Examining the impact of meaning and resilience on survivors\u27 life satisfaction after Hurricane Harvey

The experience of a traumatic event such as a natural disaster can often lead individuals to suffer a variety of negative sequelae, including the development of posttraumatic stress symptoms. However, certain positive psychological constructs like meaning and resilience have been shown to mitigate these consequences. The purpose of this study was to explore the contributions of meaning and resilience to the life satisfaction of individuals (N = 55) impacted by 2017’s Hurricane Harvey. It was hypothesized that not only would meaning and resilience be significantly and positively related to life satisfaction but that meaning would contribute more to the prediction of life satisfaction than resilience. Significant positive relationships were found between meaning and life satisfaction (r = .51, p ≤ .05) and between resilience and life satisfaction (r = .32, p ≤ .05) as was expected. After conducting a multiple regression analysis, meaning was also found to significantly predict life satisfaction (β = .46, t(54) = 3.48, p = .001, pr2 = .19), and did so to a greater extent than resilience (β = .13, t(54) = .97, p = .34, pr2 = .02), which was not a statistically significant predictor in this instance. The implications of these findings are discussed, along with study strengths, limitations, and directions for research

Examining the impact of meaning and resilience on survivors' life satisfaction after Hurricane Harvey

The experience of a traumatic event such as a natural disaster can often lead individuals to suffer a variety of negative sequelae, including the development of posttraumatic stress symptoms. However, certain positive psychological constructs like meaning and resilience have been shown to mitigate these consequences. The purpose of this study was to explore the contributions of meaning and resilience to the life satisfaction of individuals (N = 55) impacted by 2017’s Hurricane Harvey. It was hypothesized that not only would meaning and resilience be significantly and positively related to life satisfaction but that meaning would contribute more to the prediction of life satisfaction than resilience. Significant positive relationships were found between meaning and life satisfaction (r = .51, p ≤ .05) and between resilience and life satisfaction (r = .32, p ≤ .05) as was expected. After conducting a multiple regression analysis, meaning was also found to significantly predict life satisfaction (β = .46, t(54) = 3.48, p = .001, pr2 = .19), and did so to a greater extent than resilience (β = .13, t(54) = .97, p = .34, pr2 = .02), which was not a statistically significant predictor in this instance. The implications of these findings are discussed, along with study strengths, limitations, and directions for research

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

Were there losses in social support during the pandemic? Testing the impact of COVID-19 on psychological adjustment to trauma in United States adults

https://kent-islandora.s3.us-east-2.amazonaws.com/node/17615/87667-thumbnail.jpgIntroduction:&nbsp;Social support is a key protective factor in the psychological adjustment of individuals to traumatic events. However, since March 2020, extant research has revealed evidence of increased loneliness, social isolation, and disconnection, likely due to COVID-19 pandemic-related recommendations that restricted day-to-day contact with others. Methods:&nbsp;In this investigation, we applied a case-control design to test the direct impacts of the pandemic on social support in United States adults recovering from a significant injury caused by PTSD-qualifying, traumatic events (e.g., motor vehicle crashes, violence, etc.). We compared individuals who experienced trauma during the pandemic, the “cases” recruited and evaluated between December 2020 to April 2022, to trauma-exposed “controls,” recruited and evaluated pre-pandemic, from August 2018 through March 9, 2020 (prior to changes in public health recommendations in the region). Cohorts were matched on key demographics (age, sex, education, race/ethnicity, income) and injury severity variables. We tested to see if there were differences in reported social support over the first 5 months of adjustment, considering variable operationalizations of social support from social network size to social constraints in disclosure. Next, we tested to see if the protective role of social support in psychological adjustment to trauma was moderated by cohort status to determine if the impacts of the pandemic extended to changes in the&nbsp;process of adjustment. Results:&nbsp;The results of our analyses suggested that there were no significant cohort differences, meaning that whether prior to or during the pandemic, individuals reported similar levels of social support that were generally protective, and similar levels of psychological symptoms. However, there was some evidence of moderation by cohort status when examining the process of adjustment. Specifically, when examining symptoms of post-traumatic stress over time, individuals adjusting to traumatic events during COVID-19 received less benefit from social support. Discussion:&nbsp;Although negative mental health implications of the pandemic are increasingly evident, it has not been clear how the pandemic impacted normative psychological adjustment processes. These results are one of the first direct tests of the impact of COVID-19 on longitudinal adjustment to trauma and suggest some minimal impacts.</p

COPA mutations impair ER-Golgi transport and cause hereditary autoimmune-mediated lung disease and arthritis

Unbiased genetic studies have uncovered surprising molecular mechanisms in human cellular immunity and autoimmunity. We performed whole-exome sequencing and targeted sequencing in five families with an apparent mendelian syndrome of autoimmunity characterized by high-titer autoantibodies, inflammatory arthritis and interstitial lung disease. We identified four unique deleterious variants in the COPA gene (encoding coatomer subunit α) affecting the same functional domain. Hypothesizing that mutant COPA leads to defective intracellular transport via coat protein complex I (COPI), we show that COPA variants impair binding to proteins targeted for retrograde Golgi-to-ER transport. Additionally, expression of mutant COPA results in ER stress and the upregulation of cytokines priming for a T helper type 17 (TH17) response. Patient-derived CD4(+) T cells also demonstrate significant skewing toward a TH17 phenotype that is implicated in autoimmunity. Our findings uncover an unexpected molecular link between a vesicular transport protein and a syndrome of autoimmunity manifested by lung and joint disease