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Biomedical subjects

O Kato

Publications and source records attributed to O Kato.

At least 37 records · Page 2Linked to original sources

Endoscopic Nd: YAG laser therapy for gastric borderline lesions.

Endoscopic Nd:YAG laser treatment was used to eradicate 14 broad-based protruded borderline lesions of the stomach in which snare excision might be difficult and hazardous. Multiple pulse irradiations of Nd:YAG laser with a power of 40 to 50 W ablated all the lesions. During and after laser treatments, no complications were recognized. The laser-induced ulcers healed within 4 to 7 weeks after the last procedure, and the biopsy material taken from the sites of the scars showed regenerative epithelium without evidence of atypical cells. These encouraging results suggest that endoscopic laser treatment is the method of choice for therapy of the gastric borderline lesions where snare excision is not feasible.

Adult↗

[Case of yolk sac tumor decreasing in size and the normalizing of alph-fetoprotein level by anticancer chemotherapy].

A 19-year old man was hospitalized suspected of a mediastinal tumor with superior vena caval syndrome. As the chest X-ray film and thoracic CT scan on admission revealed a huge anterior mediastinal tumor, and the value of serum alpha-fetoprotein (AFP) was high, we made a diagnosis of malignant mediastinal tumor from the germ cell. Radiation therapy was not effective, but a combination chemotherapy consisted of cis-platinum, adriamycin, and vincristine was clearly effective, decreasing the size of the tumor and normalizing the value of serum AFP. As the tumor acquired tolerance to the anticancer drugs before long, the chemotherapy became ineffective and the patient died 9 months after the initiation of the treatment. This tumor had endodermal sinus structure, Schiller-Duval body, and eosinophilic hyaline globulus which were histological characteristics of yolk sac tumor, and was confirmed to be originated from anterior mediastinum.

Adult↗

Clinical significance of anomalous pancreaticobiliary union.

Anomalous pancreaticobiliary union was found in nine cases among 300 consecutive adult patients examined by endoscopic retrograde cholangiopancreatography. Three had congenital choledochal cysts: one had a cyst of the choledochus associated with a cyst of the intrahepatic bile duct, another had a fusiform dilation of the choledochus, and the third had a choledochal diverticulum. Five of the nine patients had biliary malignancies (55.6%): four carcinomas of the gallbladder and one carcinoma of the choledochus. On the other hand, 18 of 291 patients without anomalous pancreaticobiliary union had biliary malignancies (6.2%): four carcinomas of the gallbladder and 14 carcinomas of the choledochus. When anomalous pancreaticobiliary union is detected, biliary malignancy, especially carcinoma of the gallbladder, should be considered as a possible complication.

Adult↗

Experimental pancreatolithiasis in the dog.

Little is known about the pathogenesis of pancreatolithiasis, and although several theories have been proposed, no experimental models of pancreatic calculi production are documented in the literature. This study examines such a model in which partial or complete pancreatic duct obstruction was surgically created in dogs. We found that (1) pancreatic calculi were demonstrated in 46.7% of the dogs (14 of 30) with partial outflow obstruction for 4 months or longer; (2) no pancreatic calculi were found in any of the dogs with complete pancreatic duct obstruction; (3) all calculi produced were localized in the ductal system; (4) the organic and inorganic composition of canine and human pancreatic calculi were quite similar; and (5) connective tissue proliferation and mucous cell metaplasia of the ductal epithelium, often seen in association with clinical pancreatolithiasis, are also detected in the pancreata of dogs that have had partial obstruction of pancreatic excretion. These findings suggest that an experimental model of pancreatolithiasis can be accomplished in dogs by the partial obstruction of pancreatic excretion.

Animals↗

Effect of capsular polysaccharide of Klebsiella pneumoniae on host resistance to bacterial infections. III. Further study of its effects on interactions between peritoneal leukocytes and virulent Salmonella enteritidis.

The mechanism for the infection-promoting effect of the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) was investigated using the experimental system in which mice were infected intraperitoneally (i.p.) with a virulent strain of Salmonella enteritidis immediately after i.p. injection of CPS-K. In the peritoneal phagocytes of CPS-K-untreated control mice, approximately 70, 3, and 10% of phagocytized bacteria survived 6, 12, and 24 hr after challenge, respectively, when calculated from the ratio of the number of cell-associated viable bacteria, which was estimated by direct plate count, to the number of phagocytized bacteria, which was estimated by microscopic observation of stained smears. In contrast, almost all of the phagocytized bacteria were viable throughout the experimental period in mice treated with CPS-K. The electron microscopical findings of the phagocytes obtained 12 hr after challenge showed that in the cells of mice treated with CPS-K almost all of the phagocytized bacteria were morphologically intact, with some of them in the stages of cell division, whereas in those of untreated control mice, almost all of the phagocytized bacteria underwent digestive changes. When the reaction product of acid phosphatase was examined by electron microscopy in the phagocytes obtained 12 hr after challenge, the enzyme activity in the phagosomes was very low in mice treated with CPS-K in comparison with that in untreated control mice. Enzyme assays of the lysosomal and extralysosomal fractions of peritoneal cells obtained at various times after challenge also showed that release of acid phosphatase from the lysosomal fraction to the extralysosomal fraction after bacterial challenge was inhibited in peritoneal cells of mice treated with CPS-K.

Acid Phosphatase↗