IZA COVID-19 crisis response monitoring: short-run labor market impacts of COVID-19, initial policy measures and beyond

The unprecedented COVID-19 pandemic has a severe impact on societies, economies and labor markets. However, not all countries, socio-economic groups and sectors are equally affected. For example, occupational groups working in sectors where value chains have been disrupted and lockdowns have had direct impacts are affected more heavily, while the slowdown of hiring activities mostly affects young labor market entrants. As a result, there has been a steep increase in unemployment rates in many countries, but not everywhere to the same extent. Part of this difference can be related to the different role and extent of short-time work schemes, which is now being used more widely than during the Great Recession. Some countries have created or expanded these schemes, making coverage less exclusive and benefits more generous, at least temporarily. But short-time work is certainly not a panacea to “flatten the unemployment curve”. Furthermore, next to providing liquidity support to firms, unemployment benefits have been made more generous in many countries. Often, activation principles have also been temporarily reduced. Some countries have increased access to income support to some extent also for non-standard workers, such as temporary agency workers or self-employed workers, on an ad hoc basis. A major change in working conditions is the broad move towards telework arrangements and work from home. Nonetheless, it appears too early to assess the relative success of national strategies to cope with the pandemic and to revitalize the labor market as well as the medium-term fiscal viability of different support measures. Future monitoring will also have to trace policies to cope with the imminent structural changes that might result from the crisis or might be accelerated by the crisis

Neuronal Redox-Imbalance in Rett Syndrome Affects Mitochondria as Well as Cytosol, and Is Accompanied by Intensified Mitochondrial O2 Consumption and ROS Release

Rett syndrome (RTT), an X chromosome-linked neurodevelopmental disorder affecting almost exclusively females, is associated with various mitochondrial alterations. Mitochondria are swollen, show altered respiratory rates, and their inner membrane is leaking protons. To advance the understanding of these disturbances and clarify their link to redox impairment and oxidative stress, we assessed mitochondrial respiration in defined brain regions and cardiac tissue of male wildtype (WT) and MeCP2-deficient (Mecp2-/y) mice. Also, we quantified for the first time neuronal redox-balance with subcellular resolution in cytosol and mitochondrial matrix. Quantitative roGFP1 redox imaging revealed more oxidized conditions in the cytosol of Mecp2-/y hippocampal neurons than in WT neurons. Furthermore, cytosol and mitochondria of Mecp2-/y neurons showed exaggerated redox-responses to hypoxia and cell-endogenous reactive oxygen species (ROS) formation. Biochemical analyzes exclude disease-related increases in mitochondrial mass in Mecp2-/y hippocampus and cortex. Protein levels of complex I core constituents were slightly lower in Mecp2-/y hippocampus and cortex than in WT; those of complex V were lower in Mecp2-/y cortex. Respiratory supercomplex-formation did not differ among genotypes. Yet, supplied with the complex II substrate succinate, mitochondria of Mecp2-/y cortex and hippocampus consumed more O2 than WT. Furthermore, mitochondria from Mecp2-/y hippocampus and cortex mediated an enhanced oxidative burden. In conclusion, we further advanced the molecular understanding of mitochondrial dysfunction in RTT. Intensified mitochondrial O2 consumption, increased mitochondrial ROS generation and disturbed redox balance in mitochondria and cytosol may represent a causal chain, which provokes dysregulated proteins, oxidative tissue damage, and contributes to neuronal network dysfunction in RTT

The Integrated Carbon Observation System in Europe

Since 1750, land-use change and fossil fuel combustion has led to a 46% increase in the atmospheric carbon dioxide (CO2) concentrations, causing global warming with substantial societal consequences. The Paris Agreement aims to limit global temperature increases to well below 2 degrees C above preindustrial levels. Increasing levels of CO2 and other greenhouse gases (GH6s), such as methane (CH4) and nitrous oxide (N2O), in the atmosphere are the primary cause of climate change. Approximately half of the carbon emissions to the atmosphere are sequestered by ocean and land sinks, leading to ocean acidification but also slowing the rate of global warming. However, there are significant uncertainties in the future global warming scenarios due to uncertainties in the size, nature, and stability of these sinks. Quantifying and monitoring the size and timing of natural sinks and the impact of climate change on ecosystems are important information to guide policy-makers' decisions and strategies on reductions in emissions. Continuous, long-term observations are required to quantify GHG emissions, sinks, and their impacts on Earth systems. The Integrated Carbon Observation System (ICOS) was designed as the European in situ observation and information system to support science and society in their efforts to mitigate climate change. It provides standardized and open data currently from over 140 measurement stations across 12 European countries. The stations observe GHG concentrations in the atmosphere and carbon and GHG fluxes between the atmosphere, land surface, and the oceans. This article describes how ICOS fulfills its mission to harmonize these observations, ensure the related long-term financial commitments, provide easy access to well-documented and reproducible high-quality data and related protocols and tools for scientific studies, and deliver information and GHG-related products to stakeholders in society and policy.Peer reviewe

ECLAIRE: Effects of Climate Change on Air Pollution Impacts and Response Strategies for European Ecosystems. Project final report

The central goal of ECLAIRE is to assess how climate change will alter the extent to which air pollutants threaten terrestrial ecosystems. Particular attention has been given to nitrogen compounds, especially nitrogen oxides (NOx) and ammonia (NH3), as well as Biogenic Volatile Organic Compounds (BVOCs) in relation to tropospheric ozone (O3) formation, including their interactions with aerosol components. ECLAIRE has combined a broad program of field and laboratory experimentation and modelling of pollution fluxes and ecosystem impacts, advancing both mechanistic understanding and providing support to European policy makers. The central finding of ECLAIRE is that future climate change is expected to worsen the threat of air pollutants on Europe’s ecosystems. Firstly, climate warming is expected to increase the emissions of many trace gases, such as agricultural NH3, the soil component of NOx emissions and key BVOCs. Experimental data and numerical models show how these effects will tend to increase atmospheric N deposition in future. By contrast, the net effect on tropospheric O3 is less clear. This is because parallel increases in atmospheric CO2 concentrations will offset the temperature-driven increase for some BVOCs, such as isoprene. By contrast, there is currently insufficient evidence to be confident that CO2 will offset anticipated climate increases in monoterpene emissions. Secondly, climate warming is found to be likely to increase the vulnerability of ecosystems towards air pollutant exposure or atmospheric deposition. Such effects may occur as a consequence of combined perturbation, as well as through specific interactions, such as between drought, O3, N and aerosol exposure. These combined effects of climate change are expected to offset part of the benefit of current emissions control policies. Unless decisive mitigation actions are taken, it is anticipated that ongoing climate warming will increase agricultural and other biogenic emissions, posing a challenge for national emissions ceilings and air quality objectives related to nitrogen and ozone pollution. The O3 effects will be further worsened if progress is not made to curb increases in methane (CH4) emissions in the northern hemisphere. Other key findings of ECLAIRE are that: 1) N deposition and O3 have adverse synergistic effects. Exposure to ambient O3 concentrations was shown to reduce the Nitrogen Use Efficiency of plants, both decreasing agricultural production and posing an increased risk of other forms of nitrogen pollution, such as nitrate leaching (NO3-) and the greenhouse gas nitrous oxide (N2O); 2) within-canopy dynamics for volatile aerosol can increase dry deposition and shorten atmospheric lifetimes; 3) ambient aerosol levels reduce the ability of plants to conserve water under drought conditions; 4) low-resolution mapping studies tend to underestimate the extent of local critical loads exceedance; 5) new dose-response functions can be used to improve the assessment of costs, including estimation of the value of damage due to air pollution effects on ecosystems, 6) scenarios can be constructed that combine technical mitigation measures with dietary change options (reducing livestock products in food down to recommended levels for health criteria), with the balance between the two strategies being a matter for future societal discussion. ECLAIRE has supported the revision process for the National Emissions Ceilings Directive and will continue to deliver scientific underpinning into the future for the UNECE Convention on Long-range Transboundary Air Pollution

ECLAIRE third periodic report

The ÉCLAIRE project (Effects of Climate Change on Air Pollution Impacts and Response Strategies for European Ecosystems) is a four year (2011-2015) project funded by the EU's Seventh Framework Programme for Research and Technological Development (FP7)

Evaluation of an oral antioxidant therapy in a mouse model of Rett syndrome

Rett syndrome (RTT) is a severe neurodevelopmental disorder caused by spontaneous mutations in the X-chromosomal gene MECP2 encoding methyl-CpG binding protein 2 (MeCP2). Affecting almost exclusively females, it causes reduced head and brain growth, loss of speech, cognitive and motor impairment, epilepsy and breathing disturbances. MECP2 aberrations are associated with mitochondrial impairment and increased generation of reactive oxygen species. At the same time, the activity and serum levels of antioxidants seem reduced, leading to redox imbalance and oxidative burden. Accordingly, treatment with radical scavengers represents a promising therapeutic approach. The aim of this work was to evaluate an oral antioxidant therapy in a mouse model of RTT. It was recently confirmed that intraperitoneal injection of vitamin E-derivative Trolox improves cellular redox balance in male MeCP2-deficient mice. However, there was no amelioration in phenotypic symptoms like body weight and size, breathing and motor function. Due to suspected handling effects, this work investigates the less-invasive oral supplementation of antioxidants and a synergistic substance combination of vitamin E, α-lipoic acid and N-acetylcysteine. Analysing phenotypic parameters, Nissl-stained brain slices and H2O2 release by isolated cortical mitochondria in a coupled reaction of Amplex UltraRed and horseradish peroxidase, several improvements related to oral antioxidant treatment could be registered. In particular, the antioxidant diet (AOF) led to a significant increase in cortical layer thickness and the size of pyramidal neurons in male MeCP2-deficient mice at postnatal day (PD) 50. In MeCP2-deficient females at PD 50 AOF caused a significant increase in body size and brain weight. In addition, they developed significantly larger hemispherical areas and pyramidal cell somata compared to untreated Rett mice. At PD 400 Rett females showed enlarged hippocampal areas. However, they also developed an obese phenotype. Measuring H2O2 release by isolated cortical mitochondria of untreated Rett males at PD 50 showed exaggerated H2O2 releases compared to wild type (WT) mice. Even the AOF could not make this difference disappear. In addition, the AOF had unexpected effects on WT mice whose mitochondria produced significantly higher amounts of H2O2 related to AOF. Therefore, the exact individual dosage of antioxidants and restoration of cellular redox balance deserve further detailed evaluation.2021-09-1