Moulting season corticosterone correlates with winter season bodyweight in an Arctic migrant bird

In vertebrates, the endocrine system translates environmental changes into physiological responses on which natural selection can act to regulate individual fitness and, ultimately, population dynamics. Corticosterone (CORT) and dehydroepiandrosterone (DHEA) are important regulators of the avian endocrine system but relatively few studies have investigated their downstream effects on key morphological fitness‐related traits in free‐living populations. This study quantified endocrine–morphology relationships in free‐living Greenland Barnacle Geese Branta leucopsis that breed in the high Arctic. CORT and DHEA were extracted from feather and blood samples and tested for relationships with three morphological traits associated with survival and reproduction: bodyweight, body size and facial plumage coloration. We expected CORT concentration to be higher in birds with less favourable morphological traits (i.e. lighter, smaller and less attractive) and DHEA to be higher in birds with more favourable traits (i.e. heavier, bigger and more attractive). As expected, individuals with higher CORT during the post‐breeding moult (July/August) had significantly lower bodyweight during the following winter (November–April). In contrast, we found no robust DHEA–morphology relationships and no statistically significant relationship between CORT and body size or facial plumage. Overall, this study provides evidence of a negative relationship between CORT and bodyweight extending across different seasons of the annual cycle in a long‐distance migrant. This is of particular interest because bodyweight fluctuates rapidly in response to environmental resources and is closely linked to both survival and reproductive success in this species. Understanding the relationship between CORT and key morphological traits is important because endocrine‐disrupting contaminants in the Arctic increasingly interfere with CORT function in birds, including Barnacle Geese, and based on the results of this study may have consequences for bodyweight regulation

Towards a modular language curriculum for using tasks

Task-based language teaching (TBLT) and task-supported language teaching (TSLT) are often seen as incompatible as they draw on different theories of language learning and language teaching. The position adopted in this article, however, is that both approaches are needed especially in instructional contexts where ‘pure’ task-based teaching may be problematic for various reasons. The article makes a case for a modular curriculum consisting of separate (i.e. non-integrated) task-based and structure-based components. Different curriculum models are considered in the light of what is known about how a second language is learned. The model that is proposed assumes the importance of developing fluency first. It consists of a primary task-based module implemented with focus-on-form (Long, 1991) and, once a basic fluency has been achieved, supported by a secondary structural module to provide for explicit accuracy-oriented work to counteract learned selective attention (N. Ellis, 2006): one of the main sources of persistent error. The article also addresses the content and grading of the task-based and structural modules. It considers the factors that need to be considered in the vertical and horizontal grading of tasks but also points out that, for the time being, syllabus designers will have to draw on their experience and intuition as much as on research to make decisions about how to sequence tasks. An argument is presented for treating the structural component as a checklist rather than as a syllabus so as to allow teachers to address selectively those features that are found to be problematic for their students when they perform tasks

Star clusters near and far; tracing star formation across cosmic time

© 2020 Springer-Verlag. The final publication is available at Springer via https://doi.org/10.1007/s11214-020-00690-x.Star clusters are fundamental units of stellar feedback and unique tracers of their host galactic properties. In this review, we will first focus on their constituents, i.e.\ detailed insight into their stellar populations and their surrounding ionised, warm, neutral, and molecular gas. We, then, move beyond the Local Group to review star cluster populations at various evolutionary stages, and in diverse galactic environmental conditions accessible in the local Universe. At high redshift, where conditions for cluster formation and evolution are more extreme, we are only able to observe the integrated light of a handful of objects that we believe will become globular clusters. We therefore discuss how numerical and analytical methods, informed by the observed properties of cluster populations in the local Universe, are used to develop sophisticated simulations potentially capable of disentangling the genetic map of galaxy formation and assembly that is carried by globular cluster populations.Peer reviewedFinal Accepted Versio

Stratified analyses refine association between TLR7 rare variants and severe COVID-19

Despite extensive global research into genetic predisposition for severe COVID-19, knowledge on the role of rare host genetic variants and their relation to other risk factors remains limited. Here, 52 genes with prior etiological evidence were sequenced in 1,772 severe COVID-19 cases and 5,347 population-based controls from Spain/Italy. Rare deleterious TLR7 variants were present in 2.4% of young (<60 years) cases with no reported clinical risk factors (n = 378), compared to 0.24% of controls (odds ratio [OR] = 12.3, p = 1.27 × 10). Incorporation of the results of either functional assays or protein modeling led to a pronounced increase in effect size (OR = 46.5, p = 1.74 × 10). Association signals for the X-chromosomal gene TLR7 were also detected in the female-only subgroup, suggesting the existence of additional mechanisms beyond X-linked recessive inheritance in males. Additionally, supporting evidence was generated for a contribution to severe COVID-19 of the previously implicated genes IFNAR2, IFIH1, and TBK1. Our results refine the genetic contribution of rare TLR7 variants to severe COVID-19 and strengthen evidence for the etiological relevance of genes in the interferon signaling pathway

Multi-ancestry study of blood lipid levels identifies four loci interacting with physical activity

Many genetic loci affect circulating lipid levels, but it remains unknown whether lifestyle factors, such as physical activity, modify these genetic effects. To identify lipid loci interacting with physical activity, we performed genome-wide analyses of circulating HDL cholesterol, LDL cholesterol, and triglyceride levels in up to 120,979 individuals of European, African, Asian, Hispanic, and Brazilian ancestry, with follow-up of suggestive associations in an additional 131,012 individuals. We find four loci, in/near CLASP1, LHX1, SNTA1, and CNTNAP2, that are associated with circulating lipid levels through interaction with physical activity; higher levels of physical activity enhance the HDL cholesterol-increasing effects of the CLASP1, LHX1, and SNTA1 loci and attenuate the LDL cholesterol-increasing effect of the CNTNAP2 locus. The CLASP1, LHX1, and SNTA1 regions harbor genes linked to muscle function and lipid metabolism. Our results elucidate the role of physical activity interactions in the genetic contribution to blood lipid levels

Multi-ancestry study of blood lipid levels identifies four loci interacting with physical activity

Many genetic loci affect circulating lipid levels, but it remains unknown whether lifestyle factors, such as physical activity, modify these genetic effects. To identify lipid loci interacting with physical activity, we performed genome-wide analyses of circulating HDL cholesterol, LDL cholesterol, and triglyceride levels in up to 120,979 individuals of European, African, Asian, Hispanic, and Brazilian ancestry, with follow-up of suggestive associations in an additional 131,012 individuals. We find four loci, in/near CLASP1, LHX1, SNTA1, and CNTNAP2, that are associated with circulating lipid levels through interaction with physical activity; higher levels of physical activity enhance the HDL cholesterol-increasing effects of the CLASP1, LHX1, and SNTA1 loci and attenuate the LDL cholesterol- increasing effect of the CNTNAP2 locus. The CLASP1, LHX1, and SNTA1 regions harbor genes linked to muscle function and lipid metabolism. Our results elucidate the role of physical activity interactions in the genetic contribution to blood lipid levels

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 care1 or hospitalization2,3,4 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