Symbolically maintained inequality. An American case of elite higher education boundary-making

The study of elites is enjoying a revival at a time of increasing economic inequality. Sociologists of education have been leaders in this area, studying how affluent families position their children to compete favourably in a vertically stratified higher education system. However, scholars in the United States have done less research on both the horizontal stratification within the top tier of institutions and how students do symbolic work of their own to bolster elite status. In this study, the authors use qualitative interviews with 56 undergraduates at Harvard and Stanford Universities to explore how students construct the status hierarchy among elite campuses in the U. S. The authors find that Harvard and Stanford students value universities that offer a "well rounded" liberal arts education while criticizing other selective institutions for being, alternatively, too intellectual, overly connected to the old line status system, associated with partying and athletics, or having a student body too single minded about career preparation. Their findings suggest that through constructing these nuanced perceptions of elite universities\u27 distinctiveness, students justify their rarefied positions and contribute to the on-going status distinctions among social elites more generally in the United States. Comments are offered in the conclusion for how this likely differs in countries with less horizontal stratification. (DIPF/Orig.)Untersuchungen zu Eliten erleben einen Aufschwung in Zeiten steigender ökonomischer Ungleichheit. Die Bildungsssoziologie trägt entscheidend dazu bei, indem sie untersucht, wie wohlhabende Familien ihre Kinder im vertikal stratifizierten Hochschulsektor positionieren, um möglichst vorteilhaft konkurrieren zu können. Dennoch existieren in den USA nur wenige Untersuchungen zur horizontalen Stratifizierung zwischen den höchstrangigen Institutionen auf der einen Seite und andererseits zur Frage, wie Studierende selbst daran beteiligt sind, den Elitestatus symbolisch herzustellen. In der vorliegenden Untersuchung nutzen die Autorinnen 56 qualitative Interviews mit Studierenden der Universitäten Harvard und Stanford, um nachzuvollziehen wie Studierende Statusunterschiede zwischen Eliteuniversitäten konstruieren. Dabei konnte herausgefunden werden, dass Student*innen von Harvard und Stanford solche Hochschulen wertschätzen, die eine "ausgewogene" geisteswissenschaftliche Ausbildung bieten, während sie andere selektierende Institutionen beispielsweise dafür kritisieren, zu intellektuell oder zu konservativ zu sein, beziehungsweise in Verbindung mit Partys und Sport zu stehen, oder dass diese eine Studierendenschaft aufweisen, die zu sehr auf Karrierevorbereitung bedacht ist. Ihre Ergebnisse legen nah, dass die Studierenden durch Konstruktion solch nuancierter Wahrnehmungen der Besonderheiten elitärer Universitäten ihre exklusiven Positionen begründen und im großen Maße zu den fortlaufenden Statusunterscheidungen sozialer Eliten in den USA beitragen. Im Fazit dieses Artikels finden sich Anmerkungen, wie sich dies von nationalen Bildungssystemen mit geringerer horizontaler Stratifizierung unterscheidet. (DIPF/Orig.

Genomewide Association Scan of Suicidal Thoughts and Behaviour in Major Depression

Background Suicidal behaviour can be conceptualised as a continuum from suicidal ideation, to suicidal attempts to completed suicide. In this study we identify genes contributing to suicidal behaviour in the depression study RADIANT. Methodology/Principal Findings A quantitative suicidality score was composed of two items from the SCAN interview. In addition, the 251 depression cases with a history of serious suicide attempts were classified to form a discrete trait. The quantitative trait was correlated with younger onset of depression and number of episodes of depression, but not with gender. A genome-wide association study of 2,023 depression cases was performed to identify genes that may contribute to suicidal behaviour. Two Munich depression studies were used as replication cohorts to test the most strongly associated SNPs. No SNP was associated at genome-wide significance level. For the quantitative trait, evidence of association was detected at GFRA1, a receptor for the neurotrophin GDRA (p = 2e-06). For the discrete trait of suicide attempt, SNPs in KIAA1244 and RGS18 attained p-values of <5e-6. None of these SNPs showed evidence for replication in the additional cohorts tested. Candidate gene analysis provided some support for a polymorphism in NTRK2, which was previously associated with suicidality. Conclusions/Significance This study provides a genome-wide assessment of possible genetic contribution to suicidal behaviour in depression but indicates a genetic architecture of multiple genes with small effects. Large cohorts will be required to dissect this further

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

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