5 Slides in 5 Minutes: Incorporating CanMEDS Competencies on Acute Care Surgery.

BACKGROUND: The University of British Columbia (UBC) Division of General Surgery developed an initiative entitled "5-in-5s" to improve educational opportunities on the Acute Care Surgery (ACS) service. We examined whether 5-in-5s are felt to be a valuable teaching tool, and evaluated their ability to incorporate CanMEDS competencies within the General Surgery program. METHODS: A web-based survey was distributed to all general surgery trainees and staff on ACS that have participated in 5-in-5s. RESULTS: A total of 37 responses were collected (62% response rate). All respondents felt 5-in-5s were valuable overall. Four of the seven CanMEDS competencies were evaluated. About 100% felt their knowledge was positively impacted by presenting, and 80% by attending alone. About 71% of respondents agreed that 5-in5s provided opportunities for health advocacy, 50% for collaboration, and 36% for leadership. CONCLUSION: We identified 5-in-5s as a valuable teaching method and a novel approach to integrate CanMEDS competencies into ACS training.

IVIg and LPS Co-stimulation Induces IL-10 Production by Human Monocytes, Which Is Compromised by an FcγRIIA Disease-Associated Gene Variant.

Intravenous Immunoglobulin (IVIg) is used to treat autoimmune or inflammatory diseases, but its mechanism of action is not completely understood. We asked whether IVIg can induce interleukin-10 (IL-10) and reduce pro-inflammatory cytokine production in human monocytes, and whether this response is reduced in monocytes from people with an Fcγ receptor IIA (FcγRIIA) gene variant, which is associated with increased risk of inflammatory diseases and poor response to antibody-based biological therapy. IVIg increased IL-10 production and reduced pro-inflammatory cytokine production in response to bacterial lipopolysaccharide (LPS), which required FcγRI and FcγRIIB and activation of MAPKs, extracellular signal-regulated kinase 1/2 (ERK1/2), and p38. IL-10 production was lower and pro-inflammatory cytokine production was higher in monocytes from people with the FcγRIIA risk variant and the risk variant prevented IL-10 production in response to (IVIg+LPS). Finally, we show that IVIg did not induce MAPK activation in monocytes from people with the risk variant. Our results demonstrate that IVIg can skew human monocytes to an anti-inflammatory, IL-10-producing activation state, which is compromised in monocytes from people with the FcγRIIA risk variant. This research has profound implications for the use of IVIg because 25% of the population is homozygous for the FcγRIIA risk variant and its efficacy may be reduced in those individuals. In addition, this research may be useful to develop new therapeutic strategies to replace IVIg by cross-linking FcγRIs and FcγRIIBs to promote anti-inflammatory macrophage activation, independent of the FcγRIIA genotype.