An ethnographic study of knowledge sharing across the boundaries between care processes, services and organisations: the contributions to ‘safe’ hospital discharge

Background Hospital discharge is a vulnerable stage in the patient pathway. Research highlights communication failures and the problems of co-ordination as resulting in delayed, poorly timed and unsafe discharges. The complexity of hospital discharge exemplifies the threats to patient safety found ‘between’ care processes and organisations. In developing this perspective, safe discharge is seen as relying upon enhanced knowledge sharing and collaboration between stakeholders, which can mitigate system complexity and promote safety. Aim To identify interventions and practices that support knowledge sharing and collaboration in the processes of discharge planning and care transition. Setting The study was undertaken between 2011 and 2013 in two English health-care systems, each comprising an acute health-care provider, community and primary care providers, local authority social services and social care agencies. The study sites were selected to reflect known variations in local population demographics as well as in the size and composition of the care systems. The study compared the experiences of stroke and hip fracture patients as exemplars of acute care with complex discharge pathways. Design The study involved in-depth ethnographic research in the two sites. This combined (a) over 180 hours of observations of discharge processes and knowledge-sharing activities in various care settings; (b) focused ‘patient tracking’ to trace and understand discharge activities across the entire patient journey; and (c) qualitative interviews with 169 individuals working in health, social and voluntary care sectors. Findings The study reinforces the view of hospital discharge as a complex system involving dynamic and multidirectional patterns of knowledge sharing between multiple groups. The study shows that discharge planning and care transitions develop through a series of linked ‘situations’ or opportunities for knowledge sharing. It also shows variations in these situations, in terms of the range of actors, forms of knowledge shared, and media and resources used, and the wider culture and organisation of discharge. The study also describes the threats to patient safety associated with hospital discharge, as perceived by participants and stakeholders. These related to falls, medicines, infection, clinical procedures, equipment, timing and scheduling of discharge, and communication. Each of these identified risks are analysed and explained with reference to the observed patterns of knowledge sharing to elaborate how variations in knowledge sharing can hinder or promote safe discharge. Conclusions The study supports the view of hospital discharge as a complex system involving tightly coupled and interdependent patterns of interaction between multiple health and social care agencies. Knowledge sharing can help to mitigate system complexity through supporting collaboration and co-ordination. The study suggests four areas of change that might enhance knowledge sharing, reduce system complexity and promote safety. First, knowledge brokers in the form of discharge co-ordinators can facilitate knowledge sharing and co-ordination; second, colocation and functional proximity of stakeholders can support knowledge sharing and mutual appreciation and alignment of divergent practices; third, local cultures should prioritise and value collaboration; and finally, organisational resources, procedures and leadership should be aligned to fostering knowledge sharing and collaborative working. These learning points provide insight for future interventions to enhance discharge planning and care transition. Future research might consider the implementation of interviews to mediate system complexity through fostering enhanced knowledge sharing across occupational and organisational boundaries. Research might also consider in more detail the underlying complexity of both health and social care systems and how opportunities for knowledge sharing might be engendered to promote patient safety in other areas

Decoration of T-independent antigen with ligands for CD22 and Siglec-G can suppress immunity and induce B cell tolerance in vivo

Autoreactive B lymphocytes first encountering self-antigens in peripheral tissues are normally regulated by induction of anergy or apoptosis. According to the “two-signal” model, antigen recognition alone should render B cells tolerant unless T cell help or inflammatory signals such as lipopolysaccharide are provided. However, no such signals seem necessary for responses to T-independent type 2 (TI-2) antigens, which are multimeric antigens lacking T cell epitopes and Toll-like receptor ligands. How then do mature B cells avoid making a TI-2–like response to multimeric self-antigens? We present evidence that TI-2 antigens decorated with ligands of inhibitory sialic acid–binding Ig-like lectins (siglecs) are poorly immunogenic and can induce tolerance to subsequent challenge with immunogenic antigen. Two siglecs, CD22 and Siglec-G, contributed to tolerance induction, preventing plasma cell differentiation or survival. Although mutations in CD22 and its signaling machinery have been associated with dysregulated B cell development and autoantibody production, previous analyses failed to identify a tolerance defect in antigen-specific mutant B cells. Our results support a role for siglecs in B cell self-/nonself-discrimination, namely suppressing responses to self-associated antigens while permitting rapid “missing self”–responses to unsialylated multimeric antigens. The results suggest use of siglec ligand antigen constructs as an approach for inducing tolerance

Dendritic release of neurotransmitters

Release of neuroactive substances by exocytosis from dendrites is surprisingly widespread and is not confined to a particular class of transmitters: it occurs in multiple brain regions, and includes a range of neuropeptides, classical neurotransmitters and signaling molecules such as nitric oxide, carbon monoxide, ATP and arachidonic acid. This review is focused on hypothalamic neuroendocrine cells that release vasopressin and oxytocin and midbrain neurons that release dopamine. For these two model systems, the stimuli, mechanisms and physiological functions of dendritic release have been explored in greater detail than is yet available for other neurons and neuroactive substances

Extreme genome diversity in the hyper-prevalent parasitic eukaryote Blastocystis

Blastocystis is the most prevalent eukaryotic microbe colonizing the human gut, infecting approximately 1 billion individuals worldwide. Although Blastocystis has been linked to intestinal disorders, its pathogenicity remains controversial because most carriers are asymptomatic. Here, the genome sequence of Blastocystis subtype (ST) 1 is presented and compared to previously published sequences for ST4 and ST7. Despite a conserved core of genes, there is unexpected diversity between these STs in terms of their genome sizes, guanine-cytosine (GC) content, intron numbers, and gene content. ST1 has 6,544 protein-coding genes, which is several hundred more than reported for ST4 and ST7. The percentage of proteins unique to each ST ranges from 6.2% to 20.5%, greatly exceeding the differences observed within parasite genera. Orthologous proteins also display extreme divergence in amino acid sequence identity between STs (i.e., 59%–61%median identity), on par with observations of the most distantly related species pairs of parasite genera. The STs also display substantial variation in gene family distributions and sizes, especially for protein kinase and protease gene families, which could reflect differences in virulence. It remains to be seen to what extent these inter-ST differences persist at the intra-ST level. A full 26% of genes in ST1 have stop codons that are created on the mRNA level by a novel polyadenylation mechanism found only in Blastocystis. Reconstructions of pathways and organellar systems revealed that ST1 has a relatively complete membrane-trafficking system and a near-complete meiotic toolkit, possibly indicating a sexual cycle. Unlike some intestinal protistan parasites, Blastocystis ST1 has near-complete de novo pyrimidine, purine, and thiamine biosynthesis pathways and is unique amongst studied stramenopiles in being able to metabolize ?-glucans rather than ?-glucans. It lacks all genes encoding heme-containing cytochrome P450 proteins. Predictions of the mitochondrion-related organelle (MRO) proteome reveal an expanded repertoire of functions, including lipid, cofactor, and vitamin biosynthesis, as well as proteins that may be involved in regulating mitochondrial morphology and MRO/endoplasmic reticulum (ER) interactions. In sharp contrast, genes for peroxisome-associated functions are absent, suggesting Blastocystis STs lack this organelle. Overall, this study provides an important window into the biology of Blastocystis, showcasing significant differences between STs that can guide future experimental investigations into differences in their virulence and clarifying the roles of these organisms in gut health and disease

NOx storage-reduction characteristics of Ba-based lean NOx trap catalysts subjected to simulated road aging

In order to study the effect of washcoat composition on lean NOx trap (LNT) aging characteristics, fully formulated monolithic LNT catalysts containing varying amounts of La-stabilized CeO2 (5 wt% La2O3) or CeO2-ZrO2 (Ce:Zr = 70:30) were subjected to accelerated aging on a bench reactor. Subsequent catalyst evaluation revealed that aging resulted in deterioration of the NOx storage, NOx release and NOx reduction functions, whereas the observation of lean phase NO2 slip for all of the aged catalysts indicated that LNT performance was not limited by the kinetics of NO oxidation. After aging, all of the catalysts showed increased selectivity to NH3 in the temperature range 250–450 °C. TEM, H2 chemisorption, XPS and elemental analysis data revealed two main changes which can explain the degradation in LNT performance. First, residual sulfur in the catalysts, present as BaSO4, decreased catalyst NOx storage capacity. Second, sintering of the precious metals in the washcoat was observed, which can be expected to decrease the rate of NOx reduction. Additionally, sintering is hypothesized to result in segregation of the precious metal and Ba phases, resulting in less efficient NOx spillover from Pt to Ba during NOx adsorption, as well as decreased rates of reductant spillover from Pt to Ba and reverse NOx spillover during catalyst regeneration. Spectacular improvement in LNT durability was observed for catalysts containing CeO2 or CeO2-ZrO2 relative to their non-ceria containing analog. This was attributed to (i) the ability of ceria to participate in NOx storage/reduction as a supplement to the main Ba NOx storage component; (ii) the fact that Pt and CeO2(-ZrO2) are not subject to phase segregation; and (iii) the ability of ceria to trap sulfur, resulting in decreased sulfur accumulation on the Ba component

MOESM2 of Long-term variability in sugarcane bagasse feedstock compositional methods: sources and magnitude of analytical variability

Additional file 2. “R” code used to analyze data file