Racial disparities in emergency medicine: Implementation of a novel educational module in the emergency medicine clerkship.

Objectives: Despite decades of literature recognizing racial disparities (RDs) in emergency medicine (EM), published curricula dedicated to addressing them are sparse. We present details of our novel RD curriculum for EM clerkships and its educational outcomes. Methods: We created a 30-min interactive didactic module on the topic designed for third- and fourth-year medical students enrolled in our EM clerkships. Through a modified Delphi process, education faculty and content experts in RD developed a 10-question multiple-choice test of knowledge on RD that the students completed immediately prior to and 2 weeks following the activity. Students also completed a Likert-style learner satisfaction survey. Median pre- and posttest scores were compared using a paired Wilcoxon signed-rank test and presented using medians and 95% confidence intervals (CIs). Satisfaction survey responses were dichotomized into favorable and neutral/not favorable. Results: For the 36 students who completed the module, the median pretest score was 40% (95% CI 36%-50%) and the posttest score was 70% (95% CI 60%-70%) with a p-value of <0.001. Thirty-five of the 36 students improved on the posttest with a mean increase of 24.2% (95% CI 20.2-28.2). The satisfaction survey also showed a positive response, with at least 83% of participants responding favorably to all statements (overall mean favorable response 93%, 95% CI 90%-96%).ConclusionsThis EM-based module on RD led to improvement in students' knowledge on the topic and positive reception by participants. This is a feasible option for educating students in EM on the topic of RD.

Design and Evaluation of a Curriculum on Intimate Partner Violence for Medical Students in an Emergency Medicine Clerkship.

Purpose: Intimate partner violence (IPV) is a widespread public health issue that is relevant to all areas of medicine. Patients who suffer from IPV often contact the health care system via the emergency department, making this a particularly important but too often overlooked issue in this setting. Education on IPV varies in medical schools and emergency medicine (EM) educational programs, and evidence suggests that a barrier to assessing for IPV is a lack of adequate training of clinicians. In this study, we sought to design, implement and evaluate the efficacy of a curriculum on IPV geared towards medical students on an EM clerkship. Methods: We assembled a multi-disciplinary team of EM education faculty, a resident content expert on IPV, and social workers to design a two-part curriculum that was administered to medical students on an EM clerkship. The curriculum involved a 20-minute narrated slide presentation viewed asynchronously, followed by a 1-hour case-based discussion session. The curriculum was evaluated using a 13-item self-assessment survey on knowledge, comfort level and skill in managing victims of IPV, administered electronically before and after the curriculum. Survey results were compared pre- and post-curriculum using Wilcoxon signed-rank test. Results: Thirty-four students completed the curriculum and 26 completed both the pre and post self-assessment surveys. A statistically significant improvement in knowledge, comfort level and skills was observed in 11 of the 13 survey elements. Conclusion: Based on the self-assessment survey results, this curriculum was well received and successfully increased participants' comfort, knowledge and skill level regarding assessment of patients for IPV. This is a focused and feasible curriculum that can be easily incorporated into an EM clerkship to provide effective education on a relevant but often overlooked topic.

Immunoglobulin E signal inhibition during allergen ingestion leads to reversal of established food allergy and induction of regulatory T cells.

Immunoglobulin E (IgE) antibodies are known for triggering immediate hypersensitivity reactions such as food anaphylaxis. In this study, we tested whether they might additionally function to amplify nascent antibody and T helper 2 (Th2) cell-mediated responses to ingested proteins and whether blocking IgE would modify sensitization. By using mice harboring a disinhibited form of the IL-4 receptor, we developed an adjuvant-free model of peanut allergy. Mast cells and IgE were required for induction of antibody and Th2-cell-mediated responses to peanut ingestion and they impaired regulatory T (Treg) cell induction. Mast-cell-targeted genetic deletion of the FcεRI signaling kinase Syk or Syk blockade also prevented peanut sensitization. In mice with established allergy, Syk blockade facilitated desensitization and induction of Treg cells, which suppressed allergy when transferred to naive recipients. Our study suggests a key role for IgE in driving Th2 cell and IgE responses while suppressing Treg cells in food allergy.

IL-10 suppresses IL-17-mediated dermal inflammation and reduces the systemic burden of Vaccinia virus in a mouse model of eczema vaccinatum.

Individuals with atopic dermatitis (AD) are susceptible to a severe, potentially fatal, systemic infection and inflammatory response following exposure to Vaccinia virus (VV). IL-10 acts both as an inducer of Th2 responses and as a regulator of T cell activation. It has been shown to limit skin inflammation elicited by contact sensitizers. AD exacerbations have been associated with decreased IL-10 function. We used IL-10(-/-) mice to test the role of the cytokine in VV immunity. They exhibited larger primary lesions and increased cutaneous neutrophil infiltration compared to wild-type (WT) counterparts. This was associated with enhanced production of IL-17A, IL-17F and CXCL2. Paradoxically, despite intact adaptive immune responses, tissue viral burdens were increased in IL-10(-/-) mice. These findings suggest that IL-10 is important in limiting skin inflammation induced by VV and that abnormal IL-17-driven neutrophil recruitment at the primary infection site in the skin results in increased systemic viral dissemination.

An IgE receptor mimetic peptide (PepE) protects mice from IgE mediated anaphylaxis.

Crosslinking of receptor-bound Immunoglobulin E (IgE) triggers immediate hypersensitivity reactions including anaphylaxis. Blocking the interaction of IgE with its high-affinity receptor, FcεRI, on mast cells and basophils is an attractive strategy for the treatment of allergies. This approach has seen clinical success using the anti-IgE monoclonal antibody, omalizumab. We recently designed and characterized a novel FcεRI-mimetic peptide (PepE) which contains the two key FcεRI α-chain receptor loops known to interact with the ε-heavy chain of IgE, C'-E and B-C, with an optimized linker for joining them. PepE has high specificity and affinity for IgE, blocks IgE binding to FcεRI and prevents IgE-induced mediator release from RBL2H3 cells. We have now investigated the biological effects of this peptide in vivo using a line of mice (BALB/c Il4raF709) very sensitive to IgE-mediated systemic anaphylaxis. IgE-deficient (IgE-/-) Il4raF709 mice were passively sensitized with the anti-DNP IgE monoclonal antibody (SPE-7) and subsequently challenged i.v. with DNP-BSA. Mice receiving a single dose of PepE prior to sensitization with SPE-7 IgE were fully protected from anaphylaxis while vehicle control-treated mice displayed strong reactions with significant core body temperature drops and elevated levels of mouse mast cell protease-1 (mMCP-1) in the serum. However, PepE had no effect on IgE-mediated anaphylaxis if given after IgE administration in IgE-/- mice, suggesting that PepE can block binding of free IgE to FcεRI but cannot compete with the receptor for already bound IgE in vivo. A single dose of PepE treatment did not protect IgE sufficient mice from IgE mediated anaphylaxis. However, a 3 week long course of PepE treatment protected IgE sufficient Il4raF709 mice from body temperature drops and elevation of serum mMCP-1. Our findings establish the potential of this type of structure for blocking IgE binding to mast cells in vivo and suggest that related peptides might have the potential to attenuate clinical allergic reactions.