Rationale: Hypothesis-driven physical examination emphasizes the role of bedside examination in the refinement of differential diagnoses and improves diagnostic acumen. This approach has not yet been investigated as a tool to improve the ability of higher-level trainees to teach medical students.Objectives: To assess the effect of teaching hypothesis-driven physical diagnosis to pulmonary fellows on their ability to improve the pulmonary examination skills of first-year medical students.Methods: Fellows and students were assessed on teaching and diagnostic skills by self-rating on a Likert scale. One group of fellows received the hypothesis-driven teaching curriculum (the “intervention” group) and another received instruction on head-to-toe examination. Both groups subsequently taught physical diagnosis to a group of first-year medical students. An oral examination was administered to all students after completion of the course.Measurements and Main Results: Fellows were comfortable teaching physical diagnosis to students. Students in both groups reported a lack of comfort with the pulmonary examination at the beginning of the course and improvement in their comfort by the end. Students trained by intervention group fellows outperformed students trained by control group fellows in the interpretation of physical findings (P < 0.05).Conclusions: Teaching hypothesis-driven physical examination to higher-level trainees who teach medical students improves the ability of students to interpret physical findings. This benefit should be confirmed using validated testing tools.

BackgroundChronic alcohol ingestion induces the expression of transforming growth factor beta‐1(TGFβ1), inhibits nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2)‐mediated activation of the antioxidant response element (ARE), depletes alveolar glutathione pools, and potentiates acute lung injury. In this study, we examined the mechanistic relationship between TGFβ1 and Nrf2‐ARE signaling in the experimental alcoholic lung.MethodsWild‐type mice were treated ± alcohol in drinking water for 8 weeks and their lungs were assessed for Nrf2 expression. In parallel, mouse lung fibroblasts were cultured ± alcohol and treated ± sulforaphane (SFP; an activator of Nrf2), ±TGFβ1, ±TGFβ1 neutralizing antibody, and/or ±activin receptor‐like kinase 5 inhibitors (to block TGβ1 receptor signaling) and then analyzed for the expression of Nrf2, Kelch‐like ECH‐associated protein 1 (Keap1) and TGFβ1, Nrf2‐ARE activity, and the expression of the Nrf2‐ARE‐dependent antioxidants glutathione s‐transferase theta 2 (GSTT2) and glutamate‐cysteine ligase catalytic subunit (GCLC). Finally, silencing RNA (siRNA) of Nrf2 was then performed prior to alcohol exposure and subsequent analysis of TGFβ1 expression.ResultsAlcohol treatment in vivo or in vitro decreased Nrf2 expression in murine whole lung and lung fibroblasts, respectively. In parallel, alcohol exposure in vitro decreased Keap1 gene and protein expression in lung fibroblasts. Furthermore, alcohol exposure increased TGFβ1 expression but decreased Nrf2‐ARE activity and expression of the ARE‐dependent genes for GSTT2 and GCLC. These effects of alcohol were prevented by treatment with SFP; in contrast, Nrf2 SiRNA expression exacerbated alcohol‐induced TGFβ1 expression. Finally, TGFβ1 treatment directly suppressed Nrf2‐ARE activity whereas blocking TGFβ1 signaling attenuated alcohol‐induced suppression of Nrf2‐ARE activity.ConclusionsAlcohol‐induced oxidative stress is mediated by TGFβ1, which suppresses Nrf2‐ARE‐dependent expression of antioxidant defenses and creates a vicious cycle that feeds back to further increase TGFβ1 expression. These effects of alcohol can be mitigated by activation of Nrf2, suggesting a potential therapy in individuals at risk for lung injury due to alcohol abuse.

BACKGROUND Alcohol abuse increases the risk for acute lung injury (ALI). In both experimental models and in clinical studies, chronic alcohol ingestion causes airway oxidative stress and glutathione depletion and increases the expression of transforming growth factor beta-1 (TGFβ1), a potent inducer of fibrosis, in the lung. Therefore, we hypothesized that alcohol ingestion could promote aberrant fibrosis following experimental ALI and that treatment with the glutathione precursor s-adenosylmethionine (SAMe) could mitigate these effects. METHODS Three-month-old C57BL/6 mice were fed standard chow ± alcohol (20% v/v) in their drinking water for 8 weeks and ±SAMe (4% w/v) during the last 4 weeks. ALI was induced by intratracheal instillation of bleomycin (2.5 units/kg), and lungs were assessed histologically at 7 and 14 days for fibrosis and at 14 days for the expression of extracellular matrix proteins and TGFβ1. RESULTS Alcohol ingestion had no apparent effect on lung inflammation at 7 days, but at 14 days after bleomycin treatment, it increased lung tissue collagen deposition, hydroxyproline content, and the release of activated TGFβ1 into the airway. In contrast, SAMe supplementation completely mitigated alcohol-induced priming of these aberrant fibrotic changes through decreased TGFβ1 expression in the lung. In parallel, SAMe decreased alcohol-induced TGFβ1 and Smad3 mRNA expressions by lung fibroblasts in vitro. CONCLUSIONS These new experimental findings demonstrate that chronic alcohol ingestion renders the experimental mouse lung susceptible to fibrosis following bleomycin-induced ALI, and that these effects are likely driven by alcohol-mediated oxidative stress and its induction and activation of TGFβ1.

Background: Accurate medication reconciliation is a crucial aspect of inpatient as well as outpatient medicine and can prevent many medical errors. Electronic health records do not preclude significant discrepancies between documentation and actual patient practice. Thus the best source of information remains the patient himself/herself. In clinical practices worldwide, especially those that cater to populations belonging to low socio-economic groups, getting the patient to bring their medications at their health care visit remains the major challenge.Methods: Targeting patients visiting a public hospital's primary care clinic, we sought to increase their rates of bringing their medications or medication lists from under 50% to over 75%. We called our outcome of interest the SYM ("show-your-meds") rate. Through application of various quality improvement tools and models including fishbone, tally sheets and the PDSA (plan, do, study, act) technique, we employed and measured the effects of various interventions on improving the SYM rate of our patients.Results: The quality improvement exercise was carried out over six months, and various tools were employed. A SYM rate that was consistently higher than 75% (and approaching 100%) was achieved with the introduction of a specific, standardized phone message sent out to patients during the week before their healthcare visit. Several barriers to implementation of this and other interventions were also identified along the way and addressed appropriately.Conclusions: We were able to demonstrate that patients are most likely to bring their medications to clinic if verbally reminded close to the scheduled healthcare visit. Moreover, we identified several barriers to achieving a high SYM rate and also came up with their solutions. Given the considerable burden of time and effort imposed by uncertainty surrounding a patient's current medication intake, we propose that investing into an automated telephone reminder system using a standardized message is cost-effective and worth its while.