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Biomedical subjects

S Fukushima

Publications and source records attributed to S Fukushima.

At least 343 records · Page 19Linked to original sources
PubMed1989

Immunohistochemical distribution of epithelial membrane antigen in bladder carcinomas as detected with a monoclonal antibody.

Expression of epithelial membrane antigen (EMA) was investigated immunohistochemically in 27 cases of bladder carcinoma using a monoclonal antibody. Normal urothelial epithelium showed EMA staining restricted to the upper layer of the surface epithelium. G-I transitional cell carcinomas demonstrated positive EMA staining which could be divided into the following 3 types; type 1, in which highly stained cells occurred in the upper layer of the neoplastic epithelium; type 2, in which the whole tumour focus was slightly stained; and type 3, in which cells strongly positive for EMA were scattered throughout the tumour focus. G-III (undifferentiated) transitional cell lesions exhibited irregular expression of EMA whereas squamous cell demonstrated specific intense EMA staining within keratinized tumour cells.

Antibodies, Monoclonal↗
PubMed1989

Involucrin expression in urinary bladder carcinoma.

Expression of involucrin was investigated immunohistochemically in 27 cases of urinary bladder carcinoma. Although no keratinization was observed in the transitional cell carcinomas examined all displayed involucrin staining to various degrees. Involucrin expression in foci of G-I transitional cell carcinomas was classified into 3 types: type 1, a mixture of intensely stained and slightly positive cells; type 2, highly positive cells intermingled with negative tumour cells; and type 3, all tumour cells slightly positive. Undifferentiated cell carcinomas demonstrated an irregular distribution of involucrin of varying staining intensity while deposition in squamous cell carcinomas was limited to keratinized areas.

Carcinoma, Squamous Cell↗
PubMed1989

Comparison of enzyme phenotypes in human bladder tumours and experimentally induced hyperplastic and neoplastic lesions of the rat urinary bladder. A combined histochemical and immunohistochemical approach.

The expression of a number of enzymes involved in drug metabolism, membrane function etc. was compared in hyperplastic and neoplastic lesions of the rat bladder and in human bladder tumours. Transitional cell carcinomas (TCC) in both rat and Man were characterized by decreased alkaline phosphatase (ALP) and increased gamma-glutamyl transpeptidase (GGT), beta-glucuronidase (beta-G1), succinate dehydrogenase (SD) and glucose-6-phosphate dehydrogenase (G6PD) activities. In addition, binding for antibodies specific for different cytochrome P-450 species (UT50, PB3a, MC1, MC2) and microsomal epoxide hydrolase (mEHb) was elevated in both murine and human tumours. Comparison of the enzyme phenotype in hyperplastic lesions induced by freeze ulceration or uracil administration with that in preneoplastic papillary or nodular hyperplasia (PNH) and TCC suggested, however, that most of the alteration in enzyme content or activity was non-specific and related to requirements for epithelial cell proliferation. On the other hand, the decreased ALP, and increased GGT and beta-G1 activity appeared more directly related to neoplastic transformation. The results suggested that qualitative differences exist between reactive hyperplasia and preneoplastic or neoplastic lesions in the urinary bladder. The finding of increased cytochrome P-450, in clear contrast to the reduction characteristic of preneoplastic hepatic lesions, may be important with regard to the observed difference in neoplastic transformation between the bladder and liver in response to drug metabolising enzyme inducers.

Alkaline Phosphatase↗
PubMed1989

Lack of carcinogenicity of magnesium chloride in a long-term feeding study in B6C3F1 mice.

Groups of 50 male and 50 female B6C3F1 mice were given magnesium chloride (MgCl2.6H2O) at dose levels of 0 (control), 0.5 and 2% in the diet for 96 wk, after which all animals received the control diet for 8 wk and were then necropsied. In females of the high-dose group a decrease in body weight was observed. However, survival rates did not differ between the treatment and control groups for males or females. Furthermore, clinical signs and urinary, haematological or serum clinical chemistry parameters showed no treatment-related effects. On histological examination, tumours were mainly found in the skin/subcutis, liver and lymphatic system. However, with the exception of a significant decrease in the incidence of liver tumours among males of the high-dose group, no differences were noted in the tumour incidence between the treated and control animals. Thus, the study described here clearly shows a lack of carcinogenicity of MgCl2.6H2O given to B6C3F1 mice in the diet.

Animals↗
PubMed1989

Participation of urinary Na+, K+, pH, and L-ascorbic acid in the proliferative response of the bladder epithelium after the oral administration of various salts and/or ascorbic acid to rats.

Changes in urinary parameters (particularly electrolyte levels and pH), and DNA synthesis and the morphology of the bladder epithelium were investigated in rats that were fed for 4 or 8 wk on diets containing various Na, K, Mg or Ca carbonate salts, with or without L-ascorbic acid (AsA). [The carbonate salts were fed at a level of 3% in the diet, and AsA or AsA-Na was administered at 5% in the diet. NH4Cl was at 1% in the diet.] The effects of treatment with NH4Cl (used as a urine acidifier), and of combined treatment with sodium ascorbate (AsA-Na) and NH4Cl were also investigated. Urinary pH was significantly elevated in groups given NaHCO3, K2CO3, AsA + NaHCO3, AsA + K2CO3 and AsA-Na, whereas treatment with AsA or NH4Cl alone caused a significant drop in urinary pH. An increase in urinary electrolytes or ascorbic acid was associated with the corresponding dosing regimen. DNA synthesis in the bladder epithelium was increased in groups given NaHCO3, K2CO3, AsA + NaHCO3, AsA + K2CO3 or AsA-Na. Furthermore, all treatments that induced an elevation of DNA synthesis also induced some morphological alterations in the bladder epithelium. The administration of AsA in conjunction with NaHCO3 or K2CO3 induced levels of change greater than those with either salt alone. In contrast, the degree of response in the bladder epithelium of rats given AsA-Na was reduced by the simultaneous administration of NH4Cl. These results suggest that the degree of DNA synthesis and/or morphological alteration in the rat-bladder epithelium after treatment with various bases may depend on changes in urinary concentrations of Na+ or K+ ions and/or pH, and the presence of ascorbic acid in the urine. The results are discussed in relation to the possible promotion by various treatment regimens (salts +/- AsA) of urinary bladder carcinogenesis.

Administration, Oral↗
PubMed1989

Long-term feeding study of N,N'-diphenyl-p-phenylenediamine in F344 rats.

Groups of 50 F344 rats of each sex were fed a diet containing 0.5 or 2% of N,N'-diphenyl-p-phenylenediamine (DPPD) for 104 weeks and were killed 8 weeks after the cessation of DPPD administration. DPPD-treated rats of both sexes showed a dose-dependent reduction in body weight gain, but no lower survival rate, when compared with untreated control rats. Blood and urine analysis showed no remarkable changes due to the treatment. Calcium deposition in the kidney of males was the only significant histological change relating to the treatment. Tumors were found in many organs of all groups, but a significant increase of tumor induction in DPPD-treated groups was not observed.

Administration, Oral↗
PubMed1989

Modification by sodium L-ascorbate, butylated hydroxytoluene, phenobarbital and pepleomycin of lesion development in a wide-spectrum initiation rat model.

Rats were treated for 1 week each with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), 0.2% N-bis(2-hydroxypropyl)-nitrosamine (DHPN) and 0.2% N-ethyl-N-hydroxyethylnitrosamine (EHEN) in the drinking water, and then administered diet containing 5% sodium L-ascorbate (Na-AsA), 1% butylated hydroxytoluene (BHT) or 0.05% phenobarbital (PB), or weekly intraperitoneal injections of 2 mg of pepleomycin per kg body weight until week 36. Histopathological examination revealed that all exerted significant modulation effects on tumor development in the various target organs. Na-AsA was found to inhibit liver but promote renal pelvis and bladder carcinogenesis. BHT similarly decreased liver and enhanced bladder lesion development. PB, in contrast promoted hepatocarcinogenesis. However both PB and BHT were associated with increased incidences of adenomas and adenocarcinomas of the thyroid. Thus the wide-spectrum initiation model allowed confirmation of site-specific modification potential and in addition demonstrated potentiation of kidney and bladder carcinogenesis promotion by pepleomycin.

Animals↗
PubMed1989

Immunohistochemical expression of keratin proteins in urinary bladder carcinoma.

Transitional carcinomas of the urinary bladder were examined immunohistochemically for keratin proteins with the use of polyclonal antiserum (TK, 41-65 kDa) and 3 monoclonal antibodies (KL 1, 55-57 kDa; PKK 1, nos. 19, 18, 8; and K 8.12, nos. 16, 13). Umbrella cells gave particularly strong staining for TK, KL 1 and PKK 1, whereas they were negative for K 8.12. Basal- and intermediate-layer cells in urothelial epithelium were moderately positive for all keratins. Brunn's nests cells showed comparatively slight or moderate keratin staining, and K 8.12 staining of Brunn's nests was higher than in urothelial epithelial cells. Transitional carcinoma (grades I and II) indicated uniform keratin distribution, and staining was strong with TK, while that of KL 1, PKK 1 and K 8.12 varied, and grade III tumors showed the lowest intensity of staining. K 8.12 staining in papillary transitional carcinomas was strongly positive in basal located tumor cells, as compared with apical tumor cells. Squamous cell carcinoma was varying positive to keratin reactions dependent on the degree of keratinization. Heterogenity of keratin distribution in papillary transitional carcinomas was given between basal tumor cells and well differentiated tumor cells including umbrella-like cells.

Antibodies, Monoclonal↗
PubMed1989

Lack of a modifying effect by the diuretic drug furosemide on the development of neoplastic lesions in rat two-stage urinary bladder carcinogenesis.

The effect of the diuretic drug furosemide on two-stage urinary bladder carcinogenesis in F344 rats initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) was investigated with regard to possible promoting activity. BBN was administered at 2 doses, 0.01 or 0.05%, in drinking water for 4 wk, and thereafter furosemide was given by gavage 3 times weekly for 32 wk, 250 mg/kg body weight. Furosemide ingestion induced diuresis with an alkaline, hypotonic urine. No significant difference with regard to incidences of bladder lesions were apparent between furosemide and control groups. The present investigation indicated that neither furosemide nor its related polyuria acted as a promoter in two-stage urinary bladder carcinogenesis.

Animals↗
PubMed1989

Co-carcinogenic effects of NaHCO3 on o-phenylphenol-induced rat bladder carcinogenesis.

The role of urinary pH and Na+ concentration on the bladder carcinogenesis of o-phenylphenol (OPP) was examined in male F344 rats. The rats were given powdered diet containing 2% sodium o-phenylphenate (OPP-Na, group 1), 1.25% OPP plus 0.64% NaHCO3 (group 2), 1.25% OPP plus 0.32% NaHCO3 (group 3), 1.25% OPP plus 0.16% NaHCO3 (group 4), 1.25% OPP (group 5), 0.64% NaHCO3 (group 6) or no test chemical (group 7) for 104 weeks respectively. Incidences of bladder carcinoma induced were significantly higher in groups 1 (12 of 29 rats, 41.4%) and 2 (9 of 29 rats, 31.0%) than in group 7 (0 of 27 rats, 0%). Groups 3 and 4 induced bladder carcinomas in 4 of 29 rats (13.8%) and 4 of 26 rats (15.4%) respectively, whereas no tumors occurred in group 5 (0 of 27, 0%). The incidence in group 6 was 3.6% (1 of 28 rats). Groups 1 and 2 induced significant increases in urinary pH and Na+ concentrations, whereas group 5 did not. Groups 3 and 4 showed the same tendency as groups 1 and 2. Examination with a scanning electron microscope showed the appearance of pleomorphic microvilli, short, uniform microvilli, and ropy or leafy microridges on the luminal surface of the bladder in groups 1-5 of rats treated with OPP or OPP-Na for 8 weeks. The appearance and severity were the same in groups 1 and 2, followed by the groups with decreasing doses of NaHCO3. The results indicated that OPP-Na is carcinogenic for the rat bladder, but OPP is not. However, increased urinary pH and Na+ concentration play important roles in OPP-Na rat bladder carcinogenesis.

Animals↗
PubMed1989

Responses of rat urine and urothelium to bladder tumor promoters: possible roles of prostaglandin E2 and ascorbic acid synthesis in bladder carcinogenesis.

An investigation of sequential changes in urine composition, levels of DNA synthesis and morphology of bladder epithelium following administration of the tumor promoters sodium ascorbate (AsA-Na) or butylated hydroxyanisole (BHA) and the non-promoter ascorbic acid (AsA) for 36 weeks was performed. In addition, prostaglandin E2 (PGE2), cAMP and AsA content were assessed in bladder tissue after 16 weeks. While AsA-Na caused increase in pH, sodium content and volume, and a decrease in osmolality of the urine throughout the study, these changes were not observed with AsA administration which resulted in a decrease in urinary pH. BHA treatment was not associated with any urinary changes. AsA-Na brought about a significant elevation of DNA synthesis in the bladder epithelium from weeks 2 to 16 and was associated with simple hyperplasia at week 8, which, however, decreased by week 16 and was no longer evident at weeks 24 and 36 when DNA synthesis returned to normal. Under the scanning electron microscope (SEM), morphologic alterations of the urothelial surface in rats given AsA-Na were observed at weeks 8 and 16, but the appearance at week 36 was almost normal. AsA did not cause any changes in these parameters at any time point. BHA induced a significant elevation of DNA synthesis throughout the study, produced simple hyperplasia at week 36 and alterations of the epithelial surface from weeks 4 to 36. Significant increases of PGE2 and AsA in bladder tissue were noted for the AsA-Na or BHA, but not AsA groups. Moreover, cAMP levels in bladder tissue of rats exposed to AsA-Na or BHA were slightly higher than in the controls. The results suggest that changes in PGE2, cAMP and AsA may be involved in promotion of rat bladder carcinogenesis.

Animals↗
PubMed1989

Immolation after drinking kerosene.

An unusual suicide is described in which analysis of circulating kerosene components at autopsy suggested that the victim had drunk kerosene and then had poured it over his body, ignited it, and burned to death.

Burns↗
PubMed1989

Effects of age on multiple organ carcinogenesis induced by 3,2'-dimethyl-4-aminobiphenyl in rats, with particular reference to the prostate.

The effects of age on multi-organ carcinogenesis induced by 3,2'-dimethyl-4-aminobiphenyl (DMAB) in male F344 rats were examined. Groups of 5-, 35-, and 65-week-old animals were given 4 weekly sc injections of DMAB at a dose of 200 or 150 mg/kg body weight. Prostate carcinomas were induced in 8 to 19% of rats treated, no significant differences in the incidence between different ages being observed. Tumors in the small intestine, skin, pancreas and peritoneum, however, developed more frequently in young than in old animals, whereas higher incidences of testis, preputial and mammary gland lesions were found in the 35- and/or 65-week-old groups. Colon and Zymbal gland carcinogenesis did not reveal any age dependence.

Age Factors↗
PubMed1989

Lack of carcinogenicity of quercetin in F344/DuCrj rats.

Quercetin was administered at dietary levels of 0(control), 1.25 and 5.0% to groups of 50 male and 50 female rats for 104 weeks, and then all animals were maintained without quercetin supplement for a further 8 weeks. At 5.0% quercetin, both sexes showed growth retardation throughout the study. There were no treatment-ascribed effects regarding clinical signs, mortality, urinalyses or hematology. Although serum glucose in 5.0% quercetin-treated males was significantly decreased and some relative organ weights in 5.0% groups showed statistically significant increases, these latter changes seemed to be related to the growth retardation. An increased incidence of non-neoplastic hyperplastic polyps in the cecum was noted in the 5.0% males. The incidences of cystic changes and fibroadenomas of the mammary gland, and foci (areas) of hepatocellular alteration in the 5.0% females, and liver bile duct proliferations in the 5.0% males were significantly decreased. No proliferative lesions of the urinary bladder related to treatment with quercetin were found in any rats. The incidences of several other nonneoplastic and neoplastic lesions which demonstrated statistically significant changes appeared to be related to the growth retardation or to be within the normal range, and therefore none was considered to be significant biologically. Thus, the investigation did not demonstrate any clear carcinogenic effect of quercetin on F344 rats at dietary levels of up to 5.0%.

Animals↗
PubMed1989

Comparative study of urinary bladder carcinomas in Japanese and Egyptians.

One hundred six Japanese and 169 Egyptian cases of urinary bladder carcinoma treated by total cystectomy were analyzed histopathologically. Urinary bladder carcinomas in Egypt were encountered at an earlier age than those in Japan. The proportion of carcinomas in Egyptian males was higher than in Japanese males. Squamous cell carcinomas (SCCs) predominated in Egyptian cases whereas transitional cell carcinomas predominated in Japanese cases. The pathological stage of Egyptian cancers was more advanced than in Japanese cases; even grade 1 SCCs showed invasion into the muscular layer. Most carcinomas in Egypt were associated with Schistosoma haematobium infections.

Aged↗
PubMed1989

Bladder cancers. Their process of development and its modification.

Much information on the development of bladder cancers and its modification has accumulated. It is generally considered that the presence of chemicals in the environment including carcinogens and modifiers (promoters, inhibitors, anti-promoters, etc.) is responsible for the geographical variation in human neoplasia including urinary bladder cancer development. A diagrammatic representation of the possible interactions between environmental factors and tumor development in man is shown in Fig. 6. Thus if potent carcinogens or promoters are present, neoplasia results, with tumor death occurring within an individual's normal lifetime. However, lack of such substances or the existence of powerful inhibitory factors is presumed to slow down the process, so that the normal life-span is not affected. It is therefore of prime importance for thorough awareness of the factors involved to be generated.

Adult↗