Background: It is critical that medical students develop self-directed, lifelong learning skills to navigate medical school successfully and to become competent healthcare professionals. Moreover, the Liaison Committee on Medical Education (LCME), the USA medical school accrediting body, requires activities designed to help students develop self-directed learning (SDL) skills in the preclinical years. Objective: We evaluated the feasibility and effectiveness of a self-directed learning activity in a 6-week first-year medical student course. Design: The course director assigned infectious disease case studies to teams of first-year medical students who individually assessed their knowledge gaps of the case, identified scholarly sources to fill their knowledge gaps, shared the information with their teammates, and reflected on their ability to guide their own learning. Students were asked to rate workload, team effort, acquisition of new clinical knowledge, and lifelong learning skills. Students were also asked to reflect on how this assignment affected their perception of their SDL skills. Descriptive statistics were used to analyze responses to the Likert scale questions. Thematic analysis was applied to the comments. Results: Survey response rate was 80% (131/163). Students strongly or moderately agreed that 1) they spent an appropriate amount of time on the project (94%), 2) the workload was evenly distributed among their teammates (95%), 3) their teammates made significant and timely contributions to the project (97%), 4) the project contributed to learning new clinical knowledge (92%), and 5) the project contributed to the acquisition of lifelong learning skills (85%). The analysis team identified four themes from student reflections on their perception of their self-directed learning skills: self-learning skills, collaboration, application, and metacognition, Conclusions: Study results demonstrated that we successfully implemented a case-based SDL activity in a first-year medical school course and that students perceived the activity as a valuable learning experience.

Production of superoxide radicals by osteoclasts is necessary for normal bone degradation. White blood cell superoxide, needed for bacterial killing, is produced by activated NADPH oxidase. Since osteoclasts and white blood cells share a common hematopoietic origin, we initiated experiments to test the hypothesis that superoxide radicals at the osteoclast-bone interface are produced by NADPH oxidase. Diphenyl iodonium (IDP), an inhibitor of NADPH oxidase, blocked superoxide generation and decreased osteoclastic bone resorption in cultures of calvarial explants from normal mice. Interferon (IFN) gamma, a stimulant of NADPH oxidase activity, increased superoxide production and bone resorption in cultures of calvarial explants from osteopetrotic (microphthalmic) mice. IDP blocked the stimulatory effects of IFN in this bone resorption model. These data suggest that osteoclastic superoxide is produced by NADPH oxidase.

To determine the pattern of cellular expression of donor MHC class I and class II antigens during the course of rat cardiac allograft rejection, ACI cardiac allografts transplanted to BN recipients were examined from day 2 to day 6 using immunohistologic and immunoelectron microscopic methods. We used both monomorphic and donor-specific mouse anti-rat MHC class I and class II mAbs in this study. In normal ACI hearts, MHC class I reactivity was confined to the vascular endothelium and to interstitial cells. Ongoing rejection was characterized by an increased donor MHC class I staining intensity of microvascular endothelium and induction of donor class I surface reactivity on cardiac myofibers. Donor MHC class II reactivity was exclusively confined to interstitial dendritic cells (IDC) in both normal ACI hearts and in rejecting allografts, although rejection was associated with marked fluctuations in class II IDC frequency. An early numerical depression in class II IDC present in both allografts and syngeneic heart grafts was attributed to a direct effect of the transplantation procedure. By days 3-4, allografts showed an absolute overall increase in donor class II IDC frequency, which was associated with the presence of multiple localized high-density IDC-lymphocyte aggregates. The lymphocytes present in the focal areas were predominantly of the class II-reactive Th cell subpopulation. These aggregates may thus represent the in vivo homologue of dendritic cell-lymphocyte clustering, which has been shown to be required for primary class II allosensitization in the rat and mouse in vitro. During the late phase of rejection, there was a marked numerical fall in donor class II IDC, which correlated with extensive overall graft destruction. This study has shown that acute rat cardiac allograft rejection can occur in the absence of donor MHC class II expression by allograft vascular endothelium and cardiac myofibers. The IDC, which are believed to represent the principal class II alloantigen presenting cells in the rat heart, remain the sole class II-expressing cellular constituents of the graft throughout the course of rejection.

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