Radiology Residency Quality Improvement Curriculum: Lessons Learned.

Quality improvement (QI) skills in radiology are required as part of the Accreditation Council for Graduate Medical Education Diagnostic Radiology Milestones competencies. Although feasibility of QI curricula has been demonstrated in radiology before, there are still barriers to widespread implementation. Here, we share our experience with designing the curriculum structure and selecting content. We describe the QI projects that have been performed and discuss lessons learned, including successes, challenges, and future directions. This information is relevant for many radiology programs currently planning to implement or revise existing QI curricula.

Together We Learn: Analyzing the Interprofessional Internal Medicine Residents' and Master of Public Health Students' Quality Improvement Education Experience.

Although the value of interprofessional collaborative education has been promoted, it is unclear how teams of clinical and nonclinical learners perceive this experience. The authors studied an interprofessional quality improvement (QI) curriculum implemented in 2013 integrating internal medicine residents (n = 90) and Master of Public Health (MPH) students (n = 33) at an urban safety net academic medical center. Pre and post curriculum surveys assessed attitudes toward QI and interprofessional education and team performance. Resident attitudes toward learning and engaging in QI work improved at the end of the curriculum. Overall, MPH students demonstrated significantly more positive attitudes about interprofessional learning and work than residents. They also agreed more strongly than residents that patients would benefit if residents and public health students worked together. As health care organizations evolve to become more integrated, it is crucial that interprofessional educational opportunities be developed and evaluated to help encourage a culture of collaboration among health care providers.

Successful Implementation of an Automated Sedation Vacation Process in Intensive Care Units.

This quality improvement initiative sought to develop a sedation vacation (SV) protocol to increase SV performance and ensure sustainability. A standardized, nurse-driven SV protocol within the electronic medical record was implemented in adult intensive care units (ICUs) at Boston Medical Center. For 6 months, data were collected on the number of assessments performed, SV completion, SV eligibility, and reason for exclusion. Secondary outcomes included ICU length of stay (LOS) and ventilator LOS. Of 1730 patient-days during this 6-month period, SV assessments were performed 70% (n = 1211) of the time. SVs were conducted on 60.0% (n = 726) during days in which an assessment occurred. There was no significant change in ICU LOS or ventilator LOS during the study period. This SV protocol attained a 70% adherence rate, which was sustained over the 6-month period. There were no significant changes in secondary outcomes.

Increased PEA3/E1AF and decreased Net/Elk-3, both ETS proteins, characterize human NSCLC progression and regulate caveolin-1 transcription in Calu-1 and NCI-H23 NSCLC cell lines.

Caveolin-1 protein has been called a 'conditional tumor suppressor' because it can either suppress or enhance tumor progression depending on cellular context. Caveolin-1 levels are dynamic in non-small-cell lung cancer, with increased levels in metastatic tumor cells. We have shown previously that transactivation of an erythroblastosis virus-transforming sequence (ETS) cis-element enhances caveolin-1 expression in a murine lung epithelial cell line. Based on high sequence homology between the murine and human caveolin-1 promoters, we proposed that ETS proteins might regulate caveolin-1 expression in human lung tumorigenesis. We confirm that caveolin-1 is not detected in well-differentiated primary lung tumors. Polyoma virus enhancer activator 3 (PEA3), a pro-metastatic ETS protein in breast cancer, is expressed at low levels in well-differentiated tumors and high levels in poorly differentiated tumors. Conversely, Net, a known ETS repressor, is expressed at high levels in the nucleus of well-differentiated primary tumor cells. In tumor cells in metastatic lymph node sites, caveolin-1 and PEA3 are highly expressed, whereas Net is now expressed in the cytoplasm. We studied transcriptional regulation of caveolin-1 in two human lung cancer cell lines, Calu-1 (high caveolin-1 expressing) and NCI-H23 (low caveolin-1 expressing). Chromatin immunoprecipitation-binding assays and small interfering RNA experiments show that PEA3 is a transcriptional activator in Calu-1 cells and that Net is a transcriptional repressor in NCI-H23 cells. These results suggest that Net may suppress caveolin-1 transcription in primary lung tumors and that PEA3 may activate caveolin-1 transcription in metastatic lymph nodes.