577 research outputs found

    Climate sensitivity estimates – sensitivity to radiative forcing time series and observational data

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    Inferred effective climate sensitivity (ECSinf) is estimated using a method combining radiative forcing (RF) time series and several series of observed ocean heat content (OHC) and near-surface temperature change in a Bayesian framework using a simple energy balance model and a stochastic model. The model is updated compared to our previous analysis by using recent forcing estimates from IPCC, including OHC data for the deep ocean, and extending the time series to 2014. In our main analysis, the mean value of the estimated ECSinf is 2.0 °C, with a median value of 1.9 °C and a 90 % credible interval (CI) of 1.2–3.1 °C. The mean estimate has recently been shown to be consistent with the higher values for the equilibrium climate sensitivity estimated by climate models. The transient climate response (TCR) is estimated to have a mean value of 1.4 °C (90 % CI 0.9–2.0 °C), and in our main analysis the posterior aerosol effective radiative forcing is similar to the range provided by the IPCC. We show a strong sensitivity of the estimated ECSinf to the choice of a priori RF time series, excluding pre-1950 data and the treatment of OHC data. Sensitivity analysis performed by merging the upper (0–700 m) and the deep-ocean OHC or using only one OHC dataset (instead of four in the main analysis) both give an enhancement of the mean ECSinf by about 50 % from our best estimate

    Implications of differences between recent anthropogenic aerosol emission inventories for diagnosed AOD and radiative forcing from 1990 to 2019

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    This study focuses on implications of differences between recent global emissions inventories for simulated trends in anthropogenic aerosol abundances and radiative forcing (RF) over the 1990–2019 period. We use the ECLIPSE version 6 (ECLv6) and CEDS year 2021 release (CEDS21) as input to the chemical transport model OsloCTM3 and compare the resulting aerosol evolution to corresponding results derived with the first CEDS release, as well as to observed trends in regional and global aerosol optical depth (AOD). Using CEDS21 and ECLv6 results in a 3 % and 6 % lower global mean AOD compared to CEDS in 2014, primarily driven by differences over China and India, where the area average AOD is up to 30 % lower. These differences are considerably larger than the satellite-derived interannual variability in AOD. A negative linear trend over 2005–2017 in global AOD following changes in anthropogenic emissions is found with all three inventories but is markedly stronger with CEDS21 and ECLv6. Furthermore, we confirm that the model better captures the sign and strength of the observed AOD trend over China with CEDS21 and ECLv6 compared to using CEDS, while the opposite is the case for South Asia. We estimate a net global mean aerosol-induced RF in 2014 relative to 1990 of 0.08 W m−2 for CEDS21 and 0.12 W m−2 for ECLv6, compared to 0.03 W m−2 with CEDS. Using CEDS21, we also estimate the RF in 2019 relative to 1990 to be 0.10 W m−2, reflecting the continuing decreasing trend in aerosol loads post-2014. Our results facilitate more rigorous comparison between existing and upcoming studies of climate and health effects of aerosols using different emission inventories.</p

    Concentrations and radiative forcing of anthropogenic aerosols from 1750 to 2014 simulated with the Oslo CTM3 and CEDS emission inventory

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    We document the ability of the new-generation Oslo chemistry-transport model, Oslo CTM3, to accurately simulate present-day aerosol distributions. The model is then used with the new Community Emission Data System (CEDS) historical emission inventory to provide updated time series of anthropogenic aerosol concentrations and consequent direct radiative forcing (RFari) from 1750 to 2014.Overall, Oslo CTM3 performs well compared with measurements of surface concentrations and remotely sensed aerosol optical depth. Concentrations are underestimated in Asia, but the higher emissions in CEDS than previous inventories result in improvements compared to observations. The treatment of black carbon (BC) scavenging in Oslo CTM3 gives better agreement with observed vertical BC profiles relative to the predecessor Oslo CTM2. However, Arctic wintertime BC concentrations remain underestimated, and a range of sensitivity tests indicate that better physical understanding of processes associated with atmospheric BC processing is required to simultaneously reproduce both the observed features. Uncertainties in model input data, resolution, and scavenging affect the distribution of all aerosols species, especially at high latitudes and altitudes. However, we find no evidence of consistently better model performance across all observables and regions in the sensitivity tests than in the baseline configuration.Using CEDS, we estimate a net RFari in 2014 relative to 1750 of −0.17&thinsp;W&thinsp;m−2, significantly weaker than the IPCC AR5 2011–1750 estimate. Differences are attributable to several factors, including stronger absorption by organic aerosol, updated parameterization of BC absorption, and reduced sulfate cooling. The trend towards a weaker RFari over recent years is more pronounced than in the IPCC AR5, illustrating the importance of capturing recent regional emission changes.</p

    Lecithin : cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings

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    LCAT converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017 symposium where Dr. Norum recounted the history of FLD and leading experts on LCAT shared their results. The Tesmer laboratory shared structural findings on LCAT and the close homolog, lysosomal phospholipase A2. Results from studies of FLD patients in Finland, Brazil, Norway, and Italy were presented, as well as the status of a patient registry. Drs. Kuivenhoven and Calabresi presented data from carriers of genetic mutations suggesting that FLD does not necessarily accelerate atherosclerosis. Dr. Ng shared that LCAT-null mice were protected from diet-induced obesity, insulin resistance, and nonalcoholic fatty liver disease. Dr. Zhou presented multiple innovations for increasing LCAT activity for therapeutic purposes, whereas Dr. Remaley showed results from treatment of an FLD patient with recombinant human LCAT (rhLCAT). Dr. Karathanasis showed that rhLCAT infusion in mice stimulates cholesterol efflux and suggested that it could also enhance cholesterol efflux from macrophages. While the role of LCAT in atherosclerosis remains elusive, the consensus is that a continued study of both the enzyme and disease will lead toward better treatments for patients with heart disease and FLD.Peer reviewe

    Lecithin:cholesterol acyltransferase:symposium on 50 years of biomedical research from its discovery to latest findings

    Get PDF
    LCAT converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017 symposium where Dr. Norum recounted the history of FLD and leading experts on LCAT shared their results. The Tesmer laboratory shared structural findings on LCAT and the close homolog, lysosomal phospholipase A2. Results from studies of FLD patients in Finland, Brazil, Norway, and Italy were presented, as well as the status of a patient registry. Drs. Kuivenhoven and Calabresi presented data from carriers of genetic mutations suggesting that FLD does not necessarily accelerate atherosclerosis. Dr. Ng shared that LCAT-null mice were protected from diet-induced obesity, insulin resistance, and nonalcoholic fatty liver disease. Dr. Zhou presented multiple innovations for increasing LCAT activity for therapeutic purposes, whereas Dr. Remaley showed results from treatment of an FLD patient with recombinant human LCAT (rhLCAT). Dr. Karathanasis showed that rhLCAT infusion in mice stimulates cholesterol efflux and suggested that it could also enhance cholesterol efflux from macrophages. While the role of LCAT in atherosclerosis remains elusive, the consensus is that a continued study of both the enzyme and disease will lead toward better treatments for patients with heart disease and FLD.</p

    Long-term weight change and risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) study

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    BACKGROUND: The role of obesity and weight change in breast-cancer development is complex and incompletely understood. We investigated long-term weight change and breast-cancer risk by body mass index (BMI) at age 20 years, menopausal status, hormone replacement therapy (HRT) and hormone-receptor status. METHODS: Using data on weight collected at three different time points from women who participated in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, we investigated the association between weight change from age 20 years until middle adulthood and risk of breast cancer. RESULTS: In total, 150 257 women with a median age of 51 years at cohort entry were followed for an average of 14 years (standard deviation = 3.9) during which 6532 breast-cancer cases occurred. Compared with women with stable weight (±2.5 kg), long-term weight gain >10 kg was positively associated with postmenopausal breast-cancer risk in women who were lean at age 20 [hazard ratio (HR) = 1.42; 95% confidence interval 1.22-1.65] in ever HRT users (HR = 1.23; 1.04-1.44), in never HRT users (HR = 1.40; 1.16-1.68) and in oestrogen-and-progesterone-receptor-positive (ER+PR+) breast cancer (HR = 1.46; 1.15-1.85). CONCLUSION: Long-term weight gain was positively associated with postmenopausal breast cancer in women who were lean at age 20, both in HRT ever users and non-users, and hormone-receptor-positive breast cancer
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