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  • 1
    Publication Date: 2022-05-25
    Description: Author Posting. © American Meteorological Society, 2009. This article is posted here by permission of American Meteorological Society for personal use, not for redistribution. The definitive version was published in Journal of Climate 22 (2009): 5175–5204, doi:10.1175/2009JCLI2863.1.
    Description: The Massachusetts Institute of Technology (MIT) Integrated Global System Model is used to make probabilistic projections of climate change from 1861 to 2100. Since the model’s first projections were published in 2003, substantial improvements have been made to the model, and improved estimates of the probability distributions of uncertain input parameters have become available. The new projections are considerably warmer than the 2003 projections; for example, the median surface warming in 2091–2100 is 5.1°C compared to 2.4°C in the earlier study. Many changes contribute to the stronger warming; among the more important ones are taking into account the cooling in the second half of the twentieth century due to volcanic eruptions for input parameter estimation and a more sophisticated method for projecting gross domestic product (GDP) growth, which eliminated many low-emission scenarios. However, if recently published data, suggesting stronger twentieth-century ocean warming, are used to determine the input climate parameters, the median projected warming at the end of the twenty-first century is only 4.1°C. Nevertheless, all ensembles of the simulations discussed here produce a much smaller probability of warming less than 2.4°C than implied by the lower bound of the Intergovernmental Panel on Climate Change (IPCC) Fourth Assessment Report (AR4) projected likely range for the A1FI scenario, which has forcing very similar to the median projection in this study. The probability distribution for the surface warming produced by this analysis is more symmetric than the distribution assumed by the IPCC because of a different feedback between the climate and the carbon cycle, resulting from the inclusion in this model of the carbon–nitrogen interaction in the terrestrial ecosystem.
    Description: This work was supported in part by the Office of Science (BER), U.S. Department of Energy Grants DE-FG02-94ER61937 and DE-FG02-93ER61677, and by the industrial and foundations sponsors of The MIT Joint Program on the Science and Policy of Global Change (http://globalchange.mit.edu/sponsors/ current.html).
    Keywords: Probability forecasts/models ; Climate prediction ; Anthropogenic effects ; Numerical analysis/modeling ; Feedback
    Repository Name: Woods Hole Open Access Server
    Type: Article
    Format: application/pdf
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  • 2
    Publication Date: 2022-05-25
    Description: Author Posting. © American Meteorological Society, 2010. This article is posted here by permission of American Meteorological Society for personal use, not for redistribution. The definitive version was published in Journal of Climate 23 (2010): 2230–2231, doi:10.1175/2009JCLI3566.1.
    Description: Corrigendum: Sokolov, A., and Coauthors, 2009: Probabilistic forecast for twenty-first-century climate based on uncertainties in emissions (without policy) and climate parameters. J. Climate, 22, 5175–5204.
    Keywords: Probability forecasts/models ; Climate prediction ; Anthropogenic effects ; Numerical analysis/modeling ; Feedback
    Repository Name: Woods Hole Open Access Server
    Type: Article
    Format: application/pdf
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Climate dynamics 14 (1998), S. 291-303 
    ISSN: 1432-0894
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences , Physics
    Notes: Abstract  Because of significant uncertainty in the behavior of the climate system, evaluations of the possible impact of an increase in greenhouse gas concentrations in the atmosphere require a large number of long-term climate simulations. Studies of this kind are impossible to carry out with coupled atmosphere ocean general circulation models (AOGCMs) because of their tremendous computer resource requirements. Here we describe a two dimensional (zonally averaged) atmospheric model coupled with a diffusive ocean model developed for use in the integrated framework of the Massachusetts Institute of Technology (MIT) Joint Program on the Science and Policy of Global Change. The 2-D model has been developed from the Goddard Institute for Space Studies (GISS) GCM and includes parametrizations of all the main physical processes. This allows it to reproduce many of the nonlinear interactions occurring in simulations with GCMs. Comparisons of the results of present-day climate simulations with observations show that the model reasonably reproduces the main features of the zonally averaged atmospheric structure and circulation. The model’s sensitivity can be varied by changing the magnitude of an inserted additional cloud feedback. Equilibrium responses of different versions of the 2-D model to an instantaneous doubling of atmospheric CO2 are compared with results of similar simulations with different AGCMs. It is shown that the additional cloud feedback does not lead to any physically inconsistent results. On the contrary, changes in climate variables such as precipitation and evaporation, and their dependencies on surface warming produced by different versions of the MIT 2-D model are similar to those shown by GCMs. By choosing appropriate values of the deep ocean diffusion coefficients, the transient behavior of different AOGCMs can be matched in simulations with the 2-D model, with a unique choice of diffusion coefficients allowing one to match the performance of a given AOGCM for a variety of transient forcing scenarios. Both surface warming and sea level rise due to thermal expansion of the deep ocean in response to a gradually increasing forcing are reasonably reproduced on time scales of 100–150 y. However a wide range of diffusion coefficients is needed to match the behavior of different AOGCMs. We use results of simulations with the 2-D model to show that the impact on climate change of the implied uncertainty in the rate of heat penetration into the deep ocean is comparable with that of other significant uncertainties.
    Type of Medium: Electronic Resource
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  • 4
    Publication Date: 2016-06-22
    Keywords: Vascular Biology, Imaging, Prognosis, Atherosclerosis
    Print ISSN: 1941-9651
    Electronic ISSN: 1942-0080
    Topics: Medicine
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  • 5
    Publication Date: 2016-10-08
    Description: Background In-stent hyperplasia (ISH) may develop in regions of low endothelial shear stress (ESS), but the relationship between the magnitude of low ESS, the extent of ISH, and subsequent clinical events has not been investigated. Methods and Results We assessed the association of poststent ESS with neointimal ISH and clinical outcomes in patients treated with percutaneous coronary interventions (PCI). Three-dimensional coronary reconstruction was performed in 374 post-PCI patients at baseline and 6 to 10 months follow-up as part of the PREDICTION Study. Each vessel was divided into 1.5-mm-long segments, and we calculated the local ESS within each stented segment at baseline. At follow-up, we assessed ISH and the occurrence of a clinically indicated repeat PCI for in-stent restenosis. In 246 total stents (54 overlapping), 100 (40.7%) were bare-metal stents (BMS), 104 (42.3%) sirolimus-eluting stents, and 42 (17.1%) paclitaxel-eluting stents. In BMS, low ESS post-PCI at baseline was independently associated with ISH (β=1.47 mm 2 per 1-Pa decrease; 95% CI, 0.38–2.56; P 〈0.01). ISH was minimal in drug-eluting stents. During follow-up, repeat PCI in BMS was performed in 21 stents (8.5%). There was no significant association between post-PCI ESS and in-stent restenosis requiring PCI. Conclusions Low ESS after BMS implantation is associated with subsequent ISH. ISH is strongly inhibited by drug-eluting stents. Post-PCI ESS is not associated with in-stent restenosis requiring repeat PCI. ESS is an important determinant of ISH in BMS, but ISH of large magnitude to require PCI for in-stent restenosis is likely attributed to factors other than ESS within the stent.
    Keywords: Vascular Biology
    Electronic ISSN: 2047-9980
    Topics: Medicine
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  • 6
    Publication Date: 2012-10-19
    Description: The heterogeneity of plaque formation, the vascular remodelling response to plaque formation, and the consequent phenotype of plaque instability attest to the extraordinarily complex pathobiology of plaque development and progression, culminating in different clinical coronary syndromes. Atherosclerotic plaques predominantly form in regions of low endothelial shear stress (ESS), whereas regions of moderate/physiological and high ESS are generally protected. Low ESS-induced compensatory expansive remodelling plays an important role in preserving lumen dimensions during plaque progression, but when the expansive remodelling becomes excessive promotes continued influx of lipids into the vessel wall, vulnerable plaque formation and potential precipitation of an acute coronary syndrome. Advanced plaques which start to encroach into the lumen experience high ESS at their most stenotic region, which appears to promote plaque destabilization. This review describes the role of ESS from early atherogenesis to early plaque formation, plaque progression to advanced high-risk stenotic or non-stenotic plaque, and plaque destabilization. The critical implication of the vascular remodelling response to plaque growth is also discussed. Current developments in technology to characterize local ESS and vascular remodelling in vivo may provide a rationale for innovative diagnostic and therapeutic strategies for coronary patients that aim to prevent clinical coronary syndromes.
    Print ISSN: 0008-6363
    Electronic ISSN: 1755-3245
    Topics: Medicine
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  • 7
    Publication Date: 2013-06-14
    Description: Objective— The mechanisms promoting the focal formation of rupture-prone coronary plaques in vivo remain incompletely understood. This study tested the hypothesis that coronary regions exposed to low endothelial shear stress (ESS) favor subsequent development of collagen-poor, thin-capped plaques. Approach and Results— Coronary angiography and 3-vessel intravascular ultrasound were serially performed at 5 consecutive time points in vivo in 5 diabetic, hypercholesterolemic pigs. ESS was calculated along the course of each artery with computational fluid dynamics at all 5 time points. At follow-up, 184 arterial segments with previously identified in vivo ESS underwent histopathologic analysis. Compared with other plaque types, eccentric thin-capped atheromata developed more in segments that experienced lower ESS during their evolution. Compared with lesions with higher preceding ESS, segments persistently exposed to low ESS (〈1.2 Pa) exhibited reduced intimal smooth muscle cell content; marked intimal smooth muscle cell phenotypic modulation; attenuated procollagen-I gene expression; increased gene and protein expression of the interstitial collagenases matrix-metalloproteinase-1, -8, -13, and -14; increased collagenolytic activity; reduced collagen content; and marked thinning of the fibrous cap. Conclusions— Eccentric thin-capped atheromata, lesions particularly prone to rupture, form more frequently in coronary regions exposed to low ESS throughout their evolution. By promoting an imbalance of attenuated synthesis and augmented collagen breakdown, low ESS favors the focal evolution of early lesions toward plaques with reduced collagen content and thin fibrous caps—2 critical determinants of coronary plaque vulnerability.
    Keywords: Pathophysiology, Imaging, Mechanism of atherosclerosis/growth factors, Other Vascular biology
    Print ISSN: 1079-5642
    Electronic ISSN: 1524-4636
    Topics: Medicine
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  • 8
    Publication Date: 2012-07-10
    Description: Background— Atherosclerotic plaques progress in a highly individual manner. The purposes of the Prediction of Progression of Coronary Artery Disease and Clinical Outcome Using Vascular Profiling of Shear Stress and Wall Morphology (PREDICTION) Study were to determine the role of local hemodynamic and vascular characteristics in coronary plaque progression and to relate plaque changes to clinical events. Methods and Results— Vascular profiling, using coronary angiography and intravascular ultrasound, was used to reconstruct each artery and calculate endothelial shear stress and plaque/remodeling characteristics in vivo. Three-vessel vascular profiling (2.7 arteries per patient) was performed at baseline in 506 patients with an acute coronary syndrome treated with a percutaneous coronary intervention and in a subset of 374 (74%) consecutive patients 6 to 10 months later to assess plaque natural history. Each reconstructed artery was divided into sequential 3-mm segments for serial analysis. One-year clinical follow-up was completed in 99.2%. Symptomatic clinical events were infrequent: only 1 (0.2%) cardiac death; 4 (0.8%) patients with new acute coronary syndrome in nonstented segments; and 15 (3.0%) patients hospitalized for stable angina. Increase in plaque area (primary end point) was predicted by baseline large plaque burden; decrease in lumen area (secondary end point) was independently predicted by baseline large plaque burden and low endothelial shear stress. Large plaque size and low endothelial shear stress independently predicted the exploratory end points of increased plaque burden and worsening of clinically relevant luminal obstructions treated with a percutaneous coronary intervention at follow-up. The combination of independent baseline predictors had a 41% positive and 92% negative predictive value to predict progression of an obstruction treated with a percutaneous coronary intervention. Conclusions— Large plaque burden and low local endothelial shear stress provide independent and additive prediction to identify plaques that develop progressive enlargement and lumen narrowing. Clinical Trial Registration— URL: http:www.//clinicaltrials.gov . Unique Identifier: NCT01316159.
    Keywords: Pathophysiology, Coronary imaging: angiography/ultrasound/Doppler/CC, Mechanism of atherosclerosis/growth factors
    Electronic ISSN: 1524-4539
    Topics: Medicine
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  • 9
  • 10
    Publication Date: 2014-11-19
    Description: Background— Despite the exposure of the entire vasculature to the atherogenic effects of systemic risk factors, atherosclerotic plaques preferentially develop at sites with disturbed flow. This study aimed at exploring in vivo the relationship between local endothelial shear stress (ESS) and coronary plaque characteristics in humans using computational fluid dynamics and frequency-domain optical coherence tomography. Methods and Results— Three-dimensional coronary artery reconstruction was performed in 21 patients (24 arteries) presenting with acute coronary syndrome using frequency-domain optical coherence tomography and coronary angiography. Each coronary artery was divided into sequential 3-mm segments and analyzed for the assessment of local ESS and plaque characteristics. A total of 146 nonculprit segments were evaluated. Compared with segments with higher ESS [≥1 Pascal (Pa)], those with low ESS (〈1 Pa) showed higher prevalence of lipid-rich plaques (37.5% versus 20.0%; P =0.019) and thin-cap fibroatheroma (12.5% versus 2.0%; P =0.037). Overall, lipid plaques in segments with low ESS had thinner fibrous cap (115 μm [63–166] versus 170 μm [107–219]; P =0.004) and higher macrophage density (normalized standard deviation: 8.4% [4.8–12.6] versus 6.2% [4.2–8.8]; P =0.017). Segments with low ESS showed more superficial calcifications (minimum calcification depth: 93 μm [50–140] versus 152 μm [105–258]; P =0.049) and tended to have higher prevalence of spotty calcifications (26.0% versus 12.0%; P =0.076). Conclusions— Coronary regions exposed to low ESS are associated with larger lipid burden, thinner fibrous cap, and higher prevalence of thin-cap fibroatheroma in humans. Frequency-domain optical coherence tomography–based assessment of ESS and wall characteristics may be useful in identifying vulnerable coronary regions. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01110538.
    Keywords: Pathophysiology, Imaging, Endothelium/vascular type/nitric oxide
    Print ISSN: 1941-9651
    Electronic ISSN: 1942-0080
    Topics: Medicine
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