A Case of Ischemic Duodenitis Associated with Superior Mesenteric Artery Syndrome Caused by an Abdominal Aortic Aneurysm

A 74-year-old woman was admitted to our hospital with upper abdominal pain and bloody vomiting. An abdominal aneurysm compressed the third portion of the duodenum and the second portion of duodenum was distended with thickened walls as in superior mesenteric artery syndrome. Endoscopic examination showed an edematous mucosa with hemorrhagic erosions, shallow longitudinal ulcers, and star-shaped ulcers in the duodenum. We diagnosed this case as ischemic duodenitis associated with superior mesenteric artery syndrome caused by compression by an abdominal aortic aneurysm. The symptoms improved on treatment with bowel rest, total parenteral nutrition and administration of a proton pump inhibitor. We present here a rare case of ischemic duodenitis and summarize the previous medical literature on the disease

Cell competition with normal epithelial cells promotes apical extrusion of transformed cells through metabolic changes

Recent studies have revealed that newly emerging transformed cells are often apically extruded from epithelial tissues. During this process, normal epithelial cells can recognize and actively eliminate transformed cells, a process called epithelial defence against cancer (EDAC). Here, we show that mitochondrial membrane potential is diminished in RasV12-transformed cells when they are surrounded by normal cells. In addition, glucose uptake is elevated, leading to higher lactate production. The mitochondrial dysfunction is driven by upregulation of pyruvate dehydrogenase kinase 4 (PDK4), which positively regulates elimination of RasV12-transformed cells. Furthermore, EDAC from the surrounding normal cells, involving filamin, drives the Warburg-effect-like metabolic alteration. Moreover, using a cell-competition mouse model, we demonstrate that PDK-mediated metabolic changes promote the elimination of RasV12-transformed cells from intestinal epithelia. These data indicate that non-cell-autonomous metabolic modulation is a crucial regulator for cell competition, shedding light on the unexplored events at the initial stage of carcinogenesis