Delegation and supervision of health care assistants’ work in the daily management of uncertainty and the unexpected in clinical practice: invisible learning among newly qualified nurses

The invisibility of nursing work has been discussed in the international literature but not in relation to learning clinical skills. Evans and Guile’s (2012) theory of recontextualisation is used to explore the ways in which invisible or unplanned and unrecognised learning takes place as newly qualified nurses learn to delegate to and supervise the work of the health care assistant. In the British context, delegation and supervision are thought of as skills which are learnt ‘on the job’. We suggest that learning ‘on-the-job’ is the invisible construction of knowledge in clinical practice and that delegation is a particularly telling area of nursing practice which illustrates invisible learning. Using an ethnographic case study approach in three hospital sites in England from 2011-2014, we undertook participant observation, interviews with newly qualified nurses, ward managers and health care assistants. We discuss the invisible ways newly qualified nurses learn in the practice environment and present the invisible steps to learning which encompass the embodied, affective and social, as much as the cognitive components to learning. We argue that there is a need for greater understanding of the ‘invisible learning’ which occurs as newly qualified nurses learn to delegate and supervise

‘What’s it like to have ME?’ The discursive construction of ME in computer-mediated communication and face-to-face interaction

ME/CFS (chronic fatigue syndrome) is a debilitating illness for which no cause or medical tests have been identified. Debates over its nature have generated interest from qualitative researchers. However, participants are difficult to recruit because of the nature of their condition. Therefore, this study explores the utility of the internet as a means of eliciting accounts. We analyse data from focus groups and the internet in order to ascertain the extent to which previous research findings apply to the internet domain. Interviews were conducted among 49 members of internet (38 chatline, 11 personal) and 7 members of two face-to-face support groups. Discourse analysis of descriptions and accounts of ME/CFS revealed similar devices and interactional concerns in both internet and face-to-face communication. Participants constructed their condition as serious, enigmatic and not psychological. These functioned to deflect problematic assumptions about ME/CFS and to manage their accountability for the illness and its effects

Between roost contact is essential for maintenance of European bat lyssavirus type-2 in Myotis daubentonii bat reservoir: 'The Swarming Hypothesis'

Many high-consequence human and animal pathogens persist in wildlife reservoirs. An understanding of the dynamics of these pathogens in their reservoir hosts is crucial to inform the risk of spill-over events, yet our understanding of these dynamics is frequently insufficient. Viral persistence in a wild bat population was investigated by combining empirical data and in-silico analyses to test hypotheses on mechanisms for viral persistence. A fatal zoonotic virus, European Bat lyssavirus type 2 (EBLV-2), in Daubenton's bats (Myotis daubentonii) was used as a model system. A total of 1839 M. daubentonii were sampled for evidence of virus exposure and excretion during a prospective nine year serial cross-sectional survey. Multivariable statistical models demonstrated age-related differences in seroprevalence, with significant variation in seropositivity over time and among roosts. An Approximate Bayesian Computation approach was used to model the infection dynamics incorporating the known host ecology. The results demonstrate that EBLV-2 is endemic in the study population, and suggest that mixing between roosts during seasonal swarming events is necessary to maintain EBLV-2 in the population. These findings contribute to understanding how bat viruses can persist despite low prevalence of infection, and why infection is constrained to certain bat species in multispecies roosts and ecosystems

Call for emergency action to limit global temperature increases, restore biodiversity, and protect health

No Abstrac

Assessing and Strengthening African Universities' Capacity for Doctoral Programmes

Imelda Bates and colleagues developed and validated an evidence-based tool for evaluating doctoral programmes in African universities

Call for emergency action to limit global temperature increases, restore biodiversity, and protect health Wealthy nations must do much more, much faster

The UN General Assembly in September 2021 will bring countries together at a critical time for marshalling collective action to tackle the global environmental crisis. They will meet again at the biodiversity summit in Kunming, China, and the climate conference (COP26) in Glasgow, UK. Ahead of these pivotal meetings, we—the editors of health journals worldwide—call for urgent action to keep average global temperature increases below 1.5 °C, halt the destruction of nature, and protect health

Antibody-mediated disruption of the interaction between PCSK9 and the low-density lipoprotein receptor

PCSK9 (proprotein convertase subtilisin/kexin type 9) promotes degradation of the LDLR [LDL (low-density lipoprotein) receptor] through an as-yet-undefined mechanism, leading to a reduction in cellular LDLc (LDL-cholesterol) and a concomitant increase in serum LDLc. Central to the function of PCSK9 is a direct protein–protein interaction formed with the LDLR. In the present study, we investigated a strategy to modulate LDL uptake by blocking this interaction using specific antibodies directed against PCSK9. Studies using surface plasmon resonance demonstrated that direct binding of PCSK9 to the LDLR could be abolished with three different anti-PCSK9 antibodies. Two of these antibodies were raised against peptide epitopes in a region of the catalytic domain of PCSK9 that is involved in the interaction with the LDLR. Such antibodies restored LDL uptake in HepG2 cells treated with exogenous PCSK9 and in HepG2 cells engineered to overexpress recombinant PCSK9. This latter observation indicates that antibodies blocking the PCSK9–LDLR interaction can inhibit the action of PCSK9 produced endogenously in a cell-based system. These antibodies also disrupted the higher-affinity interaction between the natural gain-of-function mutant of PCSK9, D374Y, and the LDLR in both the cell-free and cell-based assays. These data indicate that antibodies targeting PCSK9 can reverse the PCSK9-mediated modulation of cell-surface LDLRs