Search PubMed⌕ Search

Biomedical subjects

T Kawachi

Publications and source records attributed to T Kawachi.

At least 91 records · Page 5Linked to original sources
PubMed1976

Effect of leupeptin, a protease inhibitor, on induction of bladder tumors in rats by n-butyl-n-(4-hydroxybutyl)nitrosamine.

Leupeptin, isolated from Actinomycetes, is a potent and specific inhibitor of proteases. We found that the administration of leupeptin enhanced that size of urinary bladder tumors induced in rats by the oral administration of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN). BBN was given as a 0.05% solution in the drinking water for 6 weeks, and then animals were fed a diet with or without 0.1% leupeptin for 30 weeks. The average weight of the bladders with tumors in rats fed a leupeptin diet was about eight times that of rats on a diet without leupeptin, though the incidences and average numbers of tumors in the bladders were similar in the two groups.

Animals↗
PubMed1976

Beta-glucuronidase isozyme patterns of experimental hepatomas of rats.

Beta-Glucuronidase isozymes in rat tissues were separated by electrophoresis on cellulose acetate membranes. Using this method, beta-glucuronidase isozyme patterns were studied in normal rat liver and experimental hepatomas with different growth rates. Changes of isozyme patterns during postnatal development were also studied in rat liver. Normal rat liver contained six types of beta-glucuronidase, numbered I to VI in order to decreasing mobility to the cathode. Type II beta-glucuronidase stained most intensely and was detected in all the cells examined. The isozyme patterns of Morris hepatomas, which are slowly growing and not highly deviated, resembled that of normal rat liver but lacked definite Type III beta-glucuronidase. Yoshida ascites hepatomas, which are rapidly growing and highly deviated, contained only Type II, but some had Types II, V, and VI beta-glucuronidase. Embryonal liver just before birth contained only Type II, but with increase in activity during development after birth, minor bands of Type I and Types III to VI beta-glucuronidase appeared successively to complete the adult pattern.

Animals↗
PubMed1976

Precancerous changes in the stomach.

Intestinal metaplasia is often associated with human gastric carcinoma. Intestinalization seems to be a typical example of abnormal differentiation and is possibly a precancerous state. For investigation of intestinal metaplasia, a method for visualizing disaccharidases using Tes-Tape was developed; this method was applied to many specimens of stomach surgically removed for the treatment of gastric carcinoma. More than 130 specimens of human stomach were investigated. Intestinalization was classified into types I and II intestinal metaplasia. In type I intestinal metaplasia, sucrase, maltase, trehalase, alkaline phosphatase, goblet cells, and Paneth cells were present; while the type II intestinal metaplasia, sucrase and maltase were present but alkaline phosphatase and trehalase were absent. In type II, goblet cells were present but not Paneth cells. The histochemical technique for sucrase was newly devised. Some of the villi with goblet cells in the area of intestinalization in the stomach were not stained by sucrase activity, although most of the villi were stained. The presence of a third type of metaplasia was suggested. Purified sucrases obtained from the intestine and one case of type I intestinal metaplasia showed blood group reactivity due to the oligosaccharide side chain. However, purified sucrases obtained from two cases of type II intestinal metaplasia were negative in blood group reactivity. A close relation between distribution of alpha-fetoprotein and carcinoembryonic antigen in gastric carcinoma and that in surrounding intestinal metaplasia is discussed.

Carcinoembryonic Antigen↗
PubMed1976

[Experimental gastric cancer (author's transl)].

Methods have been established to produce gastric cancer in rats and dogs by administration of N-methyl-N'-nitro-N-nitrosoguanidine or of the ethyl derivate. The agent is administered in drinking water or by a pellet diet soaked in the carcinogen. Histologically well differentiated and poorly differentiated types of adenocarcinoma and signet-ring cell tumors are induced in several months with greath reliability. Metastases were observed in both rats and dogs with gastric carcinoma. The carcinogenic effect could be enhanced by surface active agents, sodium chloride, iodoacetamide, insertion of plastic beads into the stomach and gastroenteroanastomosis. Follow-up studies by radiologic, endoscopic and bioptic examinations are possible in the dog. There are similarities in these experimental tumors to those in man and thus they provide means for the investigation of histogenesis, prevention, and chemotherapy of gastric cancer. An adenocarcinoma of the glandular stomach of a Wistar rat was successively transplanted to new born rats of the same strain.

Adenocarcinoma↗
PubMed1975

Purification and properties of alpha,alpha-trehalase from the mucosa of rat small intestine.

ALPHA,ALPHA-Trehalase (EC 3.2.1.28, alpha,alpha-trehalose glucohydrolase) was solubilized from the microvillous membrane of the intestinal mucosa of rats with Triton X-100 and butanol. It was purified 6350-fold by gel filtration on Sephadex G-150 and chromatography on DE-52 and hydroxyapatite. The purified enzyme, with a specific activity of about 127 units per mg of protein, showed almost a single band of protein and activity on polyacrylamide gel electrophoresis. Its molecular weight was estimated to be 96 000 on Sephadex G-150 and 90 000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Its pH optimum was 5.5-5.7 and its Km value for trehalose was 5.4 mM. Its activity was inhibited 30 and 100% by 1 mM p-chloromercuribenzoate and 0.1 mM HgCl2, respectively and 30% by 1 mM MgCl2. Moreover, its activity was inhibited completely by 10 mM tris(hydroxymethyl)aminomethane and about 60% by 10 mM sucrose and cellobiose. The enzyme showed a high specificity for trehalose.

Animals↗
PubMed1975

Changes in pepsinogen isozymes in stomach carcinogenesis induced in rats by N-methyl-N'-nitro-N-nitrosoguanidine.

Changes in the isozymes of pepsinogen (Pg) separated from the glandular stomachs of rats were studied by polyacrylamide gel electrophoresis during carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), from the beginning of MNNG administration to 3 months after the end of its 7-month regimen. In 13 of 25 rats killed successively, one (Pg 1) of the three pepsinogen isozymes (Pg 1, 3, 4) normally present in the pyloric mucosa had decreased or disappeared. It decreas was observed from 1 week after the beginning of MNNG treatment to at least 3 months after the end of the 7-month MNNG administration. Remarkable histopathologic changes were found from 8 months after MNNG was given, and rats showing such unusual histopathologic alterations also had changes in their pepsinogen isozyme pattern. In 4 of 27 rats, two (Pg 1, 2) of the four isozymes of pepsinogen (Pg 1-4) in the fundic mucosa decreased or disappeared from 3 months after the beginning of MNNG treatment to at least 2 months after the end of its 7-month administration. Histopathologic changes induced by MNNG were not as remarkable in the fundic mucosa as in the pyloric mucosa.

Adenocarcinoma↗
PubMed1974

Further studies on induction of stomach cancer in hamsters by N-methyl-N'-nitro-N-nitrosoguanidine.

Oral administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) to hamsters at a concentration of 50-83 μg/ml in the drinking water resulted in a high incidence of tumours in the glandular stomach. Short-term administration of MNNG for 4-6 months resulted in more adenocarcinomata in the glandular stomach than long-term administration for 7-8 months. One case of metastasis of an adenocarcinoma of the glandular stomach to the liver and 2 cases of metastasis to the regional lymph nodes were found. Spindle cell sarcomata in the glandular stomach and adenocarcinomata in the duodenum were also often produced.Oral administration of MNNG at the very high concentration of 500-2000 μg/ml induced a hepatic cell carcinoma, intrahepatic bile duct carcinomata, bile duct cystadenomata and cystic dilatation, and a haemangioma in the liver but no tumour in the glandular stomach.Sequential morphological studies on the glandular stomach of hamsters receiving 50 μg/ml of MNNG in the drinking water showed 3 stages of change of the mucosa. The mucosa became atrophic and eroded in the first 16 weeks. Irregular atypical glands developed at the margins of erosions and proliferation of spindle cells in the submucosa were found after 18 weeks. Spindle cell sarcomata developed in animals after 20 weeks. Adenocarcinomata developed between 25 and 32 weeks.

Adenocarcinoma↗