28 research outputs found
Global Carbon Budget 2015
Accurate assessment of anthropogenic carbon dioxide (CO2) emissions and their redistribution among the atmosphere, ocean, and terrestrial biosphere is important to better understand the global carbon cycle, support the development of climate policies, and project future climate change. Here we describe data sets and a methodology to quantify all major components of the global carbon budget, including their uncertainties, based on the combination of a range of data, algorithms, statistics, and model estimates and their interpretation by a broad scientific community. We discuss changes compared to previous estimates as well as consistency within and among components, alongside methodology and data limitations. CO2 emissions from fossil fuels and industry (E-FF) are based on energy statistics and cement production data, while emissions from land-use change (E-LUC), mainly deforestation, are based on combined evidence from land-cover-change data, fire activity associated with deforestation, and models. The global atmospheric CO2 concentration is measured directly and its rate of growth (G(ATM)) is computed from the annual changes in concentration. The mean ocean CO2 sink (S-OCEAN) is based on observations from the 1990s, while the annual anomalies and trends are estimated with ocean models. The variability in S-OCEAN is evaluated with data products based on surveys of ocean CO2 measurements. The global residual terrestrial CO2 sink (S-LAND) is estimated by the difference of the other terms of the global carbon budget and compared to results of independent dynamic global vegetation models forced by observed climate, CO2, and land-cover change (some including nitrogen-carbon interactions). We compare the mean land and ocean fluxes and their variability to estimates from three atmospheric inverse methods for three broad latitude bands. All uncertainties are reported as +/- 1 sigma, reflecting the current capacity to characterise the annual estimates of each component of the global carbon budget. For the last decade available (20052014), E-FF was 9.0 +/- 0.5 GtC yr(-1) E-LUC was 0.9 +/- 0.5 GtC yr(-1), GATM was 4.4 +/- 0.1 GtC yr(-1), S-OCEAN was 2.6 +/- 0.5 GtC yr(-1), and S LAND was 3.0 +/- 0.8 GtC yr(-1). For the year 2014 alone, E FF grew to 9.8 +/- 0.5 GtC yr(-1), 0.6% above 2013, continuing the growth trend in these emissions, albeit at a slower rate compared to the average growth of 2.2% yr(-1) that took place during 2005-2014. Also, for 2014, E-LUC was 1.1 +/- 0.5 GtC yr(-1), G(ATM) was 3.9 +/- 0.2 GtC yr(-1), S-OCEAN was 2.9 +/- 0.5 GtC yr(-1), and S-LAND was 4.1 +/- 0.9 GtC yr(-1). G(ATM) was lower in 2014 compared to the past decade (2005-2014), reflecting a larger S-LAND for that year. The global atmospheric CO2 concentration reached 397.15 +/- 0.10 ppm averaged over 2014. For 2015, preliminary data indicate that the growth in E-FF will be near or slightly below zero, with a projection of 0.6 [ range of 1.6 to C 0.5] %, based on national emissions projections for China and the USA, and projections of gross domestic product corrected for recent changes in the carbon intensity of the global economy for the rest of the world. From this projection of E-FF and assumed constant E LUC for 2015, cumulative emissions of CO2 will reach about 555 +/- 55 GtC (2035 +/- 205 GtCO(2)) for 1870-2015, about 75% from E FF and 25% from E LUC. This living data update documents changes in the methods and data sets used in this new carbon budget compared with previous publications of this data set (Le Quere et al., 2015, 2014, 2013). All observations presented here can be downloaded from the Carbon Dioxide Information Analysis Center (doi: 10.3334/CDIAC/GCP_2015)
Mismatch repair deficiency predicts response of solid tumors to PD-1 blockade.
The genomes of cancers deficient in mismatch repair contain exceptionally high numbers of somatic mutations. In a proof-of-concept study, we previously showed that colorectal cancers with mismatch repair deficiency were sensitive to immune checkpoint blockade with antibodies to programmed death receptor-1 (PD-1). We have now expanded this study to evaluate the efficacy of PD-1 blockade in patients with advanced mismatch repair-deficient cancers across 12 different tumor types. Objective radiographic responses were observed in 53% of patients, and complete responses were achieved in 21% of patients. Responses were durable, with median progression-free survival and overall survival still not reached. Functional analysis in a responding patient demonstrated rapid in vivo expansion of neoantigen-specific T cell clones that were reactive to mutant neopeptides found in the tumor. These data support the hypothesis that the large proportion of mutant neoantigens in mismatch repair-deficient cancers make them sensitive to immune checkpoint blockade, regardless of the cancers\u27 tissue of origin
Geriatrics consultation in the acute care institution: A combined experience in both the medical and psychiatric hospital
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Disparities in self-rated health across generations and through the life course.
Extensive evidence leads us to expect that health disparities by race and socioeconomic status found in one generation might be reproduced in the next. To the extent that this occurs it is important to assess life course processes responsible for the reproduction. Prospective evidence concerning such life course processes is hard to come by as it requires long-term follow-up of individuals from childhood through adult life. We present data from the Child Health and Development Disparities study that provides evidence relevant to this issue with respect to self-rated health. Mothers and offspring recruited in California's Bay Area between 1959 and 1967 were assessed during pregnancy with follow-up exams of offspring along with in-person interviews with mothers (at offspring ages 5, 9-11, 15-17) and offspring (at ages 15-17, ∼50). Available data allow us to assess the importance of three potential life course pathways in the reproduction of inequalities in self-rated health - socioeconomic pathways, cognitive pathways and pathways involving emerging health itself. As expected we found that race and SES disparities in SRH are reproduced across generations. They are evident in mothers, not strong or significant in offspring at 15-17, but present once again in offspring at age ∼50. Concerning potential pathways, we found that indicators of child health were related to adult SRH and played some role in accounting for race but not SES disparities in adult SRH. Cognitive abilities were unrelated to adult SRH with childhood SES controlled. Childhood SES was associated with adult SRH independent of other childhood factors and is reduced to non-significance only when offspring college attainment is controlled. Race and SES disparities in self-reported health in one generation are re-expressed in the next with strongest support for SES pathways in this transmission