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Y Kurata

Publications and source records attributed to Y Kurata.

At least 217 records · Page 12Linked to original sources
PubMed1986

Somatostatin-sensitive neural system in the liver.

An intraportal bolus injection of cyclic somatostatin in a dose of 3.05 pmol significantly increased the vagal afferent discharge rate in the rat. The results indicate that somatostatin facilitates the vagal sensory nerve activity in the portal venous area. The present immunohistochemical examination of the rat hepatic neural system further disclosed the encapsulated corpuscles which showed intense staining for exogenous somatostatin. They were located beneath the endothelium of the large branches of the portal vein, protruded into the lumen and contained terminal nerve arborizations in the core.

Animals↗
PubMed1986

Direct quantitation of activated C3 in human plasma with monoclonal anti-iC3b-C3d-neoantigen.

We developed a microtiter solid-phase radioimmunoassay for quantitating C3 breakdown products (iC3b, C3dg, C3d) in human plasma with a unique monoclonal antibody specific for a neoantigen present on iC3b and C3d (MoAb 130). This monoclonal antibody reacts with a neoantigen which appears when C3b is converted to iC3b. The neoantigen is also present on the C3dg and C3d fragments derived from iC3b. The concentration of the neoantigen is elevated in the plasma of most patients with rheumatoid arthritis and systemic lupus erythematosus as compared to normal volunteers. Some patients with glomerulonephritis also had elevated concentration of the neoantigen in their plasma.

Antibodies, Monoclonal↗
PubMed1986

Effect of timing of partial hepatectomy on the induction of preneoplastic liver foci in rats given hepatocarcinogens.

Beginning 2 weeks after an intraperitoneal injection of diethylnitrosamine (DEN), rats were fed diet containing either 2-acetylaminofluorene (2-AAF), 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), alpha-isomer of 1,2,3,4,5,6-hexachlorocyclohexane (alpha-HCH), or phenobarbital (PB) for 6 weeks and subjected to partial hepatectomy (PH) after various periods of chemical administration. The effect of timing of PH was most apparent in rats fed 2-AAF. The size of gamma-glutamyl transpeptidase positive foci was largest when PH was performed 1-3 weeks after the start of chemical feeding. Similar tendency was slightly observed with 3'-Me-DAB or alpha-HCH administration, but not with PB or basal diet feeding. Thus, the enhancing effect of PH on the induction of the preneoplastic liver foci was affected by the type of chemical and the timing of the operation.

2-Acetylaminofluorene↗
PubMed1986

Promoting effects of various agents in rat urinary bladder carcinogenesis initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine.

The effects of various chemicals on the development of neoplastic lesions in the urinary bladder were investigated in male F344 rats given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) as an initiator in their drinking water for 4 weeks. The compounds tested, indomethacin, acemetacin, epsilon-aminocaproic acid (EACA), diphenyl, allopurinol and acetaminophen (AAP), were added to the diet or drinking water for 32 weeks, and all animals were killed at the end of week 36. Of the chemicals tested, only diphenyl significantly increased the incidences and average numbers (per 10 cm basement membrane) of papillary or nodular hyperplasias (PN hyperplasia), papillomas and carcinomas of the urinary bladder over those in animals treated with BBN alone. These findings show that diphenyl is a promoter of urinary bladder carcinogenesis in male F344 rats.

Acetaminophen↗
PubMed1986

Sodium citrate: a promoter of bladder carcinogenesis.

Dietary administration of 5% sodium citrate to male F344 rats clearly promoted the induction of preneoplastic and neoplastic lesions of the bladder initiated with N-butyl-N-(4-hydroxybutyl)nitrosamine. Enhancement of tumorigenesis by sodium citrate was associated with changes in a number of urinary parameters: apparent elevation of pH; increase of sodium ion concentration; increase of crystalline MgNH4PO4. These results show that sodium citrate promotes bladder carcinogenesis.

Animals↗
PubMed1986

Changes in the urine and scanning electron microscopically observed appearance of the rat bladder following treatment with tumor promoters.

Urine of rats treated with promoters of urinary bladder carcinogenesis was analyzed during weeks 8 to 24 of administration. The sodium salts of several chemicals, including ascorbic acid, erythorbic acid, acid saccharin and o-phenylphenol increased the urinary pH and sodium ion concentration of the urine. In contrast, treatment with sodium hippurate did not cause elevation of urinary pH although it increased the sodium ion concentration in the urine. Butylated hydroxyanisole, butylated hydroxytoluene (BHT), and ethoxyquin did not affect the urinary pH or any electrolytes except for an increase of phosphorus in the urine of rats given BHT or ethoxyquin. Scanning electron microscopic examination showed that epithelial cells of the urinary bladder of rats given promoters of urinary bladder carcinogenesis had pleomorphic microvilli, short, uniform microvilli, and ropy or leafy microridges on their surfaces. Thus, for the class of promoters including the sodium salts of weak to moderate acids, the elevation of urinary pH and the increase of sodium ion concentration accompany the promoting activity, whereas these changes do not occur following administration of the antioxidant class of bladder tumor promoters.

Animals↗
PubMed1986

Histologic and autoradiographic studies on the forestomach of hamsters treated with 2-tert-butylated hydroxyanisole, 3-tert-butylated hydroxyanisole, crude butylated hydroxyanisole, or butylated hydroxytoluene.

The inductions of hyperplasia and neoplastic lesions in the forestomach of Syrian golden hamsters by 2-tert-butylated hydroxyanisole [(2-tert-BHA) CAS: 121-00-6], 3-tert-butylated hydroxyanisole [(3-tert-BHA) CAS: 88-32-4], crude butylated hydroxyanisole [(BHA) CAS: 25013-16-5], and butylated hydroxytoluene [(BHT) CAS: 128-37-0] were compared histopathologically and autoradiographically. In hamsters fed the 2-tert-BHA diet, severe hyperplasia developed from week 4, reaching a maximum level in week 16 of 0.56 cm/10 cm basement membrane (bm), and papillomatous lesions appeared in week 16 (0.13 cm/10 cm bm). In hamsters fed 3-tert-BHA or crude BHA, severe hyperplasia developed from week 1, which reached a maximum level in week 4 of 3.63 cm/10 cm bm with 3-tert-BHA and 5.10 cm/10 with crude BHA; it then decreased. Papillomatous lesions were found in week 3 in hamsters fed 3-tert-BHA and in week 4 in hamsters fed crude BHA; they increased to maximum levels in week 16 of 0.50 cm/10 cm bm with 3-tert-BHA and 0.29 cm/10 cm bm with crude BHA. Mild hyperplasia occurred slightly more often in hamsters fed the BHT diet than in the control group. BHT induced no severe hyperplasia and papillomatous lesions. Changes in the labeling index of the forestomach epithelium paralleled the histologic changes, except in hamsters fed the BHT diet in which no significant increase in the labeling index was observed throughout the experiment. These data suggest that the tumorigenic action of crude BHA on hamster forestomach is largely due to 3-tert-BHA and that BHT does not induce forestomach tumors in hamsters.

Animals↗
PubMed1986

[Concentrations of cefmenoxime in human bone marrow blood and osseous tissue].

One gram of cefmenoxime (CMX) was administered to each of 10 patients by a one shot intravenous injection at the beginning of surgery. At 30, 60, 90, 120 minutes after the administration, concentrations of CMX in venous blood, bone marrow blood and bone tissue were assayed by the agar-well method. CMX was smoothly transmigrated after the injection from venous blood to bone marrow blood and bone tissue, and effective concentrations higher than MIC80 values were maintained for several hours. CMX, therefore, appears to be a useful drug for the prophylaxis and the treatment of postoperative infections.

Adult↗
PubMed1986

[Evaluation of the carcinogenic risk of environmental chemicals].

Many carcinogens have been detected in our environment, and chemicals which have been shown to induce cancers in experimental animals have been largely eliminated. However, there are still many chemicals which have not been studied in rodent carcinogenicity tests. In this paper, we review the evaluation of carcinogenic risk of environmental chemicals to humans. Carcinogenic risk to humans is evaluated primarily in three different phases: carcinogenicity studies in animal experiments, in vitro short-term screening studies, and finally human epidemiological studies. There are 30 chemicals, processes or industries which have been subject to these three phases and determined to be carcinogenic to humans by the International Agency for Research on Cancer (IARC). Carcinogenic risk of chemicals should be evaluated quantitatively by their threshold doses, TD50 and virtually safe dose (VSD). Furthermore, the target organ of the carcinogen should also be taken into account, which has been emphasized by the demonstration of carcinogenicity of BHA in the forestomach of rats. Summational, synergistic, antagonistic and inhibitory effects of chemicals should also be discussed. It is important to establish a guideline for detecting and eliminating environmental carcinogens in order to prevent cancer in humans.

Animals↗
PubMed1985

Inhibitory potential of acetaminophen and o-, m-, p- aminophenols for development of gamma-glutamyltranspeptidase-positive liver cell foci in rats pretreated with diethylnitrosamine.

The inhibitory potential of treatment with acetaminophen (AAP) and 3 different isometric forms of monoaminophenols (o-, m-, p-AP) for the development of gamma-glutamyltranspeptidase-positive (gamma-GT+) liver cell foci was examined in an in vivo short-term assay system. Rats were initially given a single intraperitoneal injection of diethylnitrosamine (DEN) and fed test compounds from week 2 until they were killed at week 6, all rats being subjected to two-thirds partial hepatectomy at week 3. All 4 compounds exerted obvious inhibition of the development of gamma-GT foci with both number and area (mm2) being reduced. AAP proved the most potent agent whereas dose-related inhibitory potential was observed within the 2 doses of p-AP treated.

Acetaminophen↗