Search PubMed⌕ Search

Biomedical subjects

T Ozeki

Publications and source records attributed to T Ozeki.

At least 73 records · Page 4Linked to original sources
PubMed1987

The effect of diphenylamine derivatives on arachidonic acid metabolism in rat peritoneal macrophages.

The effect of diphenylamine derivatives such as diclofenac sodium, mefenamic acid and lobenzarit disodium on arachidonic acid metabolism in rat peritoneal macrophages was examined. Lobenzarit disodium has no effect on prostaglandin E2 production as measured by radioimmunoassay although two other diphenylamine derivatives have a potent inhibitory activity. Three diphenylamine derivatives have no effect on Ca2+ ionophore-stimulated release of radioactivity from (3H)arachidonic acid-labeled macrophages. HPLC analysis revealed that lobenzarit disodium had no effect on the synthesis of lipoxygenase products as observed in diclofenac sodium and mefenamic acid. It is concluded that lobenzarit disodium, although its fundamental chemical structure resembles diclofenac sodium and mefenamic acid, has no inhibitory activity on arachidonic acid metabolism, suggesting that immunomodulatory activities of lobenzarit disodium are manifested without interfering with arachidonic acid metabolism.

Aniline Compounds↗
PubMed1987

Analyses of glycosaminoglycans in human lung cancer.

Studies were conducted on the total amount of glycosaminoglycans and glycosaminoglycan composition in adenocarcinoma tissue of human lung. The glycosaminoglycans were prepared by exhaustive proteinase digestion of adenocarcinoma tissue from human lungs and of lung tissue without pulmonary diseases taken at autopsy as a control. The glycosaminoglycan classes were characterized by biochemical, enzymatic, and electrophoretic methods. The presence of heparin, which has until now not been found in lung cancer tissue, was demonstrated on both carcinoma and control tissues. The levels of whole glycosaminoglycans were markedly increased in cancer tissue compared to the controls. The classes of glycosaminoglycans which increased in lung carcinoma tissue were predominantly chondroitin-4-sulfate and chondroitin-6-sulfate. Both hyaluronic acid and heparin were slightly increased in cancer tissue.

Adenocarcinoma↗
PubMed1987

Interaction of silkworm larval hemolymph antitrypsin and bovine trypsin.

Antitrypsin isolated from silkworm larval hemolymph can inhibit bovine trypsin. The apparent molar ratio of silkworm antitrypsin (sw-AT) to trypsin at extrapolated null trypsin activity was determined to be 1.3 by titration of trypsin with sw-AT. The undissociability of the complex between sw-AT and trypsin on sodium dodecyl sulfate-polyacrylamide gel electrophoresis was confirmed by immunoblotting and fluorescence labeling techniques. Chemical analysis of the complex elucidated that it contained equimolar sw-AT and trypsin. Densitometric analysis of electrophoretic patterns obtained during the titration of trypsin by sw-AT suggested the presence of a suicide product formed from sw-AT. This was the reason why excess sw-AT was needed for complete inhibition of trypsin. In the complex, the sw-AT molecule was cut at one site but the fragments produced were still joined together. Trypsin in the complex was released by treatment at pH 10.0, and it was deduced that the complex formation involved acyl-bond formation between sw-AT and trypsin. The sw-AT component obtained from the alkali-treated complex possessed two kinds of NH2-terminal amino acid sequences. Non-covalent forces may bind the two fragments of sw-AT, which could be separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Amino-terminal amino acid sequence analysis of the large fragment gave a sequence identical with that of intact sw-AT. This indicated that the reactive site of sw-AT with trypsin was located at the COOH-terminal region of the molecule. These characteristics resemble those of inhibitors belonging to the serpin family.

Amino Acid Sequence↗
PubMed1987

Localization of hepatitis B core antigens in chronic active hepatitis using immunoperoxidase and chromotrope aniline blue staining.

Hepatitis B (HB) core particle, in biopsied liver specimens from patients with chronic active hepatitis (type B) were stained with immunoperoxidase and chromotrope aniline blue (a non-immunological method) and the following results were obtained. HB core particles were more clearly stained with chromotrope aniline blue than with immunoperoxidase. Numerous HB core particles were seen not only in the nuclei of hepatocytes but also in the cytoplasm in HBeAg seropositive patients with severe chronic active hepatitis. DNAase digestion indicated that the HB core particles which stained with immunoperoxidase and chromotrope aniline blue contained DNA. Small amounts of HB core particles were seen in both the nuclei and cytoplasm of all anti-HBe seropositive patients with either moderate or severe chronic active hepatitis.

Adolescent↗
PubMed1987

The effects in the excess administration of prostaglandin E1 on the indicator enzymes of organella membrane in gastric mucosa.

Administration of excess vitamin A to rats causes gastric ulceration. In this study the effects on the gastric mucosa of excess vitamin A and excess prostaglandin E1, alone and in combination, were studied. Prostaglandin E1 protected against ulceration by vitamin A. Vitamin A labilized marker enzymes from four different membrane systems, namely those of the lysosomes, mitochondria, endoplasmic reticulum and plasma membrane, whereas only the effect on lysosomes was prevented by prostaglandin E1. Indeed, the prostaglandin alone labilized the enzymes from plasma membrane and endoplasmic reticulum and also damaged mitochondrial membranes. Both vitamin A and prostaglandin E1 caused a reduction in the total number and an increase in irregularly-shaped mitochondria in the parietal cells and produced dilation of the endoplasmic reticulum in both parietal and chief cells. It is noteworthy that prostaglandin E1 effectively prevents ulceration by vitamin A despite the extent to which it damages these membrane systems. These findings lend support to the hypothesis that vitamin A ulceration of the gastric mucosa is mediated via release of lysosomal enzymes, following damage to the lysosomal membranes.

5'-Nucleotidase↗
PubMed1987

The effects of prostaglandin E1 on the pepsin activities in gastric mucosa and juice.

Prostaglandin E1 elevated pepsin activity in gastric mucosa but lowered pepsin activity in the gastric juice of rats treated by pylorus ligation and intragastric administration of hydrochloric acid. In these animals zymogen granules with low electron density were numerous in the gastric chief cells following prostaglandin E1 treatment. The prostaglandin E1-induced increase in mucosal pepsin activity was slightly inhibited by actinomycin D and there was no apparent increase in 3H-thymidine incorporation into gastric mucosa following treatment with prostaglandin E1. It is suggested that prostaglandin E1 causes an elevation of pepsin activity in the gastric mucosa by stimulating pepsin synthesis and perhaps also by facilitating pepsin release from zymogen granules. However, it also appears to inhibit pepsin release from the mucosa into the gastric cavity judging by the decrease of pepsin activity in gastric juice. The reduced pepsin activity in gastric juice may account, in part, for the reported anti-ulcerative action of prostaglandin.

Animals↗
PubMed1986

Orosomucoid as the accelerator of hepatic fibrosis.

The administration of orosomucoid to rats with chronic liver injury accelerated hepatic fibrosis. An increase of hepatic fibres was seen histologically and the content of hydroxyproline in the liver collagen fraction increased. Moreover, the incorporation of 3H-proline into the collagen fraction of injured liver was increased by the administration of orosomucoid.

Animals↗
PubMed1985

Rapid induction of cirrhosis by administration of carbon tetrachloride plus phospholipase D.

A new and rapid method for the production of liver cirrhosis in the rat is described. Rats were treated with carbon tetrachloride for 4 weeks and then injected i.p. with phospholipase D daily for 6 days. Controls received either carbon tetrachloride or phospholipase D only. Following the combined treatment cirrhosis developed rapidly; the liver developed micronodules and severe cirrhosis was accompanied by ascites and splenomegaly.

Animals↗
PubMed1982

Studies on severe hepatic damage induced by galactosamine.

Severe hepatic damage with submassive necrosis induced in rats by an intraperitoneal injection of a single dose of galactosamine hydrochloride was studied. In the severely damaged liver, the remarkable decreases of glycogen and UDPG in the damaged liver were seen. This means extreme decrease in the reserve power of glycolysis. Moreover, the activities of glucose-6-phosphatase and fructose-1,6-diphosphatase decreased. Therefore, the glucose release from liver into the blood stream decreases and the inhibition of gluconeogenesis occurs. In the damaged liver, the decrease of UTP which is essential for the synthesis of sugar moiety of polysaccharide, was seen. Further, the activities of L-glutamine: D-fructose-6-phosphate amidotransferase and UDP N-acetylglucosamine 2'-epimerase which are two key enzymes of polysaccharide synthesizing enzyme were seen to decrease remarkably. In the damaged liver, the glycoprotein fraction decreased more strikingly than the acid mucopolysaccharide fraction. Moreover, the decrease of fructose-1,6-diphosphatase activity seems also to effect on the inhibition of polysaccharide synthesis. In these respects, in the severe hepatic damage, the synthesis of glycoprotein which is essential for liver cell seems to be inhibited.

Alanine Transaminase↗