2,390 research outputs found

    Widespread changes in UK air quality observed from space

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    Previous studies have used surface observations of pollutants (e.g., nitrogen dioxide [NO₂] and aerosols) to evaluate improvements in United Kingdom (UK) air quality over recent decades. However, surface monitoring networks provide limited spatial coverage and are not always representative of air quality over a wider region. Satellite observations, such as tropospheric column NO₂ (TCNO₂), aerosol optical depth (AOD) and sub‐column (0–6 km) ozone (SCO₃), provide widespread monitoring of air quality on a national scale. In this study, we use such observations to analyse trends in UK air quality, between 2005 and 2015, finding significant decreases in TCNO₂ and AOD over UK pollution hotspots. The largest changes in short‐lived NO₂ are located over populated (i.e., source) regions, associated with large emissions of nitrogen oxides (NOₓ). AOD changes are more spread out, and less strongly associated with source regions, due to a longer aerosol lifetime, secondary aerosol formation and non‐urban aerosol sources. SCO₃ shows no significant trends over England/Wales, but significant positive trends over Scotland, which is consistent with previous studies of changes in background tropospheric ozone in other remote regions of north‐western Europe

    The site of disruption of the bronchial epithelium in asthmatic and non-asthmatic subjects

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    Attention has recently been focused on the basal cells of the tracheobronchial epithelium as the mechanism of anchorage of the tall columnar cells, which themselves do not appear to form hemidesmosomes with the basement membrane of the epithelium. Residual basal cells have been described as remaining attached to the basement membrane after epithelial denudation. This led this group to formulate the hypothesis that there may be a potential plane of cleavage between the basal cells and the overlying columnar cell layer within the bronchial epithelium, which becomes disrupted in asthma.peer-reviewe

    Determinants of voluntary audit and voluntary full accounts in micro- and non-micro small companies in the UK

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    This is an Author's Accepted Manuscript of an article published in Accounting and Business Research, 42(4), 441 - 468, 2012, copyright Taylor & Francis, available online at: http://www.tandfonline.com/10.1080/00014788.2012.667969.This study investigates the link between the auditing and filing choices made by a sample of 592 small private companies, which includes 419 micro-companies. It examines decisions made in connection with the 2006 accounts following UK's adoption of the maximum EU size thresholds in 2004, and the impact of the proposed Directive on the annual accounts of micro-companies. The research extends the model of cost, management and agency factors associated with voluntary audit, and develops a complementary model for voluntary full accounts. The results show the benefits of placing full audited accounts on public record that outweigh the costs for a significant proportion of companies. In non-micro small companies, voluntary audit is determined by cost and agency factors, whereas in micro-companies it is driven by cost, management and agency factors. In both groups, the predictors of voluntary full accounts include management and agency factors, and choosing voluntary audit is one of the key factors. The study provides models that can be tested in other jurisdictions to provide evidence of the needs of micro-companies, and the discussion of the methodological challenges for small company researchers in the UK makes further contribution to the literature

    Smoking in asthma is associated with elevated levels of corticosteroid resistant sputum cytokines—an exploratory study

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    <p>Background: Current cigarette smoking is associated with reduced acute responses to corticosteroids and worse clinical outcomes in stable chronic asthma. The mechanism by which current smoking promotes this altered behavior is currently unclear. Whilst cytokines can induce corticosteroid insensitivity in-vitro, how current and former smoking affects airway cytokine concentrations and their responses to oral corticosteroids in stable chronic asthma is unclear.</p> <p>Objectives: To examine blood and sputum cytokine concentrations in never, ex and current smokers with asthma before and after oral corticosteroids.</p> <p>Methods: Exploratory study utilizing two weeks of oral dexamethasone (equivalent to 40 mg/day prednisolone) in 22 current, 21 never and 10 ex-smokers with asthma. Induced sputum supernatant and plasma was obtained before and after oral dexamethasone. 25 cytokines were measured by multiplex microbead system (Invitrogen, UK) on a Luminex platform.</p> <p>Results: Smokers with asthma had elevated sputum cytokine interleukin (IL) -6, -7, and -12 concentrations compared to never smokers with asthma. Few sputum cytokine concentrations changed in response to dexamethasone IL-17 and IFNα increased in smokers, CCL4 increased in never smokers and CCL5 and CXCL10 reduced in ex-smokers with asthma. Ex-smokers with asthma appeared to have evidence of an ongoing corticosteroid resistant elevation of cytokines despite smoking cessation. Several plasma cytokines were lower in smokers wi</p> <p>Conclusion: Cigarette smoking in asthma is associated with a corticosteroid insensitive increase in multiple airway cytokines. Distinct airway cytokine profiles are present in current smokers and never smokers with asthma and could provide an explanatory mechanism for the altered clinical behavior observed in smokers with asthma.</p&gt

    Soluble ADAM33 initiates airway remodeling to promote susceptibility for allergic asthma in early life

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    Asthma is a chronic inflammatory airways disease that usually begins in early life and involves gene-environment interactions. Although most asthma exhibits allergic inflammation, many allergic individuals do not have asthma. Here, we report how the asthma gene A Disintegrin and Metalloprotease (ADAM)33, acts as local tissue susceptibility gene that promotes allergic asthma. We show that enzymatically active soluble (s)ADAM33 is increased in asthmatic airways and plays a role in airway remodeling, independent of inflammation. Furthermore, remodeling and inflammation are both suppressed in Adam33 null mice after allergen challenge. When induced in utero or added ex vivo, sADAM33 causes structural remodeling of the airways, which enhances post-natal airway eosinophilia and bronchial hyperresponsiveness following sub-threshold challenge with an aeroallergen. This substantial gene-environment interaction helps to explain the end-organ expression of allergic asthma in genetically susceptible individuals. Finally, we show that sADAM33-induced airway remodeling is reversible, highlighting the therapeutic potential of targeting ADAM33 in asthma

    Fairness in the Allocation of Housing: Legal and Economic Perspectives

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    Housing is an emotional, almost religious, topic. Indeed, even church groups have been active in promoting public housing in Canada and elsewhere.\u27 The housing market has also become a battleground for a struggle between vested property interests and citizens\u27 groups which insist upon a redefinition of the right to shelter. Organizations, such as the Toronto-based People\u27s Housing Coalition, Halifax\u27s Access Housing Services Association, and a host of tenants\u27 unions, ensure that housing problems are not hidden from public scrutiny. Developers and landlord associations have risen to the challenge and, under the banner of free enterprise, they steadfastly resist any charges that they are the cause of the housing crisis.2 The focus of the numerous federal programs directed towards this problem has changed direction since the 1960s, shifting more toward the middle-income home owner. However, the shift in the focus of these programs is not the result of a coherent policy decision, but is a by-product of economic restraint and a changing social mood. Indeed, a coherent policy has never been the hallmark of Canada\u27s national housing policy

    Will fire danger be reduced by using Solar Radiation Management to limit global warming to 1.5°C compared to 2.0°C

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    This is the author accepted manuscript. The final version is available from American Geophysical Union (AGU) via the DOI in this record.The commitment to limit warming to 1.5°C as set out in the Paris Agreement is widely regarded as ambitious and challenging. It has been proposed that reaching this target may require a number of actions, which could include some form of carbon removal or Solar Radiation Management in addition to strong emission reductions. Here we assess one theoretical solution using Solar Radiation Management to limit global mean warming to 1.5°C above pre‐industrial temperatures, and use the McArthur fire danger index to evaluate the change in fire danger. The results show that globally fire danger is reduced in most areas when temperatures are limited to 1.5°C compared to 2.0°C. The number of days where fire danger is ‘high’ or above is reduced by up to 30 days per year on average, although there are regional variations. In certain regions, fire danger is increased, experiencing 31 more days above ‘high’ fire danger.This work was supported by the European Commission‟s 7th Framework Programme (EU/FP7) under Grant Agreement 603864 (HELIX), and the Joint UK BEIS/Defra Met Office Hadley Centre Climate Programme (GA01101)

    Medium-term culture of normal human oral mucosa: a novel three-dimensional model to study the effectiveness of drugs administration.

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    Tissue-engineered oral mucosal equivalents have been developed for in vitro studies for a few years now. However, the usefulness of currently available models is still limited by many factors, mainly the lack of a physiological extracellular matrix (ECM) and the use of cell populations that do not reflect the properly differentiated cytotypes of the mucosa of the oral cavity. For this reason, we have developed a novel three-dimensional culture model reflecting the normal architecture of the human oral mucosa, with the main aim of creating a better in vitro model where to test cellular responses to drugs administration. This novel 3D cell culture model (3D outgrowth) was set up using an artificial extracellular matrix (MatrigelTM), allowing the interactions required for proper differentiation of the various citotypes which form the mucosal layer. Biopsies of human oral mucosa, in fragments of about 0.5 mm3, were placed onto 6.5mm Transwells, covered with MatrigelTM and grown in a specific culture medium. A gradual formation of an architectural structure similar to that of the in vivo oral mucosa was observed. Transmission electron and confocal microscopy were employed to characterize the newly developed model: the cell components (keratinocytes and fibroblasts) differentiated properly within the outgrowth and reconstituted, in vitro, the physiological structure of the human oral mucosa, including a stratified non-keratinized squamous layer composed of four different layers, a proper basal membrane and a lamina propria where fibroblasts produce ECM. Moreover, keratinocytes expressed CK5, CK13, CK19 and E-cadherin, whereas fibroblasts expressed collagen type I and IV, laminin and fibronectin. 3D outgrowths could be considered a valid alternative to animal models, and provide useful information for researchers interested in studying the responses of the human oral mucosa to locally delivered drugs or other exogenous treatments

    The respiratory research agenda in primary care in Portugal: a Delphi study

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    Background: A research agenda can help to stimulate and guide research. The International Primary Care Respiratory Group (IPCRG) published a Research Needs Statement (RNS) in 2010 in which 145 research questions were identified. In 2012, priorities for respiratory research were established, based on these questions. To date, there has been no statement on primary care respiratory research needs in Portugal. The aim of the study was to develop a national consensus on research priorities in respiratory diseases in primary care in Portugal and to assess the applicability of the priorities for respiratory research set by the IPCRG. Method: We conducted a Delphi study by electronic mail with a panel of experts on respiratory disease from primary and secondary care in Portugal. In the first round, the research needs in respiratory disease in Portugal were identified. In the second round, 196 research questions in six disease areas, derived from the first round and from the IPCRG Respiratory needs statement, were prioritised on a five-point Likert-type scale. In the third round, the questions were prioritized again with feed-back provided on the median scores for each item in the second round. Consensus was considered to have been reached when 80 % of the participants gave a score of 4 or 5 out of five on a given item. Results: The 40 experts identified 121 respiratory research questions in Round 1 and expressed their views on 196 questions in Rounds 2 and 3. Twelve research questions (6 %) reached consensus. There were five questions in the asthma domain on early diagnosis, pulmonary function tests, the use of inhalers, and adherence to treatment. There were four questions in the chronic obstructive pulmonary disease domain on vaccinations, on routine monitoring and evaluation of treatment, on diagnosis, and on adherence to treatments. There was one question in the smoking domain on the effects of brief counselling. There were two questions on respiratory tract infections on the treatment of children and on the prescription of antibiotics. An additional 23 research questions (12 %) achieved consensus between 75 and 79 %. Conclusion: The results reflect the Portuguese reality in response the international agenda for research on respiratory diseases published by the IPCRG. They can support the development of future respiratory disease research in Portugal.Financial support for this work was provided by FEDER funds through the Operational Programme Competitiveness Factors - COMPETE and National Funds through FCT - Foundation for Science and Technology under the project POCI-01-0145-FEDER-007038; and by the project NORTE-01-0145-FEDER-000013, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF). PMT is partially supported by a grant from the International Primary Care Respiratory Group

    A Consideration of Biomarkers to be Used for Evaluation of Inflammation in Human Nutritional Studies

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    To monitor inflammation in a meaningful way, the markers used must be valid: they must reflect the inflammatory process under study and they must be predictive of future health status. In 2009, the Nutrition and Immunity Task Force of the International Life Sciences Institute, European Branch, organized an expert group to attempt to identify robust and predictive markers, or patterns or clusters of markers, which can be used to assess inflammation in human nutrition studies in the general population. Inflammation is a normal process and there are a number of cells and mediators involved. These markers are involved in, or are produced as a result of, the inflammatory process irrespective of its trigger and its location and are common to all inflammatory situations. Currently, there is no consensus as to which markers of inflammation best represent low-grade inflammation or differentiate between acute and chronic inflammation or between the various phases of inflammatory responses. There are a number of modifying factors that affect the concentration of an inflammatory marker at a given time, including age, diet and body fatness, among others. Measuring the concentration of inflammatory markers in the bloodstream under basal conditions is probably less informative compared with data related to the concentration change in response to a challenge. A number of inflammatory challenges have been described. However, many of these challenges are poorly standardised. Patterns and clusters may be important as robust biomarkers of inflammation. Therefore, it is likely that a combination of multiple inflammatory markers and integrated readouts based upon kinetic analysis following defined challenges will be the most informative biomarker of inflammatio
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