Faculty Bibliography

OBJECTIVES/OBJECTIVE:Addressing minor yet significant frustrations, or "pebbles," in the workplace can reduce physician burnout, as noted by the American Medical Association. These "pebbles" are small workflow issues that are relatively easy to fix but can significantly improve the workday when resolved. This quality improvement project aimed to enhance clinician well-being in an emergency department (ED) affiliated with an academic institution through human-centered design by actively engaging clinicians to identify these "pebbles" and for a dedicated team to address them. METHODS:A task force comprised of three emergency physicians collaborating with emergency medicine leadership was established. After educating clinicians about "pebbles," clinicians were able to anonymously submit pebbles based on recall of frustrations in a baseline survey at the start of the project, as well as submit pebbles in real time by a QR code that was placed in easily noticeable areas. The task force met bimonthly to categorize, prioritize, and assign ownership of the pebbles. Progress was communicated to staff via a monthly "stop light" report. An anonymous survey assessed the impact on clinician well-being among 68 emergency clinicians within seven months of starting the project. RESULTS:Over seven months, 284 pebbles were submitted (approximately 40 per month). The feasibility of addressing pebbles was characterized by a color scale: green (easy to fix): 149 (53%); yellow (more complex): 111 (39%); and red (not feasible, "boulder"): 24 (8%). Categories of pebbles included the following: equipment/supply: 115 (40%); nursing/clinical: 86 (30%); process: 64 (23%); and information technology/technology: 19 (7%). A total of 214 pebbles (75%) were completed. Among 51 respondents (75% response rate), the self-reported impact on well-being of having pebbles addressed was as follows: extremely effective: 16 (31%); very effective: 25 (49%); moderately effective: 8 (16%); slightly effective: 2 (4%); and not effective 0 (0%). CONCLUSION/CONCLUSIONS:In addition to improving personal resilience, improving well-being in the ED involves addressing efficiency of practice. This project highlights the positive impact of resolving small, feasible issues identified by clinicians, which resulted in 80% of respondents rating the project as very to extremely effective in improving their well-being. Most pebbles were related to equipment and easily fixed, while issues involving human interactions (eg, communications between consultants and EM) were more challenging. Regular meetings and accountability facilitated progress. This approach is replicable across medical specialties and practice settings, offering a low-cost method to enhance clinician work environments and well-being.

The Yersinia enterocolitica phage-shock-protein (Psp) stress response system is activated by mislocalized outer-membrane secretin components of protein export systems and is essential for virulence. The cytoplasmic membrane proteins PspB and PspC were proposed to be dual function components of the system, acting both as positive regulators of psp gene expression and to support survival during secretin-induced stress. In this study we have uncoupled the regulatory and physiological functions of PspBC and discovered unexpected new roles, functional domains and essential amino acids. First, we showed that PspB controls PspC concentration by both pre- and post-transcriptional mechanisms. We then screened for PspBC mutants with altered transcriptional regulatory function. Unexpectedly, we identified PspB and PspC mutants that activated psp gene expression in the absence of secretin-induced stress. Together with a subsequent truncation analysis, this revealed that the PspC cytoplasmic domain plays an unforeseen role in negatively regulating psp gene expression. Conversely, mutations within the PspC periplasmic domain abolished its ability to activate psp gene expression. Significantly, PspC mutants unable to activate psp gene expression retained their ability to support survival during secretin-induced stress. These data provide compelling support for the proposal that these two functions are independent

The phage-shock-protein (Psp) system is essential for Yersinia enterocolitica virulence. Mislocalized secretins induce psp gene expression, and kill psp null strains. We used transposon mutagenesis to investigate whether other genes are required to tolerate secretin-induced stress. Our motivation included the possibility of identifying signal transducers required to activate psp gene expression. Besides Psp, only defects in the RpoE system and the TrkA potassium transporter caused secretin sensitivity. These mutations did not cause the same specific/severe sensitivity as defects in the Psp system, nor did they affect psp gene expression. The Escherichia coli Psp system was reported to be induced via the ArcB redox sensor and to activate anaerobic metabolism. Our screen did not identify arcB, or any genes involved in anaerobic metabolism/regulation. Therefore, we investigated the role of ArcB in Y. enterocolitica and E. coli. ArcB was not required for secretin-dependent induction of psp gene expression. Furthermore, microarray analysis uncovered a restricted transcriptional response to prolonged secretin stress in Y. enterocolitica. Taken together, these data do not support the proposal that the Psp system is induced via ArcB and activates anaerobic metabolism. Rather, they suggest that Psp proteins may sense an inducing trigger and mediate their physiological output(s) directly