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Aviation NOx emissions not only have an impact on global climate by changing ozone and methane levels but also contribute to the deterioration of local air quality. A new version of the LMDZ-INCA global model, including chemistry of both the troposphere and the stratosphere and the sulfate-nitrate-ammonium cycle, is applied to re-evaluate the impact of aircraft NOx and aerosol emissions on climate. The results confirm that the efficiency of NOx to produce ozone is very much dependent on the injection height; it increases with the background methane and NOx concentrations and with decreasing aircraft NOx emissions. The methane lifetime variation is less sensitive to the location of aircraft NOx emissions than the ozone change. The net NOx radiative forcing (RF) (O3+CH4) is largely affected by the revised CH4 RF formula. The ozone positive forcing and the methane negative forcing largely offset each other, resulting in a slightly positive forcing for the present day. However, in the future, the net forcing turns to negative, essentially due to higher methane background concentrations. Additional RFs involving particle formation arise from aircraft NOx emissions since the increased hydroxyl radical (OH) concentrations are responsible for an enhanced conversion of SO2 to sulfate particles. Aircraft NOx emissions also increase the formation of nitrate particles in the lower troposphere. However, in the upper troposphere, increased sulfate concentrations favour the titration of ammonia leading to lower ammonium nitrate concentrations. The climate forcing of aircraft NOx emissions is likely to be small or even switch to negative (cooling), depending on atmospheric NOx or CH4 future background concentrations, or when the NOx impact on sulfate and nitrate particles is considered. However, large uncertainties remain for the NOx net impact on climate and in particular on the indirect forcings associated with aerosols, which are even more uncertain than the other forcings from gaseous species. Hence, additional studies with a range of models are needed to provide a more consolidated view. Nevertheless, our results suggest that reducing aircraft NOx emissions is primarily beneficial for improving air quality.

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 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 modified version of CHIMERE 2009, including new methodologies in emissions modelling and an urban correction, is used to perform a simulation at high resolution (0.125° × 0.0625°) over Europe for the year 2009. The model reproduces the temporal variability of NO2, O3, PM10, PM2.5 better at rural (RB) than urban (UB) background stations, with yearly correlation values for the different pollutants ranging between 0.62 and 0.77 at RB sites and between 0.52 and 0.73 at UB sites. Also, the fractional biases (FBs) show that the model performs slightly better at RB sites than at UB sites for NO2 (RB = −33.9%, UB = −53.6%), O3 (RB = 20.1%, UB = 25.2%) and PM10 (RB = −5.50%, UB = −20.1%). The difficulties for the model in reproducing NO2 concentrations can be attributed to the general underestimation of NOx emissions as well as to the adopted horizontal resolution, which represents only partially the spatial gradient of the emissions over medium-size and small cities. The overestimation of O3 by the model is related to the NO2 underestimation and the overestimated O3 concentrations of the lateral boundary conditions. At UB sites, CHIMERE reproduces PM2.5 better than PM10. This is primarily the result of an underestimation of coarse particulate matter (PM) associated with uncertainties in secondary organic aerosol (SOA) chemistry and its precursor emissions (Po valley and Mediterranean basin), dust (south of Spain) and sea salt (western Europe). The results suggest that future work should focus on the development of national bottom-up emission inventories including a better account for semi-volatile organic compounds and their conversion to SOA, the improvement of the CHIMERE urban parameterization, the introduction into CHIMERE of the coarse nitrate chemistry and an advanced parameterization accounting for windblown dust emissions.

The first pan-European kilometre-scale atmospheric chemistry simulation is introduced. The continental-scale air pollution episode of January 2009 is modelled with the CHIMERE offline chemistry transport model with a massive grid of 2 million horizontal points, performed on 2000 CPU of a high-performance computing system hosted by the Research and Technology Computing Center at the French Alternative Energies and Atomic Energy Commission (CCRT/CEA). Besides the technical challenge, we find that model biases are significantly reduced, especially over urban areas. The high-resolution grid also allows revisiting of the contribution of individual city plumes to the European burden of pollution, providing new insights to target the appropriate geographical level of action when designing air pollution mitigation strategies.

NO2 concentrations at the street level are a major concern for urban air quality in Europe and have been regulated under the EU Thematic Strategy on Air Pollution. Despite the legal requirements, limit values are exceeded at many monitoring stations with little or no improvement in recent years. In order to assess the effects of future emission control regulations on roadside NO2 concentrations, a downscaling module has been implemented in the GAINS integrated assessment model. The module follows a hybrid approach based on atmospheric dispersion calculations and observations from the AirBase European air quality database that are used to estimate site-specific parameters. Pollutant concentrations at every monitoring site with sufficient data coverage are disaggregated into contributions from regional background, urban increment, and local roadside increment. The future evolution of each contribution is assessed with a model of the appropriate scale: 28 × 28 km grid based on the EMEP Model for the regional background, 7 × 7 km urban increment based on the CHIMERE Chemistry Transport Model, and a chemical box model for the roadside increment. Thus, different emission scenarios and control options for long-range transport as well as regional and local emissions can be analysed. Observed concentrations and historical trends are well captured, in particular the differing NO2 and total NOx = NO + NO2 trends. Altogether, more than 1950 air quality monitoring stations in the EU are covered by the model, including more than 400 traffic stations and 70% of the critical stations. Together with its well-established bottom-up emission and dispersion calculation scheme, GAINS is thus able to bridge the scales from European-wide policies to impacts in street canyons. As an application of the model, we assess the evolution of attainment of NO2 limit values under current legislation until 2030. Strong improvements are expected with the introduction of the Euro 6 emission standard for light duty vehicles; however, for some major European cities, further measures may be required, in particular if aiming to achieve compliance at an earlier time.

The compact Earth system model OSCARv2.2 is used to assess the climate impact of present and future civil aviation carbon dioxide (CO _2 ) emissions. The impact of aviation CO _2 on future climate is quantified over the 1940–2050 period, extending some simulations to 2100 and using different aviation CO _2 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 MtCO _2 /year (Factor 2 scenario) to 2338 MtCO _2 /year (ICAO based scenario) in 2050. As a reference, in 2000, the calculated impact of aviation CO _2 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 CO _2 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 CO _2 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 CO _2 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.

Background: Using metaphase spreads from human lymphoblastoid cell lines, we previously showed how immunofluorescence microscopy could define the distribution of histone modifications across metaphase chromosomes. We showed that different histone modifications gave consistent and clearly defined immunofluorescent banding patterns. However, it was not clear to what extent these higher level distributions were influenced by long-term growth in culture, or by the specific functional associations of individual histone modifications., Results: Metaphase chromosome spreads from human lymphocytes stimulated to grow in short-term culture, were immunostained with antibodies to histone H3 mono- or tri-methylated at lysine 4 (H3K4me1, H3K4me3). Chromosomes were identified on the basis of morphology and reverse DAPI (rDAPI) banding. Both antisera gave the same distinctive immunofluorescent staining pattern, with unstained heterochromatic regions and a banded distribution along the chromosome arms. Karyotypes were prepared, showing the reproducibility of banding between sister chromatids, homologue pairs and from one metaphase spread to another. At the light microscope level, we detect no difference between the banding patterns along chromosomes from primary lymphocytes and lymphoblastoid cell lines adapted to long-term growth in culture., Conclusions: The distribution of H3K4me3 is the same across metaphase chromosomes from human primary lymphocytes and LCL, showing that higher level distribution is not altered by immortalization or long-term culture. The two modifications H3K4me1 (enriched in gene enhancer regions) and H3K4me3 (enriched in gene promoter regions) show the same distributions across human metaphase chromosomes, showing that functional differences do not necessarily cause modifications to differ in their higher-level distributions.

Histone acetylation is a key modification that regulates chromatin accessibility. Here we show that treatment with butyrate or other histone deacetylase (HDAC) inhibitors does not induce histone hyperacetylation in metaphase-arrested HeLa cells. When compared to similarly treated interphase cells, acetylation levels are significantly decreased in all four core histones and at all individual sites examined. However, the extent of the decrease varies, ranging from only slight reduction at H3K23 and H4K12 to no acetylation at H3K27 and barely detectable acetylation at H4K16. Our results show that the bulk effect is not due to increased or butyrate-insensitive HDAC activity, though these factors may play a role with some individual sites. We conclude that the lack of histone acetylation during mitosis is primarily due to changes in histone acetyltransferases (HATs) or changes in chromatin. The effects of protein phosphatase inhibitors on histone acetylation in cell lysates suggest that the reduced ability of histones to become acetylated in mitotic cells depends on protein phosphorylation., (Copyright 2010 Elsevier Inc. All rights reserved.)

Background: Immunolabeling of metaphase chromosome spreads can map components of the human epigenome at the single cell level. Previously, there has been no systematic attempt to explore the potential of this approach for epigenomic mapping and thereby to complement approaches based on chromatin immunoprecipitation (ChIP) and sequencing technologies., Results: By immunostaining and immunofluorescence microscopy, we have defined the distribution of selected histone modifications across metaphase chromosomes from normal human lymphoblastoid cells and constructed immunostained karyotypes. Histone modifications H3K9ac, H3K27ac and H3K4me3 are all located in the same set of sharply defined immunofluorescent bands, corresponding to 10- to 50-Mb genomic segments. Primary fibroblasts gave broadly the same banding pattern. Bands co-localize with regions relatively rich in genes and CpG islands. Staining intensity usually correlates with gene/CpG island content, but occasional exceptions suggest that other factors, such as transcription or SINE density, also contribute. H3K27me3, a mark associated with gene silencing, defines a set of bands that only occasionally overlap with gene-rich regions. Comparison of metaphase bands with histone modification levels across the interphase genome (ENCODE, ChIP-seq) shows a close correspondence for H3K4me3 and H3K27ac, but major differences for H3K27me3., Conclusions: At metaphase the human genome is packaged as chromatin in which combinations of histone modifications distinguish distinct regions along the euchromatic chromosome arms. These regions reflect the high-level interphase distributions of some histone modifications, and may be involved in heritability of epigenetic states, but we also find evidence for extensive remodeling of the epigenome at mitosis., (© 2010 Terrenoire et al.; licensee BioMed Central Ltd.)

Consistent deficits in the cholinergic system are evident in the brains of Alzheimer's Disease (AD) patients, including reductions in the activities of acetylcholine, acetylcholinesterase (AChE), and choline acetyltransferase (ChAT), increased butyrylcholinesterase (BChE) activity, and a selective loss of nicotinic acetylcholine receptors (nAChRs). Accordingly, we have analyzed polymorphisms in the genes encoding AChE, ChAT, BChE, and several of the subunit genes from neuronal nAChRs, for genetic associations with late-onset AD. A significant association for disease was detected for a non-coding polymorphism in ChAT (allele chi(1) (2) = 12.84, P = 0.0003; genotype chi(2) (2) = 11.89, P = 0.0026). Although replication analysis did not confirm the significance of this finding when the replication samples were considered alone (allele chi(1) (2) = 1.02, P = 0.32; genotype chi(2) (2) = 1.101, P = 0.58) the trends were in the correct direction and a significant association remained when the two sample sets were pooled (allele chi(1) (2) = 12.37, P = 0.0004; genotype chi(2) (2) = 11.61, P = 0.003). Previous studies have reported significant disease associations for both the K-variant of BChE and the coding ChAT rs3810950 polymorphism with AD. Replication analyses of these two loci failed to detect any significant association for disease in our case-control samples., (Copyright 2004 Wiley-Liss, Inc.)