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S Kato

Publications and source records attributed to S Kato.

At least 1,405 records · Page 78Linked to original sources
PubMed1987

Detection of ganglioside GM2 in sera and tumor tissues of hepatoma patients.

GM2 ganglioside was detected in all five sera of hepatoma patients analyzed by thin-layer chromatography in conjunction with enzyme-immunostaining with rabbit anti-GM2 antibody and horseradish peroxidase-conjugated anti-rabbit IgG, and was quantitated by densitometry. The GM2 contents of these sera were 20 to 100 times higher than those of sera from normal adults. By the method used, an increased GM2 level could be detected with samples of less than 0.1 ml of sera from hepatoma patients. The elevated levels of serum GM2 in hepatoma patients were suggested to be due to elevated GM2 levels in the liver lesions, because the GM2 contents of the liver of five patients with liver cancer, including three with hepatoma, were higher than those of normal liver tissues.

Carcinoma, Hepatocellular↗
PubMed1987

Specific expression of unusual GM2 ganglioside with Hanganutziu-Deicher antigen activity on human colon cancers.

This paper reports the presence of GM2 ganglioside containing N-glycolylneuraminic acid (NeuGc) in human colon cancer tissues. GM2(NeuGc) was detected by two-dimensional thin layer chromatography (2d-TLC)/enzyme-immunostaining using affinity-purified chicken antibody against GM3(NeuGc) and horseradish peroxidase-conjugated rabbit anti-chicken IgG antibody. Like usual GM2 ganglioside containing N-acetylneuraminic acid (NeuAc) isolated from Tay-Sachs brain, GM2(NeuGc) in colon cancer could be converted into GM3(NeuGc) by human kidney beta-N-acetylhexosaminidase A in the presence of a GM2-specific activator protein isolated from guinea pig kidney. Three of 7 specimens of Hanganutziu-Deicher (HD) antigen-positive human colon cancer tissues so far examined expressed this unique ganglioside. In order to detect and determine specifically GM2(NeuGc) on human colon cancers, specific antibody against GM2 (NeuGc) has been prepared by immunizing chickens. By a sensitive TLC/immunostaining method using the antibody, the amounts of the antigen were determined to be 0.3-3% of total lipid-bound sialic acid. NeuGc-containing gangliosides were also detected in meconium and fetal intestinal tissues. Three species of antigenic gangliosides in pooled meconium were tentatively identified as GM3(NeuGc), sialylparagloboside and sialylhexaosylceramide on the basis of their migration positions on 2d-TLC and the results of endo-beta-galactosidase treatment. GM3(NeuGc) was the sole HD-active ganglioside in fetal intestinal tissue from one of 3 individuals tested; the other two showed no HD-active ganglioside at all. GM2(NeuGc), however, could not be detected in either meconium or fetal tissues so far examined, suggesting that this unique ganglioside is a tumor-specific antigen, at least for human intestinal tissues.

Antibodies↗
PubMed1987

Occurrence of tumor-associated ganglioside antigens with Hanganutziu-Deicher antigenic activity on human melanomas.

The specificity of antibody to NeuGc alpha 2-3Gal beta 1-4Glc-cer (GM3(NeuGc] was carefully reexamined by the method of enzyme-immunostaining on a thin layer plate. The affinity-purified antibody was found to react with NeuGc alpha 2-8NeuGc alpha 2-3Gal beta 1-4Glc-cer (GD3(NeuGc-NeuGc] and NeuGc alpha 2-8NeuAc alpha 2-3Gal beta 1-4Glc-cer (GD3(NeuGc-NeuAc], but not with NeuAc alpha 2-8NeuGc alpha 2-3Gal beta 1-4Glc-cer (GD3(NeuAc-NeuGc)) or NeuAc alpha 2-8NeuAc alpha 2-3Gal beta 1-4Glc-cer (GD3(NeuAc-NeuAc]. From this result together with the previous results, it (GD3(NeuAc-NeuAc], From this result together with the previous results, it could be concluded that the antibody recognizes the outer portion of molecular species of sialic acids in the gangliosides. By using this antibody, the expression of Hanganutziu-Deicher (HD) gangliosides could be demonstrated in human malignant melanoma. The molecular species were different among individuals examined. Among HD-antigenic gangliosides, GM3(NeuGc) was commonly found in melanoma tissues. One of the patients examined expressed GD3(NeuGc-NeuGc) and GD 3(NeuGc-NeuAc), which may be characteristic gangliosides in human melanomas, since these gangliosides could not be detected in human colon cancer or human fetal tissues.

Antigens, Heterophile↗
PubMed1987

Amplification of human immuno-deficiency virus production from a virus-producing cell line in culture at high cell density.

The amount of infectious virus released into the culture fluid from human immunodeficiency virus (HIV)-producing MOLT-4 cells (MOLT-4/HIV HTLV-III) was measured as a function of the culture conditions and cell density. After 3 days, the daily yield of infectious virus per cell in the fluid of non-growing cells cultured at high cell density was about 15 times higher than the accumulated yield from growing cells cultured at low cell density. SDS-PAGE analysis also showed a similar difference in the amounts of major gag protein p24.

Cell Line↗
PubMed1987

Suppression by neurotropin of production of human immuno-deficiency virus by the virus-producing MOLT-4 cell line.

The effect of neurotropin on human immuno-deficiency virus (HIV) production in a virus-producing MOLT-4 (MOLT-4/HTLV-III) cell line was studied. Culture of the cells for 4 days in the presence of 100 micrograms/ml of neurotropin resulted in a 72% decrease in the number of infectious virus particles released into the culture fluid. A pulse-labeling experiment to analyze the synthesis of HIV proteins suggested that neurotropin may affect the budding process of the virus.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Selective killing of human immunodeficiency virus-infected and -producing cells by liposomes containing diphtheria toxin fragment A.

Liposomes containing fragment A of diphtheria toxin killed human immunodeficiency virus (HIV)-producing MOLT-4 or TALL-1 cells, and HTLV-I-carrying MT-4 cells infected with HIV, but did not kill these cells when they were not infected with HIV. This killing was not affected by the presence of HIV antibodies. These results show that liposomes containing fragment A of diphtheria toxin selectively killed cells expressing HIV antigens or producing the virus in vitro.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Ethanol metabolism in alcohol dehydrogenase deficient deermice is mediated by the microsomal ethanol oxidizing system, not by catalase.

The participation of the microsomal ethanol oxidizing system (MEOS) and catalase in total ethanol metabolism is reviewed. Non-alcohol dehydrogenase (ADH) dependent pathways contribute to in vivo ethanol metabolism, but the respective role of each has long been debated. The principal data supporting a role for catalase is an occasionally reported moderate depression of ethanol metabolism after aminotriazole. In deermice lacking ADH, we observed a slight (though not statistically significant) decrease in basal ethanol metabolism of hepatocytes after aminotriazole. However, this decrease was found to parallel a similar inhibition of MEOS by aminotriazole, and thus may not reflect catalase mediated peroxidation in this animal. 1-butanol, a competitive inhibitor of ethanol oxidation by MEOS and not a substrate for catalase, decreased ethanol metabolism by hepatocytes in a concentration dependent manner. These results, as well as those from other investigators, indicate that MEOS mediates virtually all of non-ADH ethanol metabolism in vivo.

1-Butanol↗
PubMed1987

Significance of alcohol dehydrogenase (ADH) as a marker of hepatic centrilobular injury: a biochemical and immunohistochemical study.

Since we demonstrated previously that alcohol dehydrogenase (ADH) is distributed predominantly in zone 3 of the hepatic acinus, we have investigated the usefulness of determinations of serum ADH activity in the assessment of hepatic injuries. The measurement of serum ADH activity appears to be useful for the detection of acute and early centrilobular hepatic damage, as deduced from the results obtained from experimental hepatic injuries produced by bromobenzene, hypoxia and acute administration of ethanol. Whereas serum ADH activity increased slightly after the generation of an acute ethanol load in rats which were given ethanol chronically, the hepatic content of ADH tended to decrease. Moreover, a rather selective reduction of hepatic ADH activity was found in zone 3 of the hepatic acinus. Thus, it is conceivable that chronic alcoholic injury to the liver may result in persistent release of ADH from hepatocytes resulting in a relatively low elevation of the level of the enzyme in the blood, rather than a sudden release of the enzyme leading to a sharp increase in the serum enzyme activity.

Alanine Transaminase↗
PubMed1987

[Clinical statistics on outpatients at the Urological Clinic of Sanjukai Hospital in 1986].

A statistical study was performed on new outpatients. The total number of new outpatients in 1986 was 8,174 (male: 5,177, female: 2,997) and the male to female ratio was 1.73:1. They had urogenital diseases definitely diagnosed (7,043), urogenital diseases undefinitely diagnosed (689), no diseases (357), and diseases other than urogenital (85). Thirty percent of the outpatients were referred to us by other sources. The number of operations on new outpatients was 182, circumcision, resection of condyloma and vasectomy were representative. The peak of the age distribution was in the thirties for males and in the twenties for females. A statistical study was made on new outpatients according to the international disease classification. There were 109 malignant (urogenital) tumors (1.4%). The major diseases of the new outpatients were cystitis (acute or chronic: 21.4%), upper urinary tract stone (16.8%), prostatitis (14.1%), and benign prostatic hypertrophy (11.3%). In males the major diseases were prostatitis, upper urinary tract stone, benign prostatic hypertrophy, balanoposthitis, phimosis and in females they were cystitis, upper urinary tract stone, pyelonephritis, renoptosis and neurogenic bladder. We conclude that our hospital plays a major role as a private urological hospital.

Adolescent↗