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Abstract Recently, the oxygen potential dependence of the signal of a potentiometric CO 2 sensor, based on a cation conductor with carbonate as gas sensitive layer, has been interpreted as caused by electronic transference through the electrolyte. Though this interpretation is quite correct, the relationships on the basis of which the effect of electronic conductivity has been discussed are wrong and so are the conclusions on the electronic conduction parameter of the electrolyte material under consideration, i.e. of the lithium ion conductor Li 3 PO 4 + SiO 2 (5 mol%). In what follows, the questionable points will be corrected and the role of the electronic conductivity for the understanding of the behaviour of a CO 2 sensor will be re-examined.

As COVID-19 spreads worldwide, governments have been implementing a wide range of measures to contain it, from movement restrictions to economy-wide shutdowns. Understanding their impacts is essential to support better policies for countries still experiencing outbreaks or in case of emergence of subsequent pandemic waves. Here we show that the cumulative decline in electricity consumption within the 5 months following the stay-home orders ranges between 3% and 12% in the most affected EU countries and USA states, except Florida, which shows no significant impact. Italy, France, Spain, California, Austria, and New York have recovered baseline consumption by the end of July, whereas Great Britain and Germany remain below baseline levels. We also show that the relationship between measures stringency and daily decline in electricity consumption is nonlinear. These results illustrate the severity of the crisis across countries and can support further research on the effect of specific measures.

Air pollution and climate change are potential drivers for the increasing burden of allergic diseases. The molecular mechanisms by which air pollutants and climate parameters may influence allergic diseases, however, are complex and elusive. This article provides an overview of physical, chemical and biological interactions between air pollution, climate change, allergens, adjuvants and the immune system, addressing how these interactions may promote the development of allergies. We reviewed and synthesized key findings from atmospheric, climate, and biomedical research. The current state of knowledge, open questions, and future research perspectives are outlined and discussed. The Anthropocene, as the present era of globally pervasive anthropogenic influence on planet Earth and, thus, on the human environment, is characterized by a strong increase of carbon dioxide, ozone, nitrogen oxides, and combustion- or traffic-related particulate matter in the atmosphere. These environmental factors can enhance the abundance and induce chemical modifications of allergens, increase oxidative stress in the human body, and skew the immune system toward allergic reactions. In particular, air pollutants can act as adjuvants and alter the immunogenicity of allergenic proteins, while climate change affects the atmospheric abundance and human exposure to bioaerosols and aeroallergens. To fully understand and effectively mitigate the adverse effects of air pollution and climate change on allergic diseases, several challenges remain to be resolved. Among these are the identification and quantification of immunochemical reaction pathways involving allergens and adjuvants under relevant environmental and physiological conditions.

Opiate antagonists are promising pharmacotherapeutic agents for the treatment of alcohol dependence, reducing craving and relapse rates in weaned alcoholics. However, preclinical findings indicate that they can also increase ethanol consumption and preference in animals with a strong liking for ethanol, depending on the dose and treatment regimen.The present study examined the effects of chronic, intermittent and acute opiate antagonist treatment on the alcohol deprivation effect (ADE) in long-term ethanol- experienced rats, which is an animal model of craving and relapse.Long-term ethanol-experienced rats were either implanted with mini-osmotic pumps delivering 0, 0.5 or 1 mg/kg per hour naloxone (chronic treatment) or received intermittent naltrexone injections (2x5 mg/kg per day SC). Effects of chronic and intermittent treatment on the ADE were studied in a four-bottle home cage drinking paradigm. In a second experiment, long-term ethanol-experienced rats trained in an operant ethanol self-administration paradigm received acute naltrexone treatment (0, 0.1, 1 or 10 mg/kg SC) before a 23-h session either during basal drinking or during the ADE.Chronic naloxone treatment increased ethanol preference during the ADE. Intermittent naltrexone treatment at a dose comparable to the lower dose of chronic treatment moderately attenuated the ADE. Acute naltrexone treatment selectively reduced lever pressing for ethanol both during the ADE and during basal drinking only at the lowest dose, whereas higher doses also suppressed water intake. The ethanol-specific suppressant effect on the ADE was long lasting. Concerning basal drinking, however, naltrexone had a long lasting reductive effect only on lever pressing for water.A low dose of naltrexone and an intermittent treatment regimen seem to be necessary to maintain a specific reduction in ethanol intake in individuals with a high motivation to consume ethanol. These findings are consistent with the notion that, at low doses, opiate antagonists reduce the reward value of reinforcers.

In the 1990s, an uncommonly high percentage of glutathione S-transferase M1 (GSTM1) negative bladder cancer cases (70%) was reported in the greater Dortmund area. The question arose as to whether this uncommonly high percentage of GSTM1 negative bladder cancer cases was due to environmental and/or occupational exposure decades ago. Thus, 15 years later, another study on bladder cancer was performed in the same area after the coal, iron, and steel industries had finally closed in the 1990s. In total 196 bladder cancer patients from the St.-Josefs-Hospital Dortmund-Hörde and 235 controls with benign urological diseases were assessed by questionnaire and genotyped for GSTM1, glutathione S-transferase T1 (GSTT1), and the N-acetyltransferase 2 (NAT2) tag SNP rs1495741. The frequency of the GSTM1 negative genotype was 52% in bladder cancer cases and thus lower compared to a previous study performed from 1992 to 1995 in the same area (70%). NAT2 genotypes were distributed equally among cases and controls (63% slow acetylators). Fewer GSTT1 negative genotypes were present in cases (17%) than in controls (20%).

Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes, including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM2.5). It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary. Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010 (ref. 5), we calculate that outdoor air pollution, mostly by PM2.5, leads to 3.3 (95 per cent confidence interval 1.61-4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic, but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM2.5, with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.

Constraint-based modeling techniques have become a standard tool for the in silico analysis of metabolic networks. To further improve their accuracy, recent methodological developments focused on integration of thermodynamic information in metabolic models to assess the feasibility of flux distributions by thermodynamic driving forces. Here we present OptMDFpathway, a method that extends the recently proposed framework of Max-min Driving Force (MDF) for thermodynamic pathway analysis. Given a metabolic network model, OptMDFpathway identifies both the optimal MDF for a desired phenotypic behavior as well as the respective pathway itself that supports the optimal driving force. OptMDFpathway is formulated as a mixed-integer linear program and is applicable to genome-scale metabolic networks. As an important theoretical result, we also show that there exists always at least one elementary mode in the network that reaches the maximal MDF. We employed our new approach to systematically identify all substrate-product combinations in Escherichia coli where product synthesis allows for concomitant net CO2 assimilation via thermodynamically feasible pathways. Although biomass synthesis cannot be coupled to net CO2 fixation in E. coli we found that as many as 145 of the 949 cytosolic carbon metabolites contained in the genome-scale model iJO1366 enable net CO2 incorporation along thermodynamically feasible pathways with glycerol as substrate and 34 with glucose. The most promising products in terms of carbon assimilation yield and thermodynamic driving forces are orotate, aspartate and the C4-metabolites of the tricarboxylic acid cycle. We also identified thermodynamic bottlenecks frequently limiting the maximal driving force of the CO2-fixing pathways. Our results indicate that heterotrophic organisms like E. coli hold a possibly underestimated potential for CO2 assimilation which may complement existing biotechnological approaches for capturing CO2. Furthermore, we envision that the developed OptMDFpathway approach can be used for many other applications within the framework of constrained-based modeling and for rational design of metabolic networks.