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Biomedical subjects

M Homma

Publications and source records attributed to M Homma.

At least 289 records · Page 16Linked to original sources
PubMed1984

Dengue type 2 virus infection in human peripheral blood monocyte cultures.

Dengue type 2 virus (D2V) infection in cultured human monocytes was studied. D2V permissiveness of the monocytes was enhanced when the cells were inoculated with D2V in the presence of either polyclonal or type-specific monoclonal anti-dengue antibody. The enhancement of D2V permissiveness mediated by the antibodies was more clearly demonstrated when the monocytes had been treated with trypsin before virus inoculation, though treatment of the cells with trypsin alone decreased D2V permissiveness. The enhancement of infection by type-specific neutralizing monoclonal antibody suggests that the D2V particles possess at least two antigenic determinants closely associated with virus infectivity. Infectious center assays revealed that the infection enhancement in the presence of the antibodies was due primarily to an increase in the number of D2V-infected cells, and that only a small proportion of the monocyte population supported D2V replication. The virus-permissive monocytes did not bear HLA-DR antigens on their cell surface. The presence of nonadherent lymphocytes in the monocyte cultures before D2V inoculation did not affect the D2V permissiveness of the monocytes. Treatment of cultured monocytes with the synthetic adjuvants N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP) and its lipophilic derivative, [B30]-MDP, did not significantly affect the D2V permissiveness of the cells.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1984

Hook-associated proteins essential for flagellar filament formation in Salmonella typhimurium.

The hooks of the flagella of Salmonella typhimurium were purified by a newly developed method, using a flaL mutant without a filament, and the hook components were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. As a result, we detected three protein species in addition to hook protein. We call these three proteins hook-associated proteins (HAPs). Their molecular weights were 59,000 for HAP1, 53,000 for HAP2, and 31,000 for HAP3. The HAP1/hook protein/HAP3/HAP2 molar ratio, calculated from their relative amounts and their molecular weights, was 1:10:1.1:0.53. The compositions of HAPs were analyzed in the hooks from the other filamentless mutants which were defective in H1 H2, flaV, flaU, or flaW. Hooks from the H1 H2 mutant had the same HAP composition as hooks from the flaL mutant. Hooks from the flaV mutants contained HAP1 and HAP3. Hooks from the flaU mutants contained HAP1. Hooks from the flaW mutants contained a very small amount of HAP3. From these results, the process of hook morphogenesis and the genes responsible for each step were postulated. Electron micrographs of hooks from the filamentless mutants showed that hooks which contained all three HAPs had a sharp clawlike tip, whereas hooks lacking any HAP had a flat tip. Electron micrographs of hooks treated with antibody against the hook protein showed that each claw-shaped end was not covered with antibody. These results strongly suggest that all three HAPs or at least some of them are located at the claw-shaped end and play an essential role in filament formation.

Bacterial Proteins↗
PubMed1984

Effect of interferons on dengue virus multiplication in cultured monocytes/macrophages.

The effects of interferons on dengue virus multiplication in cultured human and mouse monocytes/macrophages were studied. Interferon treatment before, but not after virus inoculation suppressed virus multiplication dose-dependently. Recombinant human leukocyte A interferon was as effective as ordinary human fibroblast interferon in suppressing dengue virus multiplication in cultured human monocytes. Human monocytes, a population of non-proliferating cell lineage, maintained their interferon-mediated antiviral state for a few days after removal of the interferons.

Animals↗
PubMed1984

Anti-idiotypic antibodies in a patient with monoclonal rheumatoid factor after pneumococcal bacteremia.

A 51-yr-old Japanese female patient with monoclonal IgM gammopathy with rheumatoid factor activity was admitted because of pneumococcal bacteremia. About 2 wk after admission, her rheumatoid factor activity became undetectable by RAHA test and radioimmunoassay, subsequent to the initial marked elevation. The suppressive capacity of the patient's IgG fraction on the rheumatoid activity of her monoclonal IgM on January 11 was determined. The IgG fraction obtained on February 22 blocked the binding of the rheumatoid factor to rabbit IgG. The suppressive activity in the IgG fraction of February 22 was shown to be localized within the F(ab')2 fragment. Furthermore, the specificity of the suppressive serum factor was shown by the inability to block the binding of SRBC coupled with diazotized phosphorylcholine to anti-pneumococcal antibody. Thus, the marked reduction of rheumatoid factor activity was considered to result from anti-idiotypic antibody transiently appearing in her serum after pneumococcal bacteremia.

Antibodies, Anti-Idiotypic↗
PubMed1983

The synthesis of polypeptides in influenza C virus-infected cells.

The synthesis of virus-specific polypeptides was analyzed in MDCK cells infected with the JJ/50 strain of influenza C virus. In addition to three major structural proteins gp88, NP, and M, the synthesis of five polypeptides with molecular weights of 29,500 (C1), 27,500 (C2), 24,000 (C3), 19,000 (C4), and 14,000 (C5) was found in infected cells. None of these polypeptides were detected either in virions or in immunoprecipitates obtained after treatment of infected cell lysates with antiviral serum, suggesting that they are not viral structural proteins. Polypeptides C1-C5 were found to be synthesized in MDCK cells infected with different influenza C virus strains as well as in different host cell types infected with C/JJ/50. Further, it was observed that cellular protein synthesis was greatly reduced under hypertonic conditions, whereas the synthesis of C1-C5 was relatively unaffected. These results suggest that polypeptides C1-C5 are virus coded rather than host cell coded. Peptide mapping studies showed that each of polypeptides C3, C4, and C5 had a peptide composition similar to the M protein. The amount of C2 synthesized in infected cells was insufficient for mapping. This polypeptide was, however, found to rapidly disappear in pulse-chase experiments, suggesting that C2 is probably not unique but biosynthetically related to one of the other proteins. In contrast to these polypeptides, polypeptide C1 showed a map which is largely different from any major structural polypeptide. It therefore appears likely that C1 is a nonstructural protein of influenza C virus similar to the NS1 protein of influenza A and B viruses.

Animals↗
PubMed1983

The precipitating antibody to an acidic nuclear protein antigen, the Jo-1, in connective tissue diseases. A marker for a subset of polymyositis with interstitial pulmonary fibrosis.

The clinical significance of antibodies to the Jo-1 antigen in connective tissue diseases was studied. Clinical diagnoses of 11 patients who had anti-Jo-1 antibody were: polymyositis 8, dermatomyositis 1, and overlap syndrome 2 (polymyositis--systemic lupus erythematosus 1, polymyositis--scleroderma 1). All the patients who had anti-Jo-1 antibody showed interstitial pulmonary fibrosis, and in 2 patients anti-Jo-1 antibodies were detected before the appearance of lung disease.

Adult↗
PubMed1983

Evidence of proteolytic activation of Sendai virus in mouse lung.

A device was made to analyze the pneumotropism of Sendai virus in mouse. Minced lung blocks were prepared from the mouse intranasally infected with Sendai virus for 2 hours and cultured in a CO2 incubator. This culture system provided a suitable in vitro model of Sendai virus infection in mice in terms of the distribution of the viral antigens and histopathological findings. The progeny virus recovered from the lung culture was already activated and was accompanied by the cleavage of F glycoprotein into F1 and F2. This fact demonstrates that the activating mechanism is reversed in the lung culture as found in vivo infection of mouse lung. The viral activation and the cleavage of F glycoprotein were simultaneously inhibited by tosyllysylchloromethylketone, leupeptin, soybean trypsin inhibitor and antipain, but not by tosylamidophenylethylchloromethyl-ketone, chymostatin, pepstatin, iodoacetamide, phenylmethylsulfonylfluoride and p-chloromercuribenzoate. These results show that the activating enzyme of Sendai virus found in the lung culture was similar to trypsin. The existence of the activating enzyme may support the replication of Sendai virus in mouse lung in multiple-step and also result in the lung pathology.

Animals↗
PubMed1983

Importance of increased urinary calcium excretion in the development of secondary hyperparathyroidism of patients under glucocorticoid therapy.

Parathyroid function and calcium metabolism were studied in 44 patients under glucocorticoid therapy (steroid group) and in 25 control subjects. Nephrogenous cAMP and serum immunoreactive parathyroid hormone levels in the steroid group were significantly higher than those in control subjects (p less than 0.001). Nephrogenous cAMP in the steroid group correlated positively with prednisolone dosage (r = 0.424, p less than 0.01), and most patients who showed obvious elevations of nephrogenous cAMP had received over 10 mg/day of prednisolone for at least 2 mo. Fasting urinary calcium in the steroid group [166.1 +/- 78.5 (+/- SD) mg/g creatinine] was about 2 times greater than that in control subjects (74.1 +/- 35.6) (p less than 0.001). Fasting urinary calcium in control subjects correlated negatively with nephrogenous cAMP (r = -0.486, p less than 0.02). In contrast, these values in steroid group showed significant positive correlation (r = 0.631, p less than 0.001), suggesting that increased urinary calcium excretion is an important factor in the development of secondary hyperparathyroidism. Elevated nephrogenous cAMP and serum immunoreactive parathyroid hormone levels decreased after the administration of trichlormethiazide and/or 1 alpha hydroxy-vitamin D3. We conclude that increased urinary calcium excretion plays an important role in the development of secondary hyperparathyroidism in patients under glucocorticoid therapy and that the administration of thiazide and/or vitamin D could improve the secondary hyperparathyroidism caused by glucocorticoid therapy.

Adolescent↗
PubMed1983

An outbreak of type C influenza in a children's home.

During a one-year survey of a children's residence housing 20 young children and employing 29 adults, a confirmed outbreak of type C influenza unassociated with other known respiratory infections was studied. Seventeen of 20 children and two of the nine employees studied developed symptoms, which were characterized primarily by fever and nasal discharge. The three children who did not contract the disease were all under three months of age. Thirteen strains of virus were recovered from throat-swab specimens: 12 from children and one from an adult. All isolates were identified serologically as type C influenza virus. Evidence of reinfection was found in a two-year-old child and two adults who developed increases in antibody titers; the virus was recovered from a throat-swab specimen from one of these adults.

Adult↗
PubMed1983

Analyses of structural polypeptides of seven different isolates of influenza C virus.

The major structural polypeptides (gp88, NP and M) of seven different influenza C virus strains isolated between 1947 and 1981 in U.S.A. and Japan were compared by SDS-polyacrylamide gel electrophoresis and one-dimensional mapping of the peptide fragments produced after limited proteolysis with various proteases. Of the three polypeptides analysed, the membrane (M) protein appeared to be the most highly conserved since the electrophoretic mobility as well as the mapping pattern of this protein was found to be identical among all seven strains. The structure of nucleoprotein (NP) was also found to be highly conserved. The proteins of five isolates from 1964 to 1981 showed migration rates and mapping patterns indistinguishable from each other though they were slightly different in mapping patterns from the earlier isolates, C/Taylor/1233/47 and C/JJ/50. The similarities between influenza C strains were also evident with the surface glycoprotein, gp88. The gp88 proteins of the five strains isolated in 1947, 1950, 1971 and 1981 were virtually identical in migration rates as well as in mapping patterns, while the two isolates of 1964 and 1974 showed minor differences. These results strongly suggest that the surface glycoprotein of influenza C virus is structurally much more stable than the haemagglutinin and neuraminidase glycoproteins of influenza A and B viruses. Further, the findings that differences from the original influenza C strain, Taylor/1233/47 were detectable in the strains isolated in 1964 and 1974 but not in the strains isolated in 1971 and 1981 suggest that unlike the antigenic drift of types A and B influenza viruses, the structural variation of gp88 may not be a sequential event.

Electrophoresis, Polyacrylamide Gel↗
PubMed1983

Functional differences of anti-T-cell antibody in patients with systemic lupus erythematosus and ulcerative colitis.

The loss of suppressor T-cell function results in an abundant production of autoantibodies in systemic lupus erythematosus (SLE). As a cause of this suppressor T-cell defect, anti-T-cell antibody seems to be of prime importance. On the other hand, anti-T-cell antibodies can be detected in various other autoimmune diseases, but their functional characteristics have not been determined. In the present study, the functional characteristics of anti-T-cell antibody from a selected subgroup of patients with ulcerative colitis (UC) were compared with those from patients with SLE. Anti-T-cell antibody from the patients with SLE reacted with a T8 subset, resulting in a suppressor defect, whereas anti-T-cell antibody from the UC patients reacted primarily with a T4 subset. Functionally, SLE- T cells failed to proliferate in response to concanavalin A, whereas UC- T cells from UC patients failed to proliferate in response to phytohaemagglutinin. In the Ig synthesis system, both SLE- and UC- T cells increased Ig production of B cells. Since UC+ T cells did not contribute to the generation of Con-A-inducible suppressor activity, we believe that serum from the selected subgroup of patients with UC reacted with the inducer T-cell subset.

Adult↗
PubMed1983

Pneumotropism of Sendai virus in relation to protease-mediated activation in mouse lungs.

The pneumotropism of Sendai virus in mice was studied in relation to the activation and replication of the virus in the lung. Inactive Sendai virus grown in LLC-MK(2) cells, which possessed an uncleaved precursor glycoprotein, F, and was noninfectious to tissue culture cells, neither grew nor caused pathological changes in the lung of mice. When trypsin treatment was made which cleaved F into F(1) and F(2) subunits, the virus became activated so that it could initiate replication in the bronchial epithelium of the lung. In this case, the progeny virus was produced in the activated form and multiple-cycle replication occurred successively. A parallel relationship was found between the degree of the viral replication and that of clinical signs of the respiratory disease, body weight loss, and histopathological changes in the lung. A protease mutant, TR-2, which was able to be activated only by chymotrypsin but not by trypsin, could also initiate replication in the bronchial epithelium, when activated by chymotrypsin before inoculation into mice. The progeny virus, however, remained inactive, and the replication was limited to a single cycle, which resulted in the limited lung lesion. The overall results suggest that some activating mechanism for the progeny virus of wild-type Sendai virus exists in the lung of mice and the principle (activator) responsible for this phenomenon has a character similar to trypsin. The possible location of the activator is discussed.

Animals↗