3 research outputs found

    Exploring the Differences Between Domestic Homicide and Homicide-Suicide: Implications for Risk Assessment and Safety Planning

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    Domestic homicide, the killing of an individual by their current or former intimate partner, is a tragic and pervasive event. Research supports the finding that a history of domestic violence within a relationship acts as a strong predictor of domestic homicide (DH) and domestic homicide-suicide (DHS). At present, there is limited research that examines patterns in risk factors used to distinguish perpetrators of domestic homicide from domestic homicide-suicide. The present study aims to differentiate perpetrators of domestic homicide and domestic homicide-suicide according to prevalent risk factors and case characteristics. In this paper, case reports were examined from the Domestic Homicide Death Review Committee database that has been developed in collaboration with the Coroner’s Office in Ontario. A multivariate analysis using demographic information and identified risk factors within the cases was conducted in order to explore key differences between the perpetrators. The study supports the development of more refined risk assessment and risk management strategies in order to prevent deaths in similar circumstances from occurring in the future

    Genetic mechanisms of critical illness in COVID-19.

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    Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice
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