Carbon border adjustment mechanism challenges and implications: The case of Visegrád countries.

Stricter climate policies across the European Union are enhancing the phenomenon of free riding by nonacting countries, which translates into carbon leakage and loss of competitiveness. This paper investigates the trade, economic and environmental implications of the future implementation of a carbon border adjustment mechanism (CBAM) in Visegrád countries as EU member states. We exploit trade data to estimate price and income elasticities for emission-intensive trade-exposed (EITE) goods imported from non-EU trading partners to Visegrád countries. Based on these estimates, which are combined with the average carbon intensity of the EU's proposed list of EITE goods, we simulate the implications of six different configurations of restrictiveness of the CBAM imposed on imports from non-EU countries. We find that a high price elasticity and carbon intensity tend to significantly decrease import demand for EITE goods under the CBAM. Moreover, future CBAM implementation will yield a relatively small adverse impact on economic growth in Visegrád countries and a small decrease in total carbon emissions in non-EU countries.

Adding country resolution to EXIOBASE: impacts on land use embodied in trade.

Multiregional input-output (MRIO) databases are used to analyze the impact of resource use and environmental impacts along global supply chains. To accurately account for pressures and impacts that are highly concentrated in specific sectors or regions of the world, such as agricultural and land-use-related impacts, MRIO databases are being fueled by increasingly more detailed data. To date no MRIO database exists which couples a high level of harmonized sector detail with high country resolution. Currently available databases either aggregate minor countries into rest-of-the-world (WIOD and EXIOBASE 3), or the high country resolution is achieved at the cost of non-harmonized or lower sectoral detail (Eora, OECD-ICIO or the GTAP-MRIO). This aggregation can cause potentially significant differences in environmental and socioeconomic impact calculations. In this paper, we describe the development of an EXIOBASE 3 variant that expands regional coverage from 49 regions to 214 countries, while keeping the high and harmonized sectoral detail. We show the relevance of disaggregation for land-use accounting. Previous rest-of-the-world regions supply one-third of global land, which is used to produce a large range of different products under very different levels of productivity. We find that the aggregation of regions leads to a difference in the balance of land embodied in trade of up to 6% and a difference of land embodied in imports of up to 68% for individual countries and up to 600% for land-use-relevant sectors. Whilst the database can still be considered experimental, it is expected to increase the accuracy of estimates for environmental footprint studies of the original EXIOBASE countries, and provides the first estimates for the countries in the previous rest-of-the world.

Interferon-γ acutely augments inhibition of neocortical layer 5 pyramidal neurons.

BACKGROUND: Interferon-γ (IFN-γ, a type II IFN) is present in the central nervous system (CNS) under various conditions. Evidence is emerging that, in addition to its immunological role, IFN-γ modulates neuronal morphology, function, and development in several brain regions. Previously, we have shown that raising levels of IFN-ß (a type I IFN) lead to increased neuronal excitability of neocortical layer 5 pyramidal neurons. Because of shared non-canonical signaling pathways of both cytokines, we hypothesized a similar neocortical role of acutely applied IFN-γ. METHODS: We used semi-quantitative RT-PCR, immunoblotting, and immunohistochemistry to analyze neuronal expression of IFN-γ receptors and performed whole-cell patch-clamp recordings in layer 5 pyramidal neurons to investigate sub- and suprathreshold excitability, properties of hyperpolarization-activated cyclic nucleotide-gated current (Ih), and inhibitory neurotransmission under the influence of acutely applied IFN-γ. RESULTS: We show that IFN-γ receptors are present in the membrane of rat's neocortical layer 5 pyramidal neurons. As expected from this and the putative overlap in IFN type I and II alternative signaling pathways, IFN-γ diminished Ih, mirroring the effect of type I IFNs, suggesting a likewise activation of protein kinase C (PKC). In contrast, IFN-γ did neither alter subthreshold nor suprathreshold neuronal excitability, pointing to augmented inhibitory transmission by IFN-γ. Indeed, IFN-γ increased electrically evoked inhibitory postsynaptic currents (IPSCs) on neocortical layer 5 pyramidal neurons. Furthermore, amplitudes of spontaneous IPSCs and miniature IPSCs were elevated by IFN-γ, whereas their frequency remained unchanged. CONCLUSIONS: The expression of IFN-γ receptors on layer 5 neocortical pyramidal neurons together with the acute augmentation of inhibition in the neocortex by direct application of IFN-γ highlights an additional interaction between the CNS and immune system. Our results strengthen our understanding of the role of IFN-γ in neocortical neurotransmission and emphasize its impact beyond its immunological properties, particularly in the pathogenesis of neuropsychiatric disorders.

Variation in trends of consumption based carbon accounts.

The UNFCCC requires the annual reporting of greenhouse gas emissions. These inventories focus on emissions within a territory, and do not capture the effect of emissions embodied in imports. Consumption based carbon accounting (CBCA) has been proposed as a complementary method to capture these emissions, and a number of global models have been developed to operationalise CBCA. However, discrepancies in country-level CBCA results occur, which can cause concern for the practical use of CBCA. Despite these quantitative difference in results, do they provide robust results when changes over time are investigated? Here we present results of all the major global models and normalise the model results by looking at changes over time relative to a common base year value. We give an analysis of the variability across the models, both before and after normalisation in order to give insights into variance at national and regional level. A dataset of harmonised results (based on means) and measures of dispersion is presented, providing a baseline dataset for CBCA validation and analysis.

Increasing impacts of land use on biodiversity and carbon sequestration driven by population and economic growth.

Biodiversity and ecosystem service losses driven by land-use change are expected to intensify as a growing and more affluent global population requires more agricultural and forestry products, and teleconnections in the global economy lead to increasing remote environmental responsibility. By combining global biophysical and economic models, we show that, between the years 2000 and 2011, overall population and economic growth resulted in increasing total impacts on bird diversity and carbon sequestration globally, despite a reduction of land-use impacts per unit of gross domestic product (GDP). The exceptions were North America and Western Europe, where there was a reduction of forestry and agriculture impacts on nature accentuated by the 2007-2008 financial crisis. Biodiversity losses occurred predominantly in Central and Southern America, Africa and Asia with international trade an important and growing driver. In 2011, 33% of Central and Southern America and 26% of Africa's biodiversity impacts were driven by consumption in other world regions. Overall, cattle farming is the major driver of biodiversity loss, but oil seed production showed the largest increases in biodiversity impacts. Forestry activities exerted the highest impact on carbon sequestration, and also showed the largest increase in the 2000-2011 period. Our results suggest that to address the biodiversity crisis, governments should take an equitable approach recognizing remote responsibility, and promote a shift of economic development towards activities with low biodiversity impacts.

Resource footprints and their ecosystem consequences.

A meaningful environmental impact analysis should go beyond the accounting of pressures from resource use and actually assess how resource demand affects ecosystems. The various currently available footprints of nations report the environmental pressures e.g. water use or pollutant emissions, driven by consumption. However, there have been limited attempts to assess the environmental consequences of these pressures. Ultimately, consequences, not pressures, should guide environmental policymaking. The newly released LC-Impact method demonstrates progress on the path to providing this missing link. Here we present "ecosystem impact footprints" in terms of the consequences for biodiversity and assess the differences in impact footprint results from MRIO-based pressure footprints. The new perspective reveals major changes in the relative contribution of nations to global footprints. Wealthy countries have high pressure footprints in lower-income countries but their impact footprints often have their origin in higher-income countries. This shift in perspective provides a different insight on where to focus policy responses to preserve biodiversity.

Global spatially explicit CO2 emission metrics for forest bioenergy.

Emission metrics aggregate climate impacts of greenhouse gases to common units such as CO2-equivalents (CO2-eq.). Examples include the global warming potential (GWP), the global temperature change potential (GTP) and the absolute sustained emission temperature (aSET). Despite the importance of biomass as a primary energy supplier in existing and future scenarios, emission metrics for CO2 from forest bioenergy are only available on a case-specific basis. Here, we produce global spatially explicit emission metrics for CO2 emissions from forest bioenergy and illustrate their applications to global emissions in 2015 and until 2100 under the RCP8.5 scenario. We obtain global average values of 0.49 ± 0.03 kgCO2-eq. kgCO2(-1) (mean ± standard deviation) for GWP, 0.05 ± 0.05 kgCO2-eq. kgCO2(-1) for GTP, and 2.14·10(-14) ± 0.11·10(-14) °C (kg yr(-1))(-1) for aSET. We explore metric dependencies on temperature, precipitation, biomass turnover times and extraction rates of forest residues. We find relatively high emission metrics with low precipitation, long rotation times and low residue extraction rates. Our results provide a basis for assessing CO2 emissions from forest bioenergy under different indicators and across various spatial and temporal scales.

Protein kinase C activation mediates interferon-ß-induced neuronal excitability changes in neocortical pyramidal neurons.

BACKGROUND: Cytokines are key players in the interactions of the immune and nervous systems. Recently, we showed that such interplay is mediated by type I interferons (IFNs), which elevate the excitability of neocortical pyramidal neurons. A line of indirect evidence suggested that modulation of multiple ion channels underlies the effect. However, which currents are principally involved and how the IFN signaling cascade is linked to the respective ion channels remains elusive. METHODS: We tested several single and combined ionic current modulations using an in silico model of a neocortical layer 5 neuron. Subsequently we investigated resulting predictions by whole-cell patch-clamp recordings in layer 5 neurons of ex vivo neocortical rat brain slices pharmacologically reproducing or prohibiting neuronal IFN effects. RESULTS: The amount and type of modulation necessary to replicate IFN effects in silico suggested protein kinase C (PKC) activation as link between the type I IFN signaling and ion channel modulations. In line with this, PKC activation with 4ß-phorbol 12-myristate 13-acetate (4ß-PMA) or Bryostatin1 augmented the excitability of neocortical layer 5 neurons comparable to IFN-ß in our ex vivo recordings. In detail, both PKC activators attenuated the rheobase and increased the input-output gain as well as the input resistance, thereby augmenting the neuronal excitability. Similar to IFN-ß they also left the threshold of action potential generation unaffected. In further support of PKC mediating type I IFN effects, IFN-ß, 4ß-PMA and Bryostatin1 reduced the amplitude of post-train after-hyperpolarizations in a similar manner. In conjunction with this finding, IFN-ß reduced M-currents, which contribute to after-hyperpolarizations and are modulated by PKC. Finally, blocking PKC activation with GF109203X at the catalytic site or calphostin C at the regulatory site prevented the main excitatory effects of IFN-ß. CONCLUSION: Multiple ion channel modulations underlie the neuromodulatory effect of type I IFNs. PKC activation is both sufficient and necessary for mediating the effect, and links the IFN signaling cascade to the intrinsic ion channels. Therefore, we regard PKC activation as unitary mechanism for the neuromodulatory potential of type I IFNs in neocortical neurons.

Elevation in type I interferons inhibits HCN1 and slows cortical neuronal oscillations.

Central nervous system (CNS) inflammation involves the generation of inducible cytokines such as interferons (IFNs) and alterations in brain activity, yet the interplay of both is not well understood. Here, we show that in vivo elevation of IFNs by viral brain infection reduced hyperpolarization-activated currents (Ih) in cortical pyramidal neurons. In rodent brain slices directly exposed to type I IFNs, the hyperpolarization-activated cyclic nucleotide (HCN)-gated channel subunit HCN1 was specifically affected. The effect required an intact type I receptor (IFNAR) signaling cascade. Consistent with Ih inhibition, IFNs hyperpolarized the resting membrane potential, shifted the resonance frequency, and increased the membrane impedance. In vivo application of IFN-ß to the rat and to the mouse cerebral cortex reduced the power of higher frequencies in the cortical electroencephalographic activity only in the presence of HCN1. In summary, these findings identify HCN1 channels as a novel neural target for type I IFNs providing the possibility to tune neural responses during the complex event of a CNS inflammation.

HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons.

The distribution of ion channels in neurons regulates neuronal activity and proper formation of neuronal networks during neuronal development. One of the channels is the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel constituting the molecular substrate of hyperpolarization-activated current (I(h)). Our previous study implied a role for the fastest activating subunit HCN1 in the generation of Ih in rat neonatal cortical plate neurons. To better understand the impact of HCN1 in early neocortical development, we here performed biochemical analysis and whole-cell recordings in neonatal cortical plate and juvenile layer 5 somatosensory neurons of HCN1(-/-) and control HCN1(+/+) mice. Western Blot analysis revealed that HCN1 protein expression in neonatal cortical plate tissue of HCN(+/+) mice amounted to only 3% of the HCN1 in young adult cortex and suggested that in HCN1(-/-) mice other isoforms (particularly HCN4) might be compensatory up-regulated. At the first day after birth, functional ablation of the HCN1 subunit did not affect the proportion of Ih expressing pyramidal cortical plate neurons. Although the contribution of individual subunit proteins remains open, the lack of HCN1 markedly slowed the current activation and deactivation in individual I(h) expressing neurons. However, it did not impair maximal amplitude/density, voltage dependence of activation, and cAMP sensitivity. In conclusion, our data imply that, although expression is relatively low, HCN1 contributes substantially to I(h) properties in individual cortical plate neurons. These properties are significantly changed in HCN1(-/-), either due to the lack of HCN1 itself or due to compensatory mechanisms.

Distinct perinatal features of the hyperpolarization-activated non-selective cation current I(h) in the rat cortical plate.

BACKGROUND: During neocortical development, multiple voltage- and ligand-gated ion channels are differentially expressed in neurons thereby shaping their intrinsic electrical properties. One of these voltage-gated ion channels, the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel and its current I(h), is an important regulator of neuronal excitability. Thus far, studies on an early I(h) appearance in rodent neocortex are missing or conflicting. Therefore, we focused our study on perinatal neocortical I(h) and its properties. RESULTS: In the perinatal rat neocortex we observed a rapid increase in the number of neurons exhibiting I(h). Perinatal I(h) had unique properties: first, a pronounced cAMP sensitivity resulting in a marked shift of the voltage sufficient for half-maximum activation of the current towards depolarized voltages and second, an up to 10 times slower deactivation at physiological membrane potentials when compared to the one at postnatal day 30. The combination of these features was sufficient to suppress membrane resonance in our in silico and in vitro experiments. Although all four HCN subunits were present on the mRNA level we only detected HCN4, HCN3 and HCN1 on the protein level at P0. HCN1 protein at P0, however, appeared incompletely processed. At P30 glycosilated HCN1 and HCN2 dominated. By in silico simulations and heterologous co-expression experiments of a 'slow' and a 'fast' I(h) conducting HCN channel subunit in HEK293 cells, we mimicked most characteristics of the native current, pointing to a functional combination of subunit homo- or heteromeres. CONCLUSION: Taken together, these data indicate a HCN subunit shift initiated in the first 24 hours after birth and implicate a prominent perinatal role of the phylogenetically older HCN3 and/or HCN4 subunits in the developing neocortex.

Interferon-beta modulates protein synthesis in the central nervous system.

Interferon-beta (IFN-beta), acting canonically via the modulation of transcription, affects neocortical pyramidal neurons. By use of 2-D differential gel electrophoresis and subsequent mass spectrometry we identified IFN-beta regulated proteins in the central nervous system. These proteins are involved in cytoskeleton assembly, protein transport and nucleotide metabolism and, as such, serve regenerative and protective functions. Electrophysiologically, IFN-beta mediated protein synthesis is essential for part of the excitatory neuronal effects, as revealed under blockade of protein biosynthesis. This study presents novel effects of IFN-beta in the central nervous system and begins to unravel the mechanism behind the known excitability changes in neurons.