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Sökning: WFRF:(O’Connor Andy J.)

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1.
  • Smith, Christopher J., et al. (författare)
  • Effective radiative forcing and adjustments in CMIP6 models
  • 2020
  • Ingår i: Atmospheric Chemistry And Physics. - : Copernicus GmbH. - 1680-7316 .- 1680-7324. ; 20:16, s. 9591-9618
  • Tidskriftsartikel (refereegranskat)abstract
    • The effective radiative forcing, which includes the instantaneous forcing plus adjustments from the atmosphere and surface, has emerged as the key metric of evaluating human and natural influence on the climate. We evaluate effective radiative forcing and adjustments in 17 contemporary climate models that are participating in the Coupled Model Intercomparison Project (CMIP6) and have contributed to the Radiative Forcing Model Intercomparison Project (RFMIP). Present-day (2014) global-mean anthropogenic forcing relative to pre-industrial (1850) levels from climate models stands at 2.00 (+/- 0.23) W m(-2), comprised of 1.81 (+/- 0.09) Wm(-2) from CO2, 1.08 (+/- 0.21) Wm(-2) from other well-mixed greenhouse gases, -1.01 (+/- 0.23) W m(-2) from aerosols and -0.09 (+/- 0.13) W m(-2) from land use change. Quoted uncertainties are 1 standard deviation across model best estimates, and 90 % confidence in the reported forcings, due to internal variability, is typically within 0.1 W m(-2). The majority of the remaining 0.21 W m(-2) is likely to be from ozone. In most cases, the largest contributors to the spread in effective radiative forcing (ERF) is from the instantaneous radiative forcing (IRF) and from cloud responses, particularly aerosol-cloud interactions to aerosol forcing. As determined in previous studies, cancellation of tropospheric and surface adjustments means that the stratospherically adjusted radiative forcing is approximately equal to ERF for greenhouse gas forcing but not for aerosols, and consequentially, not for the anthropogenic total. The spread of aerosol forcing ranges from -0.63 to -1.37 W m(-2), exhibiting a less negative mean and narrower range compared to 10 CMIP5 models. The spread in 4 x CO2 forcing has also narrowed in CMIP6 compared to 13 CMIP5 models. Aerosol forcing is uncorrelated with climate sensitivity. Therefore, there is no evidence to suggest that the increasing spread in climate sensitivity in CMIP6 models, particularly related to high-sensitivity models, is a consequence of a stronger negative present-day aerosol forcing and little evidence that modelling groups are systematically tuning climate sensitivity or aerosol forcing to recreate observed historical warming.
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2.
  • Strickson, Sam, et al. (författare)
  • Oxidised IL-33 drives COPD epithelial pathogenesis via ST2-independent RAGE/EGFR signalling complex
  • 2023
  • Ingår i: European Respiratory Journal. - 0903-1936. ; 62:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Epithelial damage, repair and remodelling are critical features of chronic airway diseases including chronic obstructive pulmonary disease (COPD). Interleukin (IL)-33 released from damaged airway epithelia causes inflammation via its receptor, serum stimulation-2 (ST2). Oxidation of IL-33 to a non-ST2-binding form (IL-33ox) is thought to limit its activity. We investigated whether IL-33ox has functional activities that are independent of ST2 in the airway epithelium. Methods In vitro epithelial damage assays and three-dimensional, air–liquid interface (ALI) cell culture models of healthy and COPD epithelia were used to elucidate the functional role of IL-33ox. Transcriptomic changes occurring in healthy ALI cultures treated with IL-33ox and COPD ALI cultures treated with an IL-33-neutralising antibody were assessed with bulk and single-cell RNA sequencing analysis. Results We demonstrate that IL-33ox forms a complex with receptor for advanced glycation end products (RAGE) and epidermal growth factor receptor (EGFR) expressed on airway epithelium. Activation of this alternative, ST2-independent pathway impaired epithelial wound closure and induced airway epithelial remodelling in vitro. IL-33ox increased the proportion of mucus-producing cells and reduced epithelial defence functions, mimicking pathogenic traits of COPD. Neutralisation of the IL-33ox pathway reversed these deleterious traits in COPD epithelia. Gene signatures defining the pathogenic effects of IL-33ox were enriched in airway epithelia from patients with severe COPD. Conclusions Our study reveals for the first time that IL-33, RAGE and EGFR act together in an ST2-independent pathway in the airway epithelium and govern abnormal epithelial remodelling and mucoobstructive features in COPD.
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3.
  • Malavelle, Florent F., et al. (författare)
  • Strong constraints on aerosol-cloud interactions from volcanic eruptions
  • 2017
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 546:7659, s. 485-491
  • Tidskriftsartikel (refereegranskat)abstract
    • Aerosols have a potentially large effect on climate, particularly through their interactions with clouds, but the magnitude of this effect is highly uncertain. Large volcanic eruptions produce sulfur dioxide, which in turn produces aerosols; these eruptions thus represent a natural experiment through which to quantify aerosol-cloud interactions. Here we show that the massive 2014-2015 fissure eruption in Holuhraun, Iceland, reduced the size of liquid cloud droplets-consistent with expectations-but had no discernible effect on other cloud properties. The reduction in droplet size led to cloud brightening and global-mean radiative forcing of around -0.2 watts per square metre for September to October 2014. Changes in cloud amount or cloud liquid water path, however, were undetectable, indicating that these indirect effects, and cloud systems in general, are well buffered against aerosol changes. This result will reduce uncertainties in future climate projections, because we are now able to reject results from climate models with an excessive liquid-water-path response.
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