Creating Change: An Experiential Quality Improvement and Patient Safety Curriculum for Medical Students.

Introduction: Medical students are the future drivers of change in health care. The AAMC encourages quality improvement and patient safety (QI/PS) education. Unfortunately, many schools do not have a formal QI/PS curriculum. To offer the patient-centered, safe, evidence-based, and high-value care patients deserve, students will be expected to have both knowledge of and experience in QI/PS. This extracurricular experiential QI/PS curriculum is designed to prepare medical students for this role. Methods: The curriculum includes six monthly didactic and work-group sessions that cover QI/PS fundamentals and facilitate the design and implementation of student projects. Results: Twenty-two medical students, with representation from academic years 1-4, completed the curriculum. The average Quality Improvement Knowledge Application Tool-Revised score increased from 5.61 to 7.75 (p < .01). Six projects were undertaken, with teams completing an average of 2.83 plan-do-study-act cycles. Projects decreased Clostridium difficile ordering, reduced discordance between documented and true intraoperative wound classification, and increased the quantity and quality of patient sleep. Responding "Agree" or "Strongly Agree," 80.9% of students felt their practice would change due to this experience, and 96.5% planned on participating in QI/PS in the future. Four students volunteered to continue as student leaders. Many students (96.5%) felt their experience was good or very good. Discussion: This ready-to-implement curriculum offers medical students an opportunity to obtain the knowledge and experience necessary to participate meaningfully in QI/PS now and throughout their careers.

Gene silencing associated with SWI/SNF complex loss during NSCLC development.

UNLABELLED: The SWI/SNF chromatin-remodeling complex regulates gene expression and alters chromatin structures in an ATP-dependent manner. Recent sequencing efforts have shown mutations in BRG1 (SMARCA4), one of two mutually exclusive ATPase subunits in the complex, in a significant number of human lung tumor cell lines and primary non-small cell lung carcinoma (NSCLC) clinical specimens. To determine how BRG1 loss fuels tumor progression in NSCLC, molecular profiling was performed after restoration of BRG1 expression or treatment with a histone deacetylase inhibitor or a DNA methyltransferase (DNMT) inhibitor in a BRG1-deficient NSCLC cells. Importantly, validation studies from multiple cell lines revealed that BRG1 reexpression led to substantial changes in the expression of CDH1, CDH3, EHF, and RRAD that commonly undergo silencing by other epigenetic mechanisms during NSCLC development. Furthermore, treatment with DNMT inhibitors did not restore expression of these transcripts, indicating that this common mechanism of gene silencing did not account for their loss of expression. Collectively, BRG1 loss is an important mechanism for the epigenetic silencing of target genes during NSCLC development. IMPLICATIONS: Inactivation of the SWI/SNF complex provides a novel mechanism to induce gene silencing during NSCLC development.