A dedicated robotic bedside physician assistant significantly enhances trainee console operating time in general thoracic surgery.

Objective: As trainees rotate through thoracic subspecialties within their curricula, a crucial portion of their robotic training consists of actual console operating time. The more time spent on the surgeon console, the greater the development will be through the course of their training. Implementing a physician assistant at the bedside may increase the operative console time for the trainee and develop robotic skills in a more expeditious rate. The objective was to evaluate the impact a designated robotic physician assistant can have on trainee console learning opportunity. Methods: Operating room data collected consisted of all robotic general thoracic surgical cases that trainees participated in with and without a physician assistant present. Metrics regarding case efficiency included anesthesia ready-to-incision, incision-to-console, and raw resident console times. By using PRISM software, a nonparametric t test was used to analyze each averaged data group compared between when a physician assistant was present and not present. Results: The mean resident console time without and with a physician assistant assist was 45.8 minutes and 80.9 minutes, respectively (P < .0001). The average portion of a case performed by a trainee similarly without and with a physician assistant present was 28.0% and 77.1%, respectively (P < .0001). Case efficiency metrics between physician assistant presence cohorts showed no difference. Conclusions: Thoracic surgical trainees have increased opportunity for robotic skill development within a fellowship or resident program curriculum when a designated robotic physician assistant is present in the operating room. These findings are significant for the improvement of residency and fellowship robotic training models moving forward by incorporating robotic-specialized physician assistants in academic institutions.

Loss of Dis3l2 partially phenocopies Perlman syndrome in mice and results in up-regulation of Igf2 in nephron progenitor cells.

Loss of function of the DIS3L2 exoribonuclease is associated with Wilms tumor and the Perlman congenital overgrowth syndrome. LIN28, a Wilms tumor oncoprotein, triggers the DIS3L2-mediated degradation of the precursor of let-7, a microRNA that inhibits Wilms tumor development. These observations have led to speculation that DIS3L2-mediated tumor suppression is attributable to let-7 regulation. Here we examine new DIS3L2-deficient cell lines and mouse models, demonstrating that DIS3L2 loss has no effect on mature let-7 levels. Rather, analysis of Dis3l2-null nephron progenitor cells, a potential cell of origin of Wilms tumors, reveals up-regulation of Igf2, a growth-promoting gene strongly associated with Wilms tumorigenesis. These findings nominate a new potential mechanism underlying the pathology associated with DIS3L2 deficiency.