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Biomedical subjects

K Nagasako

Publications and source records attributed to K Nagasako.

At least 19 recordsLinked to original sources
PubMed1997

[Vitamin K deficiency syndrome caused by antituberculous agents].

Vitamin K deficiency caused by antituberculous agents was examined in clinical patients and in experimental rats. When antituberculous agents given to the patients who had only total elental diet because of small intestinal dysfunction, a marked increase in plasma PIVKA-II and a decrease in thrombo-test value were observed. These changes were quickly normalized by administration of vitamin K, despite of succeeding or stopping of antituberculous agents. In rat experiments, effects of four agents (ethambutol, isoniazid, paraaminosalicylate, and rifampicin) on prothrombin time were studied. Among these agents, only rifampicin prolonged prothrombin time. This prolongation depended on drug doses and duration of administration. In addition to this hypoprothrombinemia, an increase in plasma PIVKA-II was also observed, and these changes were normalized within 24 hours of vitamin K administration. These data suggest that rifampicin inhibits vitamin K epoxide reductase interfering re-use of vitamin K and caused vitamin K deficiency in patients with total elental diet.

Animals↗
PubMed1995

Expression of p53 protein related to human papillomavirus and DNA ploidy in superficial esophageal carcinoma.

We examined the p53 protein and human papilloma virus (HPV) by immunohistochemistry and DNA ploidy by cytofluorometry in paraffin-embedded esophageal carcinoma tissue specimens. Sixty-one patients with superficial esophageal carcinoma were operated on between 1983 and 1991 without any prior treatment. Immunostaining of the anti-p53 protein antibody (CM1) was positive in 32 carcinomas (52%). Patients with p53-positive tumors had a poorer outcome than those with p53-negative tumors (P < 0.05). In addition, patients with p53-positive tumors did not have any characteristic site of relapse. Only 5 of the 61 patients (8.2%) had HPV-positive tumors. One of these 5 carcinomas expressed both p53 protein and HPV. Three patients with HPV-positive tumors which had invaded the submucosal layer died of relapse. A determination of DNA ploidy revealed 30 patients with aneuploid tumors, 13 with polyploid tumors and 18 with diploid tumors. The outcome of the patients with aneuploid tumors was worse than that of the patients with diploid tumor (P < 0.05). p53 protein expression was not associated with DNA ploidy; however, the 16 patients who had both p53-positive and aneuploid tumors had a worse prognosis than patients with p53-negative and aneuploid tumors (P < 0.01). These findings suggest that p53 protein expression in conjunction with DNA ploidy may be a useful indicator in evaluating the prognosis of patients with superficial esophageal carcinoma.

Adult↗
PubMed1995

Minute flat depressed neoplastic lesions of the colon detected by contrast chromoscopy using an indigo carmine capsule.

Thirty-seven diminutive flat depressed neoplastic lesions of the colon, smaller than 5 mm, were detected by contrast chromoscopy using an indigo carmine capsule and subsequently removed by endoscopic mucosal resection. We investigated the endoscopic, macroscopic, and histologic characteristics of these lesions and also evaluated the usefulness of chromoscopy and the magnifying endoscope for detecting this type of lesion. The lesions were classified into two types according to the measured height of the histologic sections: 28 lesions were truly flat depressed and the remaining 9 lesions were flat elevated. Of the 37 lesions, 18 were adenomas with mild atypia, 14 with moderate atypia, and 5 with severe atypia. The flat depressed lesions included 12 with mild atypia, 11 with moderate atypia, and 5 with severe atypia. No invasive carcinoma was present in either type, and no adenoma with severe atypia was identified in any of the flat elevated lesions. The overall rate of severe atypia was 13.5%; the rate of severe atypia for the flat depressed type was 17.9%, which is approximately 14-fold greater than that of ordinary diminutive polypoid adenomas (1.3%). The detection of these lesions was facilitated by the use of indigo carmine dye, which clearly demonstrated the mucosal irregularities. The frequency of detection of these lesions was increased four to five times with a magnifying endoscope, as occurred in nearly 10% of all of the patients examined. These data suggest that the finding of endoscopically minute flat depressed neoplastic lesions is not at all uncommon when examination is meticulously performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1995

Multiple abdominal telangiectases and lymphangiectases. A limited form of Osler-Weber-Rendu disease?

We describe a 23-year-old man with protein-losing enteropathy, iron deficiency anemia, and recurrent gastrointestinal bleeding. The patient eventually developed disseminated intravascular coagulation, portal vein thrombosis, and extensive small bowel infarction. The autopsy showed multiple telangiectases in the intestines, mesentery, liver, gallbladder, renal pelves, and diaphragm. In addition, lymphangiectases were found in the retroperitoneal space, intestines, and liver. These lesions appeared to have been the cause of the gastrointestinal bleeding and the protein-losing enteropathy. The case most likely represents Osler-Weber-Rendu disease without the usual manifestations in the skin and oral-nasal cavities.

Adult↗
PubMed1995

Colonoscopic diagnosis of dysplasia and early cancer in longstanding colitis.

Five colitic cancers were detected among 40 patients with longstanding total colitis. The colitic cancers did not show the common polypoid or ulcerated appearance in the early stage, often being flat or plaque-like. It was not easy to detect these lesions endoscopically, and it was often impossible to do so radiologically. The flat or plaque-like early cancers were often surrounded by granular and/or red mucosa. We believed that the colonoscopic detection of this colitic cancer and dysplasia was difficult because: (1) the morphology of the lesions was difficult to determine, (2) the background mucosa was not normal. When the lesions were small, it was more difficult to detect them on the colitic mucosa than on the normal mucosa. The contrast between the lesion and the background mucosa was not clear in the latter condition. In surveillance colonoscopy (using a TV colonoscope) for longstanding ulcerative colitis, careful scrutiny throughout the large intestine is required to detect colitic cancers and dysplasia at an early state.

Adult↗
PubMed1994

Non-involvement of ras mutations in flat colorectal adenomas and carcinomas.

Ras gene mutations occur relatively early during colorectal tumor development and have been observed in 40-50% of malignant colorectal tumors. Advances in endoscopic techniques have made it possible to detect small, flat colorectal tumors that could not be detected by standard examinations. To determine whether ras gene mutations are also involved in the genesis of small, flat colorectal tumors, we examined ras point mutations in 34 cases of small polypoid or flat elevated colorectal tumors (32 adenomas, 2 carcinomas) and in 26 cases of small, flat colorectal tumors (13 adenomas, 13 carcinomas) by means of the polymerase chain reaction (PCR) and dot-blot hybridization. Ras gene point mutations were observed in 16 of the 34 tumors of the former type (47%), but in none of the 26 tumors of the latter type, even though the grade of dysplasia was severe in the flat tumors. Our results suggest that different genetic pathways for tumor progression may exist for polypoid and for flat colorectal carcinomas.

Adenoma↗
PubMed1994

Comparative clinicopathological and immunohistochemical study of ras and p53 in flat and polypoid type colorectal tumours.

Mutations in oncogenes and tumour suppressor genes may have an important oncogenic role. Although flat type tumours have been frequently detected in recent years, ras and p53 expressions have not been studied in these tumours. Using a monoclonal and polyclonal antibody to the ras p21 and p53 product, paraffin wax embedded sections of 98 colorectal tumours (43 cases of the flat type colorectal tumour and 55 cases of polypoid type tumour) were stained using the immunoperoxidase technique. Staining was evaluated by light microscopic examination. Positive staining rate of ras p21 for the flat type was 0%; for the polypoid type, it was 60% in cancer with submucosal invasion, 82% in adenoma with high grade dysplasia, and 0% in adenoma with low grade dysplasia. The positive staining rate of p53 for the flat type was 50% in submucosal cancer, 9% in adenoma with high grade dysplasia, and 0% in adenoma with low grade dysplasia. For the polypoid type, it was 40% in submucosal cancer, 12% in adenoma with high grade dysplasia, and 0% in adenoma with low grade dysplasia. The intermediate staining rate of p53 in the polypoid type was 20% in submucosal cancer and 41% in adenoma with high grade dysplasia. It was seen that p53 was commonly expressed in both flat and polypoid lesions, p21 was not expressed in flat lesions, whereas it was commonly expressed in polypoid neoplasms. In the flat type cancer, a genetic change different from that of the polypoid type cancer is suggested.

Adenoma↗
PubMed1994

[Crohn's disease].

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Crohn Disease↗
PubMed1994

[Crohn's disease].

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Crohn Disease↗
PubMed1993

Expression of oncogene products and growth factors in early gallbladder cancer, advanced gallbladder cancer, and chronic cholecystitis.

The expression of oncogene products and growth factors (epidermal growth factor, transforming growth factor-beta, erbB-2, ras p 21, and c-myc) in gallbladder cancer and chronic cholecystitis was measured by immunohistochemical staining on paraffin-embedded serial sections. Expression of these products was graded according to staining intensity in an area of positively stained cells. This study reports the detection of oncogene products and growth factors in cholecystitis as well as in early and late gallbladder cancer. The multiexpression of oncogene products and growth factors was greater for both gallbladder cancer groups as compared with the cholecystitis group. The percentage of epidermal growth factor positivity diminished with increased proportion of interstitial tissue and, conversely, the percentage of transforming growth factor positivity increased with increased proportion of interstitial tissue. The proportion of ras positivity was significantly greater in both early and advanced cholecystic cancer as compared with cholecystitis, but also was considerable even for cholecystitis. These results suggest that various oncogenes may have significant roles in gallbladder cancer and that collagen synthesis is reduced by epidermal growth factor and enhanced by transforming growth factor-beta.

Cholecystitis↗