Chiaki Uchida

Background: Intestinal knot formation is a condition wherein two segments of the intestine are knotted together; however, reports of small-intestinal ileo-ileal knot formation are rare. Case presentation: The patient was a 62-year-old Asian male with a history of endoscopic colorectal adenoma resection and a spontaneous pneumothorax. The patient had no history of a laparotomy. He consulted his local doctor with the chief complaint of abdominal pain and was admitted to our hospital with suspicion of an acute abdomen. The abdomen had muscular guarding with tenderness and rebound tenderness. Contrast-enhanced computed tomography (CT) showed torsion of the mesentery of the small intestine with poor contrast filling. The patient was referred to our department with strangulated bowel obstruction and underwent an emergency laparotomy. Intraoperative findings revealed that two segments of the ileum were wrapped around each other to form a knot, and the strangulated small bowel was necrotic. After the release of the knot, partial resection of the small intestine was performed from 220 cm distal to the ligament of Treitz to 80 cm proximal to the cecum. The patient had a good postoperative course and was discharged on the 11th postoperative day. Conclusion: Ileo-ileal knots should be considered as part of the differential diagnosis when treating strangulated bowel obstruction.

Pancreatic stellate cells (PSCs) mainly consist of cancer-associating fibroblasts in pancreatic ductal adenocarcinoma (PDAC). The receptor for advanced glycation end products (RAGE) is implicated in the pathophysiology of diabetic complications. Here, we studied the implication of RAGE in PSC activation in PDAC. The activation of cultured mouse PSCs was evaluated by qPCR. The induction of epithelial mesenchymal transition (EMT) in PDAC cell lines was assessed under stimulation with culture supernatant from activated PSCs. A total of 155 surgically resected PDAC subjects (83 nondiabetic, 18 with ≦3-years and 54 with >3-years history of diabetes) were clinicopathologically evaluated. A high-fat diet increased the expression of activated markers in cultured PSCs, which was abrogated by RAGE deletion. Culture supernatant from activated PSCs facilitated EMT of PDAC cells with elevation of TGF−β and IL−6, but not from RAGE−deleted PSCs. Diabetic subjects complicated with metabolic syndrome, divided by cluster analysis, showed higher PSC activation and RAGE expression. In such groups, PDAC cells exhibited an EMT nature. The complication of metabolic syndrome with diabetes significantly worsened disease−free survival of PDAC subjects. Thus, RAGE in PSCs can be viewed as a new promoter and a future therapeutic target of PDAC in diabetic subjects with metabolic syndrome.