4 research outputs found

    Can We Learn in the Sandbox Together?: Interprofessional Case Conferences as Facilitation Tools

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    Duke Medicine utilized interprofessional case conferences (ICCs) from 2008-2012 with the objective of modeling and facilitating development of teamwork skills among diverse health profession students, including physical therapy, physician assistant, medical doctor and nursing. The purpose of this publication was to describe the operational process used to develop and implement the ICCs and measure the success of the ICCs in order to shape future work. The ICCs were offered to develop skills and attitudes essential for participation in healthcare teams. Students were facilitated by faculty of different professions to conduct a comprehensive historical assessment of a standardized patient (SP), determine pertinent physical and lab assessments to undertake, and develop and share a comprehensive management plan. Cases included patient problems that were authentic and relevant to each professional student in attendance. The main barriers to implementation are outlined and the focus on the process of working together is highlighted. Evaluation showed high satisfaction rates among participants and the outcomes from these experiences are presented. The limitations of these results are discussed and recommendations for future assessment are emphasized. The ICCs demonstrated that students will come together voluntarily to learn in teams, even at a research-focused institution, and express benefit from the collaborative exercise

    Inhibition of renin-angiotensin system (RAS) reduces ventricular tachycardia risk by altering connexin43

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    Renin-angiotensin system (RAS) activation is associated with arrhythmias. We investigated the effects of RAS inhibition in cardiac-specific angiotensin-converting enzyme (ACE) overexpression (ACE 8/8) mice, which exhibit proclivity to ventricular tachycardia (VT) and sudden death because of reduced connexin43 (Cx43). ACE 8/8 mice were treated with an ACE inhibitor (captopril) or an angiotensin receptor type-1 blocker (losartan). Subsequently, electrophysiological studies were performed, and the hearts were extracted for Cx43 quantification using immunoblotting, immunohistochemistry, fluorescent dye spread method, and sodium current quantification using whole cell patch clamping. VT was induced in 12.5% of captopril-treated ACE 8/8 and in 28.6% of losartan-treated mice compared to 87.5% of untreated mice (P<0.01). Losartan and captopril treatment increased total Cx43 2.4-fold (P=0.01) and the Cx43 phosphorylation ratio 2.3-fold (P=0.005). Treatment was associated with a recovery of gap junctional conductance. Survival in treated mice improved to 0.78 at 10 weeks (95% confidence interval 0.64 to 0.92), compared to the expected survival of less than 0.50. In a model of RAS activation, arrhythmic risk was correlated with reduced Cx43 amount and phosphorylation. RAS inhibition resulted in increased total and phosphorylated Cx43, decreased VT inducibility, and improved survival
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