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

Technological elites, the meritocracy, and postracial myths in Silicon Valley

Entre as modernas elites tecnológicas digitais, os mitos da meritocracia e da façanha intelectual são usados como marcadores de raça e gênero por uma supremacia branca masculina que consolida recursos de forma desproporcional em relação a pessoas não brancas, principalmente negros, latinos e indígenas. Os investimentos em mitos meritocráticos suprimem os questionamentos de racismo e discriminação, mesmo quando os produtos das elites digitais são infundidos com marcadores de raça, classe e gênero. As lutas históricas por inclusão social, política e econômica de negros, mulheres e outras classes desprotegidas têm implicado no reconhecimento da exclusão sistêmica, do trabalho forçado e da privação de direitos estruturais, além de compromissos com políticas públicas dos EUA, como as ações afirmativas, que foram igualmente fundamentais para reformas políticas voltadas para participação e oportunidades econômicas. A ascensão da tecnocracia digital tem sido, em muitos aspectos, antitética a esses esforços no sentido de reconhecer raça e gênero como fatores cruciais para inclusão e oportunidades tecnocráticas. Este artigo explora algumas das formas pelas quais os discursos das elites tecnocráticas do Vale do Silício reforçam os investimentos no pós racialismo como um pretexto para a re-consolidação do capital em oposição às políticas públicas que prometem acabar com práticas discriminatórias no mundo do trabalho. Por meio de uma análise cuidadosa do surgimento de empresas de tecnologias digitais e de uma discussão sobre como as elites tecnológicas trabalham para mascarar tudo, como inscrições algorítmicas e genéticas de raça incorporadas em seus produtos, mostramos como as elites digitais omitem a sua responsabilidade por suas reinscrições pós raciais de (in)visibilidades raciais. A partir do uso de análise histórica e crítica do discurso, o artigo revela como os mitos de uma meritocracia digital baseados em um “daltonismo racial” tecnocrático emergem como chave para a manutenção de exclusões de gênero e raça.Palavras-chave: Tecnologia. Raça. Gênero.Among modern digital technology elites, myths of meritocracy and intellectual prowess are used as racial and gender markers of white male supremacy that disproportionately consolidate resources away from people of color, particularly African Americans, Latino/as and Native Americans. Investments in meritocratic myths suppress interrogations of racism and discrimination even as the products of digital elites are infused with racial, class, and gender markers. Longstanding struggles for social, political, and economic inclusion for African Americans, women, and other legally protected classes have been predicated upon the recognition of systemic exclusion, forced labor, and structural disenfranchisement, and commitments to US public policies like affirmative action have, likewise, been fundamental to political reforms geared to economic opportunity and participation. The rise of the digital technocracy has, in many ways, been antithetical to these sustained efforts to recognize race and gender as salient factors structuring technocratic opportunity and inclusion. This paper explores some of the ways in which discourses of Silicon Valley technocratic elites bolster investments in post-racialism as a pretext for re-consolidations of capital, in opposition to public policy commitments to end discriminatory labor practices. Through a careful analysis of the rise of digital technology companies, and a discussion of how technology elites work to mask everything from algorithmic to genetic inscriptions of race embedded in their products, we show how digital elites elide responsibility for their post-racial re-inscriptions of racial visibilities (and invisibilities). Using historical and critical discourse analysis, the paper reveals how myths of a digital meritocracy premised on a technocratic colorblindness emerge key to perpetuating gender and racial exclusions.Keywords: Technology. Race. Gender

First record of the Spinner Dolphin Stenella longirostris longirostris (Cetacea: Delphinidae) for Kosrae, Micronesia

The Spinner Dolphin Stenella longirostris longirostris (Gray, 1828) has been reported from most of the island groups from Micronesia, except for Kosrae. On 25 June 2014 we observed a pod of about 10 dolphins at Molsron Yela, Kosrae. Our photos of the dolphins confirm their identity as S. l. longirostris, based on the extremely long and slender snout combined with the tricolored pattern of a dark gray cape, gray sides, and white belly. This provides the first documented record for Kosrae

Ectosymbionts of the Sea Anemone Stichodactyla gigantea at Kosrae, Micronesia

We studied the ectosymbionts associating with the sea anemone Stichodactyla gigantea at Kosrae, Micronesia. Ectosymbionts of seven species associated with 60.7% of S. gigantea (n=28), with a mean of 2.4 per anemone and 3.9 per occupied anemone. Anemones hosting one or more ectosymbionts did not differ significantly in size from anemones lacking ectosymbionts and there was no significant correlation between anemone size and the number of ectosymbionts. Of 67 ectosymbionts observed, the sea cucumber Stichopus vastus comprised 23.9%, followed by the shrimp Thor amboinensis (20.9%), unidentified hermit crabs (Paguroidea; 20.9%), the cardinalfish Ostorhinchus novemfasciatus (20.9%), the shrimp Periclimenes brevicarpalis (9.0%), the sea cucumber Holothuria hilla (3.0%), and an unidentified brachyuran crab (1.5%). This study documents the first records of S. vastus, H. hilla, and O. novemfasciatus associating with S. gigantea, and the first locality records of S. gigantea, T. amboinensis, P. brevicarpalis, and S. vastus for Kosrae. Because humans often harvest S. gigantea for food at Kosrae, we recommend protecting the symbiotic assemblage of S. gigantea by establishing a sustainable system of harvesting

Altered Glutamatergic Metabolism Associated with Punctate White Matter Lesions in Preterm Infants

<div><p>Preterm infants (∼10% of all births) are at high-risk for long-term neurodevelopmental disabilities, most often resulting from white matter injury sustained during the neonatal period. Glutamate excitotoxicity is hypothesized to be a key mechanism in the pathogenesis of white matter injury; however, there has been no <i>in vivo</i> demonstration of glutamate excitotoxicity in preterm infants. Using magnetic resonance spectroscopy (MRS), we tested the hypothesis that glutamate and glutamine, i.e., markers of glutamatergic metabolism, are altered in association with punctate white matter lesions and “diffuse excessive high signal intensity” (DEHSI), the predominant patterns of preterm white matter injury. We reviewed all clinically-indicated MRS studies conducted on preterm infants at a single institution during a six-year period and determined the absolute concentration of glutamate, glutamine, and four other key metabolites in the parietal white matter in 108 of those infants after two investigators independently evaluated the studies for punctate white matter lesions and DEHSI. Punctate white matter lesions were associated with a 29% increase in glutamine concentration (<i>p</i> = 0.002). In contrast, there were no differences in glutamatergic metabolism in association with DEHSI. Severe DEHSI, however, was associated with increased lactate concentration (<i>p</i> = 0.001), a marker of tissue acidosis. Findings from this study support glutamate excitotoxicity in the pathogenesis of punctate white matter lesions, but not necessarily in DEHSI, and suggest that MRS provides a useful biomarker for determining the pathogenesis of white matter injury in preterm infants during a period when neuroprotective agents may be especially effective.</p> </div

Cases were stratified independently for analyses of pWMLs and DEHSI.

<p>Depicted above is a schematic diagram demonstrating how the 108 preterm infants were stratified with regard to both pWMLs and DEHSI following independent evaluation by two investigators and subsequent consensus classification for cases discrepant between the raters with regard to pWMLs (n = 2) or DEHSI (n = 13). Overall kappas for pWMLs and DEHSI were 0.95 and 0.84, respectively.</p

Mean metabolite concentrations (mmol/kg) [standard error].

<p>for pWML cases and non-pWML cases. Mean values above are adjusted for age.</p>a<p><i>p</i>-values listed are derived from the univariate contrasts controlling for PCA.</p