In situ simulation-based team training for post-cardiac surgical emergency chest reopen in the intensive care unit.

Emergency chest reopen of the post cardiac surgical patient in the intensive care unit is a high-stakes but infrequent procedure which requires a high-level team response and a unique skill set. We evaluated the impact on knowledge and confidence of team-based chest reopen training using a patient simulator compared with standard video-based training. We evaluated 49 medical and nursing participants before and after training using a multiple choice questions test and a questionnaire of self-reported confidence in performing or assisting with emergency reopen. Both video- and simulation-based training significantly improved results in objective and subjective domains. Although the post-test scores did not differ between the groups for either the objective (P = 0.28) or the subjective measures (P = 0.92), the simulation-based training produced a numerically larger improvement in both domains. In a multiple choice question out of 10, participants improved by a mean of 1.9 marks with manikin-based training compared to 0.9 with video training (P = 0.03). On a questionnaire out of 20 assessing subjective levels of confidence, scores improved by 3.9 with manikin training compared to 1.2 with video training (P = 0.002). Simulation-based training appeared to be at least as effective as video-based training in improving both knowledge and confidence in post cardiac surgical emergency resternotomy.

An important von Hippel-Lindau tumor suppressor domain mediates Sp1-binding and self-association.

VHL is the causative gene for both von Hippel-Lindau (VHL) disease and sporadic clear-cell renal cancer. We showed earlier that VHL downregulates vascular endothelial growth factor transcription by directly binding and inhibiting the transcriptional activator Sp1. We have now mapped the VHL Sp1-binding domain to amino acids 96-122. The 96-122 domain is disproportionately affected by substitution mutations, which interfere with the VHL-Sp1 interaction. Deletion of the 96-122 domain prevents VHL effects on Sp1 DNA binding and on VHL target gene expression, indicating the domain contributes importantly to VHL tumor suppressor activity. Nevertheless, prevention of the VHL-Sp1 interaction only partially abrogates VHL's transcriptional repressor activity, supporting the existence of VHL transcriptional effectors in addition to Sp1. VHL also directly interacts with the Sp1 zinc fingers and self-associates via the 96-122 domain, which furthermore suggest the domain may bind other metalloproteins and contribute to VHL dominant-negative effects.