The contribution of carbon dioxide emissions from the aviation sector to future climate change

The compact Earth system model OSCARv2.2 is used to assess the climate impact of present and future civil aviation carbon dioxide (CO2) emissions. The impact of aviation CO2 on future climate is quantified over the 1940–2050 period, extending some simulations to 2100 and using different aviation CO2 emission scenarios and two background Representative Concentrations Pathways (RCP2.6 and RCP6.0) for other emission sectors. Several aviation scenarios including weak to strong mitigation options are considered with emissions ranging from 386 MtCO2/year (Factor 2 scenario) to 2338 MtCO2/year (ICAO based scenario) in 2050. As a reference, in 2000, the calculated impact of aviation CO2 emissions is 9.1 ± 2 mK (0.8% of the total anthropogenic warming associated to fossil fuel emissions). In 2050, on a climate trajectory in line with the Paris Agreement limiting the global warming below 2 °C (RCP2.6), the impact of the aviation CO2 emissions ranges from 26 ± 2 mK (1.4% of the total anthropogenic warming associated to fossil fuel emissions) for an ambitious mitigation strategy scenario (Factor 2) to 39 ± 4 mK (2.0% of the total anthropogenic warming associated to fossil fuel emissions) for the least ambitious mitigation scenario of the study (ICAO based). On the longer term, if no significant emission mitigation is implemented for the aviation sector, the associated warming could further increase and reach a value of 99.5 mK ± 20 mK in 2100 (ICAO based), which corresponds to 5.2% of the total anthropogenic warming under RCP2.6. The contribution of CO2 is estimated to represent 36%–51% of the total aviation radiative forcing of climate including short-term climate forcers. However, due to its long residence time in the atmosphere, aviation CO2 will have a major contribution on decadal time scales. These additional short-terms forcers are subject to large uncertainties and will be analysed in forthcoming studies

Modelling street level PM10 concentrations across Europe: source apportionment and possible futures

Despite increasing emission controls, particulate matter (PM) has remained a critical issue for European air quality in recent years. The various sources of PM, both from primary particulate emissions as well as secondary formation from precursor gases, make this a complex problem to tackle. In order to allow for credible predictions of future concentrations under policy assumptions, a modelling approach is needed that considers all chemical processes and spatial dimensions involved, from long-range transport of pollution to local emissions in street canyons. Here we describe a modelling scheme which has been implemented in the GAINS integrated assessment model to assess compliance with PM10 (PM with aerodynamic diameter <10 um) limit values at individual air quality monitoring stations reporting to the AirBase database. The modelling approach relies on a combination of bottom up modelling of emissions, simplified atmospheric chemistry and dispersion calculations, and a traffic increment calculation wherever applicable. At each monitoring station fulfilling a few data coverage criteria, measured concentrations in the base year 2009 are explained to the extent possible and then modelled for the past and future. More than 1850 monitoring stations are covered, including more than 300 traffic stations and 80% of the stations which exceeded the EU air quality limit values in 2009. As a validation, we compare modelled trends in the period 2000-2008 to observations, which are well reproduced. The modelling scheme is applied here to quantify explicitly source contributions to ambient concentrations at several critical monitoring stations, displaying the differences in spatial origin and chemical composition of urban roadside PM10 across Europe. Furthermore, we analyse the predicted evolution of PM10 concentrations in the European Union until 2030 under different policy scenarios. Significant improvements in ambient PM10 concentrations are expected assuming successful implementation of already agreed legislation; however, these will not be large enough to ensure attainment of PM10 limit values in hot spot locations such as Southern Poland and major European cities. Remaining issues are largely eliminated in a scenario applying the best available emission control technologies to the maximal technically feasible extent

A Human TREK-1/HEK Cell Line: A Highly Efficient Screening Tool for Drug Development in Neurological Diseases

TREK-1 potassium channels are involved in a number of physiopathological processes such as neuroprotection, pain and depression. Molecules able to open or to block these channels can be clinically important. Having a cell model for screening such molecules is of particular interest. Here, we describe the development of the first available cell line that constituvely expresses the TREK-1 channel. The TREK-1 channel expressed by the h-TREK-1/HEK cell line has conserved all its modulation properties. It is opened by stretch, pH, polyunsaturated fatty acids and by the neuroprotective molecule, riluzole and it is blocked by spadin or fluoxetine. We also demonstrate that the h-TREK-1/HEK cell line is protected against ischemia by using the oxygen-glucose deprivation model

Concerted Regulation of cGMP and cAMP Phosphodiesterases in Early Cardiac Hypertrophy Induced by Angiotensin II

Left ventricular hypertrophy leads to heart failure and represents a high risk leading to premature death. Cyclic nucleotides (cAMP and cGMP) play a major role in heart contractility and cyclic nucleotide phosphodiesterases (PDEs) are involved in different stages of advanced cardiac diseases. We have investigated their contributions in the very initial stages of left ventricular hypertrophy development. Wistar male rats were treated over two weeks by chronic infusion of angiotensin II using osmotic mini-pumps. Left cardiac ventricles were used as total homogenates for analysis. PDE1 to PDE5 specific activities and protein and mRNA expressions were explored

Cyclic Nucleotide Phosphodiesterases and Compartmentation in Normal and Diseased Heart

International audienceCyclic nucleotide phosphodiesterases (PDEs) degrade the second messengers cAMP and cGMP, thereby regulating multiple aspects of cardiac function. This highly diverse class of enzymes encoded by 21 genes encompasses 11 families which are not only responsible for the termination of cyclic nucleotide signalling, but are also involved in the generation of dynamic microdomains of cAMP and cGMP controlling specific cell functions in response to various neurohormonal stimuli. In myocardium, the PDE3 and PDE4 families are predominant to degrade cAMP and thereby regulate cardiac excitation-contraction coupling. PDE3 inhibitors are positive inotropes and vasodilators in human, but their use is limited to acute heart failure and intermittent claudication. PDE5 is particularly important to degrade cGMP in vascular smooth muscle, and PDE5 inhibitors are used to treat erectile dysfunction and pulmonary hypertension. However, these drugs do not seem efficient in heart failure with preserved ejection fraction. There is experimental evidence that these PDEs as well as other PDE families including PDE1, PDE2 and PDE9 may play important roles in cardiac diseases such as hypertrophy and heart failure. After a brief presentation of the cyclic nucleotide pathways in cardiac cells and the major characteristics of the PDE superfamily, this chapter will present their role in cyclic nucleotide compartmentation and the current use of PDE inhibitors in cardiac diseases together with the recent research progresses that could lead to a better exploitation of the therapeutic potential of these enzymes in the future

Cardiomyocytes from human pluripotent stem cells: from laboratory curiosity to industrial biomedical platform

Cardiomyocytes from human pluripotent stem cells (hPSCs-CMs) could revolutionise biomedicine. Global burden of heart failure will soon reach USD $90bn, while unexpected cardiotoxicity underlies 28% of drug withdrawals. Advances in hPSC isolation, Cas9/CRISPR genome engineering and hPSC-CM differentiation have improved patient care, progressed drugs to clinic and opened a new era in safety pharmacology. Nevertheless, predictive cardiotoxicity using hPSC-CMs contrasts from failure to almost total success. Since this likely relates to cell immaturity, efforts are underway to use biochemical and biophysical cues to improve many of the ~ 30 structural and functional properties of hPSC-CMs towards those seen in adult CMs. Other developments needed for widespread hPSC-CM utility include subtype specification, cost reduction of large scale differentiation and elimination of the phenotyping bottleneck. This review will consider these factors in the evolution of hPSC-CM technologies, as well as their integration into high content industrial platforms that assess structure, mitochondrial function, electrophysiology, calcium transients and contractility. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel