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Sökning: WFRF:(Wheeler Nicola)

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11.
  • Watts, Nick, et al. (författare)
  • The Lancet Countdown : tracking progress on health and climate change
  • 2017
  • Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 389:10074, s. 1151-1164
  • Forskningsöversikt (refereegranskat)abstract
    • The Lancet Countdown: tracking progress on health and climate change is an international, multidisciplinary research collaboration between academic institutions and practitioners across the world. It follows on from the work of the 2015 Lancet Commission, which concluded that the response to climate change could be "the greatest global health opportunity of the 21st century". The Lancet Countdown aims to track the health impacts of climate hazards; health resilience and adaptation; health co-benefits of climate change mitigation; economics and finance; and political and broader engagement. These focus areas form the five thematic working groups of the Lancet Countdown and represent different aspects of the complex association between health and climate change. These thematic groups will provide indicators for a global overview of health and climate change; national case studies highlighting countries leading the way or going against the trend; and engagement with a range of stakeholders. The Lancet Countdown ultimately aims to report annually on a series of indicators across these five working groups. This paper outlines the potential indicators and indicator domains to be tracked by the collaboration, with suggestions on the methodologies and datasets available to achieve this end. The proposed indicator domains require further refinement, and mark the beginning of an ongoing consultation process-from November, 2016 to early 2017-to develop these domains, identify key areas not currently covered, and change indicators where necessary. This collaboration will actively seek to engage with existing monitoring processes, such as the UN Sustainable Development Goals and WHO's climate and health country profiles. The indicators will also evolve over time through ongoing collaboration with experts and a range of stakeholders, and be dependent on the emergence of new evidence and knowledge. During the course of its work, the Lancet Countdown will adopt a collaborative and iterative process, which aims to complement existing initiatives, welcome engagement with new partners, and be open to developing new research projects on health and climate change.
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12.
  • Watts, Nick, et al. (författare)
  • The Lancet Countdown on health and climate change : from 25 years of inaction to a global transformation for public health
  • 2018
  • Ingår i: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 391:10120, s. 581-630
  • Forskningsöversikt (refereegranskat)abstract
    • The Lancet Countdown tracks progress on health and climate change and provides an independent assessment of the health effects of climate change, the implementation of the Paris Agreement, 1 and the health implications of these actions. It follows on from the work of the 2015 Lancet Commission on Health and Climate Change, 2 which concluded that anthropogenic climate change threatens to undermine the past 50 years of gains in public health, and conversely, that a comprehensive response to climate change could be "the greatest global health opportunity of the 21st century". The Lancet Countdown is a collaboration between 24 academic institutions and intergovernmental organisations based in every continent and with representation from a wide range of disciplines. The collaboration includes climate scientists, ecologists, economists, engineers, experts in energy, food, and transport systems, geographers, mathematicians, social and political scientists, public health professionals, and doctors. It reports annual indicators across five sections: climate change impacts, exposures, and vulnerability; adaptation planning and resilience for health; mitigation actions and health co-benefits; economics and finance; and public and political engagement. The key messages from the 40 indicators in the Lancet Countdown's 2017 report are summarised below.
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13.
  • Wheeler, Michael, et al. (författare)
  • Distinct effects of acute exercise and breaks in sitting on working memory and executive function in older adults: a three-arm, randomised cross-over trial to evaluate the effects of exercise with and without breaks in sitting on cognition
  • 2020
  • Ingår i: British Journal of Sports Medicine. - : BMJ Publishing Group Ltd. - 0306-3674 .- 1473-0480. ; 54:13, s. 776-781
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Sedentary behaviour is associated with impaired cognition, whereas exercise can acutely improve cognition.Objective: We compared the effects of a morning bout of moderate-intensity exercise, with and without subsequent light-intensity walking breaks from sitting, on cognition in older adults.Methods: Sedentary overweight/obese older adults with normal cognitive function (n=67, 67±7 years, 31.2±4.1 kg/m2 ) completed three conditions (6-day washout): SIT (sitting): uninterrupted sitting (8 hours, control); EX+SIT (exercise + sitting): sitting (1 hour), moderate-intensity walking (30min), uninterrupted sitting (6.5 hours); and EX+BR (exercise + breaks): sitting (1 hour), moderate-intensity walking (30min), sitting interrupted every 30min with 3min of light-intensity walking (6.5 hours). Cognitive testing (Cogstate) was completed at four time points assessing psychomotor function, attention, executive function, visual learning and working memory. Serum brain-derived neurotrophic growth factor (BDNF) was assessed at six time points. The 8-hour net area under the curve (AUC) was calculated for each outcome.Results: Working memory net AUC z-score·hour (95%CI) was improved in EX+BR with a z-score of +28 (−26 to +81), relative to SIT, −25 (−79 to +29, p=0.04 vs EX+BR). Executive function net AUC was improved in EX+SIT, −8 (− 71 to +55), relative to SIT, −80 (−142 to −17, p=0.03 vs EX+SIT). Serum BDNF net AUC ng/mL·hour (95%CI) was increased in both EX+SIT, +171 (−449 to +791, p=0.03 vs SIT), and EX+BR, +139 (−481 to +759, p=0.045 vs SIT), relative to SIT, −227 (−851 to +396).Conclusion: A morning bout of moderate-intensity exercise improves serum BDNF and working memory or executive function in older adults, depending on whether or not subsequent sitting is also interrupted with intermittent light-intensity walking.
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14.
  • Yang, Zhijian, et al. (författare)
  • Genetic Landscape of the ACE2 Coronavirus Receptor
  • 2022
  • Ingår i: Circulation. - : Ovid Technologies (Wolters Kluwer Health). - 0009-7322 .- 1524-4539. ; 30:SUPPL 1, s. 36-36
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: SARS-CoV-2, the causal agent of COVID-19, enters human cells using the ACE2 (angiotensin-converting enzyme 2) protein as a receptor. ACE2 is thus key to the infection and treatment of the coronavirus. ACE2 is highly expressed in the heart and respiratory and gastrointestinal tracts, playing important regulatory roles in the cardiovascular and other biological systems. However, the genetic basis of the ACE2 protein levels is not well understood.Methods: We have conducted the largest genome-wide association meta-analysis of plasma ACE2 levels in >28 000 individuals of the SCALLOP Consortium (Systematic and Combined Analysis of Olink Proteins). We summarize the cross-sectional epidemiological correlates of circulating ACE2. Using the summary statistics-based high-definition likelihood method, we estimate relevant genetic correlations with cardiometabolic phenotypes, COVID-19, and other human complex traits and diseases. We perform causal inference of soluble ACE2 on vascular disease outcomes and COVID-19 severity using mendelian randomization. We also perform in silico functional analysis by integrating with other types of omics data.Results: We identified 10 loci, including 8 novel, capturing 30% of the heritability of the protein. We detected that plasma ACE2 was genetically correlated with vascular diseases, severe COVID-19, and a wide range of human complex diseases and medications. An X-chromosome cis-protein quantitative trait loci-based mendelian randomization analysis suggested a causal effect of elevated ACE2 levels on COVID-19 severity (odds ratio, 1.63 [95% CI, 1.10-2.42]; P=0.01), hospitalization (odds ratio, 1.52 [95% CI, 1.05-2.21]; P=0.03), and infection (odds ratio, 1.60 [95% CI, 1.08-2.37]; P=0.02). Tissue- and cell type-specific transcriptomic and epigenomic analysis revealed that the ACE2 regulatory variants were enriched for DNA methylation sites in blood immune cells.Conclusions: Human plasma ACE2 shares a genetic basis with cardiovascular disease, COVID-19, and other related diseases. The genetic architecture of the ACE2 protein is mapped, providing a useful resource for further biological and clinical studies on this coronavirus receptor.
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