Quantitative pediatric surgical skill assessment using a rapid-prototyped chest model.

INTRODUCTION: Though minimally invasive pediatric surgery has become more widespread, pediatric-specific surgical skills have not been quantitatively assessed. MATERIAL AND METHODS: As a first step toward the quantification of pediatric-specific surgical skills, a pediatric chest model comprising a three-dimensional rapid-prototyped pediatric ribcage with accurate anatomical dimensions, a suturing skin model with force-sensing capability, and forceps with motion-tracking sensors were developed. A skill assessment experiment was conducted by recruiting 16 inexperienced pediatric surgeons and 14 experienced pediatric surgeons to perform an endoscopic intracorporeal suturing and knot-tying task in both the pediatric chest model setup and the conventional box trainer setup. RESULTS: The instrument motion measurement was successful in only 20 surgeons due to sensor failure. The task completion time, total path length of instruments, and applied force were compared between the inexperienced and experienced surgeons as well as between the box trainer and chest model setups. The experienced surgeons demonstrated better performance in all parameters for both setups, and the pediatric chest model was more challenging due to the pediatric features replicated by the model. CONCLUSION: The pediatric chest model was valid for pediatric skill assessment, and further analysis of the collected data will be conducted to further investigate pediatric-specific skills.

Video-based skill assessment of endoscopic suturing in a pediatric chest model and a box trainer.

PURPOSE: Pediatric endoscopic surgery requires special surgical skills because of the small working space and tissue fragility. This article presents a video-based skill assessment method for endoscopic suturing using a pediatric chest model. MATERIALS AND METHODS: A commercial suture pad was placed in a rapid-prototyped pediatric chest model of a 1-year-old patient to simulate the thoracoscopic repair of esophageal atresia type C. Twenty-eight pediatric surgeons (9 experts, 9 intermediates, and 10 trainees) performed an endoscopic intracorporeal suturing and knot-tying task both in the pediatric chest model and in a box trainer. The tasks were video-recorded and rated by two blinded observers using the 29-point checklist method and a suturing errors score sheet method. The task completion time and the number of needle manipulations were measured. RESULTS: The expert group showed better performance than the intermediate and trainee groups in the pediatric chest model, and the differences were larger than those in the box trainer. Significant differences between the expert and the trainee groups were observed in the items related to safety such as the skills for keeping the needle in view at all times. Significant differences between the expert and intermediate groups were observed in the items related to task quality and efficiency such as the smoothness of knot tying and the number of needle manipulations. CONCLUSIONS: Video-based skill assessment of endoscopic suturing using the pediatric chest model and a box trainer distinguished pediatric endoscopic surgeons according to their clinical experience, and pediatric-specific skills were identified.

Arsenic trioxide augments Chk2/p53-mediated apoptosis by inhibiting oncogenic Wip1 phosphatase.

The oncogenic Wip1 phosphatase (PPM1D) is induced upon DNA damage in a p53-dependent manner and is required for inactivation or suppression of DNA damage-induced cell cycle checkpoint arrest and of apoptosis by dephosphorylating and inactivating phosphorylated Chk2, Chk1, and ATM kinases. It has been reported that arsenic trioxide (ATO), a potent cancer chemotherapeutic agent, in particular for acute promyelocytic leukemia, activates the Chk2/p53 pathway, leading to apoptosis. ATO is also known to activate the p38 MAPK/p53 pathway. Here we show that phosphatase activities of purified Wip1 toward phosphorylated Chk2 and p38 in vitro are inhibited by ATO in a dose-dependent manner. Furthermore, DNA damage-induced phosphorylation of Chk2 and p38 in cultured cells is suppressed by ectopic expression of Wip1, and this Wip1-mediated suppression can be restored by the presence of ATO. We also show that treatment of acute promyelocytic leukemia cells with ATO resulted in induction of phosphorylation and activation of Chk2 and p38 MAPK, which are required for ATO-induced apoptosis. Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. These results exemplify that Wip1 is a direct molecular target of ATO.