Biomedical subjects
Publications and source records attributed to A Miyoshi.
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To determine whether cimetidine increases serum gastrin levels by elevation of intragastric pH or by other mechanisms, the effects of two different H2-receptor antagonists, cimetidine and YM-11170, on serum gastrin levels were compared in rats with controlled intragastric pH. When the intragastric pH was maintained between 4.5 and 5.5, 2-10 mumol/kg of cimetidine increased serum gastrin levels significantly, whereas no significant increase was observed after 0.02-0.1 mumol/kg of YM-11170. This occurred despite the same extent of inhibition of histamine-stimulated acid secretion as with cimetidine. When the intragastric pH was fixed at 5.5, the serum gastrin responses to cimetidine were significantly greater than to saline or YM-11170. Therefore, the increase in serum gastrin levels by cimetidine is due neither to the elevation of intragastric pH nor the result of H2-receptor blockade, but is probably due to a direct action to release gastrin.
In this study, we have developed a reliable radioimmunoassay (RIA) for Ascaris suum protein (Asp) and have measured the serum concentration of Asp in control subjects and in patients with helminthiasis and a variety of gastrointestinal diseases. The cross-reactivities of Asp antibody with other helminth worm antigens were also measured by RIA. Ascaris lumbricoides contained approximately the same amount of Asp antigenic substance as did Ascaris suum. Toxocara canis had a high concentration of a substance partially cross-reactive with Asp. Small amounts of substance cross-reacting with Asp were also exhibited by Anisakis larvae, Schistosoma japonicum and Taenia saginata. However, no cross-reactivities of Fasciola hepatica and Paragonimus westermani with Asp were observed in this study. Almost all the serum levels of Asp from normal control subjects were below the sensitivity of this RIA (10 ng/ml). High concentrations of Asp were observed in sera from patients with ascariasis (64.5 +/- 18.8 ng/ml: mean +/- S.E.), anisakiasis (75.2 +/- 28.0 ng/ml), toxocariasis (78.4 +/- 31.3 ng/ml) and schistosomiasis japonica (14.3 +/- 3.4 ng/ml). Asp levels in sera from patients with other helminthiasis were not significantly high. From these findings, it was suggested that RIA for Asp may not be specific for diagnosis of ascariasis, but might be a suitable screening method for patients with some kinds of helminthiasis. Interestingly, high concentrations of Asp were also observed in sera from patients with ulcerative colitis (24.8 +/- 2.5 ng/ml) and Crohn's disease (19.8 +/- 5.2 ng/ml), but Asp levels from 7 other gastrointestinal diseases seemed not to be significantly high. These findings remain unexplained but may derive from cross-reactivities between helminthic and gut mucosal antigens.
Immunoreactive beta-endorphin (beta-EP) in the ventricular fluid of six carcinomatous patients was measured using a specific radioimmunoassay. The subjects were undergoing a surgical procedure for relief of chronic intractable pain. This procedure involved the focal stimulation and coagulation of the posteromedial hypothalamus. Samples of ventricular fluid were collected before and after the stimulation and serially after the coagulation. Prior to stimulation, beta-EP-like immunoreactivity (beta-EP-LI) was below 200 pg/ml. In all of the six patients with pain relief, electrical stimulation led to a marked increase in immunoreactive beta-EP. In three patients beta-EP levels remained high after electrical coagulation for 6-24 hrs. These results suggest that beta-EP-like material, released into the ventricular fluid, may contribute to the initial pain blockade that results from stimulation and coagulation of the posteromedial hypothalamus.
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To clarify the clinical efficacy of SPG, a beta-1, 3 glucan extracted from cultured Schizophyllum commune Fries, a randomized comparative study was performed in combination with mitomycin C+5-fluorouracil (MF protocol) or tegafur (F protocol). A total of 514 cases with inoperable or recurrent gastric cancer were randomly allocated to either the SPG group or the control group, 367 of which were finally assessed for clinical efficacy. SPG was intramuscularly given at a dose of 20 mg twice a week or 40 mg once a week. Significant prolongation of life span was confirmed in the SPG group (MF protocol: p less than 0.01, F protocol: p less than 0.05), although the combination of SPG did not demonstrate a remarkable antitumor effect in both MF and F protocols. Among immune response parameters tested, the positive reactions in the PHA skin test were maintained in the SPG group and decreases in lymphocyte counts were inhibited by SPG in the MF protocol. Side effects associated with SPG therapy were noted in 6 of 258 cases treated with SPG. From these results, it is indicated that the combination of SPG and the chemotherapeutic agents may be useful in treating patients with inoperable or recurrent gastric cancer.
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Lipids of HDL (high density lipoproteins) and their subfractions (HDL2 and HDL3), and LCAT activity (lecithin: cholesterol acyltransferase) were determined in hepatobiliary diseases without severe hyperbilirubinemia (less than 10 mg/dl). The decrease in major lipid constituents (cholesterol and phospholipids) of HDL was mainly attributable to the decrease in those of HDL3, except in some liver diseases of acute or severe stage (acute hepatitis in an acute stage and hepatoma) which were accompanied with a simultaneous moderate decrease in those of HDL2 and in fatty liver which showed a preferential decrease in those of HDL2. The LCAT activity also decreased in several diseases. Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. From results that HDL3- but not HDL2-cholesterol levels significantly correlated with serum total protein, albumin and choline esterase, it was suggested that the decrease in large constituents of HDL, particularly of HDL3, is caused by hepatocellular dysfunction which causes inhibition of protein and lipid syntheses in the liver in most of the hepatobiliary diseases except for fatty liver which has a preferential decrease in HDL2 lipids.
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