Ryuji Tsutsumi

A new suppressive agent against interleukin-1β and tumor necrosis factor-α enhances liver regeneration after partial hepatectomy in rats

In the present study, the effect of FR167653, a novel suppressive agent against interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), on liver regeneration was investigated in rats after partial hepatectomy (PH). Doses of 1, 3 and 5 mg/kg per h FR167653 (FR-1, FR-3 and FR-5, respectively) were given intravenously 30 min before PH, while the control was given normal saline. Serum chemistries were serially monitored, and liver regeneration was evaluated by remnant liver weight ratio, proliferating cell nuclear antigen (PCNA) labeling index and mitotic index. Accumulation of IL-1beta and TNF-alpha messenger RNA (mRNA) in the remnant liver was also measured. In FR167653-treated groups, the releases of alanine transaminase (ALT) and aspartate transaminase (AST) were lower. The PCNA labeling index was enhanced by FR167653-administration in a dose-dependent manner, FR-3 and FR-5 groups showed significantly higher peak DNA synthesis than the control group at 24 h post-PH (P<0.01). The mitotic index was also enhanced by FR167653-administration in a dose-dependent manner. In FR-5 group, the remnant liver weight ratio was significantly higher than that in the control group (P<0.05). The accumulation of IL-1beta messenger RNA (mRNA) in the remnant liver was obviously suppressed in FR-3 and FR-5 groups, but the expression of TNF-alpha mRNA was not apparently reduced. In conclusion, FR167653 ameliorates liver injury and enhances liver regeneration after PH in rats.

Situs ambiguous with gastric cancer: report of a case.

Situs ambiguous is an unpredictable anomaly characterized by disorder of the organ arrangement in the chest and abdomen. We report a case of situs ambiguous found incidentally in a 73-year-old man with gastric cancer. Preoperative imaging showed polysplenia, a bridging liver, a midline gall bladder, and pancreatic divisum. The vessels around the stomach were clearly shown by computed tomography with multiplanar reconstruction (MPR). Computed tomography with MPR proved a good diagnostic tool for identifying both the abdominal vessels and the location of the organs. Based on a precise evaluation of this unusual anatomy, we performed distal gastrectomy with dissection of the regional lymph nodes.

A Metastatic Jejunal Tumor from Squamous Cell Carcinoma of the Lung Found in an Intestinal Perforation

An 85-year-old male with advanced squamous cell carcinoma of the lung, who was diagnosed about 10 years prior to his current presentation, suddenly complained of abdominal pain and underwent an abdominal computed tomography scan, which revealed free air and massive ascites. He was admitted to our hospital for acute peritonitis and emergency surgery was performed. During the surgical procedure, a perforation of the jejunum was diagnosed and repaired. He was diagnosed to have a metastatic tumor originating from a squamous cell carcinoma of the lung. He improved and was transferred to the former hospital on the 27th postoperative day. Jejunal metastasis from squamous cell carcinoma of the lung is rare, and the prognosis of peritonitis due to a perforated intestinal metastasis from lung cancer is poor. There have been 10 reports of jejunal metastasis of squamous cell carcinoma of the lung reported in Japan between 2000 and 2011. Therefore, when patients with advanced lung cancer present with acute abdomen, it is necessary to keep in mind the possibility of a gastrointestinal metastatic tumor.

Inflammatory Polyp of the Gallbladder Mimicking Early Polypoid Carcinoma

We treated a 69-year-old male with a 16-mm polyp of the gallbladder. Enhanced computed tomography demonstrated marked enhancement. With a tentative diagnosis of early polypoid cancer of the gallbladder, open cholecystectomy was performed. Intraoperative ultrasound showed hyperechoic spots on the surface of the polyp with an inner echopenic area. The histological diagnosis was an inflammatory polyp that manifested nonneoplastic, edematous stroma, and infiltration of lymphcytes and plasmacytes.

Hamster Model of an Intraductal Papillary Mucinous Neoplasm (IPMN) of the Pancreas

The reflux of pancreatic juice into the biliary tract is a well-known risk factor for the development of biliary carcinoma. In this study, we investigated the role of bile-reflux into the pancreatic ducts in pancreatic carcinogenesis, especially in the development of carcinoma in the main pancreatic duct, in hamsters. Syrian hamsters were subjected to one of three surgical procedures: cholecystoduodenostomy with dissection of the extrahepatic bile duct on the distal end of the common duct (Model A); cholecystoduodenostomy with dissection of the common bile duct (Model B); or simple laparotomy (Model C). Four weeks after the surgery, the animals received weekly subcutaneous injections of N-nitrosobis(2-oxopropyl) amine (BOP), for 9 weeks. They were killed for pathological investigation 16 weeks after the initial BOP injection. Pancreatic carcinomas developed in 95%, 88%, and 90% of the Model A (n = 22), Model B (n = 24), and Model C (n = 21) hamsters, respectively. The induced pancreatic tumors were classified into four histological types: papillary; tubular; cystic adenocarcinoma; and intraductal carcinoma of the main pancreatic duct, consisting of intraductal papillary carcinoma (IPC) and intraductal tubular carcinoma (ITC). The number and incidence of IPCs induced in the Model A hamsters were 24 lesions and 77%, which were significantly higher than those in the Model B (7 lesions and 29%) and C hamsters (7 lesions and 33%) (P < 0.01). Bile-reflux into the pancreatic ducts was seen only in the Model A hamsters, after an indocyanine green injection via the portal vein. Proliferative cell nuclear antigen labeling indices of the epithelial cells in the main pancreatic duct, with no BOP treatment, were 3.8%, 0.8%, and 1.1% in Models A (n = 10), B (n = 10), and C (n = 10), respectively. These differences were significant (P < 0.01). Our findings suggest that bile-reflux into the pancreatic ducts is a significant factor predisposing to the development of IPC of the pancreas through the acceleration of epithelial cell kinetics of the main pancreatic duct.