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BACKGROUND: Studies have demonstrated patients hold different expectations for female physicians compared to male physicians, including higher expectations for patient-centered communication and addressing socioeconomic or emotional needs. Recent evidence indicates this gender disparity extends to the electronic health record (EHR). Similar studies have not been conducted with resident physicians. OBJECTIVE: This study seeks to characterize differences in EHR workload for female resident physicians compared to male resident physicians. DESIGN: This study evaluated 12 months of 156 Mayo Clinic internal medicine residents' inbasket data from July 2020 to June 2021 using Epic's Signal and Physician Efficiency Profile (PEP) data. Excel, BlueSky Statistics, and SAS analytical software were used for analysis. Paired t-tests and analysis of variance were used to compare PEP data by gender and postgraduate year (PGY). "Male" and "female" were used in substitute for "gender" as is precedent in the literature. SUBJECTS: Mayo Clinic internal medicine residents. MAIN MEASURES: Total time spent in EHR per day; time in inbasket and notes per day; time in notes per appointment; number of patient advice requests made through the portal; message turnaround time. KEY RESULTS: Female residents received more patient advice requests per year (p = 0.004) with an average of 86.7 compared to 68, resulting in 34% more patient advice requests per day worked (p < 0.001). Female residents spent more time in inbasket per day (p = 0.002), in notes per day (p < 0.001), and in notes per appointment (p = 0.001). Resident panel comparisons revealed equivocal sizes with significantly more female patients on female (n = 55) vs male (n = 34) resident panels (p < 0.001). There was no difference in message turnaround time, total messages, or number of results received. CONCLUSIONS: Female resident physicians experience significantly more patient-initiated messages and EHR workload despite equivalent number of results and panel size. Gender differences in inbasket burden may disproportionally impact the resident educational experience.
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Bradicardia , Eletrocardiografia , Feminino , Humanos , Bradicardia/diagnóstico , Bradicardia/etiologiaRESUMO
INTRODUCTION: Medical students find immunology difficult to understand and relate to clinically and are often frustrated by the amount of detailed material. We created PRIME Immunology: Preview or Review of Important Material for Everyone: (i) video modules, (ii) Instagram site, and (iii) vocabulary files called Immunology Language. METHODS: The self-paced modules introduced key topics in immunology for students to complete prior to their instructional block. RESULTS AND CONCLUSIONS: Use of PRIME Immunology during a 3-year period suggested that providing students with an overview of key topics before the start of their course may (i) reduce student angst about immunology and (ii) improve retention of immunology.
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Mouse Ccr1l1 (Ccr1-like 1) encodes an orphan G-protein-coupled receptor (GPCR) with the highest homology to the inflammatory and highly promiscuous chemokine receptors Ccr1 and Ccr3 (70 and 50% amino acid identity, respectively). Ccr1l1 was first cloned in 1995, yet current knowledge of this putative chemokine receptor is limited to its gene organization and chromosomal localization. Here we report that Ccr1l1 is a Rodentia-specific gene selectively expressed in eosinophils. However, eosinophil phenotypes, development, and responsiveness to chemokines were all normal in naïve Ccr1l1 knockout mice. We demonstrate for the first time that recombinant Ccr1l1 is expressed on the plasma membrane of transfected cells and contains an extracellular N terminus and an intracellular C terminus, consistent with GPCR topology. Using receptor internalization, ß-arrestin recruitment, calcium flux, and chemotaxis assays, we excluded all 37 available mouse chemokines, including Ccr1 ligands, and two viral chemokines as Ccr1l1 ligands, and demonstrated that mouse Ccr1, but not Ccr1l1, exhibits constitutive signaling activity. However, sequence analysis and structural modeling revealed that Ccr1l1 is well equipped to act as a classical signaling GPCR, with N-terminal sulfotyrosines as the only signaling and chemokine-binding determinant absent in Ccr1l1. Hereof, we show that a sulfatable N-terminal Ccr1 Y18 residue is essential for chemotaxis and calcium responses induced by Ccl3 and Ccl9/10, but substituting the corresponding Ccr1l1 F19 residue with tyrosine failed to confer responsiveness to Ccr1 ligands. Although Ccr1l1 remains an extreme outlier in the chemokine receptor family, our study supports that it might respond to unidentified mouse chemokine ligands in eosinophil-driven immune responses.