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Biomedical subjects

S Inai

Publications and source records attributed to S Inai.

At least 37 records · Page 2Linked to original sources
PubMed1987

A case of lowered eosinophilic leucocyte peroxidase activity found unexpectedly using an automated haematology analyser (the Technicon H6000 system)

The Technicon H6000 system simultaneously determines blood cell and leucocyte differential counts automatically using cytochemistry and cell size measurements. Part of the information provided by this instrument is a plot of peroxidase staining intensity against leucocyte cell size called 'the leucocyte peroxidase distribution display'. Recently, an abnormal leucocyte peroxidase distribution display was observed, on a sample from a post-operative lung cancer patient, in which eosinophilic leucocytes did not react with peroxidase. Neutrophils reacted in a normal way with this sample. The eosinophils were further examined by electron microscopy and manual peroxidase staining. Some peroxidase positive granules were observed in the eosinophilic leucocytes. The abnormal leucocyte peroxidase distribution display was found to be due to a separate group of eosinophilic leucocytes with lowered peroxidase activity.

Blood Cell Count↗
PubMed1986

Inherited deficiency of the seventh component of complement associated with meningococcal meningitis: lack of serum bactericidal activity against Neisseria meningitidis in a girl with C7 deficiency and HLA studies of a C7-deficient Japanese family.

An 8-year-old girl with meningococcal meningitis lacked serum complement activity. The seventh component of complement (C7) could not be detected in her serum by either functional or immunochemical analysis. The levels of the other components were within the normal range. Her serum complement activity was restored by the addition of purified C7. Her fresh serum showed a total absence of bactericidal activity against Neisseria meningitidis, group Y, but her serum bactericidal activity was restored by the addition of purified C7. The restoration of her serum bactericidal activity was completely inhibited in the presence of Mg2+ EGTA. These findings suggest that restoration of the bactericidal activity of her serum against N. meningitidis might be mediated by the specific antibody against N. meningitidis and the reconstituted complement system in her serum. Heterozygous deficiency of C7 was found in 10 of her family members. Genetic studies showed that the mode of inheritance might be an autosomal codominant trait. No genetic linkage between deficiency of C7 and the HLA system was found.

Blood Bactericidal Activity↗
PubMed1983

Activation of the alternative complement pathway by the immune precipitate formed with F(ab')2 fragment of human IgG antibody.

The complement fixing ability of the F(ab')2 fragment of human IgG was studied using an immune precipitate (Ippt) formed between tetanus toxoid and the F(ab')2 of high-titer IgG antibody against tetanus toxin. A major subclass of the specific IgG antibody against tetanus toxin, which was separated by affinity column chromatography, was identified as IgG1. On incubation of normal human serum (NHS) with the Ippt formed at equivalence, a dose-dependent consumption of CH50, C3 and C5 activities was observed without significant loss of the early acting complement components. A similar consumption of CH50, C3 and C5 activities was found in NHS reacted with Ippt formed at any antigen/antibody ratio. The Ippt formed at antibody excess was more efficient in complement consumption than the Ippt formed at antigen excess. An apparent consumption of C3 and C5 activities was also noted in C4-deficient guinea pig serum treated with Ippt. When Ippt was incubated with Mg2+--EGTA-treated NHS, both C3 and C5 convertases of the alternative pathway were generated on the Ippt. From these results, it was concluded the the F(ab')2 of human IgG antibody, especially IgG1 antibody, when it formed an Ippt with antigen, could activate the alternative complement pathway.

Antibody Specificity↗
PubMed1981

Hereditary deficiency of the third component of complement in two sisters with systemic lupus erythematosus-like symptoms.

We observed two sisters with lupus-like syndrome with homozygous C3 deficiencies. A 19-year-old woman and her 15-year-old sister developed malar rash, arthralgia, and photosensitivity, but antinuclear antibodies and LE cell preparations were negative. The older sister experienced recurrent bronchitis in her childhood, but the younger sister had no recurrent infections. Serum C3 was not detected immunochemically in either sister, and total complement activity and C3 hemolytic activity were extremely low.

Adolescent↗
PubMed1981

Further studies on C9 deficiency.

Further studies were carried out on the C9 deficiency (C9D). Her serum complement activity (CH50) was 15.7 units when assayed in high ionic strength buffer and 8.8 or less than 5.0 units when assayed in low ionic strength buffer containing glucose or sucrose, respectively. It was revealed that this buffer-dependent CH50 variation of C9D serum was due to the effect of the buffer on the spontaneous lysis of EAC1-8. The serum bactericidal activity of C9D was low, but the addition of specific antibody against bacteria increased the activity indicating an important role of antibody in the serum bactericidal activity. Neither C9 inactivator(s) nor antibody against C9 was detected in the serum, indicating that the case had a defect of C9 synthesis. However, the estimation of C9 levels in the sera of her family could not reveal the mode of inheritance of C9D.

Adult↗
PubMed1980

The effect of aging on complement activity (CH50) and complement protein levels.

Total complement activity (CH50), and the protein levels of C1q, C4, C3, C5, C9, factor B and C1 inactivator were measured in the 1,130 sera obtained from healthy subjects aged between 20 and 79 years old. Increase in the levels of CH50, C1q, C4, C3, C5 and C9 and decrease of factor B were found in the older age group. The level of C1 inactivator showed little variation with aging.

Adult↗
PubMed1980

The difference between serum and plasma complement activity in primary renal disease.

Low serum CH50 (s-CH50) levels were found in 16 out of 574 patients with primary renal disease. However, five of these 16 patients had normal plasma CH50 (p-CH50). The most characteristic finding in the complement profile in these sera was a marked reduction in C4 and C2 hemolytic activities with a minimal reduction in C3 and C5 activities. Sera separated at 37 degrees C showed almost normal CH50 levels, nearly equal to p-CH50, while sera prepared at room temperature and at 4 degrees C showed a remarkable decrease in their CH50 levels. Further, when the serum from one patient showing this difference was added to pooled normal human serum, the C4 activity of the mixture decreased markedly at 4 degrees C but not at 37 degrees C. It is concluded that the difference is caused by cold activation of serum complement through the classical pathway in vitro.

Adolescent↗