The Vehicle, Spring 2001

Vol. 42, No. 2 Table of Contents To Dream Without CeasingElizabeth Dedmanpage 4-5 Honoring Commandos at Spean BridgeKat Stevenspage 6 The Girl I NamelyKevin Manuspage 7 AbsolutionMike Mauritzenpage 8 Summertime SuperheroesChris Ptasnikpage 9 Flower at GlencoeKat Stevenspage 10 AddictionAdam Funkpage 11 Cornfield in JanuaryRobert Prattepage 12 MelancholyOona Margaret Burkepage 13 In PicturesAmanda McKaypage 14 Words to a Silent FilmBrianne Bolinpage 15 ManagerRobert Prattepage 16 The WellJanet Windegathpage 17 A Meal at the Personal Growth CafeAshley Kieferpage 18 Castlegate Evening at AberdeenKat Stevenspage 19 What We AreKevin Manuspage 20 Ode to My Gin-Soaked OlivesBrianne Bolinpage 21 The Six String PlayerRyan Guimondpage 22 MaxineJay Edwardspage 23 BarefootKrista Bodenpage 24 JulyAdam Funkpage 25 HopeOona Margaret Burkepage 26 UntitledLevy Wooln Dannerpage 27 The One and Only Picture I Have of YouKevin Manuspage 28 Death of a Fat ManBrianne Bolinpage 29-32https://thekeep.eiu.edu/vehicle/1075/thumbnail.jp

Mycobacterium tuberculosis peptides presented by HLA-E molecules are targets for human CD8 T-cells with cytotoxic as well as regulatory activity

Tuberculosis (TB) is an escalating global health problem and improved vaccines against TB are urgently needed. HLA-E restricted responses may be of interest for vaccine development since HLA-E displays very limited polymorphism (only 2 coding variants exist), and is not down-regulated by HIV-infection. The peptides from Mycobacterium tuberculosis (Mtb) potentially presented by HLA-E molecules, however, are unknown. Here we describe human T-cell responses to Mtb-derived peptides containing predicted HLA-E binding motifs and binding-affinity for HLA-E. We observed CD8(+) T-cell proliferation to the majority of the 69 peptides tested in Mtb responsive adults as well as in BCG-vaccinated infants. CD8(+) T-cells were cytotoxic against target-cells transfected with HLA-E only in the presence of specific peptide. These T cells were also able to lyse M. bovis BCG infected, but not control monocytes, suggesting recognition of antigens during mycobacterial infection. In addition, peptide induced CD8(+) T-cells also displayed regulatory activity, since they inhibited T-cell proliferation. This regulatory activity was cell contact-dependent, and at least partly dependent on membrane-bound TGF-beta. Our results significantly increase our understanding of the human immune response to Mtb by identification of CD8(+) T-cell responses to novel HLA-E binding peptides of Mtb, which have cytotoxic as well as immunoregulatory activity

Shared genetic risk between eating disorder- and substance-use-related phenotypes:Evidence from genome-wide association studies

First published: 16 February 202

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

Dietary macronutrient composition affects β cell responsiveness but not insulin sensitivity123

Background: Altering dietary carbohydrate or fat content may have chronic effects on insulin secretion and sensitivity, which may vary with individual metabolic phenotype