Tracey Budworth Master\u27s Portfolio

This portfolio contains examples of my work in association with familiarizing myself with the subaltern and working to incorporate the concept of the other into my teaching

The Association Between Health Care Staff Engagement and Patient Safety Outcomes: A Systematic Review and Meta-Analysis

Objectives: Despite decades of research, improving health care safety remains a global priority. Individual studies have demonstrated links between staff engagement and care quality, but until now, any relationship between engagement and patient safety outcomes has been more speculative. This systematic review and meta-analysis therefore assessed this relationship and explored if the way these variables were defined and measured had any differential effect. Methods: After systematic searches of Medline, CINAHL, PsycInfo, Embase, Cochrane Library, and National Institute for Health Research Journals databases, narrative and random-effects meta-analyses were completed, with pooled effect sizes expressed as Pearson r. Results: Fourteen studies met the inclusion criteria, 11 of which were suitable for meta-analysis. Meta-analyses indicated a small but consistent, statistically significant relationship between staff engagement and patient safety (all outcomes; 11 studies; r = 0.22; 95% confidence interval [CI], 0.07 to 0.36; n = 30,490) and 2 patient safety outcome categories: patient safety culture (7 studies;r = 0.22; 95% CI, 0.01 to 0.41; n = 27,857) and errors/adverse events (4 studies;r = −0.20; 95% CI, −0.26 to −0.13; n = 2633). The specific approach to conceptualizing engagement did not affect the strength of the findings. Conclusions: This is the first review to demonstrate a significant relationship between engagement and both safety culture scores and errors/adverse events. Despite a limited and evolving evidence base, we cautiously conclude that increasing staff engagement could be an effective means of enhancing patient safety. Further research is needed to determine causality and clarify the nature of the staff engagement/patient safety relationship at individual and unit/workgroup levels

The relationship between in-vitro endothelial permeability and molecules of the intercellular junction

Changes in endothelial permeability are known to contribute to many pathologies, including inflammation seen in skin irritation. The regulation of permeability has been linked to inter-endothelial junctions, specifically the tight and adherens junctions (TJ and AJ). The functional state of the junction is thought to be associated with numerous factors including cytoskeletal changes and the interactions between junctional components. How these factors interact and respond to inflammatory stimuli is still not fully understood. This project examined two human endothelial cell-lines for use in in-vitro permeability studies, ECV304 and HMEC-1. Changes in permeability along with arrangement of the F-actin cytoskeleton and the adherens junction molecule VE-cadherin were studied in response to a variety of compounds. Macromolecular permeability was assessed by measuring the leakage of fluorescently labelled dextrans of varying molecular weights. The F-actin and VE-cadherin were visualised using immunocytochemical techniques. TEM was undertaken to examine the ultrastructure of the junctions The ECV304 cells, whilst showing an increased permeability to a variety to vaso-active mediators, did not express some of the pertinent junctional molecules of the endothelium and thus are not recommended for use. The basal permeability of the HMEC-l cell-line was shown to act in predictable fashion, giving comparable permeability coefficients to other endothelial cells. The increase in permeability following exposure to A23187, CAPB, EGTA and PMA was shown to correlate to an altered expression of VE-cadherin and F-actin. These observations were furthered using histamine, where a quantifiable change in the levels of continuous and stitch VE-cadherin staining was demonstrated. The permeability response to histamine occurred much later than the VE-cadherin and F-actin changes. This could be due to methodology and/or the cells lack of TJs. The apparent lack of mature AJs was approached by exposing the cultures to cAMP-raising media. This significantly reduced the basal permeability and increased the expression of AJ components, apart from β-catenin, at the cell-cell contacts. Indeed α-catenin was redistributed from the triton-soluble fraction of the cells to the triton-insoluble fraction, which is proposed to contain the junctional components. These results demonstrate additional information on the role that the adherens junction molecules play in endothelial permeability and characterise the HMEC-1 cell-line for further use in this field

The relationship between in-vitro endothelial permeability and molecules of the intercellular junction

Changes in endothelial permeability are known to contribute to many pathologies, including inflammation seen in skin irritation. The regulation of permeability has been linked to inter-endothelial junctions, specifically the tight and adherens junctions (TJ and AJ). The functional state of the junction is thought to be associated with numerous factors including cytoskeletal changes and the interactions between junctional components. How these factors interact and respond to inflammatory stimuli is still not fully understood. This project examined two human endothelial cell-lines for use in in-vitro permeability studies, ECV304 and HMEC-1. Changes in permeability along with arrangement of the F-actin cytoskeleton and the adherens junction molecule VE-cadherin were studied in response to a variety of compounds. Macromolecular permeability was assessed by measuring the leakage of fluorescently labelled dextrans of varying molecular weights. The F-actin and VE-cadherin were visualised using immunocytochemical techniques. TEM was undertaken to examine the ultrastructure of the junctions The ECV304 cells, whilst showing an increased permeability to a variety to vaso-active mediators, did not express some of the pertinent junctional molecules of the endothelium and thus are not recommended for use. The basal permeability of the HMEC-l cell-line was shown to act in predictable fashion, giving comparable permeability coefficients to other endothelial cells. The increase in permeability following exposure to A23187, CAPB, EGTA and PMA was shown to correlate to an altered expression of VE-cadherin and F-actin. These observations were furthered using histamine, where a quantifiable change in the levels of continuous and stitch VE-cadherin staining was demonstrated. The permeability response to histamine occurred much later than the VE-cadherin and F-actin changes. This could be due to methodology and/or the cells lack of TJs. The apparent lack of mature AJs was approached by exposing the cultures to cAMP-raising media. This significantly reduced the basal permeability and increased the expression of AJ components, apart from β-catenin, at the cell-cell contacts. Indeed α-catenin was redistributed from the triton-soluble fraction of the cells to the triton-insoluble fraction, which is proposed to contain the junctional components. These results demonstrate additional information on the role that the adherens junction molecules play in endothelial permeability and characterise the HMEC-1 cell-line for further use in this field

Can we prepare healthcare professionals and students for involvement in stressful healthcare events? A mixed-methods evaluation of a resilience training intervention

Background Healthcare professionals are experiencing unprecedented levels of occupational stress and burnout. Higher stress and burnout in health professionals is linked with the delivery of poorer quality, less safe patient care across healthcare settings. In order to understand how we can better support healthcare professionals in the workplace, this study evaluated a tailored resilience coaching intervention comprising a workshop and one-to-one coaching session addressing the intrinsic challenges of healthcare work in health professionals and students. Methods The evaluation used an uncontrolled before-and-after design with four data-collection time points: baseline (T1); after the workshop (T2); after the coaching session (T3) and four-to-six weeks post-baseline (T4). Quantitative outcome measures were Confidence in Coping with Adverse Events (‘Confidence’), a Knowledge assessment (‘Knowledge’) and Resilience. At T4, qualitative interviews were also conducted with a subset of participants exploring participant experiences and perceptions of the intervention. Results We recruited 66 participants, retaining 62 (93.9%) at T2, 47 (71.2%) at T3, and 33 (50%) at T4. Compared with baseline, Confidence was significantly higher post-intervention: T2 (unadj. β = 2.43, 95% CI 2.08–2.79, d = 1.55, p < .001), T3 (unadj. β = 2.81, 95% CI 2.42–3.21, d = 1.71, p < .001) and T4 (unadj. β = 2.75, 95% CI 2.31–3.19, d = 1.52, p < .001). Knowledge increased significantly post-intervention (T2 unadj. β = 1.14, 95% CI 0.82–1.46, d = 0.86, p < .001). Compared with baseline, resilience was also higher post-intervention (T3 unadj. β = 2.77, 95% CI 1.82–3.73, d = 0.90, p < .001 and T4 unadj. β = 2.54, 95% CI 1.45–3.62, d = 0.65, p < .001). The qualitative findings identified four themes. The first addressed the ‘tension between mandatory and voluntary delivery’, suggesting that resilience is a mandatory skillset but it may not be effective to make the training a mandatory requirement. The second, the ‘importance of experience and reference points for learning’, suggested the intervention was more appropriate for qualified staff than students. The third suggested participants valued the ‘peer learning and engagement’ they gained in the interactive group workshop. The fourth, ‘opportunities to tailor learning’, suggested the coaching session was an opportunity to personalise the workshop material. Conclusions We found preliminary evidence that the intervention was well received and effective, but further research using a randomised controlled design will be necessary to confirm this

Crosstalk between MSH2–MSH3 and polβ promotes trinucleotide repeat expansion during base excision repair

Studies in knockout mice provide evidence that MSH2–MSH3 and the BER machinery promote trinucleotide repeat (TNR) expansion, yet how these two different repair pathways cause the mutation is unknown. Here we report the first molecular crosstalk mechanism, in which MSH2–MSH3 is used as a component of the BER machinery to cause expansion. On its own, pol β fails to copy TNRs during DNA synthesis, and bypasses them on the template strand to cause deletion. Remarkably, MSH2–MSH3 not only stimulates pol β to copy through the repeats but also enhances formation of the flap precursor for expansion. Our results provide direct evidence that MMR and BER, operating together, form a novel hybrid pathway that changes the outcome of TNR instability from deletion to expansion during the removal of oxidized bases. We propose that cells implement crosstalk strategies and share machinery when a canonical pathway is ineffective in removing a difficult lesion