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Introduction: Strengthening The Reporting Of Cohort Studies in Surgery (STROCSS) guidelines were developed in 2017 in order to improve the reporting quality of observational studies in surgery and updated in 2019. In order to maintain relevance and continue upholding good reporting quality among observational studies in surgery, we aimed to update STROCSS 2019 guidelines. Methods: A STROCSS 2021 steering group was formed to come up with proposals to update STROCSS 2019 guidelines. An expert panel of researchers assessed these proposals and judged whether they should become part of STROCSS 2021 guidelines or not, through a Delphi consensus exercise. Results: 42 people (89%) completed the DELPHI survey and hence participated in the development of STROCSS 2021 guidelines. All items received a score between 7 and 9 by greater than 70% of the participants, indicating a high level of agreement among the DELPHI group members with the proposed changes to all the items. Conclusion: We present updated STROCSS 2021 guidelines to ensure ongoing good reporting quality among observational studies in surgery.

Inflammatory bowel diseases (IBD) are chronic relapsing and remitting conditions associated with long-term gut dysfunction resulting from alterations to the enteric nervous system and a loss of enteric neurons1,2. The mechanisms underlying inflammation-induced enteric neuron death are unknown. Here we report using in vivo models of experimental colitis that inflammation causes enteric neuron death by activating a neuronal signaling complex comprised of P2X7 receptors (P2X7Rs), pannexin–1 (Panx1) channels, Asc and caspases. Inhibiting P2X7Rs, Panx1, Asc or caspase activity prevents inflammation-induced neuron cell death. Preservation of enteric neurons by inhibiting Panx1 in vivo prevented the onset of inflammation-induced colonic motor dysfunction. Panx1 expression is reduced in Crohn’s disease but not ulcerative colitis. We conclude that activation of neuronal Panx1 underlies neuron death and subsequent development of the abnormal gut motility in IBD. Targeting Panx1 represents a novel neuroprotective strategy to ameliorate the progression of IBD–associated dysmotility.