Patterns and drivers of carbohydrate budgets in ice algal assemblages from first year <scp>A</scp>rctic sea ice

AbstractOngoing changes in sea ice distribution will have major implications for the ecology of the Arctic Ocean. First year ice (FYI) supports abundant ice‐algae communities that produce dissolved and particulate carbohydrates, including extracellular polymeric substances (EPS), which are significant carbon sources, influence ice formation and microbial survival within sea ice, and water column carbon cycling following ice melt. Key drivers of the distribution and composition of these carbohydrates are poorly characterised. Carbohydrates and chlorophyll a concentrations were linearly related in springtime bottom FYI at 36 sites in the Canadian Archipelago region, with high levels of spatial heterogeneity. Nanoeukaryote cell density and phosphate concentration were strong drivers of total and dissolved carbohydrate and uronic acid concentrations. Particulate carbohydrates were strongly related to total bacterial abundance. Dissolved carbohydrates contributed 77% of total carbohydrate: the most abundant (51%) size fraction being dissolved carbohydrates &lt; 8 kDa in size, with dissolved EPS contributing 7% to total carbohydrate. Carbohydrate fractions differed in monosaccharide profiles; dissolved components being glucose rich; particulate EPS containing more mannose, xylose, fucose and arabinose. These profiles corresponded to those of cultured sea‐ice diatoms. Microbial abundance, silicate, nitrate and phosphate concentration and ice thickness were important environmental drivers, with thicker ice containing relatively more particulate EPS, with thinner ice containing high amounts of glucose‐rich smaller‐sized carbohydrate moieties. Changes in ice characteristics will alter the relative balance of labile and refractory carbohydrates generated within bottom ice layers, with implications for food webs and carbon turnover in the warming Arctic Ocean.</jats:p

Climate and juvenile recruitment as drivers of Arctic cod (Boreogadus saida) dynamics in two Canadian Arctic seas

Arctic cod (Boreogadus saida) is the most abundant forage fish species in Arctic seas and plays a pivotal role in the transfer of energy between zooplankton and top predators. The dominance of Arctic cod and the Arctic’s relatively low biodiversity interact such that changing population dynamics of Arctic cod have cascading effects on whole Arctic marine ecosystems. Over the last decades, warming in the Arctic has led to a decline in Arctic cod populations in the Barents Sea, but in the Canadian Arctic these conditions have been correlated with up to a 10-fold higher biomass of age-0 Arctic cod at the end of summer. However, whether this enhanced larval survival with warmer waters endures through age-1þ populations is unknown. A better understanding of spatial variation in the response of Arctic cod populations to environmental conditions is critical to forecast future changes in Arctic ecosystems. Here, we rely on a 17-year time series of acoustic-trawl surveys (2003–2019) to test whether ice-breakup date, sea surface temperature, zooplankton density, and Arctic climate indices during early life stages affect the subsequent recruitment of age-1þ Arctic cod in the Beaufort Sea and Baffin Bay. In the Beaufort Sea, the biomass of age-1þ Arctic cod correlated with both Arctic Oscillation indices and age-0 biomass of the previous year. In Baffin Bay, the biomass of age-1þ Arctic cod correlated with previous-year North Atlantic Oscillation indices and the timing of ice breakup. This study demonstrates that climate and environmental conditions experienced during the early life stages drive the recruitment of the age-1þ Arctic cod population and helps to quantify spatial variation in the main environmental drivers

Arctic Ocean outflow shelves in the changing Arctic: A review and perspectives

Published version. Source at http://doi.org/10.1016/j.pocean.2015.08.007. License in accordance with the journal's policy - CC-BY-NC-ND.Over the past decade or so, international research efforts, many of which were part of the International Polar Year, have accrued our understanding of the Arctic outflow shelves. The Arctic outflow shelves, namely the East Greenland Shelf (EGS) and the Canadian Arctic Archipelago (CAA), serve as conduits through which Arctic sea ice and waters and their properties are exported to the North Atlantic. These shelves play an important role in thermohaline circulation and global circulation patterns, while being influenced by basin-scale and regional changes taking place in the Arctic. Here, we synthesize the current knowledge on key forcings of primary production and ecosystem processes on the outflow shelves, as they influence their structure and functionalities and, consequently their role in Arctic Ocean productivity and global biogeochemical cycles. For the CAA, a fresh outlook on interannual and decadal physical and biological time-series reveals recent changes in productivity patterns, while an extensive analysis of sea ice conditions over the past 33 years (1980–2012) demonstrates significant declines in multi-year ice and a redistribution of ice types. For the EGS, our analysis shows that sea ice export strongly contributes to structuring spatially diverse productivity regimes. Despite the large heterogeneity in physical and biological processes within and between the outflow shelves, a conceptual model of productivity regimes is proposed, helping identify general productivity patterns and key forcings. The different productivity regimes are expected to respond differently to current and future Arctic change, providing a useful basis upon which to develop predictive scenarios of future productivity states. Current primary production estimates for both outflow shelves very likely underestimate their contribution to total Arctic production

Analysis of UK and European NOx and VOC emission scenarios in the Defra model intercomparison exercise

This is a PDF file of an unedited manuscript that has been accepted for publication. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertainSimple emission scenarios have been implemented in eight United Kingdom air quality models with the aim of assessing how these models compared when addressing whether photochemical ozone formation in southern England was NOx- or VOC-sensitive and whether ozone precursor sources in the UK or in the Rest of Europe (RoE) were the most important during July 2006. The suite of models included three Eulerian-grid models (three implementations of one of these models), a Lagrangian atmospheric dispersion model and two moving box air parcel models. The assignments as to NOx- or VOC-sensitive and to UK- versus RoE-dominant, turned out to be highly variable and often contradictory between the individual models. However, when the assignments were filtered by model performance on each day, many of the contradictions could be eliminated. Nevertheless, no one model was found to be the 'best' model on all days, indicating that no single air quality model could currently be relied upon to inform policymakers robustly in terms of NOx- versus VOC-sensitivity and UK- versus RoE-dominance on each day. It is important to maintain a diversity in model approaches.Peer reviewedFinal Accepted Versio

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-19(1,2), host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases(3-7). They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease.Peer reviewe

Detailed stratified GWAS analysis for severe COVID-19 in four European populations

Publisher Copyright: © The Author(s) 2022.Given the highly variable clinical phenotype of Coronavirus disease 2019 (COVID-19), a deeper analysis of the host genetic contribution to severe COVID-19 is important to improve our understanding of underlying disease mechanisms. Here, we describe an extended genome-wide association meta-analysis of a well-characterized cohort of 3255 COVID-19 patients with respiratory failure and 12 488 population controls from Italy, Spain, Norway and Germany/Austria, including stratified analyses based on age, sex and disease severity, as well as targeted analyses of chromosome Y haplotypes, the human leukocyte antigen region and the SARS-CoV-2 peptidome. By inversion imputation, we traced a reported association at 17q21.31 to a ∼0.9-Mb inversion polymorphism that creates two highly differentiated haplotypes and characterized the potential effects of the inversion in detail. Our data, together with the 5th release of summary statistics from the COVID-19 Host Genetics Initiative including non-Caucasian individuals, also identified a new locus at 19q13.33, including NAPSA, a gene which is expressed primarily in alveolar cells responsible for gas exchange in the lung.Peer reviewe

Diclofenac Prolongs Repolarization in Ventricular Muscle with Impaired Repolarization Reserve

Background: The aim of the present work was to characterize the electrophysiological effects of the non-steroidal anti- inflammatory drug diclofenac and to study the possible proarrhythmic potency of the drug in ventricular muscle. Methods: Ion currents were recorded using voltage clamp technique in canine single ventricular cells and action potentials were obtained from canine ventricular preparations using microelectrodes. The proarrhythmic potency of the drug was investigated in an anaesthetized rabbit proarrhythmia model. Results: Action potentials were slightly lengthened in ventricular muscle but were shortened in Purkinje fibers by diclofenac (20 mM). The maximum upstroke velocity was decreased in both preparations. Larger repolarization prolongation was observed when repolarization reserve was impaired by previous BaCl 2 application. Diclofenac (3 mg/kg) did not prolong while dofetilide (25 mg/kg) significantly lengthened the QT c interval in anaesthetized rabbits. The addition of diclofenac following reduction of repolarization reserve by dofetilide further prolonged QT c . Diclofenac alone did not induce Torsades de Pointes ventricular tachycardia (TdP) while TdP incidence following dofetilide was 20%. However, the combination of diclofenac and dofetilide significantly increased TdP incidence (62%). In single ventricular cells diclofenac (30 mM) decreased the amplitude of rapid (I Kr ) and slow (I Ks ) delayed rectifier currents thereby attenuating repolarization reserve. L-type calcium current (I Ca ) was slightly diminished, but the transient outward (I to ) and inward rectifier (I K1 ) potassium currents were not influenced. Conclusions: Diclofenac at therapeutic concentrations and even at high dose does not prolong repolarization markedly and does not increase the risk of arrhythmia in normal heart. However, high dose diclofenac treatment may lengthen repolarization and enhance proarrhythmic risk in hearts with reduced repolarization reserve

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care(1) or hospitalization(2-4) after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease.Peer reviewe