The baroclinic adjustment of time-dependent shear flows

Author Posting. © American Meteorological Society, 2010. This article is posted here by permission of American Meteorological Society for personal use, not for redistribution. The definitive version was published in Journal of Physical Oceanography 40 (2010): 1851-1865, doi:10.1175/2010JPO4217.1.Motivated by the fact that time-dependent currents are ubiquitous in the ocean, this work studies the two-layer Phillips model on the beta plane with baroclinic shear flows that are steady, periodic, or aperiodic in time to understand their nonlinear evolution better. When a linearly unstable basic state is slightly perturbed, the primary wave grows exponentially until nonlinear advection adjusts the growth. Even though for long time scales these nearly two-dimensional motions predominantly cascade energy to large scales, for relatively short times the wave–mean flow and wave–wave interactions cascade energy to smaller horizontal length scales. The authors demonstrate that the manner through which these mechanisms excite the harmonics depends significantly on the characteristics of the basic state. Time-dependent basic states can excite harmonics very rapidly in comparison to steady basic states. Moreover, in all the simulations of aperiodic baroclinic shear flows, the barotropic component of the primary wave continues to grow after the adjustment by the nonlinearities. Furthermore, the authors find that the correction to the zonal mean flow can be much larger when the basic state is aperiodic compared to the periodic or steady limits. Finally, even though time-dependent baroclinic shear on an f plane is linearly stable, the authors show that perturbations can grow algebraically in the linear regime because of the erratic variations in the aperiodic flow. Subsequently, baroclinicity adjusts the growing wave and creates a final state that is more energetic than the nonlinear adjustment of any of the unstable steady baroclinic shears that are considered.FJP was supported by NSERC and JP was supported by NSF OCE 0925061 during the research and writing of this manuscript

The Journalists of the Future meet Entrepreneurial Journalism

Journalism is undergoing a strong restructuring of its labour market due to the consequences of the economic crisis and the technological innovations. Discussions on the search for new formulas for job creation are centred on the emergence of entrepreneurial journalism. Spain is a paradigmatic example of this phenomenon because between 2008 and 2014, 454 news media outlets were created. The rise of entrepreneurial journalism raises many questions and challenges that affect all areas of journalism. One is their introduction in journalism education and the views of journalism students. The aim of this article is to analyse the perceptions regarding entrepreneurship held by those who will be future journalists and who are now receiving their education in the classroom. Our goal is to find out what knowledge journalism students have about entrepreneurship and the skills that are deemed essential. We evaluate the willingness of journalism students to develop their own business project and the major barriers and obstacles. The methodology uses a quantitative approach based on surveys in Spain (N=184). The results suggest an increase of the willingness in students to engage in entrepreneurship. However, students also have a negative and disenchanted view of journalism as they progress in their studies.This research was supported by the Universitat Jaume I de Castelló [grant number PI11A2013– 12]

The resolution sensitivity of the Asian summer monsoon and its inter-model comparison between MRI-AGCM and MetUM

In this study, we compare the resolution sensitivity of the Asian Summer Monsoon (ASM) in two Atmospheric General Circulation Models (AGCMs): the MRI-AGCM and the MetUM. We analyze the MetUM at three different resolutions, N96 (approximately 200-km mesh on the equator), N216 (90-km mesh) and N512 (40-km mesh), and the MRI-AGCM at TL95 (approximately 180-km mesh on the equator), TL319 (60-km mesh), and TL959 (20-km mesh). The MRI-AGCM and the MetUM both show decreasing precipitation over the western Pacific with increasing resolution, but their precipitation responses differ over the Indian Ocean. In MRI-AGCM, a large precipitation increase appears off the equator (5–20°N). In MetUM, this off-equatorial precipitation increase is less significant and precipitation decreases over the equator. Moisture budget analysis demonstrates that a changing in moisture flux convergence at higher resolution is related to the precipitation response. Orographic effects, intra-seasonal variability and the representation of the meridional thermal gradient are explored as possible causes of the resolution sensitivity. Both high-resolution AGCMs (TL959 and N512) can represent steep topography, which anchors the rainfall pattern over south Asia and the Maritime Continent. In MRI-AGCM, representation of low pressure systems in TL959 also contributes to the rainfall pattern. Furthermore, the seasonal evolution of the meridional thermal gradient appears to be more accurate at higher resolution, particularly in the MRI-AGCM. These findings emphasize that the impact of resolution is only robust across the two AGCMs for some features of the ASM, and highlights the importance of multi-model studies of GCM resolution sensitivity

Exome-wide association study to identify rare variants influencing COVID-19 outcomes : Results from the Host Genetics Initiative

Publisher Copyright: Copyright: © 2022 Butler-Laporte et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Host genetics is a key determinant of COVID-19 outcomes. Previously, the COVID-19 Host Genetics Initiative genome-wide association study used common variants to identify multiple loci associated with COVID-19 outcomes. However, variants with the largest impact on COVID-19 outcomes are expected to be rare in the population. Hence, studying rare variants may provide additional insights into disease susceptibility and pathogenesis, thereby informing therapeutics development. Here, we combined whole-exome and whole-genome sequencing from 21 cohorts across 12 countries and performed rare variant exome-wide burden analyses for COVID-19 outcomes. In an analysis of 5,085 severe disease cases and 571,737 controls, we observed that carrying a rare deleterious variant in the SARS-CoV-2 sensor toll-like receptor TLR7 (on chromosome X) was associated with a 5.3-fold increase in severe disease (95% CI: 2.75–10.05, p = 5.41x10-7). This association was consistent across sexes. These results further support TLR7 as a genetic determinant of severe disease and suggest that larger studies on rare variants influencing COVID-19 outcomes could provide additional insights.Peer reviewe

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 hospitalization2–4 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

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

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

Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes

publisher: Elsevier articletitle: Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes journaltitle: Cell articlelink: https://doi.org/10.1016/j.cell.2018.05.046 content_type: article copyright: © 2018 Elsevier Inc