Assessing heat exposure to extreme temperatures in urban areas using the Local Climate Zone classification

Trends of extreme-temperature episodes in cities are increasing (in frequency, magnitude and duration) due to regional climate change in interaction with urban effects. Urban morphologies and thermal properties of the materials used to build them are factors that influence spatial and temporal climate variability and are one of the main reasons for the climatic singularity of cities. This paper presents a methodology to evaluate the urban and peri-urban effect on extreme-temperature exposure in Barcelona (Spain), using the Local Climate Zone (LCZ) classification as a basis, which allows a comparison with other cities of the world characterised using this criterion. LCZs were introduced as input of the high-resolution UrbClim model (100 m spatial resolution) to create daily temperature (median and maximum) series for summer (JJA) during the period 1987 to 2016, pixel by pixel, in order to create a cartography of extremes. Using the relationship between mortality due to high temperatures and temperature distribution, the heat exposure of each LCZ was obtained. Methodological results of the paper show the improvement obtained when LCZs were mapped through a combination of two techniques (land cover-land use maps and the World Urban Database and Access Portal Tools - WUDAPT - method), and the paper proposes a methodology to obtain the exposure to high temperatures of different LCZs in urban and peri-urban areas. In the case of Barcelona, the distribution of temperatures for the 90th percentile (about 3-4 ∘C above the average conditions) leads to an increase in the relative risk of mortality of 80 %

Analysis of the common genetic component of large-vessel vasculitides through a meta- Immunochip strategy

Giant cell arteritis (GCA) and Takayasu's arteritis (TAK) are major forms of large-vessel vasculitis (LVV) that share clinical features. To evaluate their genetic similarities, we analysed Immunochip genotyping data from 1,434 LVV patients and 3,814 unaffected controls. Genetic pleiotropy was also estimated. The HLA region harboured the main disease-specific associations. GCA was mostly associated with class II genes (HLA-DRB1/HLA-DQA1) whereas TAK was mostly associated with class I genes (HLA-B/MICA). Both the statistical significance and effect size of the HLA signals were considerably reduced in the cross-disease meta-analysis in comparison with the analysis of GCA and TAK separately. Consequently, no significant genetic correlation between these two diseases was observed when HLA variants were tested. Outside the HLA region, only one polymorphism located nearby the IL12B gene surpassed the study-wide significance threshold in the meta-analysis of the discovery datasets (rs755374, P?=?7.54E-07; ORGCA?=?1.19, ORTAK?=?1.50). This marker was confirmed as novel GCA risk factor using four additional cohorts (PGCA?=?5.52E-04, ORGCA?=?1.16). Taken together, our results provide evidence of strong genetic differences between GCA and TAK in the HLA. Outside this region, common susceptibility factors were suggested, especially within the IL12B locus

A genome-wide association study identifies risk alleles in plasminogen and P4HA2 associated with giant cell arteritis

Giant cell arteritis (GCA) is the most common form of vasculitis in individuals older than 50 years in Western countries. To shed light onto the genetic background influencing susceptibility for GCA, we performed a genome-wide association screening in a well-powered study cohort. After imputation, 1,844,133 genetic variants were analysed in 2,134 cases and 9,125 unaffected controls from ten independent populations of European ancestry. Our data confirmed HLA class II as the strongest associated region (independent signals: rs9268905, P = 1.94E-54, per-allele OR = 1.79; and rs9275592, P = 1.14E-40, OR = 2.08). Additionally, PLG and P4HA2 were identified as GCA risk genes at the genome-wide level of significance (rs4252134, P = 1.23E-10, OR = 1.28; and rs128738, P = 4.60E-09, OR = 1.32, respectively). Interestingly, we observed that the association peaks overlapped with different regulatory elements related to cell types and tissues involved in the pathophysiology of GCA. PLG and P4HA2 are involved in vascular remodelling and angiogenesis, suggesting a high relevance of these processes for the pathogenic mechanisms underlying this type of vasculitis

A Large-Scale Genetic Analysis Reveals a Strong Contribution of the HLA Class II Region to Giant Cell Arteritis Susceptibility

We conducted a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated vasculitis. A case-control cohort, comprising 1,651 case subjects with GCA and 15,306 unrelated control subjects from six different countries of European ancestry, was genotyped by the Immunochip array. We also imputed HLA data with a previously validated imputation method to perform a more comprehensive analysis of this genomic region. The strongest association signals were observed in the HLA region, with rs477515 representing the highest peak (p = 4.05 × 10−40, OR = 1.73). A multivariate model including class II amino acids of HLA-DRβ1 and HLA-DQα1 and one class I amino acid of HLA-B explained most of the HLA association with GCA, consistent with previously reported associations of classical HLA alleles like HLA-DRB1∗04. An omnibus test on polymorphic amino acid positions highlighted DRβ1 13 (p = 4.08 × 10−43) and HLA-DQα1 47 (p = 4.02 × 10−46), 56, and 76 (both p = 1.84 × 10−45) as relevant positions for disease susceptibility. Outside the HLA region, the most significant loci included PTPN22 (rs2476601, p = 1.73 × 10−6, OR = 1.38), LRRC32 (rs10160518, p = 4.39 × 10−6, OR = 1.20), and REL (rs115674477, p = 1.10 × 10−5, OR = 1.63). Our study provides evidence of a strong contribution of HLA class I and II molecules to susceptibility to GCA. In the non-HLA region, we confirmed a key role for the functional PTPN22 rs2476601 variant and proposed other putative risk loci for GCA involved in Th1, Th17, and Treg cell function

Fluctuaciones de la extension del casquete glacial de la isla de Livingston (Shetland del sur) desde 1956 hasta 1996.

A partir de documentos cartográficos e imágenes de satélite se constata un 4,31% de reducción de extensión del casquete glacial de la isla Livingston desde 1956 hasta 1996. Se detecta la influencia de factores locales, fundamentalmente de tipo topogr á fico, que condicionan los avances y retrocesos del frente glacial en los diferentes sectores de la costa y se establece un modelo simple en el que se relaciona la reducción del conjunto del casquete con el calentamiento atmosférico experimentado en los últimos decenios en la zona de la Península Antártica

Fluctuaciones de la extension del casquete glacial de la isla de Livingston (Shetland del sur) desde 1956 hasta 1996.

A partir de documentos cartográficos e imágenes de satélite se constata un 4,31% de reducción de extensión del casquete glacial de la isla Livingston desde 1956 hasta 1996. Se detecta la influencia de factores locales, fundamentalmente de tipo topogr á fico, que condicionan los avances y retrocesos del frente glacial en los diferentes sectores de la costa y se establece un modelo simple en el que se relaciona la reducción del conjunto del casquete con el calentamiento atmosférico experimentado en los últimos decenios en la zona de la Península Antártica

The measurement of ice velocity, mass balance and thinning-rate on Johnsons Glacier, Livingston Island, South Shetland Islands, Antarctica

A network of twenty stakes was set up on Johnsons Glacier in order to determine its dynamics. During the austral summers from 1994-95 to 1997-98, we estimated surface velocities, mass balances and ice thickness variations. Horizontal velocity increased dow nstream from 1 m a- 1 near the ice divides to 40 m a- 1 near the ice terminus. The accumulation zone showed low accumulation rates (maximum of 0,6 m a- 1 (ice)), whereas in the lower part of the glacier, ablation rates were 4,3 m a- 1 (ice). Over the 3-year study period, both in the accumulation and ablation zones, we detected a reduction in the ice surface level ranging from 2 to 10 m from the annual ve rt ical velocities and ice-thinning data, the mass balance was obtained and compared with the mass balance field values, resulting in similar estimates. Flux values were calculated using cross-section data and horizontal velocities, and compared with the results obtained by means of mass balance and ice thinning data using the continuity equation. The two methods gave similar results

Abating heat waves in a coastal Mediterranean city: What can cool roofs and vegetation contribute?

The frequency and intensity of heat waves (HW) in cities are on the rise due to climate change as well as urban fabric materials and anthropogenic activities that affect heat accumulation. The efficacy of HW mitigation strategies depends on a city's specific and unique morphology, land use, building materials, climate and geography. In this study, we show the effectiveness of cool roofs and vegetation in reducing temperature in the Metropolitan Area of Barcelona (AMB). We use the Weather and Research Forecasting (WRF) model with the urban scheme BEP+BEM, including11 urban classes to simulate a HW that occurred in August 2015. We find that cool roofs reduce temperature best during the day (0.67 °C average and 2.22 °C maximum reductions), while additional green areas moderate temperatures to a lesser degree but also more evenly during the day and at night (average reductions of 0.15 °C and 0.17 °C, respectively). However, when irrigation is increased, the temperature reduction during the day is intensified due to the cooling effect of more evapotranspiration. The thermal regulation of combining the two strategies is the most evenly distributed over the AMB and has the highest impact, with an average and maximum reduction of 1.26 °C and 4.73 °C at 13:00UTC

The measurement of ice velocity, mass balance and thinning-rate on Johnsons Glacier, Livingston Island, South Shetland Islands, Antarctica

A network of twenty stakes was set up on Johnsons Glacier in order to determine its dynamics. During the austral summers from 1994-95 to 1997-98, we estimated surface velocities, mass balances and ice thickness variations. Horizontal velocity increased dow nstream from 1 m a- 1 near the ice divides to 40 m a- 1 near the ice terminus. The accumulation zone showed low accumulation rates (maximum of 0,6 m a- 1 (ice)), whereas in the lower part of the glacier, ablation rates were 4,3 m a- 1 (ice). Over the 3-year study period, both in the accumulation and ablation zones, we detected a reduction in the ice surface level ranging from 2 to 10 m from the annual ve rt ical velocities and ice-thinning data, the mass balance was obtained and compared with the mass balance field values, resulting in similar estimates. Flux values were calculated using cross-section data and horizontal velocities, and compared with the results obtained by means of mass balance and ice thinning data using the continuity equation. The two methods gave similar results

Erratum: Corrigendum: Analysis of the common genetic component of large-vessel vasculitides through a meta-Immunochip strategy

Giant cell arteritis (GCA) and Takayasu’s arteritis (TAK) are major forms of large-vessel vasculitis (LVV) that share clinical features. To evaluate their genetic similarities, we analysed Immunochip genotyping data from 1,434 LVV patients and 3,814 unaffected controls. Genetic pleiotropy was also estimated. The HLA region harboured the main disease-specific associations. GCA was mostly associated with class II genes (HLA-DRB1/HLA-DQA1) whereas TAK was mostly associated with class I genes (HLA-B/ MICA). Both the statistical significance and effect size of the HLA signals were considerably reduced in the cross-disease meta-analysis in comparison with the analysis of GCA and TAK separately. Consequently, no significant genetic correlation between these two diseases was observed when HLA variants were tested. Outside the HLA region, only one polymorphism located nearby the IL12B gene surpassed the study-wide significance threshold in the meta-analysis of the discovery datasets (rs755374, P = 7.54E-07; ORGCA = 1.19, ORTAK = 1.50). This marker was confirmed as novel GCA risk factor using four additional cohorts (PGCA = 5.52E-04, ORGCA = 1.16). Taken together, our results provide evidence of strong genetic differences between GCA and TAK in the HLA. Outside this region, common susceptibility factors were suggested, especially within the IL12B locus