Curricula for Teaching MRI Safety, and MRI and CT Contrast Safety to Residents: How Effective Are Live Lectures and Online Modules?

PURPOSE: The advent of the diagnostic radiology core examination and the new ACGME "milestone" evaluation system for radiology residents places new emphasis on topics in MRI and CT safety, and MRI and CT contrast agents. We evaluated whether either lecture-based teaching or online modules would improve baseline resident knowledge in these areas, and assessed which intervention was more effective. METHODS: Before didactic intervention, 2 cohorts were created from 57 radiology residents, with equal numbers and a matched level of training. The residents were tested on their baseline knowledge of MRI, MRI contrast safety, and CT contrast safety, using a multiple-choice examination. One group attended a live, 1-hour lecture on the preceding topics. The other engaged in 3 short online educational modules. After 6 weeks, the residents were again tested with the same questions to assess for improvement in their understanding. RESULTS: Both the module and lecture cohorts demonstrated a statistically significant increase in questions answered correctly on CT contrast safety (13.1%, P < .001, and 19.1%, P < .001, respectively), and on MRI and MRI contrast safety (12.9%, P < .001, and 14.4%, P < .001). The preintervention and postintervention scores, and degree of improvement postintervention, were similar for the module versus lecture groups, without a statistically significant difference (P = .70). Resident confidence improved in both groups, for both modalities. CONCLUSIONS: Focused didactic intervention improves resident knowledge of MRI and CT safety, and MRI and CT contrast agents. Live lectures and online modules can be equally effective, allowing residency programs flexibility.

Functional and phenotypic effects of AhR activation in inflammatory dendritic cells.

Aryl hydrocarbon receptor (AhR) activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces immune suppression. Dendritic cells (DCs) are key antigen presenting cells governing T cell activation and differentiation. However, the consequences of AhR activation in DCs are not fully defined. We hypothesized that AhR activation alters DC differentiation and generates dysfunctional DCs. To test this hypothesis, inflammatory bone marrow-derived DCs (BMDCs) from C57Bl/6 mice were generated in the presence of vehicle or TCDD. TCDD decreased CD11c expression but increased MHC class II, CD86 and CD25 expression on the BMDCs. The effects of TCDD were strictly AhR-dependent but not exclusively DRE-mediated. Similar effects were observed with two natural AhR ligands, 6-formylindolo[3,2-b]carbazole (FICZ) and 2-(1H-Indol-3-ylcarbonyl)-4-thiazolecarboxylic acid (ITE). TCDD increased LPS- and CpG-induced IL-6 and TNF-alpha production by BMDCs but decreased their NO production. TCDD decreased CpG-induced IL-12p70 production by BMDCs but did not affect their secretion of IL-10. TCDD downregulated LPS- and CpG-induced NF-kB p65 levels and induced a trend towards upregulation of RelB levels in the BMDCs. AhR activation by TCDD modulated BMDC uptake of both soluble and particulate antigens. Induction of indoleamine-2,3-dioxygenase (IDO) and TGF-beta3 has been implicated in the generation of regulatory T cells following AhR activation. TCDD increased IDO1, IDO2 and TGF-beta3 mRNA levels in BMDCs as compared to vehicle. Despite the induction of regulatory mediators, TCDD-treated BMDCs failed to suppress antigen-specific T cell activation. Thus, AhR activation can directly alter the differentiation and innate functions of inflammatory DCs without affecting their ability to successfully interact with T cells.

Effects of TCDD on the fate of naive dendritic cells.

The environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), causes immune suppression via activation of the aryl hydrocarbon receptor. Dendritic cells (DCs), the professional antigen-presenting cells in the immune system, are adversely affected by TCDD. We hypothesized that TCDD alters DC homeostasis, resulting in a loss of DCs in naive mice. To test this hypothesis, C57Bl/6 mice were gavaged with either vehicle or an immunosuppressive dose of TCDD (15 microg/kg). TCDD exposure decreased the frequency and number of splenic CD11c(high) DCs on day 7 when compared with vehicle-treated controls. TCDD increased the expression of CD86 and CD54, while decreasing the frequency of splenic CD11c(high) DCs expressing CD11a and major histocompatibility complex (MHC) class II. Moreover, TCDD selectively decreased the CD11c(high)CD8alpha(-)33D1(+) splenic DCs specialized at activating CD4(+) T cells but did not affect the regulatory CD11c(high)CD8alpha(+)DEC205(+) splenic DCs. TCDD did not alter the number or frequency of CD11c(low) splenic DCs but decreased their MHC class II and CD11a expression. Loss of splenic CD11c(high) DCs was independent of Fas-mediated apoptosis and was not due to alterations in the numbers of common DC precursors in the bone marrow or their ability to generate steady-state DCs in vitro. Instead, increased CCR7 expression on CD11c(high) DCs suggested involvement of a migratory event. Popliteal and brachial lymph node CD11c(+) cells showed elevated levels of MHC class II and CD40 following TCDD exposure. Collectively, this study shows the presence of a TCDD-sensitive splenic DC subpopulation in naive mice, suggesting that TCDD may induce suppression of T-cell-mediated immunity by disrupting DC homeostasis.