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Omori T.,Suzuka Chuo General Hospital | Hamada T.,Suzuka Chuo General Hospital | Noguchi D.,Suzuka Chuo General Hospital | Ito T.,Suzuka Chuo General Hospital | And 3 more authors.
Japanese Journal of Gastroenterological Surgery | Year: 2015

A 46-year-old man with a past history of gastrointestinal bypass operation was admitted to our hospital because of epigastric pain and jaundice. CT showed not only stones in both the gallbladder and common bile duct, but also anatomical anomalies, with the stomach and liver in the normal position, and the horizontal part of the duodenum running from left to right behind the superior mesenteric artery and vein, resulting in partial situs inversus distal to the duodenum. Right-sided round ligament, annular pancreas, and polysplenia were also apparent. The patient was given a diagnosis of cholangitis. We first tried biliary drainage and choledocholithotomy endoscopically, but due to difficulty approaching the papilla of Vater, this proved unsuccessful. We therefore performed cholecystectomy and choledocholithotomy as soon as possible. The gallbladder was on the left side of the round ligament and the cystic duct joined the common bile duct from the left side. No stones were found in the common bile duct, but a retrograde transhepatic biliary drainage (RTBD) tube was placed preparatory to choledocholithotomy for the remaining stones. The postoperative course was uneventful. The RTBD tube was removed 1 month postoperatively. © 2015 The Japanese Society of Gastroenterological Surgery.

Murata K.,Jichi Medical University | Suzuki H.,Jichi Medical University | Okano H.,Suzuka Chuo General Hospital | Oyamada T.,Jichi Medical University | And 2 more authors.
International Journal of Oncology | Year: 2010

Des-γ-carboxy prothrombin (DCP) is an established HCC tumor marker, but the precise mechanism of its production is still unclear. Recently, we demonstrated that cytoskeletal changes during epithelial-to-fibroblastoid conversion (EFC) or epithelial mesenchymal transition (EMT) induced by chemicals plays a critical mechanistic role in DCP production via impairment in vitamin K uptake. Our proposed mechanism of DCP production is consistent with substantial clinical evidence. Supplementary vitamin K2 analogues reduced serum DCP levels in hepatocellular carcinoma (HCC) patients. HCC patients with high serum DCP are associated with vascular invasion, metastasis and tumor recurrence. On the other hand, hypoxia has been reported to induce EMT or cytoskeletal changes. Therefore, we examined whether hypoxia induced DCP production during EFC or EMT in HCC cells. Indeed, hypoxic stimulation induced hepatoma cell lines (HepG2 or PLC/PRF/5 cells) to undergo EFC or EMT and these cells produced DCP. Immunofluorescence study demonstrated that hypoxic stimulation impaired labeled low-density lipoprotein uptake, which was a surrogate for vitamin K uptake. In addition, fine filamentous actin network, which has crucial role for clathrin-mediated endocytosis of vitamin K, was disrupted in DCP producing cells by hypoxic stimulation. Thus, hypoxic stimulation induced HCC cells to produce DCP in the same mechanism as chemicals. Furthermore, immunohistochemical study using surgically resected HCC samples showed that a positive staining of nuclear hypoxia inducible factor (HIF)-1α was more frequently observed in HCC cells with stronger staining intensity of DCP. Importantly, clinical observations that DCP as an HCC tumor marker was more useful in larger tumors, which is likely to be exposed with hypoxia during tumor development, support our results.

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