Entrustable Professional Activities (EPAs) and the Next Accreditation System reporting milestones reduce general competencies into smaller evaluable parts. However, some EPAs and reporting milestones may be too broad to use as direct assessment tools. We describe our internal medicine residency curriculum and assessment system, which uses entrustment and mapping of observable practice activities (OPAs) for resident assessment. We created discrete OPAs for each resident rotation and learning experience. In combination, these serve as curricular foundation and tools for assessment. OPA performance is measured via a 5-point entrustment scale, and mapped to milestones and EPAs. Entrustment ratings of OPAs provide an opportunity for immediate structured feedback of specific clinical skills, and mapping OPAs to milestones and EPAs can be used for longitudinal assessment, promotion decisions, and reporting. Direct assessment and demonstration of progressive entrustment of trainee skill over time are important goals for all training programs. Systems that use OPAs mapped to milestones and EPAs provide the opportunity for achieving both, but require validation.
Entrustment of milestones appears to rise progressively over time, with differences by assessor type, competency, milestone, and resident. Further research is needed to elucidate the validity of these data in promotion, remediation, and reporting decisions.
Plk1 (Polo-like kinase 1) is a critical regulator of cell cycle progression that harbors oncogenic activity and exhibits aberrant expression in multiple tumors. However, the mechanism through which Plk1 expression is regulated has not been extensively studied. Here we demonstrate that Plk1 is a target of the retinoblastoma tumor suppressor (RB) pathway. Activation of RB and related pocket proteins p107/p130 mediate attenuation of Plk1. Conversely, RB loss deregulates the control of Plk1 expression. RB pathway activation resulted in the repression of Plk1 promoter activity, and this action was dependent on the SWI/SNF chromatin remodeling complex. Although SWI/SNF subunits are lost during tumorigenesis and cooperate with RB for transcriptional repression, the mechanism through which SWI/ SNF impinges on RB action is unresolved. Therefore, we delineated the requirement of SWI/SNF for three critical facets of Plk1 promoter regulation: transcription factor binding, corepressor binding, and histone modification. We find that E2F4 and pocket protein association with the Plk1 promoter is independent of SWI/SNF. However, these analyses revealed that SWI/SNF is required for histone deacetylation of the Plk1 promoter. The importance of SWI/SNF-dependent histone deacetylation of the Plk1 promoter was evident, because blockade of this event restored Plk1 expression in the presence of active RB. In summary, these data demonstrate that Plk1 is a target of the RB pathway. Moreover, these findings demonstrate a hierarchical role for SWI/SNF in the control of promoter activity through histone modification.
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