Prompt identification of struggling candidates in near peer-led basic life support training: piloting an online performance scoring system.

BACKGROUND: Bristol Medical School has adopted a near peer-led teaching approach to deliver Basic Life Support training to first year undergraduate medical students. Challenges arose when trying to identify early in the course which candidates were struggling with their learning, in sessions delivered to large cohorts. We developed and piloted a novel, online performance scoring system to better track and highlight candidate progress. METHODS: During this pilot, a 10-point scale was used to evaluate candidate performance at six time-points during their training. The scores were collated and entered on an anonymised secure spreadsheet, which was conditionally formatted to provide a visual representation of the score. A One-Way ANOVA was performed on the scores and trends analysed during each course to review candidate trajectory. Descriptive statistics were assessed. Values are presented as mean scores with standard deviation (x̄±SD). RESULTS: A significant linear trend was demonstrated (P < 0.001) for the progression of candidates over the course. The average session score increased from 4.61 ± 1.78 at the start to 7.92 ± 1.22 at the end of the final session. A threshold of less than 1SD below the mean was used to identify struggling candidates at any of the six given timepoints. This threshold enabled efficient highlighting of struggling candidates in real time. CONCLUSIONS: Although the system will be subject to further validation, our pilot has shown the use of a simple 10-point scoring system in combination with a visual representation of performance helps to identify struggling candidates earlier across large cohorts of students undertaking skills training such as Basic Life Support. This early identification enables effective and efficient remedial support.

A webinar series to educate applicants about the UK academic foundation programme: a longitudinal cross-sectional study.

BACKGROUND: The UK academic foundation programme (AFP) is a competitive programme for medical graduates and forms the initial stage of the integrated clinical academic pathway. The application is complex and targeted education is beneficial. As online technologies improve, virtual medical education is becoming more common. Currently, webinar education, particularly that of webinar series, are poorly evidenced. An online course was created to investigate the acceptability and effectiveness of webinars for medical education. METHODS: A six-part, one-hour sessional webinar course was developed following a focus group with academic foundation doctors. A pre- and post-course cross-sectional questionnaire study evaluated participant demographics, webinar opinion and self-rated understanding of the AFP via Google Form (Google, USA). Where applicable a five-point Likert scale (1-Strongly disagree to 5-strongly agree) was utilised and analysis using non-parametric paired statistical analysis. RESULTS: Medical students (n=303) from 35 UK universities completed the pre-course questionnaire. Most students had not received targeted education on the AFP. They rated webinars useful for education (mean=4.2 s.d. 0.7). After the course, participants (n=66) expressed it was significantly convenient (mean=4.7), effective (mean=4.7) and suitably interactive (mean=4.4) (p<0.001 compared to neutral). Participants preferred short sessions over multiple days to the concept of a full-day event (mean=4.6 vs 3.1, p<0.001). Paired analysis of participants completing both forms (n=47) demonstrates a significant increase in self-rated understanding of AFP content, portfolio building, application process, acute clinical scenarios, interview technique and overall confidence in acquiring an AFP post (p<0.001). Follow-up identified 43 participants who completed the course were successful in their AFP application. This represents 7.8% of all successful AFP applicants in 2021. CONCLUSIONS: This study evidences an accessible and effective webinar series for AFP education. Comprehensive webinar courses for similar topics and demographics may provide valuable utility in the provision of future medical education. TRIAL REGISTRATION: Ethics requirements were waived for this study by Bristol University Ethics Committee. All participants in this study consented for anonymous use of their data. As such the trial is not registered.

IGFBP-1 expression is reduced in human type 2 diabetic glomeruli and modulates ß1-integrin/FAK signalling in human podocytes.

AIMS/HYPOTHESIS: Podocyte loss or injury is one of the earliest features observed in the pathogenesis of diabetic kidney disease (DKD), which is the leading cause of end-stage renal failure worldwide. Dysfunction in the IGF axis, including in IGF binding proteins (IGFBPs), is associated with DKD, particularly in the early stages of disease progression. The aim of this study was to investigate the potential roles of IGFBPs in the development of type 2 DKD, focusing on podocytes. METHODS: IGFBP expression was analysed in the Pima DKD cohort, alongside data from the Nephroseq database, and in ex vivo human glomeruli. Conditionally immortalised human podocytes and glomerular endothelial cells were studied in vitro, where IGFBP-1 expression was analysed using quantitative PCR and ELISAs. Cell responses to IGFBPs were investigated using migration, cell survival and adhesion assays; electrical cell-substrate impedance sensing; western blotting; and high-content automated imaging. RESULTS: Data from the Pima DKD cohort and from the Nephroseq database demonstrated a significant reduction in glomerular IGFBP-1 in the early stages of human type 2 DKD. In the glomerulus, IGFBP-1 was predominantly expressed in podocytes and controlled by phosphoinositide 3-kinase (PI3K)-forkhead box O1 (FoxO1) activity. In vitro, IGFBP-1 signalled to podocytes via ß1-integrins, resulting in increased phosphorylation of focal-adhesion kinase (FAK), increasing podocyte motility, adhesion, electrical resistance across the adhesive cell layer and cell viability. CONCLUSIONS/INTERPRETATION: This work identifies a novel role for IGFBP-1 in the regulation of podocyte function and that the glomerular expression of IGFBP-1 is reduced in the early stages of type 2 DKD, via reduced FoxO1 activity. Thus, we hypothesise that strategies to maintain glomerular IGFBP-1 levels may be beneficial in maintaining podocyte function early in DKD.

Prolonged exposure of mouse and human podocytes to insulin induces insulin resistance through lysosomal and proteasomal degradation of the insulin receptor.

AIMS/HYPOTHESIS: Podocytes are insulin-responsive cells of the glomerular filtration barrier and are key in preventing albuminuria, a hallmark feature of diabetic nephropathy. While there is evidence that a loss of insulin signalling to podocytes is detrimental, the molecular mechanisms underpinning the development of podocyte insulin resistance in diabetes remain unclear. Thus, we aimed to further investigate podocyte insulin responses early in the context of diabetic nephropathy. METHODS: Conditionally immortalised human and mouse podocyte cell lines and glomeruli isolated from db/db DBA/2J mice were studied. Podocyte insulin responses were investigated with western blotting, cellular glucose uptake assays and automated fluorescent imaging of the actin cytoskeleton. Quantitative (q)RT-PCR was employed to investigate changes in mRNA. Human cell lines stably overproducing the insulin receptor (IR) and nephrin were also generated, using lentiviral constructs. RESULTS: Podocytes exposed to a diabetic environment (high glucose, high insulin and the proinflammatory cytokines TNF-α and IL-6) become insulin resistant with respect to glucose uptake and activation of phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signalling. These podocytes lose expression of the IR as a direct consequence of prolonged exposure to high insulin concentrations, which causes an increase in IR protein degradation via a proteasome-dependent and bafilomycin-sensitive pathway. Reintroducing the IR into insulin-resistant human podocytes rescues upstream phosphorylation events, but not glucose uptake. Stable expression of nephrin is also required for the insulin-stimulated glucose uptake response in podocytes and for efficient insulin-stimulated remodelling of the actin cytoskeleton. CONCLUSIONS/INTERPRETATION: Together, these results suggest that IR degradation, caused by high levels of insulin, drives early podocyte insulin resistance, and that both the IR and nephrin are required for full insulin sensitivity of this cell. This could be highly relevant for the development of nephropathy in individuals with type 2 diabetes, who are commonly hyperinsulinaemic in the early phases of their disease.