Yoshiyasu Hasegawa

A Case of Adenosquamous Carcinoma of the Pancreas With a Large Cyst.

Abstract: An 81‐year‐old female was admitted to our hospital with right upper abdominal pain and an abdominal mass. She has suffered from diabetes mellitus for 10 years. She did not have other past history. In addition, her serum level of CA19–9 was remarkably high, 39,000U/ml. Investigations of ultrasonography, computed tomography and angiography were done. These radiological findings showed that a large cystic mass, including the pancreatic head and body, had hypervascularity. Endoscopic retrograde cholangiopancreatography (ERCP) suggested that this cystic mass originated from the main pancreatic duct and was malignant. These studies revealed that this tumor might its histological diagnosis of intraoperative biopsy revealed adenosquamous carcinoma. There have been no reports about adenosquamous cell carcinoma with a large cyst.

Effects of secretin on content of PGE2 and 6-keto PGF1α in gastric mucosa

To determine the involvement of prostaglandins in the action of secretin on the promotion of the healing process in injured gastric mucosa, the effect of secretin infusion on the content of PGE2 and 6-ketoPGF1α (a major metabolite of PGI2) in human gastric mucosa was investigated. Specimens of both normal and injured mucosa were obtained from each of the patients who underwent polypectomy a week prior to the study. The specimens were obtained before and 20 min after intravenous infusion of secretin [2 Crick, Harper and Raper (CHR) units/kg] or saline. The basal content of PGE2 in injured mucosa was three times higher than that in normal gastric mucosa. Secretin did not increase the PGE2 content of normal gastric mucosa. However, secretin induced a sevenfold increase in the PGE2 content of injured mucosa. The content of 6-ketoPGF1α.

Different mode of action of cimetidine and prostaglandin on the rat gastric mucosa under stress loading by restraint and water-immersion

SummaryGastric mucosal blood flow and oxygen tension in the corporal mucosa gradually declined after water immersion in the control animals. Neither cimetidine nor prostaglandin E2 had any influence on the decrease of the corporal mucosal blood flow or mucosal oxygen tension during seven hours of stress loading.The stress ulceration began to occur starting three hours after cold immersion in the control rats, and the deficit of energy metabolism was attributed to reduced oxidative phosphorylation from tissue hypoxia resulting from lowered blood flow and oxygen tension under stress. Cimetidine (4 mg/kg) maintained aerobic glycolysis, continued to produce high-energy phosphates and kept the energy charge unchanged in the gastric mucosa. In addition, PG E2-Me (100µg/kg) showed similar, but less marked and shorter-lived effects on aerobic glycolysis and ATP production, whereas the energy charge of the adenosine pool decreased significantly from that produced by cimetidine.These results indicated that cimetidine significantly reduced energy requirements as compared with the control and PG E2 groups due to marked inhibition of gastric secretion and produced inhibition of mucosal ulceration by water immersion. In addition, PG E2 reduced energy requirements through the inhibition of gastric secretion. On the other hand, increased energy requirements due to the rise of cytoprotective mucoprotein production and a resultant decrease of the energy charge were seen with PG E2 as compared with cimetidine.