Light detection enhanced by surface plasmons was confirmed in Au film/n-type Si Schottky structures. Electrons excited directly with light in Au film overflowed into the n-type silicon, and this excitation was enhanced by surface plasmons induced by Au nanorods attached to the Au film. Excitation was clearly observed in a wavelength range corresponding to the energy of less than the band gap of silicon. The feasibility of Schottky-type photodiodes, in which electrons were never generated by absorption in semiconductors but directly excited in metal, was experimentally demonstrated.

Although it has been firmly established that D-glucose inhibits glucagon secretion from pancreatic A cells, the regulatory mechanism of glucagon secretion by D-glucose has not been elucidated. To study this regulatory mechanism by D-glucose, the effects of hexoses and their derivatives on glucagon secretion from the A cells of isolated perfused rat pancreas were investigated. When these cells were perfused with D-glucose, D-fructose, D-sorbitol, D-galactose, 2-deoxy-D-glucose, D-gluconic acid sodium salt and D-glucosamine HCl salt, glucagon secretion was significantly inhibited. None of the hexoses or their derivatives tested were found to stimulate glucagon secretion. The effects of these sugars on glucagon secretion were independent of their metabolism in the cells. From the findings that the sugars both metabolized and unmetabolized in the cells demonstrated comparable inhibition of glucagon secretion from the isolated perfused rat pancreas, it is speculated that the recognition system for these sugars may be probably present on the A cell membrane and responsible for mediating these inhibitory effects of glucagon secretion.

A decrease in MAO by gastrin stimulation was observed in 13 of 20 hyperthyroid patients. Five of these 13 cases had achlorhydria. The decrease in gastric acid secretion had no relation to the duration of symptoms, serum T3 and T4 levels, serum antithyroglobulin antibody levels and serum antithyroid microsomal antibody levels. Gastroscopy with biopsy was performed in 17 cases. In patients with achlorhydria, macroscopic and histological atrophy was not observed in the body, and parietal cells were present and their succinic dehydrogenase activity was normal. Electron microscopy of the parietal cells of patients with achlorhydria showed that their cells were similar to those in the resting state of healthy subjects with the ability to secrete normal amounts of gastric acid. These findings demonstrate that the decrease in gastric acid secretion in hyperthyroidism is not caused by any structural changes in the gastric mucosa but by functional suppression. In the present experiment, this suppression was found resistant to gastrin. A rise in serum gastrin level was observed in 8 cases. Either achlorhydria or marked hypoacidity was found in 6 cases with the level more than 400 pg/ml. The HCl administration temporarily lowered elevated gastrin levels, and feedback inhibition by HCl was found to be maintained. A rise in gastric pH was considered to be one of the prerequisites for an increase in serum gastrin level.

Experimental hyperthyroidism was produced in rats by thyroxin injection, and changes in gastric acid secretion and serum gastrin level were determined to analyze the relation between these changes and hyperthyroidism. Administration of thyroxin to two groups of rats-20 micrograms per 100 g of body weight for 20 days and 75 micrograms for 7 days-brought about significant increases in serum T3 level, gastric pH and serum gastrin level. An increase in gastric pH took place later than that in serum T3 level; this time lag implies that a decrease in acid secretion was not caused by an direct effect of thyroxin on the parietal cell but by its secondary effect. In the T4-injected rats with decreased gastric acid secretion, the parietal cell remained normal in form and succinic dehydrogenase activity was also normal. The electron microscopical observations showed nothing abnormal in the parietal cells. These findings suggest that a decrease in acid secretion was not due to any structural changes in the gastric mucosa but to functional suppression. The serum gastrin level rose in correlation with an increase in gastric pH and fell by HCl administration to the stomach. Feedback inhibition by pH remained in the G cell.

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