Robotic pelvic side-wall lymph node dissection for rectal cancer: a systematic review of videos and application of the IDEAL 2A framework.

Lateral pelvic lymph node dissection (LPLND) in rectal cancer has gained increasing traction worldwide. Robotic LPLND is an emerging technique. Utilising the IDEAL (idea, development, exploration, assessment and long-term follow-up) framework for surgical innovation, robotic LPLND is currently at the IDEAL 2A stage (development) mainly limited to case reports, case series and videos. A systematic literature review was performed for videographic robotic LPLND. Pubmed, Ovid and Web of Science were searched with a predefined search strategy. The LapVEGAS score for peer review of video surgery was adapted for the robotic approach (RoVEGAS) and applied to measure video quality. Two reviewers independently reviewed videos and consensus reached on technical steps and learning points. Data are presented as a narrative synthesis of results. The IDEAL 2A framework was applied to videos to assess their content at the present stage of innovation. A total of 83 abstracts were identified. In accordance with the PRISMA statement, nine videos were analysed. Adherence to the complete IDEAL 2a framework was low. All videos demonstrated LPLND; however, reporting of clinical outcomes was heterogeneous and completed in six of nine videos. Histopathology was reported in six videos, with other outcomes variably reported. No videos presented patient-reported outcome measures. Two videos reported presence or absence of recurrence on follow-up. Video articles provide a valuable educational resource in dissemination and adoption of robotic techniques. Standardisation of reporting objectives are needed. Complete reporting of pathology and oncologic outcomes is required in videographic procedural-based publications to meet the IDEAL 2A framework criteria.

Advances in our understanding of the pathophysiology of Type 1 diabetes: lessons from the NOD mouse.

T1D (Type 1 diabetes) is an autoimmune disease caused by the immune-mediated destruction of pancreatic ß-cells. Studies in T1D patients have been limited by the availability of pancreatic samples, a protracted pre-diabetic phase and limitations in markers that reflect ß-cell mass and function. The NOD (non-obese diabetic) mouse is currently the best available animal model of T1D, since it develops disease spontaneously and shares many genetic and immunopathogenic features with human T1D. Consequently, the NOD mouse has been extensively studied and has made a tremendous contribution to our understanding of human T1D. The present review summarizes the key lessons from NOD mouse studies concerning the genetic susceptibility, aetiology and immunopathogenic mechanisms that contribute to autoimmune destruction of ß-cells. Finally, we summarize the potential and limitations of immunotherapeutic strategies, successful in NOD mice, now being trialled in T1D patients and individuals at risk of developing T1D.