Reflex regulation of the sphincter of Oddi by intrapancreatic ductal pressure in the Japanese monkey

Japanese monkey has a common ampullary channel. By a continuous injection of sterile saline (1 mL/min) into the pancreatic main duct, the pancreatic main ductal pressure increased from 8.4 +/- 1.0 (mean +/- SD) to a plateau level (16-25 mmHg) in 5 Japanese monkeys. The frequency and amplitude of the slow wave in electromyography of the sphincter of Oddi (SO) were significantly decreased from 14 to 2/min and 0.06 to 0.04 mV (p less than 0.01), and the frequency of the spike component significantly decreased from 53 to 14/min (p less than 0.05). As soon as infusion of saline ceased, the electromyography recovered to the original level. The mean value of the minimum loading pressure affecting myoelectrical activities of the SO was 19.8 +/- 3.0 mmHg. When the pancreatic duct was obstructed at the head, there was no significant change in the SO myoelectrographic activities in spite of increased pancreatic ductal pressure by infusion. These findings suggest that a homeostatic mechanism of pancreatic ductal pressure exists when the activity of the SO is regulated by the distending pressure in the pancreatic ductal system. This reflex regulation seemed to be mediated by the distension of the ampullary duct itself.     

Effect of green tea on iron absorption in elderly patients with iron deficiency anemia

The effect of green tea on iron absorption from tablets containing sodium ferrous citrate was investigated in four elderly patients with iron deficiency anemia and in eleven normal elderly subjects. In both groups, the serum iron level reached a maximum value from 2 to 4 hours after taking iron tablets and returned to the baseline value after 24 hours. No inhibitory effect of green tea on iron absorption was recognized.     

Prevalence of Helicobacter pylori in NSAID users with gastric ulcer

OBJECTIVE: Regarding the interaction of Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs), we cannot accept unanimous conclusions in inducing gastric ulcer. We therefore evaluated the role of Helicobacter pylori and NSAIDs in inducing gastric ulcer. METHODS: Dyspeptic patients receiving NSAIDs underwent endoscopic examination. Gastric ulcer formation and H. pylori status were investigated. Biopsy specimens from the antrum and lower body of the stomach were prepared for the rapid urease test and pathological evaluation. Anti-H. pylori antibody was measured by enzyme-linked immunosorbent assay. RESULTS: Two hundred and twenty-six patients receiving NSAIDs (220 chronic and six on-demand users) underwent gastrofibrescopic examination. There were 110 patients with gastric ulcer and 111 non-ulcer patients with gastritis. The remaining five patients had neither. NSAID users with gastric ulcer showed a low prevalence of H. pylori compared with those without them [55/110 (50.0%) vs 79/111 (71.2%), P < 0.01]. The same tendency was seen when patients receiving low-dose aspirin and those with rheumatoid arthritis were analysed separately [13/29 (44.8%) vs 50/62 (80.6%), P < 0.01, and 11/33 (33.3%) vs 16/26 (61.5%), P < 0.06 with Yates' correction, respectively]. CONCLUSION: Helicobacter pylori infection appeared to be a risk factor for developing gastritis, but we found no evidence that it increases gastric ulcer formation in NSAID users with dyspepsia.     

B cell lymphoma showing clinicopathological features of malignant histiocytosis

This report describes a case of B cell lymphoma, the clinicopathological features of which are quite similar to those of malignant histiocytosis. The clinical features included fever, anemia, and marked hepatosplenomegaly without lymphadenopathy. Histological findings revealed diffuse and noncohesive proliferation of cytologically atypical cells and benign-appearing histiocytes in the splenic red pulp, where the erythrophagocytosis was frequently found. Immunological studies, however, revealed a B cell nature of proliferating atypical cells. Accordingly, the histology of this patient was interpreted as a neoplastic proliferation of B cells accompanied by marked proliferation and activation of the histiocytes.     

Effect of dietary fructose on triglyceride turnover in streptozotocin-diabetic rats

The effects of fructose or glucose on plasma triglyceride kinetics in streptozotocin (40 mg/kg) diabetic rats were studied using Triton WR1339. To separate groups of diabetic rats fructose or glucose was supplied at 10% in drinking water. Diabetic rats without sugar supplementation (diabetic control) had significantly suppressed triglyceride secretion compared to non-diabetic controls. Neither fructose nor glucose supplementation increased the triglyceride secretion rate in diabetic rats. However, despite reduced secretion rates, plasma triglyceride levels in glucose-supplemented diabetic rats, diabetic controls and non-diabetic controls were essentially identical. This suggested that removal of triglyceride from the circulation was impaired in the diabetic rats. In contrast, fructose supplementation resulted in a more than 150% (significant) increase in the mean plasma triglyceride of diabetic rats. The observation of significant hypertriglyceridemia in spite of low triglyceride secretion rate in fructose-supplemented diabetic rats suggests that dietary fructose, but not glucose, interferes with triglyceride removal from the circulation of streptozotocin-diabetic rats. This impairment by dietary fructose is in addition to the impaired triglyceride removal associated with diabetes alone.