Chemical transport modeling of potential atmospheric CO2 sinks

The potential for carbon dioxide (CO2) sequestration via engineered chemical sinks is investigated using a three dimensional chemical transport model (CTM). Meteorological and chemical constraints for flat or vertical systems that would absorb CO2 from the atmosphere, as well as an example chemical system of calcium hydroxide (Ca(OH)2) proposed by Elliott et al. [Compensation of atmospheric CO2 buildup through engineered chemical sinkage, Geophys. Res. Lett. 28 (2001) 1235] are reviewed. The CTM examines land based deposition sinks, with 4° × 5° latitude/longitude resolution at various locations, and deposition velocities (v). A maximum uptake of ∼20 Gton (1015 g) Cyr-1 is attainable with v ≥ 5 cms-1 at a mid-latitude site. The atmospheric increase of CO2 (3 Gtonyr-1) can be balanced by an engineered sink with an area of no more than 75, 000 km2 at v of 1 cms-1. By building the sink upwards or splitting this area into narrow elements can reduce the active area by more than an order of magnitude as discussed in Dubey et al. © 2002 Elsevier Science Ltd. All rights reserved

Large-scale latitudinal and vertical distributions of NMHCs and selected halocarbons in the troposphere over the Pacific Ocean during the March-April 1999 Pacific Exploratory Mission (PEM-Tropics B)

Nonmethane hydrocarbons (NMHCs) and selected halocarbons were measured in whole air samples collected over the remote Pacific Ocean during NASA's Global Tropospheric Experiment (GTE) Pacific Exploratory Mission-Tropics B (PEM-Tropics B) in March and early April 1999. The large-scale spatial distributions of NMHCs and C2Cl4 reveal a much more pronounced north-south interhemispheric gradient, with higher concentrations in the north and lower levels in the south, than for the late August to early October 1996 PEM-Tropics A experiment. Strong continental outflow and winter-long accumulation of pollutants led to seasonally high Northern Hemisphere trace gas levels during PEM-Tropics B. Observations of enhanced levels of Halon 1211 (from developing Asian nations such as the PRC) and CH3Cl (from SE Asian biomass burning) support a significant southern Asian influence at altitudes above 1 km and north of 10° N. By contrast, at low altitude over the North Pacific the dominance of urban/industrial tracers, combined with low levels of Halon 1211 and CH3Cl, indicate a greater influence from developed nations such as Japan, Europe, and North America. Penetration of air exhibiting aged northern hemisphere characteristics was frequently observed at low altitudes over the equatorial central and western Pacific south to ∼5° S. The relative lack of southern hemisphere biomass burning sources and the westerly position of the South Pacific convergence zone contributed to significantly lower PEM-Tropics B mixing ratios of the NMHCs and CH3Cl south of 10° S compared to PEM-Tropics A. Therefore the trace gas composition of the South Pacific troposphere was considerably more representative of minimally polluted tropospheric conditions during PEM-Tropics B. Copyright 2001 by the American Geophysical Union

Chemical transport modeling of potential atmospheric CO2 sinks

The potential for carbon dioxide (CO2) sequestration via engineered chemical sinks is investigated using a three dimensional chemical transport model (CTM). Meteorological and chemical constraints for flat or vertical systems that would absorb CO2 from the atmosphere, as well as an example chemical system of calcium hydroxide (Ca(OH)2) proposed by Elliott et al. [Compensation of atmospheric CO2 buildup through engineered chemical sinkage, Geophys. Res. Lett. 28 (2001) 1235] are reviewed. The CTM examines land based deposition sinks, with 4° × 5° latitude/longitude resolution at various locations, and deposition velocities (v). A maximum uptake of ∼20 Gton (1015 g) Cyr-1 is attainable with v ≥ 5 cms-1 at a mid-latitude site. The atmospheric increase of CO2 (3 Gtonyr-1) can be balanced by an engineered sink with an area of no more than 75, 000 km2 at v of 1 cms-1. By building the sink upwards or splitting this area into narrow elements can reduce the active area by more than an order of magnitude as discussed in Dubey et al. © 2002 Elsevier Science Ltd. All rights reserved

Differential effects of oxidised and reduced nitrogen on vegetation and soil chemistry of species-rich acidic grasslands

Emissions and deposition of ammonia and nitrogen oxides have strongly increased since the 1950s. This has led to significant changes in the nitrogen (N) cycle, vegetation composition and plant diversity in many ecosystems of high conservation value in Europe. As a consequence of different regional pollution levels and of the increased importance of reduced N in the near future, determining the effect of different forms of N is an important task for understanding the consequences of atmospheric N inputs. We have initiated three replicated N addition experiments in species-rich, acidic grasslands spanning a climatic gradient in the Atlantic biogeographic region of Europe in Norway, Wales and France at sites with low levels of pollution. N was added in two doses (0 and 70 kg N ha−1 year−1 above background) and in three forms (oxidised N, reduced N and a 50–50 combination). After 2.5 years of N additions, the effects of these treatments on plant biomass, plant nutritional status, soil pH and soil nutrient availability were determined. Impacts of the N additions were observed within the 2.5-year research period. In some cases, the first signs of differential effects of N form could also be demonstrated. In the French site, for example, grass biomass was significantly increased by the oxidised N treatments but decreased by the reduced N treatments. In the Norwegian site, the reduced N treatments significantly reduced soil pH, whereas oxidised N did not. Effects on nutrient availability were also observed. These experiments will be continued to elucidate the longer term impacts of N deposition on these grasslands

GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19

Data availability: Downloadable summary data are available through the GenOMICC data site (https://genomicc.org/data). Summary statistics are available, but without the 23andMe summary statistics, except for the 10,000 most significant hits, for which full summary statistics are available. The full GWAS summary statistics for the 23andMe discovery dataset will be made available through 23andMe to qualified researchers under an agreement with 23andMe that protects the privacy of the 23andMe participants. For further information and to apply for access to the data, see the 23andMe website (https://research.23andMe.com/dataset-access/). All individual-level genotype and whole-genome sequencing data (for both academic and commercial uses) can be accessed through the UKRI/HDR UK Outbreak Data Analysis Platform (https://odap.ac.uk). A restricted dataset for a subset of GenOMICC participants is also available through the Genomics England data service. Monocyte RNA-seq data are available under the title ‘Monocyte gene expression data’ within the Oxford University Research Archives (https://doi.org/10.5287/ora-ko7q2nq66). Sequencing data will be made freely available to organizations and researchers to conduct research in accordance with the UK Policy Framework for Health and Social Care Research through a data access agreement. Sequencing data have been deposited at the European Genome–Phenome Archive (EGA), which is hosted by the EBI and the CRG, under accession number EGAS00001007111.Extended data figures and tables are available online at https://www.nature.com/articles/s41586-023-06034-3#Sec21 .Supplementary information is available online at https://www.nature.com/articles/s41586-023-06034-3#Sec22 .Code availability: Code to calculate the imputation of P values on the basis of SNPs in linkage disequilibrium is available at GitHub (https://github.com/baillielab/GenOMICC_GWAS).Acknowledgements: We thank the members of the Banco Nacional de ADN and the GRA@CE cohort group; and the research participants and employees of 23andMe for making this work possible. A full list of contributors who have provided data that were collated in the HGI project, including previous iterations, is available online (https://www.covid19hg.org/acknowledgements).Change history: 11 July 2023: A Correction to this paper has been published at: https://doi.org/10.1038/s41586-023-06383-z. -- In the version of this article initially published, the name of Ana Margarita Baldión-Elorza, of the SCOURGE Consortium, appeared incorrectly (as Ana María Baldion) and has now been amended in the HTML and PDF versions of the article.Copyright © The Author(s) 2023, Critical illness in COVID-19 is an extreme and clinically homogeneous disease phenotype that we have previously shown1 to be highly efficient for discovery of genetic associations2. Despite the advanced stage of illness at presentation, we have shown that host genetics in patients who are critically ill with COVID-19 can identify immunomodulatory therapies with strong beneficial effects in this group3. Here we analyse 24,202 cases of COVID-19 with critical illness comprising a combination of microarray genotype and whole-genome sequencing data from cases of critical illness in the international GenOMICC (11,440 cases) study, combined with other studies recruiting hospitalized patients with a strong focus on severe and critical disease: ISARIC4C (676 cases) and the SCOURGE consortium (5,934 cases). To put these results in the context of existing work, we conduct a meta-analysis of the new GenOMICC genome-wide association study (GWAS) results with previously published data. We find 49 genome-wide significant associations, of which 16 have not been reported previously. To investigate the therapeutic implications of these findings, we infer the structural consequences of protein-coding variants, and combine our GWAS results with gene expression data using a monocyte transcriptome-wide association study (TWAS) model, as well as gene and protein expression using Mendelian randomization. We identify potentially druggable targets in multiple systems, including inflammatory signalling (JAK1), monocyte–macrophage activation and endothelial permeability (PDE4A), immunometabolism (SLC2A5 and AK5), and host factors required for viral entry and replication (TMPRSS2 and RAB2A).GenOMICC was funded by Sepsis Research (the Fiona Elizabeth Agnew Trust), the Intensive Care Society, a Wellcome Trust Senior Research Fellowship (to J.K.B., 223164/Z/21/Z), the Department of Health and Social Care (DHSC), Illumina, LifeArc, the Medical Research Council, UKRI, a BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070 and BBS/E/D/30002275) and UKRI grants MC_PC_20004, MC_PC_19025, MC_PC_1905 and MRNO2995X/1. A.D.B. acknowledges funding from the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z), the Edinburgh Clinical Academic Track (ECAT) programme. This research is supported in part by the Data and Connectivity National Core Study, led by Health Data Research UK in partnership with the Office for National Statistics and funded by UK Research and Innovation (grant MC_PC_20029). Laboratory work was funded by a Wellcome Intermediate Clinical Fellowship to B.F. (201488/Z/16/Z). We acknowledge the staff at NHS Digital, Public Health England and the Intensive Care National Audit and Research Centre who provided clinical data on the participants; and the National Institute for Healthcare Research Clinical Research Network (NIHR CRN) and the Chief Scientist’s Office (Scotland), who facilitate recruitment into research studies in NHS hospitals, and to the global ISARIC and InFACT consortia. GenOMICC genotype controls were obtained using UK Biobank Resource under project 788 funded by Roslin Institute Strategic Programme Grants from the BBSRC (BBS/E/D/10002070 and BBS/E/D/30002275) and Health Data Research UK (HDR-9004 and HDR-9003). UK Biobank data were used in the GSMR analyses presented here under project 66982. The UK Biobank was established by the Wellcome Trust medical charity, Medical Research Council, Department of Health, Scottish Government and the Northwest Regional Development Agency. It has also had funding from the Welsh Assembly Government, British Heart Foundation and Diabetes UK. The work of L.K. was supported by an RCUK Innovation Fellowship from the National Productivity Investment Fund (MR/R026408/1). J.Y. is supported by the Westlake Education Foundation. SCOURGE is funded by the Instituto de Salud Carlos III (COV20_00622 to A.C., PI20/00876 to C.F.), European Union (ERDF) ‘A way of making Europe’, Fundación Amancio Ortega, Banco de Santander (to A.C.), Cabildo Insular de Tenerife (CGIEU0000219140 ‘Apuestas científicas del ITER para colaborar en la lucha contra la COVID-19’ to C.F.) and Fundación Canaria Instituto de Investigación Sanitaria de Canarias (PIFIISC20/57 to C.F.). We also acknowledge the contribution of the Centro National de Genotipado (CEGEN) and Centro de Supercomputación de Galicia (CESGA) for funding this project by providing supercomputing infrastructures. A.D.L. is a recipient of fellowships from the National Council for Scientific and Technological Development (CNPq)-Brazil (309173/2019-1 and 201527/2020-0)