27 research outputs found

    The Leverage of Demographic Dynamics on Carbon Dioxide Emissions: Does Age Structure Matter?

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    This article provides a methodological contribution to the study of the effect of changes in population age structure on carbon dioxide (CO2) emissions. First, I propose a generalization of the IPAT equation to a multisector economy with an age-structured population and discuss the insights that can be obtained in the context of stable population theory. Second, I suggest a statistical model of household consumption as a function of household size and age structure to quantitatively evaluate the extent of economies of scale in consumption of energy-intensive goods, and to estimate age-specific profiles of consumption of energy-intensive goods and of CO2 emissions. Third, I offer an illustration of the methodologies using data for the United States. The analysis shows that per-capita CO2 emissions increase with age until the individual is in his or her 60s, and then emissions tend to decrease. Holding everything else constant, the expected change in U.S. population age distribution during the next four decades is likely to have a small, but noticeable, positive impact on CO2 emissions

    Onset dynamics of type A botulinum neurotoxin-induced paralysis

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    Experimental studies have demonstrated that botulinum neurotoxin serotype A (BoNT/A) causes flaccid paralysis by a multi-step mechanism. Following its binding to specific receptors at peripheral cholinergic nerve endings, BoNT/A is internalized by receptor-mediated endocytosis. Subsequently its zinc-dependent catalytic domain translocates into the neuroplasm where it cleaves a vesicle-docking protein, SNAP-25, to block neurally evoked cholinergic neurotransmission. We tested the hypothesis that mathematical models having a minimal number of reactions and reactants can simulate published data concerning the onset of paralysis of skeletal muscles induced by BoNT/A at the isolated rat neuromuscular junction (NMJ) and in other systems. Experimental data from several laboratories were simulated with two different models that were represented by sets of coupled, first-order differential equations. In this study, the 3-step sequential model developed by Simpson (J Pharmacol Exp Ther 212:16–21,1980) was used to estimate upper limits of the times during which anti-toxins and other impermeable inhibitors of BoNT/A can exert an effect. The experimentally determined binding reaction rate was verified to be consistent with published estimates for the rate constants for BoNT/A binding to and dissociating from its receptors. Because this 3-step model was not designed to reproduce temporal changes in paralysis with different toxin concentrations, a new BoNT/A species and rate (kS) were added at the beginning of the reaction sequence to create a 4-step scheme. This unbound initial species is transformed at a rate determined by kS to a free species that is capable of binding. By systematically adjusting the values of kS, the 4-step model simulated the rapid decline in NMJ function (kS ≥0.01), the less rapid onset of paralysis in mice following i.m. injections (kS = 0.001), and the slow onset of the therapeutic effects of BoNT/A (kS < 0.001) in man. This minimal modeling approach was not only verified by simulating experimental results, it helped to quantitatively define the time available for an inhibitor to have some effect (tinhib) and the relation between this time and the rate of paralysis onset. The 4-step model predicted that as the rate of paralysis becomes slower, the estimated upper limits of (tinhib) for impermeable inhibitors become longer. More generally, this modeling approach may be useful in studying the kinetics of other toxins or viruses that invade host cells by similar mechanisms, e.g., receptor-mediated endocytosis

    Relating industrial symbiosis and circular economy to the sustainable development debate

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    Industrial Symbiosis (IS) is a business-focused collaborative approach oriented towards resource efficiency that has been theorised and studied mainly over the last twenty-five years. Recently, IS seems to have found a renewed impetus in the framework of the Circular Economy (CE), a novel approach to sustainability and Sustainable Development (SD) that has been rapidly gaining momentum world-wide. This opening chapter of the book provides an introduction to the concepts of IS, CE and SD, and summarizes their complex evolutionary paths, recalling the rel-evant developments and implementation challenges. In addition, the authors point out the divergences and interrelations of these concepts, both among themselves and with other related concepts and research fields, such as industrial ecology, eco-logical modernization and the green economy. Furthermore, the potential contribu-tion of IS and the CE to SD is briefly discussed, also highlighting critical issues and trade-offs, as well as gaps in research and application, especially relating to the so-cial component of sustainability. Particular attention is given to the potential role of IS in the achievement of targets connected to the Sustainable Development Goals set in the UN Agenda 2030. The recent advances in the IS and CE discussion in the context of the SD research community are further explored, with particular empha-sis on the contribution of the International Sustainable Development Research So-ciety (ISDRS) and its 24th annual conference organised in Messina, Italy, in 2018. The programme of that conference, indeed, included specific tracks on the above-mentioned themes, the contents of which are briefly commented on here, after an overview on the whole conference and the main cross-cutting concepts emerged. In the last part of the chapter, a brief description of the chapters collected in the book is presented. These contributions describe and discuss theoretical frameworks, methodological approaches and/or experiences and case studies where IS and the principles of CE are applied in different geographical context and at different scales to ultimately improve the sustainability of the current production patterns

    Alteration in Superoxide Dismutase 1 Causes Oxidative Stress and p38 MAPK Activation Following RVFV Infection

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    Rift Valley fever (RVF) is a zoonotic disease caused by Rift Valley fever virus (RVFV). RVFV is a category A pathogen that belongs to the genus Phlebovirus, family Bunyaviridae. Understanding early host events to an infectious exposure to RVFV will be of significant use in the development of effective therapeutics that not only control pathogen multiplication, but also contribute to cell survival. In this study, we have carried out infections of human cells with a vaccine strain (MP12) and virulent strain (ZH501) of RVFV and determined host responses to viral infection. We demonstrate that the cellular antioxidant enzyme superoxide dismutase 1 (SOD1) displays altered abundances at early time points following exposure to the virus. We show that the enzyme is down regulated in cases of both a virulent (ZH501) and a vaccine strain (MP12) exposure. Our data demonstrates that the down regulation of SOD1 is likely to be due to post transcriptional processes and may be related to up regulation of TNFα following infection. We also provide evidence for extensive oxidative stress in the MP12 infected cells. Concomitantly, there is an increase in the activation of the p38 MAPK stress response, which our earlier published study demonstrated to be an essential cell survival strategy. Our data suggests that the viral anti-apoptotic protein NSm may play a role in the regulation of the cellular p38 MAPK response. Alterations in the host protein SOD1 following RVFV infection appears to be an early event that occurs in multiple cell types. Activation of the cellular stress response p38 MAPK pathway can be observed in all cell types tested. Our data implies that maintaining oxidative homeostasis in the infected cells may play an important role in improving survival of infected cells

    Rationale and design of the Sodium Lowering In Dialysate (SoLID) trial: a randomised controlled trial of low versus standard dialysate sodium concentration during hemodialysis for regression of left ventricular mass

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    Which method of estimating renal function is the best predictor of mortality after coronary artery bypass grafting?

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    Objectives Definitions of renal function in patients undergoing coronary artery bypass graft surgery (CABG) vary in the literature. We sought to investigate which method of estimating renal function is the best predictor of mortality after CABG. Methods We analysed the preoperative and postoperative renal function data from all patients undergoing isolated CABG from January 1998 through December 2007. Preoperative and postoperative renal function was estimated using serum creatinine (SeCr) levels, creatinine clearance (CrCl) determined by the Cockcroft-Gault formula and the glomerular filtration rate (e-GFR) estimated by the Modification of Diet in Renal Disease (MDRD) formula. Receiver operator characteristic (ROC) curves and area under the ROC curves were calculated. Results In 9987 patients, CrCl had the best discriminatory power to predict early as well as late mortality, followed by e-GFR and finally SeCr. The odds ratios for preoperative parameters for early mortality were closer to 1 than those of the postoperative parameters. Conclusions Renal function determined by the Cockcroft-Gault formula is the best predictor of early and late mortality after CABG. The relationship between renal function and mortality is non-linear. Renal function as a variable in risk scoring systems such as the EuroSCORE needs to be reconsidered
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