Can fatigue affect acquisition of new surgical skills? A prospective trial of pre- and post-call general surgery residents using the da Vinci surgical skills simulator.

OBJECTIVE: To study the effects of fatigue on general surgery residents' performance on the da Vinci Skills Simulator (dVSS). METHODS: 15 General Surgery residents from various postgraduate training years (PGY2, PGY3, PGY4, and PGY5) performed 5 simulation tasks on the dVSS as recommended by the Robotic Training Network (RTN). The General Surgery residents had no prior experience with the dVSS. Participants were assigned to either the Pre-call group or Post-call group based on call schedule. As a measure of subjective fatigue, residents were given the Epworth Sleepiness Scale (ESS) prior to their dVSS testing. The dVSS MScore™ software recorded various metrics (Objective Structured Assessment of Technical Skills, OSATS) that were used to evaluate the performance of each resident to compare the robotic simulation proficiency between the Pre-call and Post-call groups. RESULTS: Six general surgery residents were stratified into the Pre-call group and nine into the Post-call group. These residents were also stratified into Fatigued (10) or Nonfatigued (5) groups, as determined by their reported ESS scores. A statistically significant difference was found between the Pre-call and Post-call reported sleep hours (p = 0.036). There was no statistically significant difference between the Pre-call and Post-call groups or between the Fatigued and Nonfatigued groups in time to complete exercise, number of attempts, and high MScore™ score. CONCLUSION: Despite variation in fatigue levels, there was no effect on the acquisition of robotic simulator skills.

Zinc Finger and X-Linked Factor (ZFX) Binds to Human SET Transcript 2 Promoter and Transactivates SET Expression.

SET (SE Translocation) protein carries out multiple functions including those for protein phosphatase 2A (PP2A) inhibition, histone modification, DNA repair, and gene regulation. SET overexpression has been detected in brain neurons of patients suffering Alzheimer's disease, follicle theca cells of Polycystic Ovary Syndrome (PCOS) patients, and ovarian cancer cells, indicating that SET may play a pathological role for these disorders. SET transcript 2, produced by a specific promoter, represents a major transcript variant in different cell types. In this study, we characterized the transcriptional activation of human SET transcript 2 promoter in HeLa cells. Promoter deletion experiments and co-transfection assays indicated that ZFX, the Zinc finger and X-linked transcription factor, was able to transactivate the SET promoter. A proximal promoter region containing four ZFX-binding sites was found to be critical for the ZFX-mediated transactivation. Mutagenesis study indicated that the ZFX-binding site located the closest to the transcription start site accounted for most of the ZFX-mediated transactivity. Manipulation of ZFX levels by overexpression or siRNA knockdown confirmed the significance and specificity of the ZFX-mediated SET promoter activation. Chromatin immunoprecipitation results verified the binding of ZFX to its cognate sites in the SET promoter. These findings have led to identification of ZFX as an upstream factor regulating SET gene expression. More studies are required to define the in vivo significance of this mechanism, and specifically, its implication for several benign and malignant diseases related to SET dysregulation.