Background and Objectives: Cultural barriers and patient-provider language discordance exert deleterious effects on patient care. One solution has been the integration of medical interpreters into the care of patients with limited English proficiency. While medical schools and residency programs have started developing training programs on how to work with medical interpreters, no similar endeavor has been reported by student-run free clinics. Methods: Over 1 year, 76 third-year medical students (MS3s) were enrolled in control and intervention groups, and evaluated by in-person interpreters during interpreted real-patient encounters. MS3s in the intervention group received a lesson- and reminder-based training program on how to work with in-person interpreters. Results: MS3s who received the intervention were more likely to ask the patient one question at a time (odds ratio [OR] 3.54, P=.0079), listen to the interpreter without unnecessary interruption (OR 3.30, P=.022), and speak in short, simple sentences with pauses for interpretation (OR 3.08, P=.017). Conclusions: Our lesson- and reminder-based training program on provider-interpreter collaboration can improve the performance of MS3s within a select skill set with minimal cost and time investment.

Ribosomal Protein (Rp) gene haploinsufficiency affects overall translation rate, leads to cell elimination by competition with wild type cells in mosaic tissues, and sometimes leads to accumulation of protein aggregates. The changes in ribosomal subunit levels observed are not sufficient for these effects, which all depend on the AT-hook, bZip domain protein Xrp1. In Rp+/− cells, Xrp1 reduced global translation through PERK-dependent phosphorylation of eIF2α. eIF2α phosphorylation was sufficient to reduce translation in, and also enable cell competition of, otherwise wild type cells. Unexpectedly, however, many other defects reducing ribosome biogenesis or function (depletion of TAF1B, eIF2, eIF4G, eIF6, eEF2, eEF1α1, or eIF5A), also increased eIF2α phosphorylation and enabled cell competition. In all cases this was through the Xrp1 expression that was induced, placing Xrp1 as the downstream instigator of cell competition that also contributed to overall translation deficits. In the absence of Xrp1, translation differences between cells were not themselves sufficient to trigger cell competition. Thus, Xrp1, which is shown here to be a sequence-specific transcription factor, is the master regulator that triggers cell competition and other consequences of multiple ribosomal stresses.