COVID-Well: Evaluation of the Implementation of Supported Wellbeing Centres for Hospital Employees during the COVID-19 Pandemic

Supported Wellbeing Centres have been set up in UK hospital trusts in an effort to mitigate the psychological impact of COVID-19 on healthcare workers, although the extent to which these are utilised and the barriers and facilitators to access are not known. The aim of the study was to determine facility usage and gather insight into employee wellbeing and the views of employees towards this provision. The study included (i) 17-week service use monitoring, (ii) employee online survey with measures of wellbeing, job stressfulness, presenteeism, turnover intentions, job satisfaction, and work engagement, as well as barriers and facilitators to accessing the Wellbeing Centres. Over 17 weeks, 14,934 facility visits were recorded across two sites (peak attendance in single week n = 2605). Facilities were highly valued, but the service model was resource intensive with 134 wellbeing buddies supporting the centres in pairs. 819 hospital employees completed an online survey (88% female; 37.7% working in COVID-19 high risk areas; 52.4% frontline workers; 55.2% had accessed a wellbeing centre). There was moderate-to-high job stress (62.9%), low wellbeing (26.1%), presenteeism (68%), and intentions to leave (31.6%). Wellbeing was higher in those that accessed a wellbeing centre. Work engagement and job satisfaction were high. Healthcare organisations are urged to mobilise access to high-quality rest spaces and psychological first aid, but this should be localised and diversified. Strategies to address presenteeism and staff retention should be prioritised, and the high dedication of healthcare workers should be recognised

Covid-well study: Qualitative evaluation of supported wellbeing centres and psychological first aid for healthcare workers during the covid-19 pandemic

Supported wellbeing centres were set up in UK hospital trusts as an early intervention aimed at mitigating the psychological impact of COVID-19 on healthcare workers. These provided high quality rest spaces with peer-to-peer psychological support provided by National Health Service (NHS) staff volunteers called ‘wellbeing buddies’, trained in psychological first aid. The aim of the study was to explore the views of centre visitors and operational staff towards this COVID-19 workforce wellbeing provision. Qualitative semi-structured interviews were undertaken with twenty-four (20F, 4M) employees from an acute hospital trust in the UK. Interviews were digitally recorded and transcribed, data were handled and analysed using thematic analysis. Interviews generated 3 over-arching themes, and 13 sub-themes covering ‘exposure and job roles’, ‘emotional impacts of COVID-19 and ‘the wellbeing centres’. Supported wellbeing centres were viewed as critical for the wellbeing of hospital employees during the first surge of COVID-19 in the UK. Wellbeing initiatives require managerial advocacy and must be inclusive. Job-related barriers to work breaks and accessing staff wellbeing provisions should be addressed. High quality rest spaces and access to peer-to-peer support are seen to benefit individuals, teams, organisations and care quality. Training NHS staff in psychological first aid is a useful approach to supporting the wellbeing of the NHS workforce during and beyond the COVID-19 pandemic

The Lantern Vol. 40, No. 2, Spring 1974

• Response • Roads • Ghost Dance • Natator • Make Believe • An English Sonnet • A Cinquain • Icarus • Alchemy • Pain • Love • Scramblen\u27 Zone • In the Gathering Wind • The Circus • Streams • The Showdown on the Corner of Main Street and Koscuisko Drive!!! • Fandango • Ode to an Orange Orangutan • Nauseahttps://digitalcommons.ursinus.edu/lantern/1104/thumbnail.jp

Synchronous seasonality in the gut microbiota of wild mouse populations

The gut microbiome performs many important functions in mammalian hosts, with community composition shaping its functional role. However, the factors that drive individual microbiota variation in wild animals and to what extent these are predictable or idiosyncratic across populations remains poorly understood. Here, we use a multi-population dataset from a common rodent species (the wood mouse, Apodemus sylvaticus), to test whether a consistent “core” gut microbiota is identifiable in this species, and to what extent the predictors of microbiota variation are consistent across populations. Between 2014 and 2018 we used capture-mark-recapture and 16S rRNA profiling to intensively monitor two wild wood mouse populations and their gut microbiota, as well as characterising the microbiota from a laboratory-housed colony of the same species. Although the microbiota was broadly similar at high taxonomic levels, the two wild populations did not share a single bacterial amplicon sequence variant (ASV), despite being only 50km apart. Meanwhile, the laboratory-housed colony shared many ASVs with one of the wild populations from which it is thought to have been founded decades ago. Despite not sharing any ASVs, the two wild populations shared a phylogenetically more similar microbiota than either did with the colony, and the factors predicting compositional variation in each wild population were remarkably similar. We identified a strong and consistent pattern of seasonal microbiota restructuring that occurred at both sites, in all years, and within individual mice. While the microbiota was highly individualised, some seasonal convergence occurred in late winter/early spring. These findings reveal highly repeatable seasonal gut microbiota dynamics in multiple populations of this species, despite different taxa being involved. This provides a platform for future work to understand the drivers and functional implications of such predictable seasonal microbiome restructuring, including whether it might provide the host with adaptive seasonal phenotypic plasticity

Loss of PTEN expression is associated with IGFBP2 expression, younger age, and late stage in triple-negative breast cancer

© American Society for Clinical Pathology. Objectives: To investigate the association between PTEN loss and IGFBP2 expression in a series of triple-negative breast cancers and to relate this expression to basal cytokeratin expression and clinicopathologic features. Methods: One hundred and one formalin-fixed and paraffin-processed triple-negative breast cancer cases from the University of Malaya Medical Centre were tested immunohistochemically for cytokeratins 5/6 and 14, PTEN, and IGFBP2. The resulting slides were scored for proportion and intensity of staining. Results: Loss of tumor nuclear and cytoplasmic staining for PTEN occurred in 48.3% of cases and was significantly associated with younger age at diagnosis (47 years compared with 57 years in those without PTEN loss; P = .005). Independent predictors of PTEN loss were late stage at presentation ( P = .026), cytokeratin 5/6 positivity ( P = .028), and IGFBP2 expression ( P = .042). High levels of IGFBP2 expression were seen in 32% of cases; an independent predictor of high levels was cytokeratin 14 negativity ( P = .005). PTEN loss and high levels of IGFBP2 expression were associated with poorer survival, but neither of these trends was significant. Conclusions: PTEN loss is a frequent event in triple-negative breast cancers and is significantly associated with younger age at onset of breast cancer, late stage, and IGFBP2 expression

Percussion Convocation

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Correction: Exome Sequencing of Phenotypic Extremes Identifies CAV2 and TMC6 as Interacting Modifiers of Chronic Pseudomonas aeruginosa Infection in Cystic Fibrosis

Discovery of rare or low frequency variants in exome or genome data that are associated with complex traits often will require use of very large sample sizes to achieve adequate statistical power. For a fixed sample size, sequencing of individuals sampled from the tails of a phenotype distribution (i.e., extreme phenotypes design) maximizes power and this approach was recently validated empirically with the discovery of variants in DCTN4 that influence the natural history of P. aeruginosa airway infection in persons with cystic fibrosis (CF; MIM219700). The increasing availability of large exome/genome sequence datasets that serve as proxies for population-based controls affords the opportunity to test an alternative, potentially more powerful and generalizable strategy, in which the frequency of rare variants in a single extreme phenotypic group is compared to a control group (i.e., extreme phenotype vs. control population design). As proof-of-principle, we applied this approach to search for variants associated with risk for age-of-onset of chronic P. aeruginosa airway infection among individuals with CF and identified variants in CAV2 and TMC6 that were significantly associated with group status. These results were validated using a large, prospective, longitudinal CF cohort and confirmed a significant association of a variant in CAV2 with increased age-of-onset of P. aeruginosa airway infection (hazard ratio = 0.48, 95% CI=[0.32, 0.88]) and variants in TMC6 with diminished age-of-onset of P. aeruginosa airway infection (HR = 5.4, 95% CI=[2.2, 13.5]) A strong interaction between CAV2 and TMC6 variants was observed (HR=12.1, 95% CI=[3.8, 39]) for children with the deleterious TMC6 variant and without the CAV2 protective variant. Neither gene showed a significant association using an extreme phenotypes design, and conditions for which the power of an extreme phenotype vs. control population design was greater than that for the extreme phenotypes design were explored

Hypoxia and TGF-β Drive Breast Cancer Bone Metastases through Parallel Signaling Pathways in Tumor Cells and the Bone Microenvironment

BACKGROUND: Most patients with advanced breast cancer develop bone metastases, which cause pain, hypercalcemia, fractures, nerve compression and paralysis. Chemotherapy causes further bone loss, and bone-specific treatments are only palliative. Multiple tumor-secreted factors act on the bone microenvironment to drive a feed-forward cycle of tumor growth. Effective treatment requires inhibiting upstream regulators of groups of prometastatic factors. Two central regulators are hypoxia and transforming growth factor (TGF)- beta. We asked whether hypoxia (via HIF-1alpha) and TGF-beta signaling promote bone metastases independently or synergistically, and we tested molecular versus pharmacological inhibition strategies in an animal model. METHODOLOGY/PRINCIPAL FINDINGS: We analyzed interactions between HIF-1alpha and TGF-beta pathways in MDA-MB-231 breast cancer cells. Only vascular endothelial growth factor (VEGF) and the CXC chemokine receptor 4 (CXCR4), of 16 genes tested, were additively increased by both TGF-beta and hypoxia, with effects on the proximal promoters. We inhibited HIF-1alpha and TGF-beta pathways in tumor cells by shRNA and dominant negative receptor approaches. Inhibition of either pathway decreased bone metastasis, with no further effect of double blockade. We tested pharmacologic inhibitors of the pathways, which target both the tumor and the bone microenvironment. Unlike molecular blockade, combined drug treatment decreased bone metastases more than either alone, with effects on bone to decrease osteoclastic bone resorption and increase osteoblast activity, in addition to actions on tumor cells. CONCLUSIONS/SIGNIFICANCE: Hypoxia and TGF-beta signaling in parallel drive tumor bone metastases and regulate a common set of tumor genes. In contrast, small molecule inhibitors, by acting on both tumor cells and the bone microenvironment, additively decrease tumor burden, while improving skeletal quality. Our studies suggest that inhibitors of HIF-1alpha and TGF-beta may improve treatment of bone metastases and increase survival