237 research outputs found

    The processes and practices of sustainable cities

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    As concentrations of population and consumption, cities are fundamental to the sustainable transition that is urgently needed to resolve the ecological crisis we are facing. Cities have responded to this challenge with a large number committing to sustainable visions and/or initiatives such as the Global Covenant of Mayors (GCoM), C40 Cities Climate Leadership Group or ICLEI Local Governments for Sustainability network. Whilst there are pockets of best practice we are not seeing the speed or scale of change required in terms of resource use, carbon emissions or well-being. There is an implementation gap between cities’ long-term sustainable visions and the short-term actions realised to achieve them; cities are struggling to achieve long-term goals in the face of short-term pressures. To accelerate sustainable urban transitions a greater understanding of the regime-level processes that enable or constrain translation between long-term visions and short-term action is required. Transition research to date has neglected regime processes, especially non-technical institutional processes and cultural-cognitive habits and heuristics, as well as the role of power and agency. This thesis aims to critically explore the processes of regime-level change to gain insights into how urban transitions occur and under what circumstances they can be accelerated. To achieve this a novel analytical framework is proposed, with transition theory as the foundation, additionally drawing on institutional and quasi-evolutionary theory. This framework is tested using three leading sustainable cities case studies, London, New York and Copenhagen, including interviews with sustainable city network actors. Analysis using the framework generates important insights into how urban transitions might be steered and accelerated. In particular that normative institutional processes are an effective means for regime actors to coordinate power, affect resource allocation, and impact selection pressures and adaptive capacity. The findings suggests that unless the institutional and quasi-evolutionary processes that drive action are re-configured in line with sustainable city visions then progress will be limited

    Sex Differences in the Excess Risk of Cardiovascular Diseases Associated with Type 2 Diabetes: Potential Explanations and Clinical Implications

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    Strong evidence suggests that type 2 diabetes confers a stronger excess risk of cardiovascular diseases in women than in men; with women having a 27 % higher relative risk of stroke and a 44 % higher relative risk of coronary heart disease compared with men. The mechanisms that underpin these sex differences in the associations between diabetes and cardiovascular disease risk are not fully understood. Some of the excess risk may be the result of a sex disparity in the management and treatment of diabetes, to the detriment of women. However, accruing evidence suggests that real biological differences between men and women underpin the excess risk of diabetes-related cardiovascular risk in women such that there is a greater decline in risk factor status in women than in men in the transition from normoglycemia to overt diabetes. This greater risk factor decline appears to be associated with women having to put on more weight than men, and thus attain a higher body mass index, to develop diabetes. Further studies addressing the mechanisms responsible for sex differences in the excess risk of cardiovascular diseases associated with diabetes are needed to improve the prevention and management of diabetes in clinical practise

    The association between indoor air quality and adult blood pressure levels in a high-income setting

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    Background: Indoor air pollution is still considered one of the leading causes of morbidity and mortality worldwide. We aimed to investigate the potential association between indoor particulate matter (PM) and fasting clinic blood pressure in adult Australians. Methods: Sixty-three participants residing within the Perth metropolitan area were studied. Participants were aged between 18 and 65 years and free of major medical conditions. We conducted 24-h monitoring of residential PM concentrations, including the size fractions PM1, PM2.5, PM4, and PM10. All participants attended a clinical assessment at Curtin University following a 10–12 h overnight fast. Results: In this study we found that PM1 and PM2.5 were significantly associated with heart rate: a one interquartile range (IQR) increase in PM1 or PM2.5 was associated with a 4–6 beats per minute (bpm) increase in heart rate. Both PM10 and total PM exposure had a significant impact on systolic blood pressure (SBP): a one IQR increase in PM10 and total PM were associated with a 10 mmHg (95% CI: 0.77–20.05) and 12 mmHg (2.28–22.43 mmHg) increase in SBP, respectively. Conclusion: The study findings provide additional support to the thesis that indoor air pollution is an important modifiable factor in the risk of hypertension

    Smoking as a risk factor for lung cancer in women and men: A systematic review and meta-analysis

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    Published by BMJ. Objectives To investigate the sex-specific association between smoking and lung cancer. Design Systematic review and meta-analysis. Data sources We searched PubMed and EMBASE from 1 January 1999 to 15 April 2016 for cohort studies. Cohort studies before 1 January 1999 were retrieved from a previous meta-analysis. Individual participant data from three sources were also available to supplement analyses of published literature. Eligibility criteria for selecting studies Cohort studies reporting the sex-specific relative risk (RR) of lung cancer associated with smoking. Results Data from 29 studies representing 99 cohort studies, 7 million individuals and >50 000 incident lung cancer cases were included. The sex-specific RRs and their ratio comparing women with men were pooled using random-effects meta-analysis with inverse-variance weighting. The pooled multiple-adjusted lung cancer RR was 6.99 (95% Confidence Interval (CI) 5.09 to 9.59) in women and 7.33 (95% CI 4.90 to 10.96) in men. The pooled ratio of the RRs was 0.92 (95% CI 0.72 to 1.16; I 2 =89%; p<0.001), with no evidence of publication bias or differences across major pre-defined participant and study subtypes. The women-to-men ratio of RRs was 0.99 (95% CI 0.65 to 1.52), 1.11 (95% CI 0.75 to 1.64) and 0.94 (95% CI 0.69 to 1.30), for light, moderate and heavy smoking, respectively. Conclusions Smoking yields similar risks of lung cancer in women compared with men. However, these data may underestimate the true risks of lung cancer among women, as the smoking epidemic has not yet reached full maturity in women. Continued efforts to measure the sex-specific association of smoking and lung cancer are required

    The development of a national salt reduction strategy for Australia

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    Excess dietary salt is a well established cause of high blood pressure and vascular disease. National and international bodies recommend a significant reduction in population salt intakes on the basis of strong evidence for health gains that population salt reduction strategies could achieve. The Australian Division of World Action on Salt and Health (AWASH) coordinates the Drop the Salt! campaign in Australia. This aims to reduce the average amount of salt consumed by Australians to six grams per day over five years through three main implementation strategies targeting the food industry, the media and government. This strategy has the potential to achieve a rapid and significant reduction in dietary salt consumption in Australia. With industry and government engagement, this promises to be a highly effective, low cost option for preventing chronic disease.<br /

    The Association between Exposure to Residential Indoor Volatile Organic Compounds and Measures of Central Arterial Stiffness in Healthy Middle-Aged Men and Women

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    It is well reported that individuals spend up to 90% of their daily time indoors, with between 60% to 90% of this time being spent in the home. Using a cross-sectional study design in a population of 111 healthy adults (mean age: 52.3 ± 9.9 years; 65% women), we investigated the association between exposure to total volatile organic compounds (VOCs) in indoor residential environments and measures of central arterial stiffness, known to be related to cardiovascular risk. Indoor VOC concentrations were measured along with ambulatory measures of pulse pressure (cPP), augmentation index (cAIx) and cAIx normalized for heart rate (cAIx75 ), over a continuous 24-h period. Pulse wave velocity (cfPWV) was determined during clinical assessment. Multiple regression analysis was performed to examine the relationship between measures of arterial stiffness and VOCs after adjusting for covariates. Higher 24-h, daytime and night-time cAIx was associated with an interquartile range increase in VOCs. Similar effects were shown with cAIx75 . No significant effects were observed between exposure to VOCs and cPP or cfPWV. After stratifying for sex and age (≤50 years; >50 years), effect estimates were observed to be greater and significant for 24-h and daytime cAIx in men, when compared to women. No significant effect differences were seen between age groups with any measure of arterial stiffness. In this study, we demonstrated that residential indoor VOCs exposure was adversely associated with some measures of central arterial stiffness, and effects were different between men and women. Although mechanistic pathways remain unclear, these findings provide a possible link between domestic VOCs exposure and unfavourable impacts on individual-level cardiovascular disease risk

    Residential indoor exposure to fine and ultrafine particulate air pollution in association with blood pressure and subclinical central haemodynamic markers of cardiovascular risk among healthy adults living in Perth, Western Australia

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    Despite that large percentages of individual daily time is spent in the home, few studies have examined the relationship between indoor particulate matter (PM) exposure in residential settings with subclinical indicators of cardiovascular risk. This cross-sectional study investigated associations between exposure to fine (PM2.5) and ultrafine (UFP) PM in domestic indoor environments, with central blood pressure (BP) and component BP measures (pulse pressure, augmented pressure [AP], augmentation index [AIx], mean arterial pressure, pulse wave velocity [PWV]) in 40 non-smoking, otherwise healthy adults (58% women) living in Perth, Western Australia. Overall, in adjusted models, an interquartile range (IQR) increase in PM2.5 was associated with a 3.2 mmHg (95% confidence interval [CI]: 0.99, 5.45) higher diastolic BP, and a 1.8 mmHg lower AP (95%CI: − 3.63, − 0.01) and 0.4 m/s PWV (95%CI: − 0.80, − 0.08), respectively. For the UFP fraction, an IQR increase was associated with a 5.2% higher AIx (95%CI: 0.51, 9.97) and a 0.6 m/s lower PWV (95%CI: − 1.00, − 0.11). When stratified by sex, higher UFP concentrations were associated with higher DBP and lower PWV among women. Among men, higher UFP concentrations were associated with lower AP. Exposure to domestic indoor fine and ultrafine PM was associated with preclinical indicators of cardiovascular risk and some of these relationships were affected by sex. These findings contribute important evidence linking low-level residential indoor PM exposure with measurable impacts on cardiovascular physiology and may inform preventative recommendations as part of risk profiles for susceptible individuals

    The TriTryp Phosphatome: analysis of the protein phosphatase catalytic domains

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    <p>Abstract</p> <p>Background</p> <p>The genomes of the three parasitic protozoa <it>Trypanosoma cruzi</it>, <it>Trypanosoma brucei </it>and <it>Leishmania major </it>are the main subject of this study. These parasites are responsible for devastating human diseases known as Chagas disease, African sleeping sickness and cutaneous Leishmaniasis, respectively, that affect millions of people in the developing world. The prevalence of these neglected diseases results from a combination of poverty, inadequate prevention and difficult treatment. Protein phosphorylation is an important mechanism of controlling the development of these kinetoplastids. With the aim to further our knowledge of the biology of these organisms we present a characterisation of the phosphatase complement (phosphatome) of the three parasites.</p> <p>Results</p> <p>An ontology-based scan of the three genomes was used to identify 86 phosphatase catalytic domains in <it>T. cruzi</it>, 78 in <it>T. brucei</it>, and 88 in <it>L. major</it>. We found interesting differences with other eukaryotic genomes, such as the low proportion of tyrosine phosphatases and the expansion of the serine/threonine phosphatase family. Additionally, a large number of atypical protein phosphatases were identified in these species, representing more than one third of the total phosphatase complement. Most of the atypical phosphatases belong to the dual-specificity phosphatase (DSP) family and show considerable divergence from classic DSPs in both the domain organisation and sequence features.</p> <p>Conclusion</p> <p>The analysis of the phosphatome of the three kinetoplastids indicates that they possess orthologues to many of the phosphatases reported in other eukaryotes, including humans. However, novel domain architectures and unusual combinations of accessory domains, suggest distinct functional roles for several of the kinetoplastid phosphatases, which await further experimental exploration. These distinct traits may be exploited in the selection of suitable new targets for drug development to prevent transmission and spread of the diseases, taking advantage of the already extensive knowledge on protein phosphatase inhibitors.</p

    Co-benefits of urban climate action: a framework for cities

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    Why do climate co-benefits matter for cities? • The evidence suggests that citizens are more likely to take action on climate change, or more likely to support governments that take action on climate change, if the wider co-benefits of those actions are emphasised. • At the same time, policies that are aimed at supporting innovation, delivering economic benefits and enhancing the quality of life of citizens can potentially lead to major climate cobenefits (e.g. reduced greenhouse gas emissions) which would be more challenging to achieve if climate action were the primary objective. • At the city level, the potential of co-benefits is particularly great as citizens can often witness the results of policy actions more directly on their daily lives. Definition and taxonomy of co-benefits • The term co-benefits has a wide range of definitions in the climate literature, with over 20 terms identified in the literature that are used synonymously or in a similar context. • The term co-benefits varies in intentionality (e.g. is climate the primary or secondary objective, or simply an unintentional benefit?), scope (e.g. does it include mitigation benefits, adaptation benefits or both?), and scale (e.g. are the benefits short term and local, or long term and global?). • Co-benefits may be (1) secondary benefits from climate policy action, (2) secondary climate benefits from other policy actions, or (3) the combination of climate and non-climate benefits; both of which are targeted under an integrated policy programme. • The wide range of established definitions of co-benefits used by authoritative organisations means that formulating a taxonomy of co-benefits with broad buy-in from policy makers is challenging. Results of literature review • Health, Land Use and Transport were the top three sectors for the number of co-benefits, with over 40 co-benefits identified in each. • Waste, Air Quality, Transport and Energy had particularly high numbers of mitigation cobenefits in the literature reviewed. Adaptation co-benefits were particularly strong for Disaster and Emergency, Food Security and Tourism, Culture and Sport. Land Use, Health, Water and Education tended to be strong for both mitigation and adaptation co-benefits

    Associations between sub-clinical markers of cardiometabolic risk and exposure to residential indoor air pollutants in healthy adults in Perth, Western Australia: A study protocol

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    © 2019 by the authors. Licensee MDPI, Basel, Switzerland. Background: A growing body of epidemiological and clinical evidence has implicated air pollution as an emerging risk factor for cardiometabolic disease. Whilst individuals spend up to two-thirds of daily time in their domestic residential environment, very few studies have been designed to objectively measure the sub-clinical markers of cardiometabolic risk with exposure to domestic indoor air pollutants. This cross-sectional study aims to investigate associations between the components of domestic indoor air quality and selected sub-clinical cardiometabolic risk factors in a cohort of healthy adults living in Perth,Western Australia. Methods: One hundred and eleven non-smoking adults (65% female) living in non-smoking households who were aged between 35-69 years were recruited for the project. Study subjects were invited to participate in all sections of the study, which included: Domestic indoor air monitoring along with the concurrent 24 h ambulatory monitoring of peripheral and central blood pressure and measures of central hemodynamic indices, standardized questionnaires on aspects relating to current health status and the domestic environment, a 24 h time-activity diary during the monitoring period, and clinic-based health assessment involving collection of blood and urine biomarkers for lipid and glucose profiles, as well as measures of renal function and an analysis of central pulse wave and pulse wave velocity. Results: This study provides a standardized approach to the study of sub-clinical cardiometabolic health effects that are related to the exposure to indoor air pollution. Conclusion: The findings of this study may provide direction for future research that will further contribute to our understanding of the relationship that exists between indoor air pollution and sub-clinical markers of cardiometabolic risk
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