Supporting bereaved parents : A phenomenological study of a telephone intervention programme in a paediatric oncology unit

Aims and objectives. This study sought to discover bereaved parents' perspectives and experiences of a nurse-led, ward-based, telephone support programme in a children's oncology unit. Background. Parental grief is especially intense and long-lasting, and many parents can experience serious psychological problems. The oncology team learned that some parents felt 'forgotten' or 'abandoned' following their child's death and addressed this concern by initiating and subsequently evaluating a telephone bereavement support programme. Design. An interpretive phenomenological investigation of the experiences of six parents who participated in the programme. Methods. Parents shared their experiences and perceptions of the programme in individual interviews. Interpretive phenomenology and thematic analysis guided the interviews' interpretation to ascertain both the parents' experiences of the programme and their understandings of everyday clinical terms such as 'support' or 'reassurance'. Results. Parents found the programme supportive, especially valuing ongoing contact with a nurse who 'knew them'. Telephone contact was preferred to visiting the hospital, which brought back painful memories. Calls were important elements in helping parents create meaning and memory around their deceased child. Conclusions. Regular telephone contact over an agreed period from a familiar member of the child's treating team can create a more positive and supportive bereavement experience for parents in the year following their child's death. The specific findings are discussed in the context of the death of a child as a crisis of meaning. Relevance to clinical practice. Clinical nurses are ideally placed to use existing close relationships to extend care and support to bereaved parents. This study shows how nurses can identify service gaps, work with interdisciplinary team colleagues to initiate appropriate actions and participate in the essential evaluation subsequently required. © 2012 Blackwell Publishing Ltd

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