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Biomedical subjects

S Kozuka

Publications and source records attributed to S Kozuka.

At least 55 records · Page 3Linked to original sources

Relation of adenoma to carcinoma in the gallbladder.

In order to clarify the relation of adenoma to carcinoma in the gallbladder, histopathologic examination was made on surgical specimens of 1605 cholecystectomies. Among them, 11 benign adenomas, seven adenomas with malignant change, and 79 invasive carcinomas were found. All of the benign adenomas were 12 mm or less in diameter (average diameter, 5.5 +/- 3.1 mm), while the adenomas having cancerous foci were 12 mm or more in diameter (average diameter, 17.6 +/- 4.4 mm). Most invasive carcinomas were more than 30 mm in diameter. The average patient age was 50.5 +/- 16.3 years for benign adenomas, 58.3 +/- 12.6 years for adenomas with malignant change, and 64.8 +/- 9.6 years for invasive carcinomas. Transition of benign adenoma into carcinoma was histologically traceable. Adenomatous residue was found in 15 (19.0%) of 79 cases of invasive carcinoma.

Adenoma↗

DNA content of pancreatic duct hyperplasia and carcinoma.

The DNA content of epithelial nuclei of hyperplastic and carcinomatous ducts of the pancreas was examined cytophotometrically. The materials were obtained from 2 cases of nonpapillary hyperplasia, 3 of papillary hyperplasia, 2 of atypical hyperplasia and 2 of tubular adenocarcinoma, which were selected by reviewing the pancreata of about 1,600 human autopsy cases. A gradual shift was observed in the DNA content from the normal level to a carcinomatous level through various stages of hyperplasia. Based on these findings, the hypothesis that pancreatic duct hyperplasia is a potent precursor of pancreatic carcinoma is discussed.

Adenocarcinoma↗

Mutual relationship between antibiotics and resting spores of Bacillus subtilis: morphological changes and macromolecular synthesis after germination of spores treated with cyclic polypeptide and aminoglycoside antibiotics.

Morphological changes and synthesis of DNA, RNA, protein, and cell wall were investigated during germination of resting spores of Bacillus subtilis exposed transiently to the cyclic polypeptide antibiotics, polymyxin B and gramicidin S, and the aminoglycoside antibiotics, streptomycin, kanamycin, and gentamicin. Normal germinated spores showed breaks of the spore coat, a diminution in size and a fibrillar appearance of the cortex, a swelling core, a cell wall as thick as that of vegetable cells, some mesosomes and DNA fibrils. On the other hand, no breaks of the spore coat, a spore core with a slight swelling and irregular form, a thin cell wall, no demonstration of the nuclear material and no granularity in the cytoplasm were characteristic of the germinated spores derived from polymyxin B- and gramicidin S-treated resting spores. With gramicidin S-treated germinated spores a few vacuoles were formed in the cytoplasm. Both polymyxin B- and gramicidin S-treated germinated spores showed little or no synthesis of DNA, RNA, and protein. The vegetative cells derived from streptomycin-treated resting spores demonstrated several finely granular regions in the cytoplasm and a disorder of the fibrillar nucleoid, and their autolysis occurred early. Their DNA and RNA synthesis was normal, whereas protein synthesis was low. In spite of no occurrence of cell division and very low protein synthesis, the most striking characteristics of the outgrowing cells derived from kanamycin-treated resting spores were a markedly thickened cell wall and a continuous incorporation of labeled D-alanine suggesting cell wall synthesis; RNA synthesis was slightly lower and DNA synthesis was almost normal. The outgrowing cells from gentamicin-treated resting spores also revealed relatively thick cell walls and a very slight incorporation of labeled D-alanine. Their DNA and RNA synthesis was fairly low and protein synthesis was almost completely inhibited. These results coincide with the growth curves of individual antibiotic-treated resting spores.

Aminoglycosides↗

Adenomatous residue in cancerous papilla of Vater.

Surgical specimens of carcinoma in the papilla of Vater were studied histologically. Adenomatous residue which suggested that the carcinoma was derived from a pre-existing adenoma was found in 18 cases (81.8%) out of 22. The histological transition of adenoma into carcinoma was also frequently seen.

Adenocarcinoma↗

Pathogenesis of duct hyperplasia in the pancreas.

Causative factors in duct hyperplasia were histologically examined by using 1,388 autopsied pancreases. Duct hyperplasia was frequent in pancreases having primary carcinoma and in those having necrotizing pancreatitis, but it was not frequent in those with interstitial pancreatitis, ductal pancreatitis, and other disorders. Duct hyperplasia was almost always found in ducts which connected with small ducts having a feature of adenomatous hyperplasia or ductular aggregation in foci of intralobular fibrosis. A histologic examination revealed that these fibrous foci are likely the vestiges of fat necrosis, mostly of a subclinical one.

Adolescent↗

Relation of pancreatic duct hyperplasia to carcinoma.

In order to find a relationship between ductal hyperplasia and carcinoma of the pancreas, histological and histochemical examinations were made on pancreatic specimens of 1,174 autopsy patients with special attention to the age incidence of the former. Ductal hyperplasia was divided into 3 types; nonpapillary, papillary, and atypical hyperplasia. All three types of hyperplasia and ductal carcinoma showed a similar tinctorial property in mucous histochemistry. In general, atypical hyperplasia was seen in the pancreas having papillary hyperplasia which was found in the pancreas associated with nonpapillary hyperplasia. All three types of hyperplasia were apparently more frequent in cancerous pancreases than in non-cancerous ones. They were also more common in the head of the pancreas than in the body and tail. Age incidence also suggests a sequential change from nonpapillary hyperplasia through papillary and atypical ones to carcinoma.

Adolescent↗

Cerebral aneurysm induced by giant cell arteritis: a case report.

A rare case of giant cell arteritis inducing an aneurysmal dilatation in the peripheral branch of the middle cerebral artery was presented. The lesion was solitary and no extra-cerebral vasculature was involved. The literature of giant cell arteritis and of similar disorders involving the intracranial arteries was reviewed.

Cerebral Arteries↗

Gastric gland metaplasia in the small and large intestine.

Fifty-six surgical specimens with various ulcerative intestinal disorders were microscopically investigated for evidence of gastric gland metaplasia. Thiry-one specimens (55-4%) showed pyloric gland metaplasia. Among the 31 patients with pyloric gland metaplasia, five showed true gastric metaplasia, consisting of parietal cells, chief cells, and mucous neck cells. The percentage of true gastric metaplasia among pyloric gland metaplasia was as high as 16%, an overall frequency of 9% among various ulcerative intestinal disorders. The mechanism of pyloric gland metaplasia and true gastric metaplasia is not understood, but may occur secondary to submucosal response to ulcer healing and subsequent alteration of the intraluminal condition in the intestine.

Adolescent↗

Nature of juvenile polyps in the large intestine.

Forty-five juvenile polyps were found among approximately 390 mucosal polyps of the large intestine. Various degrees of epithelial pseudostratification were found among juvenile polyps and the larger-sized polyps of both juvenile type and adult one tended to have a more advanced degree of epithelial pseudostratification. The glands of both juvenile polyps and adult ones revealed a closely resembled or almost identical pattern of size-distribution-pattern of the glandular size in both normal mucosae and hyperplastic mucosae of long-standing ulcerative colitis. Transition of juvenile polyps into adult ones was suggested by the cases with increase in numbers of glands and their orifices to the surface of the polyp and there were some polyps showing an intermediate form between juvenile polyps and adult ones. On the basis of histologic characteristics and age incidence of the patients, it may be said that a juvenile polyp is an immature variant of an adult polyp.

Adolescent↗

Acceleration of hepatocarcinogenesis of 2,7-bis(acetamido)fluorene by carbon tetrachloride and time relation of treatment.

The role of period between administration of CCl4 and feeding of 2,7-bis-(acetamido)fluorene in the hepatocarcinogenesis of mice was analyzed by using 14 groups of different feeding schedules. Simultaneous treatment with CCl4 and either continuous or intermittent feeding of 2,7-bis(acetamido)fluorene increased the average number of hepatic nodules and the incidence of hepatomas, while separation of 8-week feeding of 2,7-bis(acetamido)fluorene from 8 week treatment with CCl4 did not accelerate the hepatocarcinogenesis. Alternate treatment with CCl4 and 2,7-bis(acetamido)fluorene increased the average number of hepatic nodules but failed to induce hepatomas. Allyl alcohol, which is a hepatotoxic substance as is CCl4, also failed to accelerate hepatocarcinogenesis of 2,7-bis(acetamido)fluorene. Concerning the feeding schedule of 2,7-bis(acetamido)fluorene alone, the intermittent one-week feeding of the carcinogen with 3-week intervals decreased the average number of hepatic nodules as compared with the continuous feeding of the carcinogen.

2-Acetylaminofluorene↗

An enormous intrahepatic shunt between portal vein and hepatic one.

An autopsy case of an enormous shunt between intrahepatic portal vein and hepatic vein in a 57-year-old man who showed an Inose's type of hepatocerebral disorder for 6 years is described. The shunt measuring up to more than 1 cm in diameter was located in the right-upper angle of the right liver lobe. The wall of the shunt lacked both the muscular layer and the elastic lamellae. Based upon the histopathology and the clinical history, this shunt was considered not to be a congenital malformation but a vascular disorder resulted from the parenchymal collapse of the liver.

Atrophy↗