Simulation of integrative physiology for medical education.

Medical education is founded on the understanding of physiology. While lecture materials and reading contribute to the learning of physiology, the richness and complexity of the subject suggest that more active learning methods may provide a richer introduction to the science as it applies to the practice of medicine. Simulation has been previously used in basic science to better understand the interaction of physiological systems. In the current context, simulation generally refers to interactive case studies performed with a manikin or anatomic device. More recently, simulation has grown to encompass computational simulation: virtual models of physiology and pathophysiology where students can see in a mechanistic setting how tissues and organs interact with one another to respond to changes in their environment. In this manuscript, we discuss how simulation fits into the overall history of medical education, and detail two computational simulation products designed for medical education. The first of these is an acute simulator, JustPhysiology, which reduces the scope of a large model, HumMod, down to a more focused interface. The second is Sycamore, an electronic health record-delivered, real time simulator of patients designed to teach chronic patient care to students. These products represent a new type of tool for medical and allied health students to encourage active learning and integration of basic science knowledge into clinical situations.

JAM-A as a prognostic factor and new therapeutic target in multiple myeloma.

Cell adhesion in the multiple myeloma (MM) microenvironment has been recognized as a major mechanism of MM cell survival and the development of drug resistance. Here we addressed the hypothesis that the protein junctional adhesion molecule-A (JAM-A) may represent a novel target and a clinical biomarker in MM. We evaluated JAM-A expression in MM cell lines and in 147 MM patient bone marrow aspirates and biopsies at different disease stages. Elevated JAM-A levels in patient-derived plasma cells were correlated with poor prognosis. Moreover, circulating soluble JAM-A (sJAM-A) levels were significantly increased in MM patients as compared with controls. Notably, in vitro JAM-A inhibition impaired MM migration, colony formation, chemotaxis, proliferation and viability. In vivo treatment with an anti-JAM-A monoclonal antibody (αJAM-A moAb) impaired tumor progression in a murine xenograft MM model. These results demonstrate that therapeutic targeting of JAM-A has the potential to prevent MM progression, and lead us to propose JAM-A as a biomarker in MM, and sJAM-A as a serum-based marker for clinical stratification.