprotein E and the Amyloid β Peptide Interaction: Misfolding Induced by Frustration of the Salt Bridge Network

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    The relationship between Apolipoprotein E (ApoE) and the aggregation processes of the amyloid β (Aβ) peptide has been shown to be crucial for Alzheimer's disease (AD). The presence of the ApoE4 isoform is considered to be a contributing risk factor for AD. However, the detailed molecular properties of ApoE4 interacting with the Aβ peptide are unknown, although various mechanisms have been proposed to explain the physiological and pathological role of this relationship. Here, computer simulations have been used to investigate the process of Aβ interaction with the N-terminal domain of the human ApoE isoforms (ApoE2, ApoE3 and ApoE4). Molecular docking combined with molecular dynamics simulations have been undertaken to determine the Aβ peptide binding sites and the relative stability of binding to each of the ApoE isoforms. Our results show that from the several ApoE isoforms investigated, only ApoE4 presents a misfolded intermediate when bound to Aβ. Moreover, the initial α-helix used as the Aβ peptide model structure also becomes unstructured due to the interaction with ApoE4. These structural changes appear to be related to a rearrangement of the salt bridge network in ApoE4, for which we propose a model. It seems plausible that ApoE4 in its partially unfolded state is incapable of performing the clearance of Aβ, thereby promoting amyloid forming processes. Hence, the proposed model can be used to identify potential drug binding sites in the ApoE4-Aβ complex, where the interaction between the two molecules can be inhibited

    Inducible and constitutive heat shock gene expression responds to modification of Hsp70 copy number in Drosophila melanogaster but does not compensate for loss of thermotolerance in Hsp70 null flies

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    <p>Abstract</p> <p>Background</p> <p>The heat shock protein Hsp70 promotes inducible thermotolerance in nearly every organism examined to date. Hsp70 interacts with a network of other stress-response proteins, and dissecting the relative roles of these interactions in causing thermotolerance remains difficult. Here we examine the effect of <it>Hsp70 </it>gene copy number modification on thermotolerance and the expression of multiple stress-response genes in <it>Drosophila melanogaster</it>, to determine which genes may represent mechanisms of stress tolerance independent of Hsp70.</p> <p>Results</p> <p><it>Hsp70 </it>copy number in four strains is positively associated with <it>Hsp70 </it>expression and inducible thermotolerance of severe heat shock. When assayed at carefully chosen temperatures, <it>Hsp70 </it>null flies are almost entirely deficient in thermotolerance. In contrast to expectations, increasing <it>Hsp70 </it>expression levels induced by thermal pretreatment are associated with increasing levels of seven other inducible <it>Hsps </it>across strains. In addition, complete <it>Hsp70 </it>loss causes upregulation of the inducible <it>Hsps </it>and six constitutive stress-response genes following severe heat shocks.</p> <p>Conclusion</p> <p>Modification of <it>Hsp70 </it>copy number quantitatively and qualitatively affects the expression of multiple other stress-response genes. A positive association between absolute expression levels of <it>Hsp70 </it>and other <it>Hsps </it>after thermal pretreatment suggests novel regulatory mechanisms. Severe heat shocks induce both novel gene expression patterns and almost total mortality in the <it>Hsp70 </it>null strain: alteration of gene expression in this strain does not compensate for <it>Hsp70 </it>loss but suggests candidates for overexpression studies.</p

    Observation of an Exotic S=+1S=+1 Baryon in Exclusive Photoproduction from the Deuteron

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    In an exclusive measurement of the reaction γdK+Kpn\gamma d \to K^+ K^- p n, a narrow peak that can be attributed to an exotic baryon with strangeness S=+1S=+1 is seen in the K+nK^+n invariant mass spectrum. The peak is at 1.542±0.0051.542\pm 0.005 GeV/c2^2 with a measured width of 0.021 GeV/c2^2 FWHM, which is largely determined by experimental mass resolution. The statistical significance of the peak is 5.2±0.6σ5.2 \pm 0.6 \sigma. The mass and width of the observed peak are consistent with recent reports of a narrow S=+1S=+1 baryon by other experimental groups.Comment: 5 pages, 5 figure

    Measurement of the Polarized Structure Function σLT\sigma_{LT^\prime} for p(e,ep)πop(\vec{e},e'p)\pi^o in the Δ(1232)\Delta(1232) Resonance Region

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    The polarized longitudinal-transverse structure function σLT\sigma_{LT^\prime} has been measured in the Δ(1232)\Delta(1232) resonance region at Q2=0.40Q^2=0.40 and 0.65 GeV2^2. Data for the p(e,ep)πop(\vec e,e'p)\pi^o reaction were taken at Jefferson Lab with the CEBAF Large Acceptance Spectrometer (CLAS) using longitudinally polarized electrons at an energy of 1.515 GeV. For the first time a complete angular distribution was measured, permitting the separation of different non-resonant amplitudes using a partial wave analysis. Comparison with previous beam asymmetry measurements at MAMI indicate a deviation from the predicted Q2Q^2 dependence of σLT\sigma_{LT^{\prime}} using recent phenomenological models.Comment: 5 pages, LaTex, 4 eps figures: to be published in PRC/Rapid Communications. Version 2 has revised Q^2 analysi
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