RESUMO
BACKGROUND: Concerns persist about the effect of current duty hour reforms on resident educational outcomes. We investigated whether a flexible, less-restrictive duty hour policy (Flexible Policy) was associated with differential general surgery examination performance compared with current ACGME duty hour policy (Standard Policy). STUDY DESIGN: We obtained examination scores on the American Board of Surgery In-Training Examination, Qualifying Examination (written boards), and Certifying Examination (oral boards) for residents in 117 general surgery residency programs that participated in the Flexibility in Duty Hour Requirements for Surgical Trainees (FIRST) Trial. Using bivariate analyses and regression models, we compared resident examination performance across study arms (Flexible Policy vs Standard Policy) for 2015 and 2016, and 1 year of the Qualifying Examination and Certifying Examination. Adjusted analyses accounted for program-level factors, including the stratification variable for randomization. RESULTS: In 2016, FIRST trial participants were 4,363 general surgery residents. Mean American Board of Surgery In-Training Examination scores for residents were not significantly different between study groups (Flexible Policy vs Standard Policy) overall (Flexible Policy: mean [SD] 502.6 [100.9] vs Standard Policy: 502.7 [98.6]; p = 0.98) or for any individual postgraduate year level. There was no difference in pass rates between study arms for either the Qualifying Examination (Flexible Policy: 90.4% vs Standard Policy: 90.5%; p = 0.99) or Certifying Examination (Flexible Policy: 86.3% vs Standard Policy: 88.6%; p = 0.24). Results from adjusted analyses were consistent with these findings. CONCLUSIONS: Flexible, less-restrictive duty hour policies were not associated with differences in general surgery resident performance on examinations during the FIRST Trial. However, more years under flexible duty hour policies might be needed to observe an effect.
Assuntos
Certificação/estatística & dados numéricos , Avaliação Educacional/estatística & dados numéricos , Cirurgia Geral/educação , Internato e Residência/organização & administração , Admissão e Escalonamento de Pessoal/normas , Carga de Trabalho/normas , Certificação/normas , Cirurgia Geral/organização & administração , Humanos , Modelos Lineares , Modelos Logísticos , Guias de Prática Clínica como Assunto , Estudos Prospectivos , Estados UnidosRESUMO
A number of receptors and signaling pathways can influence the ability of dendritic cells (DC) to promote CD4(+) Th type 1 (Th1) responses. In contrast, the regulatory pathways and signaling events that govern the ability of DC to instruct Th2 cell differentiation remain poorly defined. In this report, we demonstrate that NF-kappaB1 expression within DC is required to promote optimal Th2 responses following exposure to Schistosoma mansoni eggs, a potent and natural Th2-inducing stimulus. Although injection of S. mansoni eggs induced production of IL-4, IL-5, and IL-13 in the draining lymph node of wild-type (WT) mice, NF-kappaB1(-/-) hosts failed to express Th2 cytokines and developed a polarized Ag-specific IFN-gamma response. In an in vivo adoptive transfer model in which NF-kappaB-sufficient OVA-specific DO11.10 TCR transgenic T cells were injected into OVA-immunized WT or NF-kappaB1(-/-) hosts, NF-kappaB1(-/-) APCs efficiently promoted CD4(+) T cell proliferation and IFN-gamma responses, but failed to promote Ag-specific IL-4 production. Further, bone marrow-derived DC from NF-kappaB1(-/-) mice failed to promote OVA-specific Th2 cell differentiation in in vitro coculture studies. Last, S. mansoni egg Ag-pulsed NF-kappaB1(-/-) DC failed to prime for Th2 cytokine responses following injection into syngeneic WT hosts. Impaired Th2 priming by NF-kappaB1(-/-) DC was accompanied by a reduction in MAPK phosphorylation in Ag-pulsed DC. Taken together, these studies identify a novel requirement for DC-intrinsic expression of NF-kappaB1 in regulating the MAPK pathway and governing the competence of DC to instruct Th2 cell differentiation.