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Biomedical subjects

H Nishimukai

Publications and source records attributed to H Nishimukai.

12 recordsLinked to original sources
PubMed1992

Activation of complement in normal serum by hydrogen peroxide and hydrogen peroxide-related oxygen radicals produced by activated neutrophils.

Neutrophils activated by soluble particulate stimuli generate superoxide anion and subsequently form hydrogen peroxide and other oxygen radicals. The effect of hydrogen peroxide on the complement system in normal serum was investigated. Treatment of normal serum with hydrogen peroxide resulted in a diminution of the haemolytic activity of the total and alternative complement pathways and the haemolytic titres of C3 and C5 but not of C2, in normal serum. These decreases in complement activity depended on the concentration of hydrogen peroxide added to the serum. Immunoelectrophoretic analysis of hydrogen peroxide-treated serum showed that C3 and C5 proteins were activated. Complement degradation products C3a and C5a were produced in normal serum treated with hydrogen peroxide, and 20 mM EDTA abolished C3a and C5a production in hydrogen peroxide-treated serum but 20 mM Mg-EGTA did not. Catalase completely abolished and dimethylsulphoxide and D-mannitol, hydroxyl radical scavengers, partially inhibited the hydrogen peroxide-mediated complement activation. Hypochlorite, incubated with normal serum, significantly inhibited serum haemolytic activity, and sodium thiosulphate, a reducing agent, abolished the effect of hypochlorite. Normal serum incubated with activated neutrophils showed neutrophil chemotactic activity and decreased serum haemolytic activity, and the addition of catalase or methionine (5 mM) completely abolished the effects of activated neutrophils. These results suggest that hydrogen peroxide activates complement via an alternative pathway of complement activation and that hydroxyl radicals and other hydrogen peroxide-related species such as hypochlorite are most likely involved in hydrogen peroxide-mediated complement activation. Complement activation by oxygen radicals produced by activated neutrophils may be one of the mechanisms by which complement is activated in human immune complex diseases.

Complement Activation↗
PubMed1991

Polymorphisms of serum proteins in Japanese patients with vascular diseases. I. Factor XIIIB, plasminogen and complement types in primary varicose veins.

The polymorphisms of the B subunit of coagulation factor XIII (F13B), plasminogen (PLG), complement C6, C7, factor B (BF) and factor I (IF) were studied among 21 unrelated Japanese patients with primary varicose veins (PVV) by isoelectric focusing followed by immunoblotting. The allele frequencies for F13B*2 and IF*A in PVV patients were significantly higher (F13B*2, p = 0.0047; IF*A, p = 0.0006) than those in healthy controls (n = 60). Significant associations of F13B 2 allotype [p = 0.0220, relative risk (RR) = 13.9] and IF A allotype (p = 0.0006, RR = 10.0) with PVV were observed; however, no significant association of PLG, C6, C7 or BF allotype with the disease was found.

Adult↗
PubMed1991

Complement allotypes in Japanese patients with pemphigus and bullous pemphigoid.

The allotypes of C6, C7, factor B (BF) and factor I (IF) of the human complement system were studied in 11 Japanese patients with pemphigus (5 with pemphigus vulgaris and 6 with pemphigus foliaceus) and 17 with bullous pemphigoid (BP) to investigate the genetic background of these diseases. The allotypes were detected by using isoelectric focusing and immunoblotting. The frequency for IF*A allele in the pemphigus patients was significantly higher (p = 0.009) than that in healthy controls (n = 60). A significant association of IF A allotype with pemphigus was also observed (p = 0.027), with a relative risk of 6.3. There was no association between the C6, C7, BF or IF allotypes and BP. These data suggest that IF A allotype may be an etiological genetic factor in the development of pemphigus.

Alleles↗
PubMed1990

A new complement factor B variant (BF S075) in Japanese.

A new slow-moving variant of the complement factor B, named BF S075, was found in a Japanese patient with cerebral thrombosis and urticaria. The variant was inherited in a codominant manner. The protein concentration and functional hemolytic activity of the complement factor B in the patient's serum were within normal limits. The BF S075 is the fourth rare BF variant found in the Japanese population.

Complement Factor B↗
PubMed1990

C6 reference typing report.

Various C6 protein allotypes were examined using polyacrylamide gel isoelectric focusing followed by immunoblotting or hemolytic overlay. For several 'difficult' allotypes, neuraminidase treatment of samples and long-distance isoelectric focusing gels were applied. Nineteen different allotypes were distinguished besides the two common allotypes C6 A and C6 B. They were designated basically according to the previous statement on C6 nomenclature [Mauff et al., 1980].

Complement C6↗
PubMed1990

Factor I reference typing report.

Complement factor I (IF) reference typing has been examined using polyacrylamide gel isoelectric focusing followed by electroblotting with enzyme immunoassay. The submitted samples could be classified into three common and two new variants, and these were controlled by two common and two rare alleles. Two common alleles were IF*B (the most common allele) and IF*A, and two new rare alleles were designated IF*A1 and IF*B1, respectively.

Alleles↗
PubMed1989

Complement C6 and C7 polymorphisms in Japanese patients with chronic glomerulonephritis.

C6 and C7 types were studied in 158 Japanese patients with different types of chronic glomerulonephritis: 75 patients with IgA nephropathy (IgA-N); 49 patients with idiopathic membranous nephropathy (IMN), and 34 patients with minimal-change nephrotic syndrome (MCNS). There were significant differences in the C6 and C7 allele and phenotype frequencies between the patient groups and controls. A strong association was found between IgA-N and C7 5 phenotype (p less than 0.001, RR = 12.71), and between MCNS and C7 5 phenotype (p less than 0.001, RR = 14.20). A significant association between MCNS and C6 B2 phenotype (p less than 0.05, RR = 2.42) was also found. In the IMN patient group, a significant association with C7 4 phenotype (p less than 0.05, RR = 2.42) was observed. Thus, C6 and C7 phenotypes may be causative factors in the development of chronic glomerulonephritis.

Complement C6↗
PubMed1988

Activation of human complement by rat peritoneal mast cells and its inhibition by a rat serum factor.

The effects of normal sera from humans, rats, and guinea pigs on unsensitized rat peritoneal mast cells were studied in vitro. Five to 20% fresh human sera induced mast cell death and substantial histamine release. The factor was heat labile. Neither hereditary C3-deficient sera nor experimentally C1q-depleted sera showed cytotoxicity. The CH50 activity of human serum was decreased to about one half after a 15-min incubation with 2 X 10(6) mast cells/ml at 37 degrees C. The cytotoxic activity and CH50 reduction were completely eliminated by an addition of 10 mM Mg-EGTA to the serum. These data demonstrated that unsensitized rat mast cells served as both the initiator and target of complement activity when human serum was used as a complement source. Requirements of both Ca++ and C1q suggested the activation of the classical pathway of complement. Fresh 5-20% sera from rats and guinea pigs, on the other hand, showed neither cytotoxicity nor CH50 reduction. Furthermore, these sera strongly inhibited the human serum-induced reaction. The latter results indicated the presence of a modulating factor in rat and guinea pig sera, which inhibits mast cell associated complement activation.

Animals↗
PubMed1988

Three Japanese families with members carrying C7 silent allele (C7*Q0). Possibility for an association between C7*Q0 and C6*B.

Three Japanese families with members carrying C7 silent allele(s) (C7*Q0) are presented. C6 types in the family members were also examined, and it was found that C7*Q0 was transmitted from a parent to offsprings as a haplotype, C7*Q0-C6*B. In another study of C6 types in sera from 3 volunteer blood donors with homozygous C7 deficiencies, the C6 phenotypes were found to be C6 B (homozygote). It seems remarkable that C7*Q0 can be associated with C6*B.

Alleles↗
PubMed1988

Factor B subtypes in Japanese patients with IgA nephropathy and with idiopathic membranous nephropathy.

The present paper describes a method of subtyping of properdin factor B (BF) using polyacrylamide gel isoelectric focusing followed by immunoblotting, and the distribution of BF subtypes in Japanese patients with IgA nephropathy or idiopathic membranous nephropathy (IMN) along with controls. BF*F allele was splitted into two suballeles, named BF*FA and BF*FB. There were significant differences in the BF suballele frequencies between the IMN patient group and the control group. A significant association of IMN with the BF FA subtype (p less than 0.05) and with the BF FB subtype (p less than 0.001) was also found. BF*FB may be a susceptibility suballele to IMN rather than BF*FA.

Adult↗
PubMed1979

Purification and partial characterization of aldehyde dehydrogenase from human erythrocytes.

Human erythrocyte aldehyde dehydrogenase (aldehyde:NAD+ oxidoreductase, EC 1.2.1.3) was purified to apparent homogeneity. The native enzyme has a molecular weight of about 210,000 as determined by gel filtration, and SDS-polyacrylamide gel electrophoresis of this enzyme yields a single protein and with a molecular weight of 51,500, suggesting that the native enzyme may be a tetramer. The enzyme has a relatively low Km for NAD (15 microM) and a high sensitivity to disulfiram. Disulfiram inhibits the enzyme activity rapidly and this inhibition is apparently of a non-competitive nature. In kinetic characteristic and sensitivity to disulfiram, erythrocyte aldehyde dehydrogenase closely resembles the cytosolic aldehyde dehydrogenase found in the liver of various species of mammalians.

Aldehyde Oxidoreductases↗