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Biomedical subjects

E Uchida

Publications and source records attributed to E Uchida.

At least 163 records · Page 9Linked to original sources
PubMed1985

Lateral flagellar antigen of Vibrio alginolyticus and Vibrio harveyi: existence of serovars common to the two species.

The antigenicity of lateral (L-) flagella of two marine vibrios, Vibrio alginolyticus and V. harveyi, was studied, and the two species were found to have common antigenicity of their flagella. Antisera against L-flagella were prepared by immunizing rabbits with highly purified L-flagellar filaments. H-Agglutination tests with the anti-L-flagella antisera showed that four H-serovars existed in these species and that two of them were shared by the two species. Cross reactivity between H-serovars of these two species and other vibrios having lateral flagella, such as V. parahaemolyticus, V. campbellii, V. proteus, or V. fluvialis, was not observed in the H-agglutination test, although partial common antigenicity was observed in the gel diffusion test with flagellin monomers. These observations suggest that surface antigenic determinants of the lateral flagella of V. alginolyticus and V. harveyi are specific to these two species but internal antigenic determinants buried in the flagellar filaments are partially shared with other vibrio species.

Antigens, Bacterial↗
PubMed1984

Histochemical investigation of criteria for the distinction between monoamine oxidase A and B in various species.

The superior cervical ganglion (SCG), pineal body (PB), and liver (L) of the rat, rabbit and cat were stained for monoamine oxidase (MAO) A and B by the tetranitro blue tetrazolium (TNBT) and coupled peroxidase ( PerOx ) methods, using 5-hydroxytryptamine (5HT), tryptamine ( Tryp ), tyramine (Tyr), and benzylamine (Bz) as substrates, and clorgyline (Cl) and deprenyl (Dep), both at 10(-7) M, as selective inhibitors. The nodose ganglion (NG) and dorsal root ganglion (DRG) of the rabbit and cat were also studied. The results with rat tissues were consistent with published quantitative findings (SCG, MAO-A much greater than B; PB, MAO-A less than or equal to B; L, MAO-A = B). In the rabbit, the findings with the SCG were similar; the MAO activities of the PB were relatively resistant to both inhibitors; the MAO of the liver required 10(-4) M concentrations of both inhibitors to produce near total inhibition, suggesting that the liver contains an MAO distinct from MAO A and B. All cat tissues examined appeared to contain almost exclusively MAO-B. In this species 5HT, which is generally considered a selective substrate for MAO-A, was oxidized by MAO-B. The findings indicate that criteria for MAO-A, -B, and other subgroups must be defined for each species and tissue.

Animals↗
PubMed1983

Effects of sodium pentobarbital anesthesia and neurotrophic factor on the maintenance of acetylcholinesterase and butyrylcholinesterase in the preganglionically denervated superior cervical ganglion of the cat.

In continuation of a previously reported study, the superior cervical ganglia of cats were preganglionically denervated bilaterally under sodium pentobarbital anesthesia. The following day cats were reanesthetized and infused via the common carotid artery with an aqueous extract of cat brain, spinal cord, and sciatic nerves for periods of 24, 12, 6, and 3 hr, without ligation of the external carotid or lingual arteries as was done previously. Values for acetylcholinesterase and butyrylcholinesterase of superior cervical ganglia at 48 hr postdenervation were all considerably above those of denervated controls. However, values for cats infused with 0.9% NaCl solution and for noninfused cats in which sodium pentobarbital anesthesia was maintained during the 24- to 48-hr postdenervation period were similarly elevated, to approximately twice the values in denervated controls. Ligation of the external carotid and lingual arteries at 24 hr postdenervation was found to oppose the preservation of acetylcholinesterase and butyrylcholinesterase contents of the ganglia induced by barbiturate anesthesia. When arterially ligated cats were infused with extract for periods of 12, 6, or 3 hr, beginning 24 hr postdenervation, acetylcholinesterase contents of superior cervical ganglia were elevated significantly above those of reanesthetized, arterially ligated controls after 12 and 6 hr but not after 3 hr of infusion, at 48 hr postdenervation.

Acetylcholinesterase↗
PubMed1983

Identification of the probable site of synthesis of butyrylcholinesterase in the superior cervical and ciliary ganglia of the cat.

The source of butyrylcholinesterase (acylcholine acylhydrolase, EC 3.1.1.8) in the ganglion cells of the cat superior cervical and ciliary ganglia has been elusive, inasmuch as the enzyme is present in high concentrations in the neuropil, where it is confined largely to the dendritic and perikaryonal plasma membranes, but appears to be absent from the perikarya. In the present study, ganglionic butyrylcholinesterase was near-totally inactivated by the injection of tetramonoisopropyl pyyrophosphoramide (6.0 mumol/kg of body weight) intravenously. During the ensuing 72 hr, the regenerating enzyme became detectable by the copper thiocholine histochemical method in the somata of essentially all ganglion cells and in the neuropil. Results were similar in preganglionically denervated superior cervical ganglia and in normal ciliary ganglia. These findings suggest (i) that butyrylcholinesterase indeed is synthesized in the ganglion cell perikarya (presumably, the rough endoplasmic reticulum) and transported extremely rapidly to more peripheral cellular sites and (ii) that the synthesis is largely independent of control by any neurotrophic factor provided by the preganglionic axonal terminals. Similar studies were conducted in the rat. In this species, in contrast to the cat, the somata of essentially all ganglion cells of the superior cervical ganglion contain various but at least moderate concentrations of acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.7) and propionylcholinesterase (acylcholine acylhydrolase, EC 3.1.1.8). After injection of tetramonoisopropyl pyrophosphoramide, propionylcholinesterase reappeared in the ganglion cell somata before its accumulation in the neuropil, as would be expected.

Acetylcholinesterase↗
PubMed1981

Effect of phenobarbital on the development of neoplastic lesions in the liver of cycasin-treated rats.

The effect of phenobarbital on the development of neoplastic lesions by cycasin was examined in inbred ACI rats. Tumor development in the liver and the kidney was observed in groups of rats treated with a single oral administration of cycasin (100 mg/kg body weight) and maintained on either a control diet or one supplemented with 0.05% phenobarbital. The feeding of phenobarbital diet after the application of cycasin significantly increased the incidence of liver tumors in female rats, but not in male rats. On the other hand, the administration of phenobarbital did not affect the incidence of kidney tumors in either sex. In addition, many large gamma-glutamyltranspeptidase (GGT)-positive foci, which were thought to be preneoplastic lesions, developed in the liver of rats treated with cycasin and then phenobarbital, whereas a small number of tiny foci were seen in rats treated with cycasin alone. Long-term feeding of the 0.05% phenobarbital diet without treatment of cycasin induced many GGT-positive foci which, however, were small-sized. These data indicated phenobarbital to possess a tumor-promoting effect in terms of induction of neoplastic lesions in the liver but not in the kidney.

Animals↗
PubMed1980

Induction of liver tumors in Wistar rats by sodium nitrite given in pellet diet.

Sodium nitrate was given to male noninbred Wistar rats at levels of 800 ppm and 1,600 ppm in a pellet diet for 646 experimental days. The first tum or was found on day 441 in the liver of a rat given a diet containing 800 ppm sodium nitrite. On day 646, liver tumors were found in 1 of 22 rats (4.5%) on an 800-ppm sodium nitrite diet and in 5 of 19 rats (26.3%) on a 1,600-ppm sodium nitrite diet. The incidence of liver tumors in the rats fed 1,600 ppm sodium nitrite was significantly different from that in controls as judged by the t-test (P < 0.05). A hepatocellular carcinoma and a hemangioendothelial sarcoma of the liver were found on day 646 in 2 rats fed 1,600 ppm sodium nitrite. One mammary tumor but no liver tumors were found in the 19 control rats. The concentration of sodium nitrite decreased after preparation of the pellet diet, but it was still at least 70% of the initial amount when the pellets were given to the rats. Volatile N-nitroso compounds, especially dimehylnitrosamine, at ppm levels were detected in the pellet diet with a gas chromatography-thermal energy analyzer.

Adenoma↗
PubMed1980

Chemotherapeutic study on canine gastric cancer induced by N-ethyl-N'-nitro-N-nitrosoguanidine.

Studies were made on the chemotherapy of gastric cancer in dogs induced by N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG). Four male Beagle dogs were given a solution of ENNG at 100 approximately 150 microgram/ml with or without 0.4% Tween 60 to drink for 5 approximately 8 months. They all developed gastric adenocarcinomas, which were confirmed by histological examination of biopsy specimens taken in months 13 approximately 32 of the experiment. After confirming the presence of gastric cancer, 1-n-hexylcarbamoyl-5-fluorouracil (HCFU), a derivative of 5-fluorouracil, was given to the dogs orally as capsules at a daily dose of 5 or 10 mg/kg body weight. One dog died from adverse effects of HCFU 12 days after the beginning of chemotherapy. The other 3 dogs were treated with CHFU for 82 approximately 424 days. In these dogs, the tumor size, measured by X-ray examination, increased during chemotherapy. On autopsy, the tumors in the stomach were found to be restricted to the antrum, and metastases of the gastric adenocarcinomas to the regional lymph nodes and/or liver were found in 2 dogs. No degenerative changes of tumor cells were found in the stomach or metastasized organs, except for necrosis of cells in a perigastric regional lymph node of the dog. The value of using canine gastric cancer in studies on chemotherapy is discussed.

Adenocarcinoma↗
PubMed1979

Induction of hepatic tumors in rats by senkirkine and symphytine.

The carcinogenicity of the pyrrolizidine alkaloids senkirkine and symphytine was studied in male inbred ACI rats. Animals were divided into 3 groups: Group I received ip injections of freshly prepared senkirkine at a dose of 10% of the median lethal dose (LD50) twice weekly for 4 weeks and then once a week for 52 weeks. Group II received ip injections of symphytine at a dose of 10% of the LD50 by the same injection schedule as in group I. The control group was given ip injections of a 0.9% NaCl solution following the same injection schedule as in experimental groups. All group I rats survived for more than 290 days after the start of injections, and 9 of 20 rats developed liver cell adenoma. All group II animals survived for more than 330 days after the start of injections. Of 20 rats, 4 had liver tumors, 3 had hemangioendothelial sarcomas, and 1 had liver cell adenoma. The hemangioendothelial sarcomas showed metastasis in the lungs of 2 rats. The control group had no liver tumors.

Animals↗
PubMed1979

Effect of phenobarbital on induction of liver and lung tumors by dimethylnitrosamine in newborn mice.

The effect of phenobarbital on simultaneous induction of liver and lung tumors was examined in inbred DDD mice. Group 1 of newborn mice received a single intraperitoneal (ip) injection of dimethylnitrosamine (DMN) and after weaning they were given 0.05% phenobarbital solution to drink. Group 2 received an injection of DMN like Group 1 but were then given normal water. Group 3 were injected ip with 0.9% NaCl solution and then given phenobarbital solution to drink as in Group 1, and Group 4 were injected with 0.9% NaCl solution like Group 3, and then given tap water to drink. The animals were examined 16 weeks after birth. In Group 1, 27 of 35 mice (77%) had liver tumor and 15 (43%) had lung tumor. In Group 2, 8 of 24 mice (33%) had liver tumor and 16 (67%) had lung tumor. Animals in Groups 3 and 4 did not develop tumors. The difference in the incidences of liver tumor, but not lung tumor, in Groups 1 and 2 was statistically significant (P less than 0.01); that is, a promoting effect of phenobarbital was observed in induction of liver tumor, but not lung tumor.

Adenoma↗