Availability analysis of post-combustion carbon capture systems: minimum work input

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Application of Structure-from-Motion photogrammetry to river restoration

This research is funded by the Environment Agency and United Utilities whose support is gratefully acknowledged. Some of the methods employed in this work have been tested on the background of the results obtained in MorphSed (www.morphsed.es), a research project funded by the Spanish Ministry of Economy and Competiveness and the European Regional Development Fund Scheme (FEDER; CGL2012-36394). The second author is funded by a Ramon y Cajal Fellowship (RYC-2010-06264). Authors acknowledge the support from the Economy and Knowledge Department of the Catalan Government through the Consolidated Research Group ‘Fluvial Dynamics Research Group’ (2014 SGR 645). The authors thank Manel Llena from the University of Lleida for his help and contribution to the camera calibration experiments. We are also grateful to the three anonymous reviewers and the editors for their comments that greatly improved the manuscript.Peer reviewedPostprin

Post-combustion carbon dioxide capture cost reduction to 2030 and beyond

Post-combustion CO2 capture (PCC) can be achieved using a variety of technologies. Importantly it is applicable to a wide range of processes and may also be retrofitted in certain cases. This paper covers the use of PCC for low carbon power generation from new natural gas combined cycle (NGCC) plants that are expected to be built in the UK in the 2020s and 2030s and that will run into the 2050s. Costs appear potentially comparable with other low carbon and controllable generation sources such as nuclear or renewables plus storage, especially with the lower gas prices that can be expected in a carbon-constrained world. Non-fuel cost reduction is still, however, desirable and, since CO2 capture is a new application, significant potential is likely to exist. For the NGCC+PCC examples shown in this paper, moving from ‘first of a kind’ (FOAK) to ‘nth of a kind’ (NOAK) gives significant improvements through both reduced financing costs and capital cost reductions. To achieve this the main emphasis needs to be on ‘commercial readiness’, rather than on system-level ‘technical readiness’, and on improvements through innovation activities, supported by underpinning research, that develop novel sub-processes; this will also maintain NOAK status for cost-effective financing. Feasible reductions in the energy penalty for PCC capture have much less impact, reflecting the inherently high levels of efficiency for modern NGCC+PCC plants

The association between cognitive impairment and functional outcome in hospitalised older patients: a systematic review and meta-analysis

BACKGROUND: in hospitalised older adults, cognitive impairments are common and may be associated with functional outcomes. Our aim was to systematically review this association. METHOD: we systematically searched MEDLINE, CINAHL, AMED and PsycINFO from inception to April 2016. Non-English language studies were filtered out at search stage. All types of studies were considered for inclusion except reviews, conference abstracts, dissertations and case studies. Population: community-dwelling or institutionalised older adults aged 65 years or more, who are acutely hospitalised and have information on history of dementia and/or cognitive scores on admission. Setting: acute hospital (excluding critical care and subacute or intermediate care). Outcome of interest: change in a measure of physical function or disability between pre-admission or admission, and discharge or post-discharge. This review was registered on PROSPERO (CRD42016035978). RESULTS: the search returned 5,988 unique articles, of which 34 met inclusion criteria. All studies were observational, with 30 prospective and 4 retrospective from 14 countries, recruiting from general medicine (n = 11), geriatric medicine (n = 11) and mixed (n = 12) wards. Twenty-six studies (54,637 participants) were suitable for the quantitative synthesis. The meta-analysis suggested that cognitive impairment was associated with functional decline in hospitalised older adults (risk ratio (RR): 1.64; 95% confidence interval (CI): 1.45–1.86; P < 0.01). Results were similar in subanalyses focusing on diagnosis of dementia (RR: 1.36; 95% CI: 1.05–1.76; P = 0.02; n= 2,248) or delirium (RR: 1.55; 95% CI: 1.31–1.83; P < 0.01; n= 1,677). CONCLUSION: cognitive impairments seem associated with functional decline in hospitalised older people. Causality cannot be inferred, and limitations include low quality of studies and possible confounding

Ibrutinib inhibits platelet integrin αIIbβ3 outside-in signaling and thrombus stability but not adhesion to collagen

OBJECTIVE: Ibrutinib is an irreversible Bruton tyrosine kinase inhibitor approved for treatment of Waldenstrom macroglobulinemia, chronic lymphocytic leukemia, and mantle cell lymphoma that increases the risk of bleeding among patients. Platelets from ibrutinib-treated patients exhibit deficiencies in collagen-evoked signaling in suspension; however, the significance of this observation and how it relates to bleeding risk is unclear, as platelets encounter immobile collagen in vivo. We sought to clarify the effects of ibrutinib on platelet function to better understand the mechanism underlying bleeding risk. APPROACH AND RESULTS: By comparing signaling in suspension and during adhesion to immobilized ligands, we found that the collagen signaling deficiency caused by ibrutinib is milder during adhesion to immobilized collagen. We also found that platelets in whole blood treated with ibrutinib adhered to collagen under arterial shear but formed unstable thrombi, suggesting that the collagen signaling deficiency caused by ibrutinib may not be the predominant cause of bleeding in vivo. However, clot retraction and signaling evoked by platelet adhesion to immobilized fibrinogen were also inhibited by ibrutinib, indicating that integrin αIIbβ3 outside-in signaling is also effected in addition to GPVI signaling. When ibrutinib was combined with the P2Y12 inhibitor, cangrelor, thrombus formation under arterial shear was inhibited additively. CONCLUSIONS: These findings suggest that (1) ibrutinib causes GPVI and integrin αIIbβ3 platelet signaling deficiencies that result in formation of unstable thrombi and may contribute toward bleeding observed in vivo and (2) combining ibrutinib with P2Y12 antagonists, which also inhibit thrombus stability, may have a detrimental effect on hemostasis

Unique genetic and histological signatures of mouse pericardial adipose tissue

Obesity is a major risk factor for a plethora of metabolic disturbances including diabetes and cardiovascular disease. Accumulating evidence is showing that there is an adipose tissue depot-dependent relationship with obesity-induced metabolic dysfunction. While some adipose depots, such as subcutaneous fat, are generally metabolically innocuous, others such as visceral fat, are directly deleterious. A lesser known visceral adipose depot is the pericardial adipose tissue depot. We therefore set out to examine its transcriptional and morphological signature under chow and high-fat fed conditions, in comparison with other adipose depots, using a mouse model. Our results revealed that under chow conditions pericardial adipose tissue has uncoupling-protein 1 gene expression levels which are significantly higher than classical subcutaneous and visceral adipose depots. We also observed that under high-fat diet conditions, the pericardial adipose depot exhibits greatly upregulated transcript levels of inflammatory cytokines. Our results collectively indicate, for the first time, that the pericardial adipose tissue possesses a unique transcriptional and histological signature which has features of both a beige (brown fat-like) but also pro-inflammatory depot, such as visceral fat. This unique profile may be involved in metabolic dysfunction associated with obesity