[Changes in beta-glucuronidase activity recognized in granulocytes from patients with carcinomas of the gastrointestinal tract].
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Biomedical subjects
Publications and source records attributed to H Okabe.
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We ascertained the relationship between the relaxation time of magnetic resonance imaging and the protein concentration of subretinal fluid, by examining rhegmatogenous and nonrhegmatogenous retinal detachments with a 0.15 tesla nuclear magnetic resonance system, and we calculated T1 and T2 relaxation times of subretinal fluid. The protein concentration of subretinal fluid obtained at the time of surgery was determined by a biochemical method. The subretinal fluid in a fresh rhegmatogenous retinal detachment had a low protein concentration and relaxation times equal to those of vitreous. Conversely, increased protein concentrations and shortened relaxation times were noted in subretinal fluid from long-standing rhegmatogenous retinal detachments. Subretinal fluid in a nonrhegmatogenous retinal detachment with a high concentration of protein showed much shorter relaxation times. The relaxation times and protein concentration of the subretinal fluid correlated closely. It may be possible to measure the protein concentration of subretinal fluid in vivo with nuclear magnetic resonance imaging.
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Among various tannins tested, Areca II-5-C, a fraction isolated from seeds of Areca catechu L., showed the most potent angiotensin-converting enzyme (ACE) inhibitory activity in vitro. Its antihypertensive activity was therefore investigated in normotensive and spontaneous hypertensive rats (SHR) after both oral and intravenous (i.v.) administration. The activity was compared with that of captopril (D-3-mercapto-2-methylpropanoyl-L-proline), a potent ACE inhibitor. Oral administration of Areca II-5-C to SHR produced a lasting, dose-related antihypertensive effect, and the responses obtained with doses of 100 and 200 mg/kg were comparable to those of captopril at doses of 30 and 100 mg/kg. Intravenous administration of Areca II-5-C to SHR produced a rapid and marked reduction in blood pressure at doses of 10 and 15 mg/kg. The maximum antihypertensive effect of Areca II-5-C in SHR, at an i.v. dose of 15 mg/kg, was about 5 times as large as that of captopril at the same dose. Although the vasopressor response to norepinephrine and vasodepressor responses to bradykinin and acetylcholine were not appreciably changed by i.v. treatment with Areca II-5-C at a dose of 5 mg/kg, it did produce dose-related inhibition of the pressor responses to angiotensin I and II. It is suggested that Areca II-5-C has favorable properties as a hypotensive drug through its ability to inhibit the pressor responses to both angiotensin I and II.
Using the peroxidase-antiperoxidase (PAP) immunohistochemical method, we studied the epithelial component of Warthin's tumor of the human salivary gland with respect to the presence of S-100-protein-positive cells. The tumor epithelium consisted of two layers of oxyphilic cells (an apical layer of tall columnar cells and a basal layer of small cuboidal cells) and irregularly shaped, dendritic cells scattering throughout the neoplastic epithelial cells. Two types of the oxyphilic cells were devoid of the immunoreaction products for S-100 protein. However, in the epithelial layer of Warthin's tumor, S-100-protein-positive material was observed in the cytoplasm and nuclei of dendritic cells. They were more abundant in the lymphoid tissue than in the neoplastic epithelium. The morphologic appearance of these cells was identical to that of Langerhans' cells, which were absent from the normal human salivary glands. The presence of these cells, which have a special function of antigen presentation in immune responses, indicates that delayed hypersensitivity may be the main pathogenic factor in the development of Warthin's tumor.
Filling of the gastric lumen of rats with 1.0 M NaCl solution (5 ml) for 10 min under urethane anesthesia caused an increase in the gastric fluid concentrations of prostaglandin (PG) E2, 13,14-dihydro-15-keto-PGE2 and 6-keto-PGF1 alpha as determined by radioimmunoassay. PGE2 was the major PG generated. The levels of PGE2 in the gastric fluid were increased dose-dependently after filling the lumen with 0.3, 0.5, 0.7 or 1.0 M NaCl solutions. The pH of the gastric fluid increased similarly after 0.5 to 1.0 M NaCl solutions. Indomethacin (10 mg/kg, i.p.) suppressed the PGE2 increase caused by 1.0 M NaCl solution, but did not prevent the increase of the pH of the gastric fluid induced by intragastric 1.0 M NaCl. Infusion of tetragastrin (62.5 micrograms/kg/hr, i.v., for 10 min) caused a marked increase of acid secretion without modifying intragastric concentration of PGE2. The acid secretion due to tetragastrin was completely inhibited after intragastric administration of 1.0 M NaCl solution, while indomethacin restored the tetragastrin-induced acid secretion, with prevention of a rise of intragastric PGE2 levels. These observations suggest that 1.0 M NaCl solutions suppress basal intragastric acid through a mechanism which is independent of prostaglandins. In contrast, the suppression of tetragastrin-induced acid secretion by intragastric 1.0 M NaCl solution appears to be mediated through a release of prostaglandins.
The authors devised a new method using measure plates for the endoscopic measurement of gastric ulcer area. A grid composed of 2.5-mm squares was photographed by the endoscope with lens-object-distance (LOD) being changed every 2.5 mm precisely, and the obtained images of the square pattern were printed on glass plates, which were used as measure plates. The ulcer size was determined by mounting an endoscopic photograph of the ulcer on the corresponding glass plate with the same LOD, projecting them on the screen by a projector and counting the number of squares within the ulcer area. In this way the gastric ulcer size could be determined with an average aberration ratio of 5.6% or less, irrespective of LOD.
The effects of cimetidine on gastric mucus glycoprotein biosynthesis in rat gastric mucosa were investigated using organ culture technique. 2 h following oral administration of cimetidine (40 mg/kg body weight), corpus tissue was placed in the organ culture. Mucus glycoprotein synthesis was accelerated to 137% of control (p less than 0.01). In order to investigate the direct effect of cimetidine on mucus glycoprotein biosynthesis, corpus tissue was cultured in the medium containing cimetidine. 100 microM cimetidine enhanced mucus glycoprotein biosynthesis to 174% (p less than 0.01). Cimetidine was found to stimulate gastric mucus glycoprotein biosynthesis both in vivo and in vitro.
In the Salivary Gland Register (University of Hamburg), 9883 cases were recorded from 1965 to 1984. Among these cases there were 3,326 neoplasms, of which 3,017 were epithelial in origin. In this latter group, 80 neoplasms arose in children and adolescents. Among these 80 persons, there was a slight predominance of females; 57 tumors (71%) were localized in the parotid gland, and only 6 (8%) in the submandibular gland. The incidence of the tumor types was different in children and adolescents as compared to the incidence in adults: monomorphic adenomas were virtually absent in children (only 1 patient), and benign tumors were also less common (65%). The incidence of mucoepidermoid tumors was remarkable (12 cases, 15%). Acinic cell tumors occurred more frequently (5 cases, 6%). The neoplasms have been analyzed histologically. Two very rare tumors, a monomorphic salivary duct adenoma and an embryonal carcinoma, were also studied by electron microscopy and immunohistochemistry.
The effects of diphenylhydantoin and phenobarbital on lipids metabolism were studied by quantification of lipids in human serum with GC-MS. The ratios of palmitic acid to stearic, oleic and linoleic acids decreased in patients on diphenylhydantoin therapy. Increases of free palmitic, stearic and oleic acids concentrations as well as higher cholesterol ester levels were observed in patients receiving either diphenylhydantoin or phenobarbital. With respect to fatty acids composition of cholesterol esters and phosphatidyl-choline, higher concentrations of palmitic, oleic and linoleic acids were observed in patients on diphenylhydantoin and phenobarbital therapy. Although the concentration of palmitic acid in serum phosphatidylcholine remained the same for all groups, a marked decrease in stearic, oleic and linoleic acids concentrations in serum phosphatidylcholine was observed in diphenylhydantoin treated group, and oleic acid in phenobarbital treated group. These results suggested the relationship to lecithin-cholesterol acyltransferase activity by these drugs.
The localization of carcinoembryonic antigen (CEA) and lysozyme (LZM) was immunohistochemically studied in 34 carcinomas arising in benign pleomorphic adenomas and 25 normal salivary glands in order to assess its potential diagnostic value. CEA in the normal salivary gland was located in luminal cell membranes of intercalated duct cells and serous acinar cells. Strongly positive cell surface and intraluminal staining of CEA appeared in the areas of gland-forming pattern in pleomorphic adenoma. CEA activity was detected in 7/9 cases (78%) of adenocarcinoma, 10/11 cases (91%) of epidermoid carcinoma, 3/8 cases (38%) of anaplastic carcinoma, 5/5 cases (100%) of mucoepidermoid carcinoma, and 1/1 case (100%) of adenoid cystic carcinoma. CEA was always present in the cytoplasm of epithelial cells and luminal contents of neoplastic glands. CEA in epidermoid carcinoma may occasionally react strongly in the cytoplasm. Lysozyme-immunoreactivity was detected in the cytoplasm of intercalated duct cells and serous acinar cells of the normal salivary gland but little or no LZM was observed in any of the tumors. These results suggest that the presence of CEA could be a useful marker that provides valuable information for the differential diagnosis between benign and malignant areas of carcinoma in pleomorphic adenoma of the salivary gland. Moreover, LZM could be of valuable use for discriminating neoplastic from non-neoplastic tissue of salivary glands.
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Glycyrrhetic acid suppressed tumor promoter-induced effects in vitro, such as stimulation of 32Pi-incorporation into phospholipids of cultured cells and down-regulation of the epidermal growth factor receptor. Glycyrrhetic acid inhibited the promoting activity of both 12-O-tetradecanoylphorbol-13-acetate (TPA) and teleocidin on skin tumor formation in mice initiated with 7,12-dimethylbenz[a]anthracene (DMBA). The percentage of tumor-bearing mice in the group treated with DMBA plus teleocidin was 88% at week 18, whereas that in the group treated with DMBA plus teleocidin and glycyrrhetic acid (10 mumol/painting) was 6%. Similarly, the percentage of tumor-bearing mice of the group treated with DMBA plus TPA was 97% at week 20, whereas that of the group treated with DMBA plus TPA and glycyrrhetic acid was 40%. Therefore, glycyrrhetic acid was proved to inhibit the activity of two different tumor promoters, teleocidin and TPA, in mouse skin.
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