Resident-Driven Clinical Decision Support Governance to Improve the Utility of Clinical Decision Support.

OBJECTIVES: This resident-driven quality improvement project aimed to better understand the known problem of a misaligned clinical decision support (CDS) strategy and improve CDS utilization. METHODS: An internal survey was sent to all internal medicine (IM) residents to identify the most bothersome CDS alerts. Survey results were supported by electronic health record (EHR) data of CDS firing rates and response rates which were collected for each of the three most bothersome CDS tools. Changes to firing criteria were created to increase utilization and to better align with the five rights of CDS. Findings and proposed changes were presented to our institution's CDS Governance Committee. Changes were approved and implemented. Postintervention firing rates were then collected for 1 week. RESULTS: Twenty nine residents participated in the CDS survey and identified sepsis alerts, lipid profile reminders, and telemetry renewals to be the most bothersome alerts. EHR data showed action rates for these CDS as low as 1%. We implemented changes to focus emergency department (ED)-based sepsis alerts to the right provider, better address the right information for lipid profile reminders, and select the right time in workflow for telemetry renewals to be most effective. With these changes we successfully eliminated ED-based sepsis CDS reminders for IM providers, saw a 97% reduction in firing rates for the lipid profile CDS, and noted a 55% reduction in firing rates for telemetry CDS. CONCLUSION: This project highlighted that alert improvements spearheaded by resident teams can be completed successfully using robust CDS governance strategies and can effectively optimize interruptive alerts.

Sab concentrations indicate chemotherapeutic susceptibility in ovarian cancer cell lines.

The occurrence of chemotherapy-resistant tumors makes ovarian cancer (OC) the most lethal gynecological malignancy. While many factors may contribute to chemoresistance, the mechanisms responsible for regulating tumor vulnerability are under investigation. Our analysis of gene expression data revealed that Sab, a mitochondrial outer membrane (MOM) scaffold protein, was down-regulated in OC patients. Sab-mediated signaling induces cell death, suggesting that this apoptotic pathway is diminished in OC. We examined Sab expression in a panel of OC cell lines and found that the magnitude of Sab expression correlated to chemo-responsiveness; wherein, OC cells with low Sab levels were chemoresistant. The Sab levels were reflected by a corresponding amount of stress-induced c-Jun N-terminal kinase (JNK) on the MOM. BH3 profiling and examination of Bcl-2 and BH3-only protein concentrations revealed that cells with high Sab concentrations were primed for apoptosis, as determined by the decrease in pro-survival Bcl-2 proteins and an increase in pro-apoptotic BH3-only proteins on mitochondria. Furthermore, overexpression of Sab in chemoresistant cells enhanced apoptotic priming and restored cellular vulnerability to a combination treatment of cisplatin and paclitaxel. Contrariwise, inhibiting Sab-mediated signaling or silencing Sab expression in a chemosensitive cell line resulted in decreased apoptotic priming and increased resistance. The effects of silencing on Sab on the resistance to chemotherapeutic agents were emulated by the silencing or inhibition of JNK, which could be attributed to changes in Bcl-2 protein concentrations induced by sub-chronic JNK inhibition. We propose that Sab may be a prognostic biomarker to discern personalized treatments for OC patients.