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Biomedical subjects

M Shingu

Publications and source records attributed to M Shingu.

At least 91 records · Page 5Linked to original sources
PubMed1989

Laboratory diagnosis of viral myocarditis. A review.

This review delineates the impact of molecular biology on the diagnosis and pathogenesis of coxsackie B viral myocarditis. The etiological role of the coxsackie B viruses in acute myocarditis is well established. A hallmark of most coxsackie B virus infections is extension cytopathology of the host cell. Recent evidence from studies of a nonlytic infection show that a coxsackie B virus can alter an infected cell which results from persistent infection. There are two other mechanisms for cardiac injury during coxsackie B virus infection. The first phase usually occurs during the first week after infection, and is probably a direct result of lytic infection to the myocytes and of the accompanying inflammatory response. The second phase of coxsackie B virus-induced myocarditis is accompanied by an autoimmune response to heart tissue, which occurs 2 weeks after infection. Genetic factors probably play a role, but their contribution has not yet been evaluated.

Antibodies, Viral↗
PubMed1989

Comparative analysis of herpes simplex virus type 1 mutants that are defective in fusion function by using restriction endonuclease.

Mutants derived from herpes simplex virus type 1 (HSV-1) strains, YH and KOS, that were defective in cell fusion function (r mutants) were examined for DNA structure using a restriction endonuclease and gel electrophoresis. A distinct difference in the restriction patterns was found in some r mutants. One which was derived from strain YH and belonged to complementation group A lost the BamHI cleavage site in the long inverted repeat regions. But the site could not be associated with the gene that was related to the cell fusion event, inasmuch as the other mutants belonging to the same complementation group had a normal BamHI site. The others, which belonged to complementation group G of strain KOS, had a deletion of approximately 2 kb (kilobase-pair) in the BamHI B fragment. A mixed infection was carried out with r410 and r426 which belonged to groups A and G of strain KOS, respectively, and the viruses of parental and recombinant types were isolated from the progeny. The BamHI restriction fragment patterns of the DNAs showed that all recombinants, which carried the cell fusion ability, had the normal BamHI fragment B. Thus, one of the genes associated with cell fusion function must be located in BamHI fragment B.

Cloning, Molecular↗
PubMed1989

The effect of cimetidine on survival of mice infected with herpes simplex virus type 2, murine encephalomyelitis virus and vesicular stomatitis virus infections.

The effect of cimetidine on survival was investigated in mice infected with herpes simplex virus type 2 (HSV-2), murine encephalomyelitis virus (GD-VII), and vesicular stomatitis virus (VSV). BALB/c mice, 5 weeks of age, were injected intraperitoneally (i.p.) with 5.5 x 10(5) plaque-forming units (PFU) of virus/0.5 ml, and cimetidine (1 mg/0.5 ml) was administered simultaneously. The survival rates of 80% and 85% in the cimetidine groups were significantly greater than the 10% and 23% for the control groups. The GD-VII- and VSV-infected control mice were dead at 3 days after virus inoculation. However, more cimetidine-treated mice survived than control mice. When anti-mouse T-cell serum or cyclosporine, which is a helper T-cell suppressor, was administered to BALB/c mice; the effect of cimetidine against the HSV-2 infection could be observed. When injected with anti-asialo GM1, BALB/c mice or beige mice with low natural killer (NK) cell activity were not affected by cimetidine. Lastly, cimetidine was shown to activate the cytotoxic action on NK cells. The above results indicate that the antiviral effects of cimetidine depend on NK cell activation.

Animals↗
PubMed1988

Correlation between plaque size and genetic variation of type 3 poliovirus from a vaccinate.

Vaccine strain derivatives could be serially isolated from the feces of a healthy infant for about 30 days after the second administration of a trivalent poliovirus vaccine. These were all identified as poliovirus type 3, and no other types were detected. The titer in feces increased gradually until day 19, when it reached a maximum, after which it decreased. The plaque size altered roughly in parallel with the changes in the titer. On day 11 it began to increase, becoming the highest abruptly on day 15, and then fell again. Oligonucleotide mapping analysis of RNAs of isolated viruses showed that the samples from days 1 and 11 exhibited the same patterns as those shown by the vaccine strain RNA. However, on day 15 many of the preexisting spots had decreased, and new ones appeared. On day 27, the pattern was again similar to that of the original virus, rather than that of the day-15 virus. A nonmetric distance scaling and cluster analysis suggested that all the strains were derived from the same origin and that the polioviruses on days 1, 11, 21, and 27 had closer relationships, but the poliovirus on day 15 was different.

Feces↗
PubMed1988

Complement-activating properties of immune complexes are suppressed by IgM rheumatoid factor and enhanced by IgG rheumatoid factor.

The effect of rheumatoid factor (RF) on complement-activating capacity of aggregated IgG was investigated. The degree of complement activation induced by the addition of specific amounts of aggregated IgG to patients' sera and normal sera was demonstrated by the inhibition of hemolytic activity (%IHA). The %IHA was significantly lower in rheumatoid arthritis (RA) sera and higher in systemic lupus erythematosus (SLE) sera, compared with normal sera. There was a negative correlation between %IHA and IgMRF/IgGRF ratio in RA and SLE sera, and RA synovial fluid. The %IHA and IgGRF were positively correlated in RA sera. The IgMRF/IgGRF ratio was significantly lower in SLE sera than in RA sera and systemic sclerosis sera, and was significantly lower in RA synovial fluid than in osteoarthritis synovial fluid. Isolated RF, consisting of mostly IgMRF class, inhibited complement-activating properties of aggregated IgG, depending on the concentration of RF. Isolated RF was further purified by the fractionation using high pressure liquid chromatography, and IgGRF and IgMRF were obtained. IgMRF significantly suppressed the complement-activating capacity of aggregated IgG, whereas IgGRF promoted it. These observations suggest that IgMRF acts protectively, while IgGRF induces inflammation. Thus, the expression of the biological activity of RF with special reference to immune complex interaction mainly depends on the IgMRF/IgGRF ratio.

Antigen-Antibody Complex↗
PubMed1987

Generation of superoxide by immunologically stimulated normal human neutrophils and possible modulation by intracellular and extracellular SOD and rheumatoid factors.

Rheumatoid synovial fluids generated significantly greater amounts of superoxide, lysosomal enzymes, and superoxide dismutase from neutrophils into extracellular fluid than osteoarthritic synovial fluids. Rheumatoid factors isolated from serum suppressed superoxide-generating activity of performed immune complexes, but did not suppress that of intermediate-sized immune complexes isolated from RA serum. Synovial fluid neutrophils has a greater capacity to generate superoxide and lower intracellular superoxide dismutase activity, compared with peripheral neutrophils of the corresponding patients. These results suggest that neutrophil superoxide release may be modulated, both by rheumatoid factor and by intracellular and extracellular superoxide dismutase.

Acetylglucosaminidase↗
PubMed1987

Studies on the classification of bovine enteroviruses.

Bovine enteroviruses isolated from cattle and other ruminants in various areas of the world were classified into three distinct serotypes by cross-neutralization tests using criteria established for the differentiation of human enteroviruses. According to Western blot analysis, however, immunodominant structural polypeptides VP1 of the viruses tested have common epitopes, recognized by antisera to each of the three serotypes. These findings indicate that non-neutralizing epitopes on VP1 are generally conserved. It is, therefore, conjectured that bovine enteroviruses were derived from a common ancestor.

Animals↗
PubMed1987

Detection of low molecular weight IgM by immunoblot analysis in rheumatoid arthritis.

The immunoblot technique was used to detect low molecular weight IgM (LMWIgM) in the serum and synovial fluid (SF) of patients with rheumatoid arthritis (RA). LMWIgM was detected in 64% of 58 RA sera and in 47% of 17 RA SF. The levels of IgM and rheumatoid factor (RF) were significantly higher in the positive sera of LMWIgM. Sequential studies revealed that LMWIgM appeared in the serum while the titer of RF was high. Our analysis also suggested the presence of several other oligomeric LMWIgM with monomeric IgM.

Arthritis, Rheumatoid↗
PubMed1986

Superoxide generation by synovial fluid neutrophils enhanced by immune complexes and suppressed by rheumatoid factor in synovial fluid.

Synovial fluid (SF) from patients with rheumatoid arthritis (RA) enhanced superoxide generation by neutrophils isolated from RA SF, in contrast to SF from patients with osteoarthritis. These superoxide generation-enhancing substances may be intermediate-sized immune complexes and a complement C5-derived fragment. Rheumatoid factor (RF) isolated from RA SF suppressed superoxide generation-enhancing activity of aggregated IgG. Therefore, biologically active RF may block the interaction of the immune complexes with neutrophils accumulating in RA SF, and protect the joint tissue from the effects of oxygen radicals or proteases.

Antigen-Antibody Complex↗
PubMed1986

Serum alkaline ribonuclease derived from vascular endothelial cells is raised in patients with rheumatoid vasculitis.

We investigated the mechanisms of the marked increase of alkaline ribonuclease (RNase) in the sera of patients with rheumatoid arthritis associated with vasculitis. Among various tissues examined, blood vessels contained higher levels of alkaline RNase than acid RNase. Cultured human endothelial cells contained significantly higher amounts of alkaline RNase than acid RNase. In contrast, acid RNase was predominant in most other tissues and cells. Endothelial cells cultured with sera from patients with vasculitis released alkaline RNase into the extracellular medium. The phosphocellulose chromatographic profile of these sera differed from that of sera from healthy subjects. These results imply that the alkaline RNase in sera of patients with vasculitis is derived from blood vessels, probably from endothelial cells.

Arthritis, Rheumatoid↗
PubMed1985

Human vascular smooth muscle cells and endothelial cells lack catalase activity and are susceptible to hydrogen peroxide.

51Cr release as lytic and cell detachment as nonlytic injury were employed to estimate neutrophil-mediated injury of cultured human vascular smooth muscle cells and endothelial cells. The reagents hydrogen peroxide or hypoxanthine-xanthine oxidase produced dose-dependent killing and nonlytic cell detachment, which were specifically inhibited by catalase but not by superoxide dismutase. The concentration of hydrogen peroxide or xanthine oxidase to induce cell detachment was less than lytic dose, suggesting that cell detachment was a much more sensitive assay of injury. Neutrophil-mediated cell lysis averaged 15% at most and was mostly dependent on hydrogen peroxide, while neutrophil-mediated cell detachment was nearly 100% and its dependency on hydrogen peroxide varied from 46% to 60%. These results suggest that vascular smooth muscle cells and endothelial cells in neutrophil-mediated events are destroyed by a hydrogen peroxide-dependent process, mainly via a nonlytic cell detachment mechanism. There was no striking difference of sensitivity to hydrogen peroxide between vascular smooth muscle cells and endothelial cells. Vascular smooth muscle cells and endothelial cells contained fairly high concentrations of superoxide dismutase, but not catalase, activity. The sensitivity of these cells to hydrogen peroxide but not to superoxide may arise from the fact that these cells lack intracellular catalase activity. The injury of vascular cells, which constitute important components of blood vessels, may lead to vascular injury and subsequent tissue damage.

Blood Vessels↗
PubMed1985

Role of stimulated neutrophils from patients with systemic lupus erythematosus in tissue injury, with special reference to serum factors and increased active oxygen species generated by neutrophils.

To examine the possible correlation between tissue injury and neutrophil-produced active oxygen (AO) species in patients with systemic lupus erythematosus (SLE), we studied the capacity of the serum from six patients with untreated, active SLE to generate AO and release lysosomal enzymes by normal neutrophils. Cultured endothelial cells from human umbilical cord vein were incubated with serum-stimulated neutrophils to assess AO-induced tissue injury. Serum from patients with bacterial infections and healthy individuals served as controls. AO production was highest in the neutrophils stimulated with SLE patient-derived serum, while lysosomal enzyme release was only slightly increased. SLE neutrophils with or without stimulation and SLE serum-stimulated normal neutrophils produced significantly high levels of cytotoxicity upon coincubation with 51Cr-labeled human endothelial cells. These excessive cytotoxicities were reversed by the presence of superoxide dismutase and catalase, indicating the specificity of the AO effect on endothelial cell damage. These findings suggest that tissue damage in SLE may be partially due to excessive production of AO and that both neutrophils themselves and a serum factor which activates neutrophils are involved in the mechanism for vascular injury.

Adolescent↗