Using Simulations to Train Medical Students for Unanticipated Technology Failures in Telemedicine.

Simulations offer a safe environment for health professional training and the opportunity to predictably and consistently introduce events or variables that may be rare or dangerous in a live setting. Exposing trainees to unanticipated events during simulations can improve their ability to adapt and improvise. The COVID-19 pandemic accelerated the adoption of telehealth worldwide and highlighted the need for better training in health professional schools. In the United States, the Association of American Medical Colleges (AAMC) published new telehealth competency standards in 2021. The AAMC stated that health care providers should be aware of the risks of technology failures, capable of troubleshooting them, and lead systems interventions to improve safety. However, the AAMC does not provide guidance on the specific failures or solutions. In this study, we developed a set of technology failures that can be simulated in a telehealth curriculum. We incorporated one technology failure into a simulated telehealth encounter and gathered students' (N = 53) feedback on the exercise. Students' feedback was overwhelmingly positive. They agreed that integrating technology failures into telehealth simulations provides important practice managing these events during clinical encounters. While telehealth is an important healthcare delivery modality that can improve access-to-care, it is imperative to train medical students to navigate technology failures so that can adeptly manage these issues in clinical practice.

Macrophage colony-stimulating factor receptor c-fms is a novel target of imatinib.

Imatinib is a tyrosine kinase inhibitor that suppresses the growth of bcr-abl-expressing chronic myeloid leukemia (CML) progenitor cells by blockade of the adenosine triphosphate (ATP)-binding site of the kinase domain of bcr-abl. Imatinib also inhibits the c-abl, platelet-derived growth factor (PDGF) receptor, abl-related gene (ARG) and stem-cell factor (SCF) receptor tyrosine kinases, and has been used clinically to inhibit the growth of malignant cells in patients with CML and gastrointestinal stromal tumors (GISTs). Although initially considered to have minimal effects of normal hematopoiesis, recent studies show that imatinib also inhibits the growth of some nonmalignant hematopoietic cells, including monocyte/macrophages. This inhibition could not be attributed to the known activity profile of imatinib. Here, we demonstrate for the first time that imatinib targets the macrophage colony-stimulating factor (M-CSF) receptor c-fms. Phosphorylation of c-fms was inhibited by therapeutic concentrations of imatinib, and this was not due to down-regulation in c-fms expression. Imatinib was also found to inhibit M-CSF-induced proliferation of a cytokine-dependent cell line, further supporting the hypothesis that imatinib affects the growth and development of monocyte and/or macrophages through inhibition of c-fms signaling. Importantly, these results identify an additional biologic target to those already defined for imatinib. Imatinib should now be assessed for activity in diseases where c-fms activation is implicated, including breast and ovarian cancer and inflammatory conditions.