12 research outputs found

    Psychosocial characteristics and social networks of suicidal prisoners: towards a model of suicidal behaviour in detention

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    Prisoners are at increased risk of suicide. Investigation of both individual and environmental risk factors may assist in developing suicide prevention policies for prisoners and other high-risk populations. We conducted a matched case-control interview study with 60 male prisoners who had made near-lethal suicide attempts in prison (cases) and 60 male prisoners who had not (controls). We compared levels of depression, hopelessness, self-esteem, impulsivity, aggression, hostility, childhood abuse, life events (including events occurring in prison), social support, and social networks in univariate and multivariate models. A range of psychosocial factors was associated with near-lethal self-harm in prisoners. Compared with controls, cases reported higher levels of depression, hopelessness, impulsivity, and aggression, and lower levels of self-esteem and social support (all p values <0.001). Adverse life events and criminal history factors were also associated with near-lethal self-harm, especially having a prior prison spell and having been bullied in prison, both of which remained significant in multivariate analyses. The findings support a model of suicidal behaviour in prisoners that incorporates imported vulnerability factors, clinical factors, and prison experiences, and underscores their interaction. Strategies to reduce self-harm and suicide in prisoners should include attention to such factors

    Microsomal Oxidation and Insecticide Metabolism

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    Effects of Ionizing Radiation

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    Ankylosing spondylitis: an autoimmune or autoinflammatory disease?

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    Ankylosing spondylitis (AS) is a chronic inflammatory disorder of unknown aetiology. Unlike other systemic autoimmune diseases, in AS, the innate immune system has a dominant role characterized by aberrant activity of innate and innate-like immune cells, including γδ T cells, group 3 innate lymphoid cells, neutrophils, mucosal-associated invariant T cells and mast cells, at sites predisposed to the disease. The intestine is involved in disease manifestations, as it is at the forefront of the interaction between the mucosal-associated immune cells and the intestinal microbiota. Similarly, biomechanical factors, such as entheseal micro-trauma, might also be involved in the pathogenesis of the articular manifestation of AS, and sentinel immune cells located in the entheses could provide links between local damage, genetic predisposition and the development of chronic inflammation. Although these elements might support the autoinflammatory nature of AS, studies demonstrating the presence of autoantibodies (such as anti-CD74, anti-sclerostin and anti-noggin antibodies) and evidence of activation and clonal expansion of T cell populations support an autoimmune component to the disease. This Review presents the evidence for autoinflammation and the evidence for autoimmunity in AS and, by discussing the pathophysiological factors associated with each, aims to reconcile the two hypotheses.</p
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