42 research outputs found

    Examining individual social status using the MacArthur Scale of Subjective Social Status: : Findings from the Born in Bradford study

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    Subjective social status is how a person perceives their social class relative to other people and has frequently been associated with people's health and well-being. A frequently used measure of subjective social status is the MacArthur Scale of Subjective Social Status that depicts social status as a 10 rung ladder, asking individuals to rank themselves on this ladder relative to other people, either in their local neighbourhood or wider society. The Born in Bradford's Better Start birth cohort study aims to understand the lives, relationships, wellbeing, and social and economic circumstances of pregnant women and their children in three inner city areas of Bradford, UK. Pregnant mothers were asked to report their subjective social status, using the MacArthur subjective social status scales, comparing themselves to other people in their local neighbourhood and in England as a whole. This paper explores the characteristics of the women who gave responses, examines associations between the MacArthur subjective social status measures and other subjective and objective measures and looks specifically at the characteristics of women who reported either very low or very high subjective social status. On average, women reported that they had a higher social status compared to others within their local neighbourhood (mean ladder rung = 6) and, although participants were from areas of Bradford with very high levels of deprivation, 23% placed themselves on the top three rungs, 8–10. Respondents reported that they had an average social status when comparing themselves to people in all of England (mean ladder rung = 5) and 13% placed themselves on the top rungs 8–10. These findings raise important questions about the interpretation of the MacArthur scale of subjective social status

    Pathogenesis of HIV-associated sensory neuropathy: evidence from in vivo and in vitro experimental models

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    HIV-associated sensory neuropathy (HIV-SN) is a frequent neurological complication of HIV infection and its treatment with some antiretroviral drugs. We review the pathogenesis of the viral- and drug-induced causes of the neuropathy, and its primary symptom, pain, based on evidence from in vivo and in vitro models of HIV-SN. Viral coat proteins mediate nerve fibre damage and hypernociception through direct and indirect mechanisms. Direct interactions between viral proteins and nerve fibres dominate axonal pathology, while somal pathology is dominated by indirect mechanisms that occur secondary to virus-mediated activation of glia and macrophage infiltration into the dorsal root ganglia. The treatment-induced neuropathy and resulting hypernociception arise primarily from drug-induced mitochondrial dysfunction, but the sequence of events initiated by the mitochondrial dysfunction that leads to the nerve fibre damage and dysfunction are still unclear. Overall, the models that have been developed to study the pathogenesis of HIV-SN, and hypernociception associated with the neuropathy, are reasonable models and have provided useful insights into the pathogenesis of HIV-SN. As new models are developed they may ultimately lead to identification of therapeutic targets for the prevention or treatment of this common neurological complication of HIV infection

    Vaccinia virus gene F3L encodes an intracellular protein that affects the innate immune response

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    The Vaccinia virus BTB/kelch protein F3 has been characterized and its effects on virus replication in vitro and virus virulence in vivo have been determined. The loss of the F3L gene had no effect on virus growth, plaque phenotype or cytopathic effect in cell culture under the conditions tested. However, the virulence of a virus lacking F3L in an intradermal model was reduced compared with controls, and this was demonstrated by a significantly smaller lesion and alterations to the innate immune response to infection. The predicted molecular mass of the F3 protein is 56 kDa; however, immunoblotting of infected cell lysates using an antibody directed against recombinant F3 revealed two proteins of estimated sizes 37 and 25 kDa

    A pilot validation of a modified Illness Perceptions Questionnaire designed to predict response to cognitive therapy for psychosis

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    Background and objectives: Clinical responsiveness to cognitive behavioural therapy for psychosis (CBTp) varies. Recent research has demonstrated that illness perceptions predict active engagement in therapy, and, thereby, better outcomes. In this study, we aimed to investigate the psychometric properties of a modification of the Illness Perceptions Questionnaire (M-IPQ) designed to predict response following CBTp. Methods: Fifty-six participants with persistent, distressing delusions completed the M-IPQ; forty before a brief CBT intervention targeting persecutory ideation and sixteen before and after a control condition. Additional predictors of outcome (delusional conviction, symptom severity and belief inflexibility) were assessed at baseline. Outcomes were assessed at baseline and at follow-up four to eight weeks later. Results: The M-IPQ comprised two factors measuring problem duration and therapy-specific perceptions of Cure/Control. Associated subscales, formed by summing the relevant items for each factor, were reliable in their structure. The Cure/Control subscale was also reliable over time; showed convergent validity with other predictors of outcome; predicted therapy outcomes; and differentially predicted treatment effects. Limitations: We measured outcome without an associated measure of engagement, in a small sample. Findings are consistent with hypothesis and existing research, but require replication in a larger, purposively recruited sample. Conclusions: The Cure/Control subscale of the M-IPQ shows promise as a predictor of response to therapy. Specifically targeting these illness perceptions in the early stages of cognitive behavioural therapy may improve engagement and, consequently, outcomes

    Psychological characteristics of religious delusions

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    Purpose Religious delusions are common and are considered to be particularly difficult to treat. In this study we investigated what psychological processes may underlie the reported treatment resistance. In particular, we focused on the perceptual, cognitive, affective and behavioural mechanisms held to maintain delusions in cognitive models of psychosis, as these form the key treatment targets in cognitive behavioural therapy. We compared religious delusions to delusions with other content. Methods Comprehensive measures of symptoms and psychological processes were completed by 383 adult participants with delusions and a schizophrenia spectrum diagnosis, drawn from two large studies of cognitive behavioural therapy for psychosis. Results Binary logistic regression showed that religious delusions were associated with higher levels of grandiosity (OR 7.5; 95 % CI 3.9–14.1), passivity experiences, having internal evidence for their delusion (anomalous experiences or mood states), and being willing to consider alternatives to their delusion (95 % CI for ORs 1.1–8.6). Levels of negative symptoms were lower. No differences were found in delusional conviction, insight or attitudes towards treatment. Conclusions Levels of positive symptoms, particularly anomalous experiences and grandiosity, were high, and may contribute to symptom persistence. However, contrary to previous reports, we found no evidence that people with religious delusions would be less likely to engage in any form of help. Higher levels of flexibility may make them particularly amenable to cognitive behavioural approaches, but particular care should be taken to preserve self-esteem and valued aspects of beliefs and experiences

    Quantitative analysis of MicroRNAs in vaccinia virus infection reveals diversity in their susceptibility to modification and suppression

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    Vaccinia virus (VACV) is a large cytoplasmic DNA virus that causes dramatic alterations to many cellular pathways including microRNA biogenesis. The virus encodes a poly(A) polymerase which was previously shown to add poly(A) tails to the 3' end of cellular miRNAs, resulting in their degradation by 24 hours post infection (hpi). Here we used small RNA sequencing to quantify the impact of VACV infection on cellular miRNAs in human cells at both early (6 h) and late (24 h) times post infection. A detailed quantitative analysis of individual miRNAs revealed marked diversity in the extent of their modification and relative change in abundance during infection. Some miRNAs became highly modified (e.g. miR-29a-3p, miR-27b-3p) whereas others appeared resistant (e.g. miR-16-5p). Furthermore, miRNAs that were highly tailed at 6 hpi were not necessarily among the most reduced at 24 hpi. These results suggest that intrinsic features of human cellular miRNAs cause them to be differentially polyadenylated and altered in abundance during VACV infection. We also demonstrate that intermediate and late VACV gene expression are required for optimal repression of some miRNAs including miR-27-3p. Overall this work reveals complex and varied consequences of VACV infection on host miRNAs and identifies miRNAs which are largely resistant to VACV-induced polyadenylation and are therefore present at functional levels during the initial stages of infection and replication
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