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Biomedical subjects

C Furihata

Publications and source records attributed to C Furihata.

At least 109 records · Page 6Linked to original sources
PubMed1982

Radioimmunoassay of serum group I and group II pepsinogens in normal controls and patients with various disorders.

A radioimmunoassay (RIA) for human group I pepsinogens (PgI) in serum was developed, using PgI purified from gastric mucosa. The sensitivity (0.7 micrograms/l) and reproducibility of the assay were satisfactory for clinical use. In normal controls, total serum pepsinogen (T-Pg) level was 58.9 +/- 31.7 micrograms/l (mean +/- SD) (PgI, 43.6 +/- 25.0 micrograms/l; PgII, 15.3 +/- 11.1 micrograms/l). Peptic ulcer cases had elevated T-Pg levels (gastric ulcer, gastroduodenal ulcer and duodenal ulcer, in increasing order of magnitude). T-Pg levels were not useful for diagnosis of peptic ulcer because of a large overlap with normal controls. T-Pg levels were low in patients with gastric polyp and in aged subjects. In these groups, the decrease of PgI was more marked than that of PgII.

Adult↗
PubMed1982

Radioimmunoassay of group II pepsinogen in human serum.

A new radioimmunoassay (RIA) using a double antibody method for human Group II pepsinogens in serum was developed. (1) Sensitivity of this assay system was of the order of 1 microgram per 1 of serum and optimal assay range was 10 to 50 microgram per 1; (2) no effect of interference of human serum was detected and there was no cross-reaction with human Group I pepsinogens within the optimal assay range; (3) satisfactory results were obtained for both within- and between-assay reproducibility (coefficient of variation was 3.9% and 3.7-15.3%, respectively); (4) the mean (+/- SEM) serum Pg II level in healthy donors was 15.9 +/- 0.7 microgram/l for males and 12.8 +/- 1.3 microgram/l for females; the difference between males and females was statistically significant (p less than 0.05); (5) the mean serum Pg II level in 10 patients with total gastrectomy was 1.2 +/- 0.05 microgram/l. These results suggest that most of Pg II in human serum is derived from the gastroduodenal system.

Adult↗
PubMed1982

Potential peptic activity of pepsinogen of human gastroduodenal mucosa determined by fluorescent microassay method using succinyl albumin.

Pepsinogen level, expressed as the potential peptic activity of pepsinogen was determined by a fluorescent microassay using succinyl albumin as substrate, in biopsy specimens from the gastroduodenal mucosa of 95 subjects. The following results were obtained: (1) pepsinogen level in the gastric mucosa becomes progressively higher from pylorus to corpus (p less than 0.001); (2) pepsinogen level in the gastroduodenal mucosa of duodenal ulcer was significantly higher than that of normal mucosa or gastric ulcer (p less than 0.001); (3) the difference in pepsinogen level between the gastric mucosa with and without intestinal metaplasia was statistically significant (p less than 0.01); (4) the correlation between the histology of gastric glands and pepsinogen level was fundic gland greater than intermediate gland greater than pyloric gland (p less than 0.001).

Adult↗
PubMed1982

Effect of X-ray irradiation on pepsinogen and on induction of intestinal-type crypts in the pyloric mucosa of the Wistar rat stomach.

The effects of X-ray irradiation on the content and isozyme pattern of pepsinogen and on the induction of intestinal-type crypts in the pyloric mucosa of rat stomach were compared with the previously reported effects of chemical carcinogens, N-methyl-N'-nitro-N-nitrosoguanidine, N-ethyl-N'-nitro-N-nitrosoguanidine and N-propyl-N'-nitro-N-nitrosoguanidine. The gastric regions of 6-week-old male Wistar rats were irradiated with X-rays (1,000 rad) twice at an interval of 3 days. A decrease in pepsinogen content in the pyloric mucosa was observed between 2 and 52 weeks after the irradiation, as had been found in the previous experiments using chemical stomach carcinogens. However, in contrast to the latter experiment, in which the isozyme pattern was altered, the pepsinogen isozyme pattern did not change throughout the observation period after irradiation. Morphologically, intestinal-type crypts appeared and increased gradually after irradiation as after the administration of chemical stomach carcinogens. However, Paneth cells were either not observed or only rarely observed in rats treated with carcinogens, whereas they were found in crypts in the stomachs of the irradiated rats.

Animals↗
PubMed1981

Preservation of gastric gland character in transplantable gastric adenocarcinoma (SG2B) of rats.

The morphological and biochemical characteristics of a transplantable tumor line of rat gastric carcinoma (SG2B), that developed in a Wistar strain rat after treatment with N-methyl-N'-nitro-N-nitrosoguanidine and then 4-nitro-quinoline 1-oxide were examined at the 60th passage. The tumor was serially transplanted into newborn rats by subcutaneous and intraperitoneal routes and has been passed through 60 transplant generations over a 4-year period. The tumors appeared to be well-differentiated tubular adenocarcinomas throughout successive passages, and at each generation transplants were almost identical to the original gastric adenocarcinoma as judged by light and electron microscopic observation. Ultrastructurally, the neoplastic cell contained abundant free ribosomes and exhibited few mucin granules. The microville on the apical cell surface were short and irregularly spaced. Electrophoresis showed that pepsinogens (Pg) 3 and 4 were present but no Pg 1 was detectable at the 60th passage, as was the case in the tissue at the 2nd and 5th passages. The pepsinogen content of the tissue at the 60th passage was similar to that at the 5th passage. The tumor tissue has thus retained the morphological and biochemical character of a pyloric gland type tumor for a long time (over 4 years) during serial transplantation.

4-Nitroquinoline-1-oxide↗
PubMed1981

Induction of changes in the pepsinogen content and the pepsinogen isoenzyme pattern of the pyloric mucosa of the rat stomach by short-term administration of stomach carcinogens.

Changes in pepsinogen isoenzyme patterns were examined in the pyloric mucosae of the stomachs of noninbred male Wistar rats after short-term administration of gastric carcinogens. N-Methyl-N-nitro-N-nitrosoquanidine, N-ethyl-N1-nitro-N-nitrosoguanidine, and N-propyl-N-nitro-N-nitrosoguanidine, which induce stomach cancer in rats, decreased the content of pepsinogen isoenzyme 1 )Pg 1), which was separated by poly-acrylamide gel electrophoresis. They also decreased the pepsingoen content of the pyloric mucosa. 4-Nitroguinoline 1-oxide, which induces a low incidence of stomach cancer in rats, rarely decreased the Pg 1 content or the pepsinogen content of the pyloric mucosa, and the incidence of such decreases was not statistically significant. However, diethylnitrosamine and dimethylnitrosamine, which do not induce stomach cancer in rats, did not cause any decrease in pepsinogen content. Ethyl methanesulfonate, a direct-acting carcinogen used as a control, also did not decrease the pepsinogen content.

4-Nitroquinoline-1-oxide↗
PubMed1981

Transplantation of untreated glandular stomach of fetal and newborn rats and their malignant conversion.

Untreated fetal and newborn glandular stomachs of Wistar rats were transplanted into the subcutis, testis, peritoneal cavity and subcapsular spaces of the kidney or spleen of syngeneic adult rats. The recipients were sacrificed one year after transplantation. Transplantability was very high and the grafted tissues were recovered from more than 80% of the animals at almost all transplantation sites. The transplanted gastric mucosa was well-differentiated morphologically and biochemically. Malignant conversion occurred in 6 of 118 transplants (5%); the tumors were a fibrosarcoma (1), a ganglioneuroblastoma (1), leiomyosarcomas (2) and squamous cell carcinomas (2). No malignant transformation of glandular stomach epithelium was observed.

Animals↗
PubMed1980

Purification and characterization of pepsinogens and a unique pepsin from rat stomach.

Four pepsinogens (1, 2, 3 and 4) (zymogens of pepsin A, EC 3.4.23.1, or pepsin C, EC 3.4.23.3) were purified from the fundic mucosa of rat stomach to homogeneous states as judged by sodium dodecyl sulfate/polyacrylamide gel electrophoresis and a unique pepsin was purified from pepsinogen 1. The molecular weights of pepsinogens 1, 2, 3 and 4 were 42 000, 40 000, 40 500 and 39 000, respectively, and those of the respective activated pepsins (1, 2, 3 and 4) were 35 500, 40 000, 35 500 and 37 000, respectively, as estimated by polyacrylamide gel electrophoresis. The amino acid compositions of these four zymogens differed, but resembled those of pepsinogen Cs from various animal species. Rabbit antiserum prepared against pepsinogen 1 reacted with pepsinogen 2, but not with pepsinogens 3 or 4. The precipitin line against pepsinogen 1 fused completely with that against pepsinogen 2. Purified pepsin 1 was a unique pepsin showing remarkable stability in alkali. It resembled pepsin A with respect to inhibition by pepstatin and pepsin C with respect to its amino acid composition, but had properties intermediate between those of pepsin A and C with respect to its optimal pH (2.1 to 3.1) with hemoglobin and activity on N-acetyl-L-phenylalanyl-L-diiodotyrosine.

Amino Acids↗
PubMed1980

Inhibition of experimental blood-borne lung metastasis by protease inhibitors.

The inhibitory effects of protease inhibitors on blood-borne metastasis in male Donryu rat lung were studied. Injection i.v. of 10(6) Yoshida ascites hepatoma AH7974 cells induced about 118 +/- 92 (S.D.) metastatic foci in rat lung after 3 weeks. Leupeptin (50 mg/kg body weight twice a day), injected i.p. from 2 days before to 4 days after the inoculation of tumor cells, reduced the number of metastatic foci to about 49 +/- 45 (p less than 0.005). Leupeptin also suppressed the formation of metastatic foci of Yoshida ascites hepatoma AH100B cells (p less than 0.001). Elastatinal (100 mg/kg body weight twice a day) and chymostatin (100 mg/kg body weight once a day) did not inhibit formation of metastatic foci of AH7974 cells. Injection i.v. of 10(6) AH7974 cells induced pulmonary thrombi within 1 hr. Leupeptin (50 mg/kg body weight twice a day) reduced the number of thrombi from 1298 +/- 395 to 646 +/- 218, when injected i.p. for 2 days before the inoculation of the cells (p less than 0.005). Chymostatin and elastatinal did not significantly change the number of pulmonary thrombi. These results indicate that leupeptin inhibited metastasis formation and suggest that this effect may be due to the inhibition of thrombus formation after the arrest of circulating tumor cells.

Animals↗