90 research outputs found
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Net carbon dioxide emissions from central London
Carbon dioxide (CO2) emissions from cities drive increased global atmospheric CO2 concentrations and associated climate change. Urban CO2 emissions can be evaluated using an inventory approach (summing all know emissions and sequestrations of CO 2 within a defined area), and/or a micrometeorological approach (summing the exchanges of CO2 through the sides of a defined volume of air, and the change in the total stored within the volume). Generally the micrometeorological approach, with the assumption that only the net turbulent vertical flux of CO2 is significant on annual timescales, is preferred. This study evaluates that assumption with respect to storage and vertical advection of CO2, and calculates net CO 2 emissions in central London using both methods
for June 2012 to May 2013. Data sources include an eddy covariance system, switched horizontal and vertical CO 2 profiles, traffic counts and vegetation surveys. Annual total emissions were 51.4 and 53.5 kg CO2 m−2 y−1, (micrometeorological and inventory methods, respectively), i.e., within 4%, (1.3% with the assumption that the net vertical turbulent flux is the only non-negligible micrometeorological term). This study supports the use of vertical fluxes calculated from eddy covariance measurements at a single location to estimate total emissions from high density urban environments
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Impact of meal fatty acid composition on postprandial lipaemia, vascular function and blood pressure in postmenopausal women
Cardiovascular diseases (CVD) are the leading cause of death in women globally, with aging associated with progressive endothelial dysfunction and increased CVD risk. Natural menopause is characterised by raised non-fasting triacylglycerol (TAG) concentrations and impairment of vascular function compared with premenopausal women. However, the mechanisms underlying the increased CVD risk after women have transitioned through the menopause are unclear. Dietary fat is an important modifiable risk factor relating to both postprandial lipaemia and vascular reactivity. Meals rich in saturated (SFA) and monounsaturated fatty acids (MUFA) are often associated with greater postprandial TAG responses compared with those containing n-6 polyunsaturated fatty acids (PUFA), but studies comparing their effects on vascular function during the postprandial phase are limited, particularly in postmenopausal women. This review aimed to evaluate the acute effects of test meals rich in SFA, MUFA and n-6 PUFA on postprandial lipaemia, vascular reactivity and other CVD risk factors in postmenopausal women. The systematic literature search identified 778 publications. The impact of fat-rich meals on postprandial lipaemia was reported in seven relevant studies, of which meal fat composition was compared in one study described by three papers. An additional study determined the impact of a high fat meal on vascular reactivity. Although moderately consistent evidence suggests detrimental effects of high fat meals on postprandial lipaemia in postmenopausal (than premenopausal) women, there is insufficient evidence to establish the impact of meals of differing fat composition. Furthermore, there is no robust evidence to conclude the effect of meal fatty acids on vascular function or blood pressure. In conclusion, there is an urgent requirement for suitably powered robust randomised controlled trials to investigate the impact of meal fat composition on postprandial novel and established CVD risk markers in postmenopausal women, an understudied population at increased cardiometabolic risk
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Effects of urban density on carbon dioxide exchanges: observations of dense urban, suburban and woodland areas of southern England
Anthropogenic and biogenic controls on the surface–atmosphere exchange of CO2 are explored for three different environments. Similarities are seen between suburban and woodland sites during summer, when photosynthesis and respiration determine the diurnal pattern of the CO2 flux. In winter, emissions from human activities dominate urban and suburban fluxes; building emissions increase during cold weather, while traffic is a major component of CO2 emissions all year round. Observed CO2 fluxes reflect diurnal traffic patterns (busy throughout the day (urban); rush-hour peaks (suburban)) and vary between working days and non-working days, except at the woodland site. Suburban vegetation offsets some anthropogenic emissions, but 24-h CO2 fluxes are usually positive even during summer. Observations are compared to estimated emissions from simple models and inventories. Annual CO2 exchanges are significantly different between sites, demonstrating the impacts of increasing urban density (and decreasing vegetation fraction) on the CO2 flux to the atmosphere
DAF-16/FOXO requires Protein Phosphatase 4 to initiate transcription of stress resistance and longevity promoting genes
In C. elegans, the conserved transcription factor DAF-16/FOXO is a powerful aging regulator, relaying dire conditions into expression of stress resistance and longevity promoting genes. For some of these functions, including low insulin/IGF signaling (IIS), DAF-16 depends on the protein SMK-1/SMEK, but how SMK-1 exerts this role has remained unknown. We show that SMK-1 functions as part of a specific Protein Phosphatase 4 complex (PP4(SMK-1)). Loss of PP4(SMK-1) hinders transcriptional initiation at several DAF-16-activated genes, predominantly by impairing RNA polymerase II recruitment to their promoters. Search for the relevant substrate of PP4(SMK-1) by phosphoproteomics identified the conserved transcriptional regulator SPT-5/SUPT5H, whose knockdown phenocopies the loss of PP4(SMK-1). Phosphoregulation of SPT-5 is known to control transcriptional events such as elongation and termination. Here we also show that transcription initiating events are influenced by the phosphorylation status of SPT-5, particularly at DAF-16 target genes where transcriptional initiation appears rate limiting, rendering PP4(SMK-1) crucial for many of DAF-16's physiological roles
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Urban signals in high-resolution weather and climate simulations: role of urban land-surface characterisation
Two urban schemes within the Joint UK Land Environment Simulator
(JULES) are evaluated offline against multi-year flux observations in the densely
built-up city centre of London and in suburban Swindon (UK): (i) the 1-tile slab
model, used in climate simulations, (ii) the 2-tile canopy model MORUSES (Met
Office–Reading Urban Surface Exchange Scheme), used for numerical weather pre-
diction over the UK. Offline, both models perform better at the suburban site,
where differences between the urban schemes are less pronounced due to larger
vegetation fractions. At both sites, the outgoing short- and longwave radiation is
more accurately represented than the turbulent heat fluxes. The seasonal varia-
tions of model skill are large in London, where the sensible heat flux in autumn and
winter is strongly under-predicted if the large city-centre magnitudes of anthro-
pogenic heat emissions are not represented. The delayed timing of the sensible heat flux in the 1-tile model in London results in large negative bias in the morning.
The partitioning of the urban surface into canyon and roof in MORUSES improves
this as the roof-tile is modelled with a very low thermal inertia, but phase and
amplitude of the gridbox-averaged flux critically depend on accurate knowledge of
the plan-area fractions of streets and buildings. Not representing non-urban land-
cover (e.g. vegetation, inland water) in London results in severely under-predicted
latent heat fluxes. Control runs demonstrate that the skill of both models can be
greatly improved by providing accurate land-cover and morphology information
and using representative anthropogenic heat emissions, which is essential if the
model output is intended to inform integrated urban services
Variation in the SERPINA6SERPINA1 locusalters morning plasma cortisol, hepatic corticosteroid binding globulin expression, gene expressionin peripheral tissues, and risk of cardiovascular disease
The stress hormone cortisol modulates fuel metabolism, cardiovascular homoeostasis, mood, inflammation and cognition. The CORtisol NETwork (CORNET) consortium previously identified a single locus associated with morning plasma cortisol. Identifying additional genetic variants that explain more of the variance in cortisol could provide new insights into cortisol biology and provide statistical power to test the causative role of cortisol in common diseases. The CORNET consortium extended its genome-wide association meta-analysis for morning plasma cortisol from 12,597 to 25,314 subjects and from ~2.2 M to ~7 M SNPs, in 17 population-based cohorts of European ancestries. We confirmed the genetic association with SERPINA6/SERPINA1. This locus contains genes encoding corticosteroid binding globulin (CBG) and α1-antitrypsin. Expression quantitative trait loci (eQTL) analyses undertaken in the STARNET cohort of 600 individuals showed that specific genetic variants within the SERPINA6/SERPINA1 locus influence expression of SERPINA6 rather than SERPINA1 in the liver. Moreover, trans-eQTL analysis demonstrated effects on adipose tissue gene expression, suggesting that variation
Meta-Analysis of Genome-Wide Association Studies for Abdominal Aortic Aneurysm Identifies Four New Disease-Specific Risk Loci
Rationale: Abdominal aortic aneurysm (AAA) is a complex disease with both genetic and environmental risk factors. Together, 6 previously identified risk loci only explain a small proportion of the heritability of AAA. Objective: To identify additional AAA risk loci using data from all available genome-wide association studies (GWAS). Methods and Results: Through a meta-analysis of 6 GWAS datasets and a validation study totalling 10,204 cases and 107,766 controls we identified 4 new AAA risk loci: 1q32.3 (SMYD2), 13q12.11 (LINC00540), 20q13.12 (near PCIF1/MMP9/ZNF335), and 21q22.2 (ERG). In various database searches we observed no new associations between the lead AAA SNPs and coronary artery disease, blood pressure, lipids or diabetes. Network analyses identified ERG, IL6R and LDLR as modifiers of MMP9, with a direct interaction between ERG and MMP9. Conclusions: The 4 new risk loci for AAA appear to be specific for AAA compared with other cardiovascular diseases and related traits suggesting that traditional cardiovascular risk factor management may only have limited value in preventing the progression of aneurysmal disease
Cardiac Expression of Microsomal Triglyceride Transfer Protein Is Increased in Obesity and Serves to Attenuate Cardiac Triglyceride Accumulation
Obesity causes lipid accumulation in the heart and may lead to lipotoxic heart disease. Traditionally, the size of the cardiac triglyceride pool is thought to reflect the balance between uptake and β-oxidation of fatty acids. However, triglycerides can also be exported from cardiomyocytes via secretion of apolipoproteinB-containing (apoB) lipoproteins. Lipoprotein formation depends on expression of microsomal triglyceride transfer protein (MTP); the mouse expresses two isoforms of MTP, A and B. Since many aspects of the link between obesity-induced cardiac disease and cardiac lipid metabolism remain unknown, we investigated how cardiac lipoprotein synthesis affects cardiac expression of triglyceride metabolism-controlling genes, insulin sensitivity, and function in obese mice. Heart-specific ablation of MTP-A in mice using Cre-loxP technology impaired upregulation of MTP expression in response to increased fatty acid availability during fasting and fat feeding. This resulted in cardiac triglyceride accumulation but unaffected cardiac insulin-stimulated glucose uptake. Long-term fat-feeding of male C57Bl/6 mice increased cardiac triglycerides, induced cardiac expression of triglyceride metabolism-controlling genes and attenuated heart function. Abolishing cardiac triglyceride accumulation in fat-fed mice by overexpression of an apoB transgene in the heart prevented the induction of triglyceride metabolism-controlling genes and improved heart function. The results suggest that in obesity, the physiological increase of cardiac MTP expression serves to attenuate cardiac triglyceride accumulation albeit without major effects on cardiac insulin sensitivity. Nevertheless, the data suggest that genetically increased lipoprotein secretion prevents development of obesity-induced lipotoxic heart disease
Subnormal vitamin B12 concentrations and anaemia in older people: a systematic review
<p>Abstract</p> <p>Background</p> <p>Pernicious anaemia is undeniably associated with vitamin B12 deficiency, but the association between subnormal vitamin B12 concentrations and anaemia in older people is unclear. The aim of this systematic review was to evaluate the association between subnormal vitamin B12 concentrations and anaemia in older people.</p> <p>Methods</p> <p>Clinical queries for aetiology and treatment in bibliographic databases (PubMed [01/1949-10/2009]; EMBASE [01/1980-10/2009]) were used. Reference lists were checked for additional relevant studies. Observational studies (≥50 participants) and randomized placebo-controlled intervention trials (RCTs) were considered.</p> <p>Results</p> <p>25 studies met the inclusion criteria. Twenty-one observational cross-sectional studies (total number of participants n = 16185) showed inconsistent results. In one longitudinal observational study, low vitamin B12 concentrations were not associated with an increased risk of anaemia (total n = 423). The 3 RCTs (total n = 210) were well-designed and showed no effect of vitamin B12 supplementation on haemoglobin concentrations during follow-up in subjects with subnormal vitamin B12 concentrations at the start of the study. Due to large clinical and methodological heterogeneity, statistical pooling of data was not performed.</p> <p>Conclusions</p> <p>Evidence of a positive association between a subnormal serum vitamin B12 concentration and anaemia in older people is limited and inconclusive. Further well-designed studies are needed to determine whether subnormal vitamin B12 is a risk factor for anaemia in older people.</p
Variation in the SERPINA6/SERPINA1 locus alters morning plasma cortisol, hepatic corticosteroid binding globulin expression, gene expression in peripheral tissues, and risk of cardiovascular disease
The stress hormone cortisol modulates fuel metabolism, cardiovascular homoeostasis, mood, inflammation and cognition. The CORtisol NETwork (CORNET) consortium previously identified a single locus associated with morning plasma cortisol. Identifying additional genetic variants that explain more of the variance in cortisol could provide new insights into cortisol biology and provide statistical power to test the causative role of cortisol in common diseases. The CORNET consortium extended its genome-wide association meta-analysis for morning plasma cortisol from 12,597 to 25,314 subjects and from similar to 2.2 M to similar to 7 M SNPs, in 17 population-based cohorts of European ancestries. We confirmed the genetic association with SERPINA6/SERPINA1. This locus contains genes encoding corticosteroid binding globulin (CBG) and alpha 1-antitrypsin. Expression quantitative trait loci (eQTL) analyses undertaken in the STARNET cohort of 600 individuals showed that specific genetic variants within the SERPINA6/SERPINA1 locus influence expression of SERPINA6 rather than SERPINA1 in the liver. Moreover, trans-eQTL analysis demonstrated effects on adipose tissue gene expression, suggesting that variations in CBG levels have an effect on delivery of cortisol to peripheral tissues. Two-sample Mendelian randomisation analyses provided evidence that each genetically-determined standard deviation (SD) increase in morning plasma cortisol was associated with increased odds of chronic ischaemic heart disease (0.32, 95% CI 0.06-0.59) and myocardial infarction (0.21, 95% CI 0.00-0.43) in UK Biobank and similarly in CARDIoGRAMplusC4D. These findings reveal a causative pathway for CBG in determining cortisol action in peripheral tissues and thereby contributing to the aetiology of cardiovascular disease.</p
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