Jeremy B. Richards

A randomized pilot study of the use of concept maps to enhance problem-based learning among first-year medical students

Background: Medical student education is challenging, and concept maps (CMs) can help students link new and existing knowledge, promote critical thinking and identify knowledge gaps. Aims: To study the feasibility, acceptability, and effectiveness of CMs in problem-based learning (PBL) tutorials. Method: Students and tutors were randomized to tutorials that used or did not use CMs. A mixed-methods approach generated qualitative and quantitative results of participants’ perspectives on and the effects of CMs in PBL tutorials. Results: Student survey response rate was 71% (122/172). Most students (82.6%) planned to use CMs in the future at least occasionally, and students in CM tutorials endorsed increased likelihood of using CMs in the future (p = 0.02) versus students in non-CM tutorials. Qualitative analyses identified consistent associations between CMs and recurrent themes: integration of physiological mechanisms, challenging students’ knowledge of the material, and identification of knowledge gaps. Quantitative assessment of final exam scores revealed a statistically significant increase in the students’ scores in CM tutorials versus students in non-CM tutorials with an a priori α of <0.10. Conclusions: CMs are well accepted by students and faculty, feasible to incorporate into PBL tutorials, and may result in improved exam performance and student learning of physiologic concepts.

Endogenous osteopontin promotes ozone-induced neutrophil recruitment to the lungs and airway hyperresponsiveness to methacholine

Inhalation of ozone (O₃), a common environmental pollutant, causes pulmonary injury, pulmonary inflammation, and airway hyperresponsiveness (AHR) in healthy individuals and exacerbates many of these same sequelae in individuals with preexisting lung disease. However, the mechanisms underlying these phenomena are poorly understood. Consequently, we sought to determine the contribution of osteopontin (OPN), a hormone and a pleiotropic cytokine, to the development of O₃-induced pulmonary injury, pulmonary inflammation, and AHR. To that end, we examined indices of these aforementioned sequelae in mice genetically deficient in OPN and in wild-type, C57BL/6 mice 24 h following the cessation of an acute (3 h) exposure to filtered room air (air) or O₃ (2 parts/million). In wild-type mice, O₃ exposure increased bronchoalveolar lavage fluid (BALF) OPN, whereas immunohistochemical analysis demonstrated that there were no differences in the number of OPN-positive alveolar macrophages between air- and O₃-exposed wild-type mice. O₃ exposure also increased BALF epithelial cells, protein, and neutrophils in wild-type and OPN-deficient mice compared with genotype-matched, air-exposed controls. However, following O₃ exposure, BALF neutrophils were significantly reduced in OPN-deficient compared with wild-type mice. When airway responsiveness to inhaled acetyl-β-methylcholine chloride (methacholine) was assessed using the forced oscillation technique, O₃ exposure caused hyperresponsiveness to methacholine in the airways and lung parenchyma of wild-type mice, but not OPN-deficient mice. These results demonstrate that OPN is increased in the air spaces following acute exposure to O₃ and functionally contributes to the development of O₃-induced pulmonary inflammation and airway and lung parenchymal hyperresponsiveness to methacholine.

Procedural instruction in invasive bedside procedures: a systematic review and meta-analysis of effective teaching approaches

Importance Optimal approaches to teaching bedside procedures are unknown. Objective To identify effective instructional approaches in procedural training. Data sources We searched PubMed, EMBASE, Web of Science and Cochrane Library through December 2014. Study selection We included research articles that addressed procedural training among physicians or physician trainees for 12 bedside procedures. Two independent reviewers screened 9312 citations and identified 344 articles for full-text review. Data extraction and synthesis Two independent reviewers extracted data from full-text articles. Main outcomes and measures We included measurements as classified by translational science outcomes T1 (testing settings), T2 (patient care practices) and T3 (patient/public health outcomes). Due to incomplete reporting, we post hoc classified study outcomes as ‘negative’ or ‘positive’ based on statistical significance. We performed meta-analyses of outcomes on the subset of studies sharing similar outcomes. Results We found 161 eligible studies (44 randomised controlled trials (RCTs), 34 non-RCTs and 83 uncontrolled trials). Simulation was the most frequently published educational mode (78%). Our post hoc classification showed that studies involving simulation, competency-based approaches and RCTs had higher frequencies of T2/T3 outcomes. Meta-analyses showed that simulation (risk ratio (RR) 1.54 vs 0.55 for studies with vs without simulation, p=0.013) and competency-based approaches (RR 3.17 vs 0.89, p<0.001) were effective forms of training. Conclusions and relevance This systematic review of bedside procedural skills demonstrates that the current literature is heterogeneous and of varying quality and rigour. Evidence is strongest for the use of simulation and competency-based paradigms in teaching procedures, and these approaches should be the mainstay of programmes that train physicians to perform procedures. Further research should clarify differences among instructional methods (eg, forms of hands-on training) rather than among educational modes (eg, lecture vs simulation).

Teaching during consultation: factors affecting the resident-fellow teaching interaction.

The subspecialty consultation represents a potentially powerful opportunity for resident learning, but barriers may limit the educational exchanges between fellows (subspecialty registrars) and residents (house officers). We conducted a focus group study of internal medicine (IM) residents and subspecialty fellows to determine barriers against and factors facilitating resident–fellow teaching interactions on the wards, and to identify opportunities for maximising teaching and learning.

Effect of antigen sensitization and challenge on oscillatory mechanics of the lung and pulmonary inflammation in obese carboxypeptidase E-deficient mice.

Atopic, obese asthmatics exhibit airway obstruction with variable degrees of eosinophilic airway inflammation. We previously reported that mice obese as a result of a genetic deficiency in either leptin (ob/ob mice) or the long isoform of the leptin receptor (db/db mice) exhibit enhanced airway obstruction in the presence of decreased numbers of bronchoalveolar lavage fluid (BALF) eosinophils compared with lean, wild-type mice following antigen (ovalbumin; OVA) sensitization and challenge. To determine whether the genetic modality of obesity induction influences the development of OVA-induced airway obstruction and OVA-induced pulmonary inflammation, we examined indices of these sequelae in mice obese as a result of a genetic deficiency in carboxypeptidase E, an enzyme that processes prohormones and proneuropeptides involved in satiety and energy expenditure (Cpe(fat) mice). Accordingly, Cpe(fat) and lean, wild-type (C57BL/6) mice were sensitized to OVA and then challenged with either aerosolized PBS or OVA. Compared with genotype-matched, OVA-sensitized and PBS-challenged mice, OVA sensitization and challenge elicited airway obstruction and increased BALF eosinophils, macrophages, neutrophils, IL-4, IL-13, IL-18, and chemerin. However, OVA challenge enhanced airway obstruction and pulmonary inflammation in Cpe(fat) compared with wild-type mice. These results demonstrate that OVA sensitization and challenge enhance airway obstruction in obese mice regardless of the genetic basis of obesity, whereas the degree of OVA-induced pulmonary inflammation is dependent on the genetic modality of obesity induction. These results have important implications for animal models of asthma, as modeling the pulmonary phenotypes for subpopulations of atopic, obese asthmatics critically depends on selecting the appropriate mouse model.

Assessing the Effectiveness of Case-based Collaborative Learning via Randomized Controlled Trial

Purpose Case-based collaborative learning (CBCL) is a novel small-group approach that borrows from team-based learning principles and incorporates elements of problem-based learning (PBL) and case-based learning. CBCL includes a preclass readiness assurance process and case-based in-class activities in which students respond to focused, open-ended questions individually, discuss their answers in groups of 4, and then reach consensus in larger groups of 16. This study introduces CBCL and assesses its effectiveness in one course at Harvard Medical School. Method In a 2013 randomized controlled trial, 64 medical and dental student volunteers were assigned randomly to one of four 8-person PBL tutorial groups (control; n = 32) or one of two 16-person CBCL tutorial groups (experimental condition; n = 32) as part of a required first-year physiology course. Outcomes for the PBL and CBCL groups were compared using final exam scores, student responses to a postcourse survey, and behavioral coding of portions of video-recorded class sessions. Results Overall, the course final exam scores for CBCL and PBL students were not significantly different. However, CBCL students whose mean exam performance in prior courses was below the participant median scored significantly higher than their PBL counterparts on the physiology course final exam. The most common adjectives students used to describe CBCL were “engaging,” “fun,” and “thought-provoking.” Coding of observed behaviors indicated that individual affect was significantly higher in the CBCL groups than in the PBL groups. Conclusions CBCL is a viable, engaging, active learning method. It may particularly benefit students with lower academic performance.

Performance characteristics of measurement instruments of epistemic curiosity in third-year medical students

Epistemic curiosity is theorized to underlie the adoption of learning goals, studying strategies, and skill development critical to becoming a successful physician. However, there is relatively little research regarding the measurement of epistemic curiosity in medical learners. We administered the I- and D-type curiosity and Need For Cognition (NFC) scales to assess individual differences in epistemic curiosity, and the Study Processes Questionnaire to measure tendencies to employ “Deep” or “Surface” learning goals and strategies to 90 third-year medical students in academic years 2010 and 2011. The performance characteristics of these instruments were characterized, and path analyses were conducted to examine the relationships between these instruments. Individual differences in I- and D-type curiosity were positively associated with tendencies to set goals and use strategies aimed at developing a deeper understanding of knowledge. NFC was negatively associated with goals and strategies that involved seeking only a surface understanding of new information. Our results demonstrate that in a population of medical learners, I- and D-type curiosity scale scores significantly predict seeking a deeper understanding of new information, while NFC scale scores may be better considered as a marker of avoiding superficial study processes but not necessarily engaging in deeper approaches.

Lectures for Adult Learners: Breaking Old Habits in Graduate Medical Education

AAIM is the largest academically focused specialty organization representing departments of internal medicine at medical schools and teaching hospitals in the United States and Canada. As a consortium of five organizations, AAIM represents department chairs and chiefs; clerkship, residency, and fellowship program directors; division chiefs; and academic and business administrators as well as other faculty and staff in departments of internal medicine and their divisions.

Noninvasive carbon monoxide detection: insufficient evidence for broad clinical use.

Carbon monoxide (CO) poisoning is an important public health issue, as this colorless, odorless gas is a common cause of unintentional poisoning and leads to over 400 deaths each year in the United States.[1][1] Detection of CO poisoned patients may be difficult, as even classic symptoms, including

Resistin deficiency in mice has no effect on pulmonary responses induced by acute ozone exposure

Acute exposure to ozone (O3), an air pollutant, causes pulmonary inflammation, airway epithelial desquamation, and airway hyperresponsiveness (AHR). Pro-inflammatory cytokines-including IL-6 and ligands of chemokine (C-X-C motif) receptor 2 [keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-2], TNF receptor 1 and 2 (TNF), and type I IL-1 receptor (IL-1α and IL-1β)-promote these sequelae. Human resistin, a pleiotropic hormone and cytokine, induces expression of IL-1α, IL-1β, IL-6, IL-8 (the human ortholog of murine KC and MIP-2), and TNF. Functional differences exist between human and murine resistin; yet given the aforementioned observations, we hypothesized that murine resistin promotes O3-induced lung pathology by inducing expression of the same inflammatory cytokines as human resistin. Consequently, we examined indexes of O3-induced lung pathology in wild-type and resistin-deficient mice following acute exposure to either filtered room air or O3. In wild-type mice, O3 increased bronchoalveolar lavage fluid (BALF) resistin. Furthermore, O3 increased lung tissue or BALF IL-1α, IL-6, KC, TNF, macrophages, neutrophils, and epithelial cells in wild-type and resistin-deficient mice. With the exception of KC, which was significantly greater in resistin-deficient compared with wild-type mice, no genotype-related differences in the other indexes existed following O3 exposure. O3 caused AHR to acetyl-β-methylcholine chloride (methacholine) in wild-type and resistin-deficient mice. However, genotype-related differences in airway responsiveness to methacholine were nonexistent subsequent to O3 exposure. Taken together, these data demonstrate that murine resistin is increased in the lungs of wild-type mice following acute O3 exposure but does not promote O3-induced lung pathology.