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Biomedical subjects

N Ito

Publications and source records attributed to N Ito.

At least 631 records · Page 35Linked to original sources
PubMed1987

Histochemical reactivity of soybean agglutinin with blood group antigens and their precursor substances in acinar cells of human pancreas.

In human pancreas, soybean agglutinin (SBA) conjugated to horseradish peroxidase reacted with the acinar cells secreting blood group A and/or H antigen, but not with those secreting only B antigen. For detailed histochemical characterization of SBA staining, the effects of treatment with unlabeled lectins and of digestion of certain enzymes on SBA staining were investigated in formalin-fixed, paraffin-embedded pancreatic tissue from individuals of different blood groups. Pre-incubation of sections with unlabeled Dolichos biflorus agglutinin to block A antigen eliminated subsequent SBA staining in the cells secreting A antigen, although failing to induce any effects in those secreting H antigen. In contrast, pre-incubation with unlabeled Ulex europaeus agglutinin-I (UEA-I) to block H antigen abolished SBA staining in cells secreting H antigen but not in those secreting A antigen. Treatment with galactose oxidase yielded the same results as those with unlabeled UEA-I, i.e., SBA reactivity was significantly diminished in cells secreting H antigen but not in those secreting A antigen. Digestion with beta-galactosidase resulted in a slight decrease of SBA staining in the cells secreting H antigen. Accompanying the decrease of SBA staining, reactivity with Griffonia simplicifolia agglutinin-II (GSA-II) appeared for the first time in the enzyme-susceptible, SBA-reactive cells secreting H antigen. Pre-treatment with galactose oxidase abolished this effect of beta-galactosidase. The GSA-II reactivity disclosed by treatment with galactosidase was completely eliminated by digestion with beta-N-acetylhexosaminidase, indicating that GSA-II staining after digestion with galactosidase is due to exposed penultimate beta-N-acetyl-D-glucosamine residues. These results demonstrate that at least two substances react with SBA in acinar cells of human pancreas, one being terminal beta-N-acetyl-D-galactosamine residues of A antigen, and the other being terminal beta-D-galactose-(1----3 or 1----4)-beta-N-acetyl-D-glucosamine dimers in the precursor of blood group H antigen. Such dimers may exist in close proximity to L-fucose residues of H antigen, since unlabeled UEA-I blocked SBA staining.

ABO Blood-Group System↗
PubMed1987

Experimental induction of renal tumors.

Renal tumors have been reported to be induced by natural products, chemical carcinogens, viruses, or radiation. Species or strain specificity and sex also appear to play significant roles in their development. In man, it is also likely that the heredity existence of other diseases, smoking, food habits, and irradiation may be etiological factors. It also appears that hormonal, chemical, and other environmental factors can play a role. Nephrotoxin modifies two-stage chemical carcinogenesis in rat kidney. Some nephrotoxins without carcinogenicity promote the development of renal tumors in rats pretreated with subcarcinogenic doses of chemical carcinogens. The importance of nephrotoxin in development of renal adenocarcinomas needs elucidation. Preneoplastic lesions in the kidneys can be recognized by histochemical methods with specific antibodies. It is hoped that further research will be continued, so that data obtained from experimental work will provide a better understanding of the etiology and induction of renal cancer in man.

Animals↗
PubMed1987

Induction of tumors in the liver, urinary bladder, esophagus and forestomach by short-term treatment with different doses of N,N'-dibutylnitrosamine in rats.

The multipotential carcinogen N,N'-dibutylnitrosamine (DBN) was given to F344 male rats for 2 weeks at three dose levels to study the concentration dependence of its organ specificity. Groups of 20 rats were given water containing 0.25, 0.125 or 0.063% DBN for 2 weeks and then tap water only to drink until they were killed 52 weeks after the start of the experiment. DBN induced preneoplastic lesions in the liver, esophagus, forestomach and urinary bladder. Carcinoma was found only in the liver. Induction of preneoplastic focal hepatocyte lesions positive for the P-form of glutathione S-transferase (GST-P) was quantitatively dependent on the dose of DBN. In the urinary bladder, the incidences of papillary or nodular hyperplasia (PNH) and papilloma of transitional cells tended to increase at higher doses. The incidence and number per unit length of basal cell-type hyperplasias of the esophageal epithelium were significantly higher in all DBN groups than in the control group, through the increase did not show a clear dose-dependency. The incidence of epithelial basal cell hyperplasia of the forestomach was significantly increased at all doses and the increase was apparently dose-related. These results indicate that even in a short-term experiment, DBN exerted multipotential carcinogenic effects. Thus, this system could be used for assay of the modifying effects of compounds administered subsequently on carcinogenesis in different organs.

Animals↗
PubMed1987

A rapid and sensitive analytical procedure for human plasminogen subspecies. Combination of high-performance affinity chromatography and specific monitoring of proenzymes.

Human plasminogens specifically separated by high-performance affinity chromatography were specifically detected by a newly devised, on-line monitoring system, in which the proenzymes were activated by urokinase and plasmin activity thus generated was assayed. Presence of Lys-plasminogen as a constituent in the blood was demonstrated by both chromatographic patterns and biochemical experiments. This system made it possible to estimate rapidly not only Glu-plasminogen but also Lys-plasminogen in the plasma without any pretreatment. Its utility as a tool for clinical analysis of fibrinolytic system was suggested.

Chromatography, High Pressure Liquid↗
PubMed1987

Activation of N-ras gene in a rat hepatocellular carcinoma induced by dibutylnitrosamine and butylated hydroxytoluene.

DNA samples from eighteen rat hepatocellular carcinomas, including those induced by oral administration of dibutylnitrosamine (DBN) with butylated hydroxytoluene (BHT), or DBN with butylated hydroxyanisole (BHA), have been tested for the presence of transforming activity by transfection assay with NIH3T3 cells. Of the eighteen samples, only one from a tumor induced by DBN and BHT gave transformants. the activated oncogene was identified as rat N-ras by Southern blot analysis.

Animals↗
PubMed1987

[Effect of intravesical instillation of the antitumor chemotherapeutic agents mitomycin C and cytosine arabinoside on rat bladder carcinogenesis initiated by N-butyl-N-(4-hydroxybutyl) nitrosamine].

The effects of intravesical instillation of cytosine arabinoside (CA), mitomycin C (MMC) and combination of CA and MMC were examined in rats pretreated with N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN). Rats were given initial treatment with BBN for 4 weeks followed by intravesical instillation of drugs once a week for 12 weeks. The total observation period was 36 weeks. Instillation of MMC markedly increased the development of bladder tumors, although CA did not. Moreover, tumor incidence in the combination group was less than that with MMC only. The results indicate that the intravesical instillation of MMC promotes 2-stage bladder carcinogenesis, whereas CA does not. Moreover, it is suggested that CA inhibits the promoting effect of MMC.

Administration, Intravesical↗
PubMed1987

[Lymphocyte cytotoxicity against autologous tumor cells and the effect of interferon-beta on their activities. (2) Evaluation of large granular lymphocytes (LGL)].

Large granular lymphocytes (LGL) were obtained by Percoll density gradient centrifugation of peripheral mononuclear cells from 15 patients with hematological malignancies (10 acute leukemias and 5 non-Hodgkin's lymphomas). Five-hour 51Cr-release cytotoxic assay by LGL was performed against frozen autologous tumor cells in these patients. Mean percentage cytotoxicity by LGL was 5.6%, and this was enhanced to 15.0% by the addition of IFN-beta to the culture medium. A decrease of cytotoxicity was observed when LGL was treated with anti-Leu 11b antibody plus complement, or when LGL was pretreated with the unlabelled K562 as a competitive inhibition assay. The addition of monocytes also induced a decrease of cytotoxicity, suggesting that monocytes may act as a suppressive agent in autologous tumor cell killing by LGL.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1987

Enhancing effects of N-ethyl-N'-nitro-N-nitrosoguanidine and sodium taurocholate on development of pepsinogen 1 decreased pyloric glands in rats initiated with N-methyl-N'-nitro-N-nitrosoguanidine.

Sequential quantitative analyses were made of pepsinogen 1 (Pg 1) decreased pyloric glands after treating male WKY rats first with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and then with N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) as a second gastric carcinogen or sodium taurocholate (Na-TC) as a gastric promoter. Animals received a single dose of MNNG (160 mg/kg body weight) by gastric intubation followed two weeks later by either ENNG in drinking water (100 micrograms/ml) (group 1), basal diet containing 0.25% Na-TC (group 2), or basal diet and tap water (group 3), from weeks 3 to 24. Animals were sacrificed at weeks 8, 12, 16, 20 and 24. Sections of the pyloric mucosa were investigated for Pg 1 immunostaining. In comparison with group 3, induction of Pg 1 decreased pyloric glands was significantly enhanced by ENNG from week 8 and by Na-TC from week 16. The former exerted a significantly stronger effect at each time point. The results suggest that Pg 1 decreased pyloric glands represent a good marker for early detection of gastric carcinogens and promoters in in vivo test systems.

Animals↗
PubMed1987

Induction of forestomach lesions in rats by oral administrations of naturally occurring antioxidants for 4 weeks.

The effects of naturally occurring antioxidants on rat forestomach epithelium were compared with those of synthetic antioxidants, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT), of which the former is a known forestomach carcinogen. Groups of five F344 male rats were given diet containing BHA, BHT, gallic acid, syringic acid, sesamol, caffeic acid, chlorogenic acid, ferulic acid, eugenol or esculin for 4 weeks at a level of 0.7% for BHT or 2% for other compounds. Histological examination of the forestomach showed that BHA induced hyperplasia mainly in the prefundic region near the esophageal orifice, caffeic acid induced pronounced hyperplasia throughout the forestomach epithelium, and sesamol induced large ulcers and hyperplasia in the central region. Thus, these naturally occurring antioxidants showed different toxicities and abilities to induce hyperplasia in the rat forestomach.

Animals↗
PubMed1987

Patterns of epithelial proliferation revealed by continuous administration of bromodeoxyuridine during urinary bladder carcinogenesis in rats.

The patterns of epithelial proliferation in the urinary bladder during carcinogenesis were examined sequentially in rats given drinking water supplemented with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for 12 weeks and then water without BBN for 18 weeks. Animals received 120 micrograms of bromodeoxyuridine (BrdU) per hour continuously via an osmotic minipump for 4 days before sacrifice and labeled cells were detected immunohistochemically using monoclonal antibody against BrdU. Two types of BBN-induced epithelial lesions were distinguishable: reversible changes characterized by proliferation of basal cells only, and irreversible changes with high and irregularly distributed incorporation of label throughout the epithelium. Simple hyperplasia, and papillary or nodular hyperplasia consisted of areas of reversible and/or irreversible changes, whereas papilloma and cancer consisted of areas of irreversible changes.

Animals↗
PubMed1987

Epithelial lesions of the urinary bladder in three hundred and thirteen autopsy cases.

Urinary bladders that appeared normal macroscopically were obtained from 313 autopsy cases of both sexes and examined microscopically. Proliferative lesions such as Brunn's nests and cystitis glandularis were frequent in cases of all ages and both sexes. Metaplastic lesions such as columnar or cuboidal metaplasia and squamous metaplasia were less frequent. These two types of lesions were not related to age, but squamous metaplasia was more common in females than in males. The sites of predilection for these 4 types of lesions were the trigone and anterior wall. Hyperplasia was observed in 16.3% of the male and 10.6% of the female cases, and dysplasia in 6.8% of the male and 5.7% of the female cases. Both types of lesions were more frequent in older than younger cases. Neither type of lesions was related to chronic inflammation. One case of carcinoma in situ was found in a male. These data and mapping of the bladders indicated that none of these benign proliferative and metaplastic lesions were related with the development of dysplasia or carcinoma in situ.

Adult↗
PubMed1987

Catechol strongly enhances rat stomach carcinogenesis: a possible new environmental stomach carcinogen.

Catechol (CAS: 120-80-9) is present in the environment, being a major industrial chemical as well as a major phenolic component of cigarette smoke. Continuous oral treatment of rats with 0.8% catechol for 51 weeks after a single intragastric dose of 150 mg/kg of N-methyl-N'-nitro-N-nitrosoguanidine strongly enhanced both forestomach and glandular stomach carcinogenesis. In addition, and more importantly, catechol alone induced adenocarcinoma and adenomatous hyperplasia in the pyloric region of the glandular stomach. These results clearly indicate that this environmental contaminant merits classification as an enhancer of forestomach and glandular stomach carcinogenesis with complete carcinogenic potential for the glandular stomach. Its significance for gastric tumor development in man requires elucidation.

Adenocarcinoma↗
PubMed1987

[A case of renal angiomyolipoma treated with partial nephrectomy. Diagnostic value of ultrasonography and computed tomography].

A 62-year-old woman with renal angiomyolipoma is reported. Ultrasonogram revealed a hyperechoic renal mass and computed tomography showed a fatty density area in the tumor. Preoperative diagnosis of renal angiomyolipoma was made and was confirmed by frozen section during the operation. Partial nephrectomy was performed subsequently. Renal angiomyolipoma is known by its fat content causing high echogenicity in the ultrasonogram and fatty density area in computed tomography. Renal angiomyolipoma, therefore, could be suspected by this combination of findings and conservative surgery should be planned preoperatively.

Female↗
PubMed1987

Differential modification of development of preneoplastic lesions in the Syrian golden hamster initiated with a single dose of 2,2'-dioxo-N-nitrosodipropylamine: influence of subsequent butylated hydroxyanisole, alpha-tocopherol, or carbazole.

The effects of butylated hydroxyanisole [(BHA) CAS: 25013-16-5], alpha-tocopherol [(TC) CAS: 59-02-9], and carbazole [(CA) CAS: 86-74-8] administered subsequent to a single dose of 2,2'-dioxo-N-nitrosodipropylamine [(DOPN) CAS: 60599-38-4] on the development of putative preneoplastic lesions were investigated in Syrian golden hamsters. Whereas the 2 antioxidants BHA and TC inhibited the incidence of both liver and pancreatic lesions, CA, itself giving rise to considerable numbers of enzyme-altered foci, enhanced carcinogenesis in the liver while inhibiting carcinogenesis in the pancreas. All 3 of these agents induced hyperplastic and papillomatous lesions in the forestomachs of treated animals, independent of prior DOPN treatment; these forestomach lesions were not evident in controls. Cellular atypia and invasive growth characteristics signifying malignant change were also observed in BHA-induced forestomach lesions. The results demonstrate that hepatocarcinogenesis in the Syrian golden hamster, like that in the rat, can be inhibited by antioxidants. The similar decrease in putative preneoplastic lesion yield evident in the pancreas of BHA- or TC-treated hamsters, considered in the light of similarities in altered enzyme phenotype in carcinogen-induced lesions of both organs, suggests that common biochemical changes can be an underlying factor in the modification of neoplastic development in liver and pancreas. The present results also provide further evidence that CA has carcinogenic potential for the liver and forestomach of experimental animals.

Animals↗
PubMed1987

Comparison of lesions induced in the Syrian golden hamster by diethylnitrosamine, dimethylhydrazine, and dibutylnitrosamine: influence of subsequent butylated hydroxyanisole treatment.

The target organ specificity of the carcinogens diethylnitrosamine [(DENA) CAS: 55-18-5], dimethylhydrazine [(DMH) CAS: 57-14-7], and dibutylnitrosamine [(DBN) CAS: 924-16-3] was examined in Syrian golden hamsters. Groups of male animals were given 8 weekly injections of one of these carcinogens and then were maintained on a basal diet or a diet supplemented with 1% butylated hydroxyanisole [(BHA) CAS: 25013-16-5], or they were given the respective carcinogens in the drinking water until they were sacrificed at week 34. While DENA specifically induced tracheal polyps and hepatocellular foci and nodules, DMH administration was associated with development of both hepatocellular and hemangiocellular liver lesions as well as forestomach papillomas and adenocarcinomas of the large intestine. DBN induced lesions in the urinary bladder, forestomach, and trachea, in addition to a few preneoplastic foci in the liver and lungs. In all organs studied, preneoplastic and neoplastic populations were essentially similar to those observed in other experimental animals, with colon and tracheal lesions demonstrating alteration in polysaccharide metabolism. While inhibiting the development of hepatocellular lesions, especially in the group initiated with DENA, and while itself inducing extensive papillomatous forestomach hyperplasia, BHA administration did not exert a significant modifying influence on tumorigenesis in other organs. The present results demonstrate the efficacy of Syrian golden hamster studies for investigation of comparative neoplasia. Of particular interest in this respect were differences in the degree of phenotypic instability demonstrated by glutathione S-transferase placental form-positive foci induced by the 3 carcinogens, which indicated a possible qualitative variation in "initiation."

Animals↗