Efficacy of quality improvement and patient safety workshops for students: a pilot study.

BACKGROUND: While the Association of American Medical Colleges encourages medical schools to incorporate quality improvement and patient safety (QI/PS) into their curriculum, medical students continue to have limited QI/PS exposure. To prepare medical students for careers that involve QI/PS, the Institute for Healthcare Improvement chapter at an allopathic medical school and school of allied health professions initiated self-directed learning by offering student-led workshops to equip learners with skills to improve the quality and safety of healthcare processes. METHODS: In this prospective cohort study, workshops were hosted for medical students between 2015 and 2018 on five QI/PS topics: Process Mapping, Root-Cause Analysis (RCA), Plan-Do-Study-Act (PDSA) Cycles, Evidence Based Medicine (EBM), and Patient Handoffs. Each workshop included a hands-on component to engage learners in practical applications of QI/PS skills in their careers. Change in knowledge, attitudes, and behaviors was assessed via pre- and post-surveys using 5-point Likert scales, and analyzed using either the McNemar test or non-parametric Wilcoxon signed-rank test. Surveys also gathered qualitative feedback regarding strengths, future areas for improvement, and reasons for attending the workshops. RESULTS: Data was collected from 88.5% of learners (n = 185/209); 19.5% of learners reported prior formal instruction in these topics. Statistically significant improvements in learners' confidence were observed for each workshop. Additionally, after attending workshops, learners felt comfortable teaching the learned QI/PS skill to colleagues (mean pre/post difference 1.96, p < 0.0001, n = 139) and were more likely to pursue QI/PS projects in their careers (mean pre/post difference 0.45, p < 0.0001, n = 139). Lastly, learners demonstrated a statistically significant increase in knowledge in four out of five skills workshop topics. CONCLUSION: Few medical students have formal instruction in QI/PS tools. This pilot study highlights advantages of incorporating an innovative, student-directed modified 'flipped classroom' methodology, with a focus on active experiential learning and minimal didactic instruction.

Endothelial Cell Senescence Increases Traction Forces due to Age-Associated Changes in the Glycocalyx and SIRT1.

Endothelial cell (EC) aging and senescence are key events in atherogenesis and cardiovascular disease development. Age-associated changes in the local mechanical environment of blood vessels have also been linked to atherosclerosis. However, the extent to which cell senescence affects mechanical forces generated by the cell is unclear. In this study, we sought to determine whether EC senescence increases traction forces through age-associated changes in the glycocalyx and antioxidant regulator deacetylase Sirtuin1 (SIRT1), which is downregulated during aging. Traction forces were higher in cells that had undergone more population doublings and changes in traction force were associated with altered actin localization. Older cells also had increased actin filament thickness. Depletion of heparan sulfate in young ECs elevated traction forces and actin filament thickness, while addition of heparan sulfate to the surface of aged ECs by treatment with angiopoietin-1 had the opposite effect. While inhibition of SIRT1 had no significant effect on traction forces or actin organization for young cells, activation of SIRT1 did reduce traction forces and increase peripheral actin in aged ECs. These results show that EC senescence increases traction forces and alters actin localization through changes to SIRT1 and the glycocalyx.

The Effect of Stress-Induced Senescence on Aging Human Cord Blood-Derived Endothelial Cells.

PURPOSE: We sought to determine the effect of stress-induced senescence on the permeability to albumin of aging endothelial progenitor cells. METHODS: Human umbilical cord blood derived endothelial cells (hCB-ECs) and human aortic endothelial cells (HAECs) were treated with 200 µM H2O2 and permeability to FITC-bovine serum albumin was measured. Some samples were subsequently treated with 100µM 8-pCPT-2'-O-Me-cAMP, a cAMP analog that activates the Epac1-Rap1 pathway. Cell proliferation was measured with the EdU assay. Phase contrast, and immunofluorescence images were taken to observe morphological changes in cells after exposure to H2O2. RESULTS: hCB-ECs exposed to H2O2 exhibited a significant increase in permeability, but their response differed from the HAECs. Low passage hCB-ECs had a permeability increase of about 82% (p<0.01) compared to aged cells which had a permeability increase of about 37% (p<0.05). This increase in permeability was reduced by treating the cells with 100 µM 8-pCPT-2'-O-Me-cAMP. The younger cells exhibited a significant decrease in proliferation after being subjected to various concentrations of H2O2 whereas the aged cells exhibited a more gradual decrease in the percent of cells in S-phase. These changes also correlated with changes in cell morphology and junction staining. When placed back in the original media, the morphology and permeability of the hCB-ECs returned to the control condition, while the HAECs did not. CONCLUSIONS: The permeability of low and high passage hCB-ECs and HAECs initially increases in response to oxidative stress. hCB-ECs, but not HAECs, were able to recover from the stress 24 hours later. Early passage hCB-ECs were more susceptible to exogenous H2O2 than late passage hCB-ECs. The increase in permeability of hCB-ECs to H2O2 also correlated with decreased cell proliferation and changes in cell junctions.