Application of the Denitrification-Decomposition Model to Predict Carbon Dioxide Emissions under Alternative Straw Retention Methods

Straw retention has been shown to reduce carbon dioxide (CO2) emission from agricultural soils. But it remains a big challenge for models to effectively predict CO2 emission fluxes under different straw retention methods. We used maize season data in the Griffith region, Australia, to test whether the denitrification-decomposition (DNDC) model could simulate annual CO2 emission. We also identified driving factors of CO2 emission by correlation analysis and path analysis. We show that the DNDC model was able to simulate CO2 emission under alternative straw retention scenarios. The correlation coefficients between simulated and observed daily values for treatments of straw burn and straw incorporation were 0.74 and 0.82, respectively, in the straw retention period and 0.72 and 0.83, respectively, in the crop growth period. The results also show that simulated values of annual CO2 emission for straw burn and straw incorporation were 3.45 t C ha−1 y−1 and 2.13 t C ha−1 y−1, respectively. In addition the DNDC model was found to be more suitable in simulating CO2 mission fluxes under straw incorporation. Finally the standard multiple regression describing the relationship between CO2 emissions and factors found that soil mean temperature (SMT), daily mean temperature (Tmean), and water-filled pore space (WFPS) were significant

Trade-offs in agricultural outcomes across various farm sizes

Farm size plays a critical role in agriculture, influencing productivity, resource use efficiency, and environmental impacts. Smallholder farms, compared to large farms, often face constraints such as limited mechanisation and advanced technology, leading to lower efficiency and potential environmental degradation. Transitioning from a system dominated by smallholders to one featuring large-scale farming holds potential for sustainable agricultural intensification, especially in regions currently reliant on smallholder systems. However, the benefits and potential unintended consequences of such a transition remain contentious and require further exploration. This review examines the multifaceted role of farm size, highlighting the essential contributions of smallholders to food security, poverty alleviation, crop diversity, and biodiversity despite their limitations in machinery, technology and efficiency. While acknowledging the potential for increased sustainability through scaling up farm size, we also identify the risks associated with large-scale farming, such as biodiversity loss, increased market volatility, and adverse environmental impacts. We emphasise the importance of tailored strategies for managing different farm size to optimise agricultural productivity, economic viability, human well-being, and sustainable development. Our study provides a new perspective that complements the conventional advocacy for large-scale agriculture, revealing trade-offs of agricultural outcomes across different farm sizes. It offers a comprehensive evaluation of the significance of farm size in shaping future sustainable agricultural systems

Elevated CO2_{2} negates O3_{3} impacts on terrestrial carbon and nitrogen cycles

Increasing tropospheric concentrations of ozone (e[O$_{3}$]) and carbon dioxide (e[CO$_{2}$]) profoundly perturb terrestrial ecosystem functions through carbon and nitrogen cycles, affecting beneficial services such as their capacity to combat climate change and provide food. However, the interactive effects of e[O$_{3}$] and e[CO$_{2}$] on these functions and services remain unclear. Here, we synthesize the results of 810 studies (9,109 observations), spanning boreal to tropical regions around the world, and show that e[O$_{3}$] significantly decreases global net primary productivity and food production as well as the capacity of ecosystems to store carbon and nitrogen, which are stimulated by e[CO$_{2}$]. More importantly, simultaneous increases in [CO$_{2}$] and [O$_{3}$] negate or even overcompensate the negative effects of e[O$_{3}$3] on ecosystem functions and carbon and nitrogen cycles. Therefore, the negative effects of e[O$_{3}$] on terrestrial ecosystems would be overestimated if e[CO$_{2}$] impacts are not considered, stressing the need for evaluating terrestrial carbon and nitrogen feedbacks to concurrent changes in global atmospheric composition

Toward a generic analytical framework for sustainable nitrogen management: application for China

Managing reactive nitrogen (Nr) to achieve a sustainable balance between production of food, feed and fiber, and environmental protection is a grand challenge in the context of an increasingly affluent society. Here, we propose a novel framework for national nitrogen (N) assessments enabling a more consistent comparison of the uses, losses and impacts of Nr between countries, and improvement of Nr management for sustainable development at national and regional scales. This framework includes four key components: national scale N budgets, validation of N fluxes, cost-benefit analysis and Nr management strategies. We identify four critical factors for Nr management to achieve the sustainable development goals: N use efficiency (NUE), Nr recycling ratio (e.g., ratio of livestock excretion applied to cropland), human dietary patterns and food waste ratio. This framework was partly adopted from the European Nitrogen Assessment and now is successfully applied to China, where it contributed to trigger policy interventions toward improvements for future sustainable use of Nr. We demonstrate how other countries can also benefit from the application our framework, in order to include sustainable Nr management under future challenges of growing population, hence contributing to the achievement of some key sustainable development goals (SDGs)

The warming climate aggravates atmospheric nitrogen pollution in Australia

Australia is a warm country with well-developed agriculture and a highly urbanized population. How these specific features impact the nitrogen cycle, emissions, and consequently affect environmental and human health is not well understood. Here, we find that the ratio of reactive nitrogen () losses to air over losses to water in Australia is 1.6 as compared to values less than 1.1 in the USA, the European Union, and China. Australian emissions to air increased by more than 70% between 1961 and 2013, from 1.2 Tg N yr-1 to 2.1 Tg N yr-1. Previous emissions were substantially underestimated mainly due to neglecting the warming climate. The estimated health cost from atmospheric emissions in Australia is 4.6 billion US dollars per year. Emissions of to the environment are closely correlated with economic growth, and reduction of losses to air is a priority for sustainable development in Australia

Cleaning up nitrogen pollution may reduce future carbon sinks

Biosphere carbon sinks are crucial for reducing atmospheric carbon dioxide (CO2) concentration to mitigate global warming, but are substantially affected by the input of reactive nitrogen (Nr). Although the effects of anthropogenic CO2 emission and nitrogen deposition (indicated by Nr emission to atmosphere) on carbon sink have been studied, it is unclear how their ratio (C/N) changes with economic development and how such change alters biosphere carbon sinks. Here, by compiling datasets for 132 countries we find that the C/N ratio continued to increase despite anthropogenic CO2 and Nr emissions to atmosphere both showing an asymmetric para-curve with economic growth. The inflection points of CO2 and Nr emissions are found at around $15,000 gross domestic product per capita worldwide. Economic growth promotes the use of Nr and energy, while at the same time increases their use efficiencies, together resulting in occurrences of inflection points of CO2 and Nr emissions. Nr emissions increase slower but decrease faster than that of CO2 emissions before and after the inflection point, respectively. It implies that there will be relatively more anthropogenic CO2 emission but less N deposition with economic growth. This may limit biosphere carbon sink because of relative shortage of Nr. This finding should be integrated/included in global climate change modelling. Efforts, such as matching N deposition with carbon sequestration on regional scale, to manage CO2 and Nr emissions comprehensively to maintain a balance are critical

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.Peer reviewedPublisher PD

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Abstract Background Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding Information: GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file : Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services. Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe