Social Workers’ Philosophical Attitudes Towards Harm Reduction Services in Housing First Organizations

AbstractOver the past three decades, harm reduction has gradually become more prevalent among social workers and is now viewed as an instrumental approach in treating people with drug and alcohol problems. Although there have been several studies that described how harm reduction approaches were applied in Housing First (HF) settings, there are few studies that have described social workers’ perspectives of their philosophical attitudes regarding harm reduction in HF settings. The purpose of this study was to understand social workers’ perspectives of their philosophical attitudes toward harm reduction services and how those attitudes were apparent in their interactions with substance-using HF clients. A generic qualitative research design was employed with a purposive sample of six social workers with work experience in HF settings. Data were collected through individual, semistructured interviews comprised of 10 interview questions. Thematic analysis revealed three emergent themes in the data set: support of HF and a positive philosophical attitude about harm reduction in HF settings, programmatic challenges exist in HF settings, and HF programs align with the concept of social justice. The findings from this study support positive social change by identifying micro, mezzo, and macro implications that could be used to support the provision of harm reduction services to clients living in HF programs

Social Workers’ Philosophical Attitudes Towards Harm Reduction Services in Housing First Organizations

AbstractOver the past three decades, harm reduction has gradually become more prevalent among social workers and is now viewed as an instrumental approach in treating people with drug and alcohol problems. Although there have been several studies that described how harm reduction approaches were applied in Housing First (HF) settings, there are few studies that have described social workers’ perspectives of their philosophical attitudes regarding harm reduction in HF settings. The purpose of this study was to understand social workers’ perspectives of their philosophical attitudes toward harm reduction services and how those attitudes were apparent in their interactions with substance-using HF clients. A generic qualitative research design was employed with a purposive sample of six social workers with work experience in HF settings. Data were collected through individual, semistructured interviews comprised of 10 interview questions. Thematic analysis revealed three emergent themes in the data set: support of HF and a positive philosophical attitude about harm reduction in HF settings, programmatic challenges exist in HF settings, and HF programs align with the concept of social justice. The findings from this study support positive social change by identifying micro, mezzo, and macro implications that could be used to support the provision of harm reduction services to clients living in HF programs

Social Workers’ Philosophical Attitudes Towards Harm Reduction Services in Housing First Organizations

AbstractOver the past three decades, harm reduction has gradually become more prevalent among social workers and is now viewed as an instrumental approach in treating people with drug and alcohol problems. Although there have been several studies that described how harm reduction approaches were applied in Housing First (HF) settings, there are few studies that have described social workers’ perspectives of their philosophical attitudes regarding harm reduction in HF settings. The purpose of this study was to understand social workers’ perspectives of their philosophical attitudes toward harm reduction services and how those attitudes were apparent in their interactions with substance-using HF clients. A generic qualitative research design was employed with a purposive sample of six social workers with work experience in HF settings. Data were collected through individual, semistructured interviews comprised of 10 interview questions. Thematic analysis revealed three emergent themes in the data set: support of HF and a positive philosophical attitude about harm reduction in HF settings, programmatic challenges exist in HF settings, and HF programs align with the concept of social justice. The findings from this study support positive social change by identifying micro, mezzo, and macro implications that could be used to support the provision of harm reduction services to clients living in HF programs

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease