Role of Radiology in the Preoperative Detection of Arterial Calcification and Celiac Trunk Stenosis and Its Association with Anastomotic Leakage Post Esophagectomy, an Up-to-Date Review of the Literature.

Surgical resection of the esophagus remains a critical component of the multimodal treatment of esophageal cancer. Anastomotic leakage (AL) is the most significant complication following esophagectomy, in terms of clinical implications. Identifying risk factors for AL is important for modifying patient management and improving surgical outcomes. This review aims to examine the role of radiological risk factors for AL after esophagectomy, and in particular, arterial calcification and celiac trunk stenosis. Eligible publications prior to 25 August 2021 were retrieved from Medline and Google Scholar using a predefined search algorithm. A total of 68 publications were identified, of which 9 original studies remained for in-depth analysis. The majority of these studies found correlations between calcifications in the aorta, celiac trunk, and right post-celiac arteries and AL following esophagectomy. Some studies suggest celiac trunk stenosis as a more appropriate surrogate. Our up-to-date review highlights the need for automated quantification of aortic calcifications, as well as the degree of celiac trunk stenosis in preoperative computed tomography in patients undergoing esophagectomy, to obtain robust and reproducible measurements that can be used for a definite correlation.

Obesity and hyperinsulinemia drive adipocytes to activate a cell cycle program and senesce.

Obesity is considered an important factor for many chronic diseases, including diabetes, cardiovascular disease and cancer. The expansion of adipose tissue in obesity is due to an increase in both adipocyte progenitor differentiation and mature adipocyte cell size. Adipocytes, however, are thought to be unable to divide or enter the cell cycle. We demonstrate that mature human adipocytes unexpectedly display a gene and protein signature indicative of an active cell cycle program. Adipocyte cell cycle progression associates with obesity and hyperinsulinemia, with a concomitant increase in cell size, nuclear size and nuclear DNA content. Chronic hyperinsulinemia in vitro or in humans, however, is associated with subsequent cell cycle exit, leading to a premature senescent transcriptomic and secretory profile in adipocytes. Premature senescence is rapidly becoming recognized as an important mediator of stress-induced tissue dysfunction. By demonstrating that adipocytes can activate a cell cycle program, we define a mechanism whereby mature human adipocytes senesce. We further show that by targeting the adipocyte cell cycle program using metformin, it is possible to influence adipocyte senescence and obesity-associated adipose tissue inflammation.