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Biomedical subjects

O Sakaguchi

Publications and source records attributed to O Sakaguchi.

At least 19 recordsLinked to original sources
PubMed1985

[Pancreas head carcinoma associated with situs inversus viscerum totalis].

The patient was a seventy seven years old male whose chief complaint was jaundice. Chest and abdomen roentgenogram showed situs inversus viscerum totalis. Echographically, pancreas head tumor was showed. Stenosis of inferior bile duct and dilatation of main pancreatic duct were showed by percutaneous transhepatic cholangiography and endoscopic retrograde cholangio pancreaticography. So, pancreas head carcinoma associated with situs inversus viscerum totalis was diagnosed. Pancreaticoduodenectomy and modified Child method was undergone. At the time of operation, liver was recognized left side of abdomen. The tumor was diagnosed well or moderately differentiated papillotubular adenocarcinoma by pathological study. This unusual combination of situs inversus viscerum totalis and pancreas head carcinoma was reported.

Adenocarcinoma, Papillary↗
PubMed1984

Studies on the toxin of Aspergillus fumigatus. XVIII. Photooxidation of asp-hemolysin in the presence of various dyes and its relation to the site of hemolytic activity.

The site of hemolytic activity of a toxin isolated from Aspergillus fumigatus designated Asp-hemolysin was determined by photooxidation techniques. The hemolytic activity of this toxin was strongly inhibited by photooxidation with methylene blue, rose bengal, riboflavin, or eosin G as a sensitizer, whereas crystal violet, hematoxylin, naphthol yellow S, bromothymol blue, methyl orange, and cresol red had no effect. pH dependence of the inactivation with methylene blue was observed in the narrow range of pH values from 7.0 to 8.0, like that of the inactivation with rose bengal or riboflavin. The histidine, cysteine, methionine, tryptophan, and tyrosine content of methylene blue-photooxidized Asp-hemolysin was significantly decreased, while other amino acids were not affected. The hemolytic activity of the toxin was lost more slowly than the histidine residue, being maintained at about 50% even at the time when the histidine residue was completely lost after 30 min. Photooxidation of Asp-hemolysin in the presence of rose bengal also caused a decrease in histidine, methionine, and threonine content. These findings suggest that residues of cysteine, methionine, threonine, tryptophan, and/or tyrosine but not histidine may play an important role through stereostructure in the manifestation of the hemolytic activity of Asp-hemolysin.

Amino Acids↗
PubMed1984

Calcium behavior in endotoxin-poisoned mice: especially calcium accumulation in mitochondria.

A possible role of intracellular Ca2+ and participation of calmodulin in cellular metabolism in endotoxin-poisoned mice were investigated. The levels of calcium in liver cytosol and liver mitochondria fractions in poisoned mice were markedly higher 18-48 hr after endotoxin injection than in the control mice. On the other hand, the levels of serum calcium in the poisoned mice were about 20% lower at 18 hr than in the controls. The serum calcium levels in mice injected with 50 and 100 micrograms of endotoxin showed no dose-response effect, but a dose-response effect was observed at a dose of 200-400 micrograms. The serum Ca2+ levels in endotoxin-tolerant mice were similar to those in the control mice. The levels in mice injected with glucocorticoid-antagonizing factor mice were about 14% lower at 3 hr than in the controls. The mice fed a vitamin D3- and calcium-free diet showed a higher mortality rate in the early stage (12-18 hr) of endotoxication than that of the mice fed a normal diet. The lipid peroxide levels and Ca2+-ATPase activity in the liver mitochondria fraction in endotoxin-poisoned mice showed a higher level than those of the control mice. There was little or no difference in the levels of serum glucose between the mice injected with calmodulin antagonist (trifluoperazine, TFP) plus endotoxin and those given endotoxin alone. However, the liver glycogen levels in TFP plus endotoxin-treated mice were markedly higher than that in mice given endotoxin alone. Furthermore, calcium antagonist (verapamil) plus endotoxin-treated mice had about a 40% higher survival rate after 72 hr than those given endotoxin alone. The findings suggest that there is a possibility of participation of the Ca2+-calmodulin system in carbohydrate metabolic disorders during endotoxemia and that the changes in intracellular Ca2+ may result in various metabolic disorders.

Animals↗
PubMed1982

Effect of lead acetate on superoxide anion generation and its scavengers in mice given endotoxin.

The administration of endotoxin to mice rendered hypersensitive by lead acetate resulted in profound lipid peroxide formation in the liver 6 hr postintoxication. Endotoxin plus lead acetate administration depressed glutathione peroxidase and superoxide dismutase activities in mouse liver, whereas superoxide anion generation significantly increased in the livers of endotoxin plus lead acetate-treated mice compared with that in mice treated with endotoxin alone. Serum acid phosphatase and lactate dehydrogenase isozyme exhibited much more leakage in endotoxin plus lead acetate-injected mice than in sera of mice given endotoxin alone. Nonprotein SH level in the liver was reduced markedly in endotoxin-lead treated mice compared with those receiving endotoxin alone. The plasma vitamin E level was found to decline by 6 hr postintoxication in both endotoxin-lead and endotoxin alone-treated mice, and the transient elevation of the plasma level at 18 hr may be considered to indicate mobilization from other tissues into the blood.

Acid Phosphatase↗
PubMed1981

Lipid peroxide formation and membrane damage in endotoxin-poisoned mice.

Lipid peroxide formation and plasma membrane damage in mouse liver following the administration of Salmonella endotoxin were examined. The liver lipoperoxide level was markedly elevated in animals given endotoxin compared with that in the controls, and returned to its normal range after 2 days. On the other hand, superoxide dismutase activity was decreased by 18--48 hr after endotoxin injection, thereafter tending to increase. Glutathione reductase and glutathione peroxidase activities declined in the liver 18 hr after the injection. The endotoxin resulted in much lower lipoperoxide formation in the livers of tolerant mice than in those of the poisoned mice. The lipoperoxide level in endotoxin-poisoned mice after the administration of alpha-tocopherol was lower than that in the controls, and alpha-tocopherol administration prevented completely the membrane protein damage that arose from endotoxin challenge. After glutathione administration the membranes of the poisoned mice also returned to almost the normal disk electrophoretic profile. These results suggest that lipid peroxide formation in the liver plasma membrane caused by free radicals might occur in a tissue ischemic state in endotoxicosis.

Adenosine Triphosphate↗
PubMed1981

Effect of alpha-Tocopherol on endotoxicosis.

The effect of alpha-tocopherol in endotoxicosis was studied. The alpha-tocopherol level significantly decreased in mouse liver 18 hr after endotoxin administration, thereafter tending to increase to approach the normal range. In endotoxin-tolerant mouse liver, the lipid peroxide level was reduced to less than half of that in nontolerant animals following endotoxin challenge. The liver lipid peroxide level and serum lactate dehydrogenase or acid phosphatase leakage were studied in mice fed a vitamin E-deficient (ED) diet and a vitamin E-supplemented (ES) diet for 40 days. ED mouse liver exhibited a higher formation of lipid peroxide after endotoxin was given while there was a markedly lower level in ES mouse liver. There was significantly more serum lactate dehydrogenase or acid phosphatase leakage in ED mice than in ES mice after endotoxin administration. There was about a 25% decrease in liver superoxide dismutase (SOD) activity in endotoxin-poisoned mice fed both the normal and the ED diets, while the activity was at a higher level in ES-fed mice. These results suggest that alpha-tocopherol may be helpful in preventing membrane instability in endotoxin poisoning.

Acid Phosphatase↗
PubMed1980

Metabolic aspects in mice administered live Salmonella typhimurium.

The influence of intraperitoneal inoculation of live Salmonella typhimurium on carbohydrate and lipid metabolisms in mice was investigated at doses of 9.2 x 10(7) cells, 1.9 x 10(8) cells, and 3.8 x 10(8) cells. The hepatic glycogen content in mice at 18 hr after the inoculation decreased in inverse proportion to an increase in the injection dose. The activities of hepatic phosphorylase and G-6-Pase increased significantly after 2 hr, but after 18 hr the levels of both enzyme activities, especially G-6-Pase, declined in inverse proportion to an increase in dose of viable cells administered to the mice. The levels of serum glucose and free fatty acids (FFA) in mice markedly decreased at doses of 1.9 x 10(8) and 3.8 x 10(8) cells after a transient rise at early stage (1 hr) after the injection. Marked hypertriglyceridemia was seen in infected mice. However, the activity in serum lipoprotein lipase (LPL) was reduced by an increase in the injection dose. The effect of intraperitoneal administration of viable cells on the serum triglyceride level was prevented in mice immunized with S. typhimurium endotoxin or administered with the anti-endotoxin serum. These results indicate that hypertriglyceridemia mainly results from the action of endotoxin in the pathogen. Serum lactate dehydrogenase (LDH) activity markedly increased at the dose of 3.8 x 10(8) cells within 8--16 hr, and the infected mice exhibited a leakage of isozymes LDH-3 and 5 in the serum 16 hr post-inoculation.

Animals↗
PubMed1979

Alterations of lipid metabolism in mice injected with endotoxin.

Some alterations in lipid metabolism in mice were observed by the intraperitoneal injection of endotoxin from Salmonella typhimurium. The content of serum triglyceride increased markedly in poisoned mice 16-24 hr postintoxication. The level of free fatty acid (FFA) in the serum of endotoxin-administered mice decreased in inverse proportion to an increase in the injected dose of endotoxin. The electrophoretic analysis of the serum lipoprotein on cellulose acetate membrane showed that pre beta-lipoprotein increased markedly and that FFA fraction in the poisoned mice sera disappeared 18 hr postintoxication. The activity of hormone-sensitive lipase in adipose tissue was elevated appreciably 2 hr after injection, but decreased more significantly after 18 hr than that in fasted control mice. On the other hand, the activity of lipoprotein lipase decreased in the post-heparin serum and adipose tissue 3 hr postintoxication, and decreased significantly after 16 hr. There were no significant differences between changes in the formation of active glycerol (alpha-GP) and in the activity of alpha glycerophosphate dehydrogenase (alpha-GPDH) in the mice liver with or without administration of endotoxin, and after 16 hr levels of both hepatic alpha-GP content and alpha-GPDH activity in poisoned mice showed a tendency to be slightly lower than those in fasted control mice.

Animals↗