2 resultados para Five-factor model

em QSpace: Queen's University - Canada


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OBJECTIVES: (1) Describe the population of mentally ill offenders over whom Ontario Review Board (ORB) held jurisdiction. (2) Assess the influences of psychopathology and criminal factors on criminal career. METHOD: This study was a retrospective case series design that reviewed all offenders who were court ordered for psychiatric evaluation at Mental Health Services Site of Providence Care in Kingston, Ontario from 1993 to 2007 (N=347). Eighty five subjects were found not criminally responsible on the account of mental disorder and were included in statistical analysis (n=85). Bivariate associations between five key variables and two outcome variables, seriousness of crime and recidivism, were examined. Logistic regressions were conducted to test the role of the predictor variables on the outcome variables. RESULTS: Age and change in principal psychiatric diagnosis over time were shown to be associated with seriousness of crime. Timing of psychiatric onset, early signs of deviance and change in diagnosis were shown to be associated with recidivism. On the whole, study population did not markedly vary in their distribution of variables by the outcome variables. Regression model included timing of psychiatric onset; psychiatric history; existence of criminal associate; child abuse history; and early signs of deviance. Recidivism was shown to be predicted by early signs of deviance (OR=8.154, p<0.05). Existence of criminal associates was shown to have substantial values of odds ratio at marginal significance (OR=7.577, p=0.13). CONCLUSION: Seriousness of crime is a complex factor that could not be sufficiently predicted by any one or combinations of study variables. Recidivism is better predicted by criminality factors than psychopathology. In the future, an exploratory analysis that more broadly examines the psychopathology and criminal factors in Canadian forensic population is needed. Findings from this study have important clinical and legal implications.

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Endometriosis affects 5-10% of women and is characterized by the growth of endometrial tissue outside of the uterus. Treatment for endometriosis primarily focuses on symptom relief, is short term with severe side effects and often leads to recurrence of the condition. Establishing new blood supply is a fundamental requirement for endometriosis lesions growth. This has led to the idea that antiangiogenic therapy may be a successful approach for inhibiting endometriosis. Recent evidence indicates that endothelial progenitor cells (EPCs) contribute to neoangiogenesis of endometriotic lesions. These EPCs are recruited to the lesion site by stromal cell-derived factor-1 (SDF-1). We hypothesize that SDF-1 is central to the neoangiogenesis and survival of endometriotic lesions and that administration of SDF-1 blocking antibody will inhibit lesion growth by inhibiting angiogenesis in a murine model of endometriosis. Immunohistochemistry for SDF-1 and CD34 was performed on human endometriosis and normal endometrial samples. Quantification of SDF-1 and EPCs was performed in the blood of endometriosis patients and controls using ELISA and flow cytometry, respectively. A new mouse model of endometriosis was developed using BALB/c-Rag2-/-/IL2rg-/- mice to investigate role of SDF-1 in neoangiogenesis. Either SDF-1 blocking antibody or an isotype control was administered on a weekly basis for four weeks. Weekly samples of peripheral blood from mice were analyzed for SDF-1, other cytokines of interest and EPCs. Mice were euthanized at seven weeks to observe lesion growth and blood vessel development. Our results indicate overabundance of SDF-1 and CD34+ progenitor cells in human endometriotic lesions compared to eutopic endometrium. In the mouse model, SDF-1 and circulating EPC levels decreased from pre-treatment levels after one week, and remained constant over the course of the treatment in both SDF-1 blocking antibody and isotype control groups. In the SDF-1 blocking group, reduced vascularity of lesions, identified by immunofluorescence staining for CD31, was revealed compared to isotype controls. These findings suggest that SDF-1 may be responsible for CD34+ progenitor cell recruitment to the neoangiogenic sites in endometriosis. Blocking of SDF-1 reduces neovascularization of human endometriotic lesions in a mouse model. Further studies on blocking SDF-1 in combination with other antiangiogenic agents are needed.