Background The COVID-19 pandemic has led to widespread cancelation of electively scheduled surgeries, including for colorectal, pancreatic, and gastric cancer. The American College of Surgeons and the Society of Surgical Oncology have released guidelines for triage of these procedures. We seek to synthesize available evidence on delayed resection and oncologic outcomes, while also providing a critical assessment of the released guidelines. Methods A systematic review was conducted to identify literature between 2005 and 2020 investigating the impact of time to surgery on oncologic outcomes in colorectal, pancreatic, and gastric cancer. Results For colorectal cancer, 1066 abstracts were screened and 43 papers were included. In primarily resected colon cancer, delay over 30 to 40 days is associated with lower survival. In rectal cancer, time to surgery over 7 to 8 weeks following neoadjuvant therapy is associated with decreased survival. Three hundred ninety-four abstracts were screened for pancreatic cancer and nine studies were included. Two studies demonstrate increased unexpected progression with delayed surgery over 30 days. Out of 633 abstracts screened for gastric cancer, six studies were included. No identified study demonstrated worse survival with increased time to surgery. Conclusion Moderate evidence suggests that delayed resection of colorectal cancer worsens survival; the impact of time to surgery on gastric and pancreatic cancer outcomes is uncertain. Early resection of gastrointestinal malignancies provides the best chance for curative therapy. During the COVID-19 pandemic, prioritization of procedures should account for available evidence on time to surgery and oncologic outcomes.

Acute respiratory distress syndrome is the most severe form of acute lung injury (ALI) and is associated with significant mortality. Lipopolysaccharide (LPS)-induced injury is a valuable murine model of ALI but there is a paucity of data on lung regeneration and the role of angiogenic signaling involving vascular endothelial growth factor (VEGF). Eight-week-old male C57BL/6J mice were randomized to receive intratracheal instillation of either LPS or isovolumetric phosphate buffered saline as a vehicle control. Mice were observed at a single follow-up time-point that was either short-term (24 h or 4 days) or long-term (7 days or 4 weeks). On pulmonary function testing, LPS-treated mice had increased compliance at 4 weeks post-instillation, which correlated with decreased vascularization and with time-dependent, progressive decrease in alveolarization. Treadmill exercise tolerance testing demonstrated impaired performance at 24 h, 4 days and 4 weeks following LPS exposure. On lung protein analysis, LPS instillation decreased VEGF expression at up to 4 weeks, and decreased activation of its key receptor, VEGFR2 at 7 days and 4 weeks post-instillation. Together, these data provide insight on long-term pulmonary functional outcomes 4 weeks after ALI and identify angiogenic proteins as possible therapeutic targets following lung injury.

Free fatty acid receptors (FFARs) are a class of G protein-coupled receptors (GPCRs) that have wide-ranging effects on human physiology. The four well-characterized FFARs are FFAR1/GPR40, FFAR2/GPR43, FFAR3/GPR41, and FFAR4/GPR120. Short-chain (<6 carbon) fatty acids target FFAR2/GPR43 and FFAR3/GPR41. Medium- and long-chain fatty acids (6–12 and 13–21 carbon, respectively) target both FFAR1/GPR40 and FFAR4/GPR120. Signaling through FFARs has been implicated in non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), intestinal failure-associated liver disease (IFALD), and a variety of other liver disorders. FFARs are now regarded as targets for therapeutic intervention for liver disease, diabetes, obesity, hyperlipidemia, and metabolic syndrome. In this review, we provide an in-depth, focused summary of the role FFARs play in liver health and disease.