Cytotoxicity of streptolysin "O" in tissue culture.
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Biomedical subjects
Publications and source records attributed to A Mathur.
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In dengue type 2 virus (DV)-infected mice, the virus-specific immunosuppression is mediated by a two-step mechanism: (1) induction of T suppressor cells (Ts1) by by virus to produce a suppressor factor (SF) which (2) stimulates another subpopulation of T cells (Ts2) to produce prostaglandin which finally mediates suppression. SF suppresses DV-specific IgM plaque-forming cells (PFC) in the spleen cells sensitized in vivo or in vitro, as detected by Jerne's haemolytic plaque technique. The present study enabled us to investigate the role of an intermediary cell in transmission of the suppressor signal from Ts1 to Ts2. It was observed that SF was adsorbed on the surface of peritoneal macrophages. Live macrophages adsorbed SF, retrieved it from that adsorbed on heat-killed macrophages and presented it to the target cells. Heat-killed macrophages adsorbed SF to the same extent as live ones, but could present it to the target cells by themselves. The target cells of SF were unprimed splenic T lymphocytes. SF suppressed DV-specific PFC in syngeneic spleen cells and was adsorbed on syngeneic macrophages, but not on those from allogenic animals. The findings described here show that the presence of live macrophages is obligatory for transmission of the suppressor signal to the target Ts2.
Our earlier studies reported that the cytotoxic factor (CF) produced in the spleen of dengue virus type 2-infected mice killed the lymphoid cells of many species of animals and induced normal mouse splenic and peritoneal macrophages to produce a cytotoxin (CF2). In the present study, it has been observed that pretreatment of target cells with cell plasma membrane stabilizers--2,4-dinitrophenol, ouabain and reduced glutathione--prevents the cytotoxicity of CF and blocks the production of CF2, but does not abolish the cytotoxic effect of the latter. CF thus appears to act on target cells through damage to the plasma membrane.
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PURPOSE: Our goal was to use high resolution (HR) CT images combined with texture analysis to investigate the trabecular structure of human vertebral specimens and to compare these techniques with bone mineral density (BMD) in the prediction of bone strength. METHOD: HR CT images with a slice thickness of 1 mm were obtained of 28 bone cubes. Four different groups of texture analysis techniques were used to assess these images. In addition, quantitative CT (QCT) was performed and elastic modulus (EM) was determined biomechanically. RESULTS: R2 between EM and BMD was 0.78 (p < 0.01). R2 values for EM versus most of the texture measures were also significant. Texture measures in addition to measures of BMD in a multivariate regression model significantly increased R2 up to 0.87. CONCLUSION: In an experimental setting, texture parameters calculated using HR CT images correlated significantly with EM. Combining texture measures with BMD improved the prediction of EM significantly.
AIMS AND BACKGROUND: We have found that polyclonally stimulated T cells from mice bearing ascitic plasma cell tumors demonstrate specific decreases in Th1 cytokine production. In this study we investigated whether loss of Th1 responses in the plasma cell tumor system was associated with alterations in the Vbeta T cell receptor repertoire. METHODS: We examined the cell surface expression of specific Vbeta expressing splenic CD4+ or CD8+ T cells from normal and tumor bearing mice using direct three-color flowcytometry. In order to determine the Th phenotype of Vbeta expressing T cells, we enriched for Vbeta6, Vbeta14 or Vbeta8.1,8.2 cells, polyclonally stimulated them and measured the levels of the sytokines interleukin-4 (IL-4), IL-2 and interferon-gamma (IFN-gamma). RESULTS: We find there is a statistically significant decrease in the frequency of Vbeta6+ and Vbeta14+ CD8+ T cells in mice bearing a plasma cell tumor (B53) as compared to normal (p<0.05). Stimulated Vbeta6+ and Vbeta14+ T cells exhibit an exclusively Th1 phenotype. Stimulated Vbeta6+ and Vbeta14+ T cells from B53 mice are deficient in production of the Th1 cytokines. In contrast, stimulated Vbeta8.1,8.2+ T cells, which are not altered in B53 mice, reveal a Th2 phenotype. CONCLUSIONS: The significance of this study is our demonstration that decreased expression and function of Vbeta6+ and Vbeta14+ T cells may be, at least in part, responsible for the decrease in the production of IL-2 and/or IFN-gamma observed in hosts with tumors.
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Eighty-eight patients underwent surgery for various cardiac tumours from January 1978 to June 1998 at our Institute. Seventy-seven tumours were myxomas, 10 were non-myxomatous and one was secondary cardiac tumour. Case records of the patients with non-myxomatous primary cardiac tumours and one secondary tumour were reviewed. Six of these primary tumours were benign and four, malignant. Age of the patients ranged from 26 days to 47 years. Among patients (3 children, 8 adults) with non-myxomatous primary cardiac tumours, dyspnoea on exertion was the commonest symptom and was the cause of presentation in seven out of 11 patients. Of the eight adults, six were in New York Heart Association functional class II/III and two in class IV. Echocardiographic diagnosis was possible in all the patients. Complete excision of the tumour was possible in all benign and two of the four malignant tumours. Incomplete resection was done in the secondary tumour. Of the six benign tumours, three were rhabdomyomas and one each of fibroma, haemangioma and lipoma. The malignant tumours were one each of fibrosarcoma, angiosarcoma, unclassified sarcoma and malignant mesothelioma. The secondary tumour was a malignant thymoma. Follow-up ranged from 1 to 10 years (mean 7.2 years). Of the patients with benign tumours, four out of six are alive; one patient died on the first post-operative day and one lost to follow-up. Two of the four patients with malignant cardiac tumours died, one was lost to follow-up and one is alive two years after surgery. The patient with secondary malignant thymoma to the superior vena cava was lost to follow-up three months after an uneventful recovery from surgery.
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A case with pinhole rupture of the balloon of a Probe (USCI) coronary angioplasty catheter with resultant dissection and occlusion of the coronary artery is presented. The possible mechanism, predictors and precautions to prevent this complication are discussed.
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Since Japanese encephalitis virus (JEV) induces the generation of suppressor T cells in mouse spleen which, through the production of a soluble suppressor factor (SF), suppress IgM plaque-forming cells (IgM-PFC) the present study was undertaken to further characterize these suppressor cells and the SF. The suppressor cells were Ly1-2+ and sensitive to hydrocortisone and a high dose of irradiation. SF was trypsin-sensitive, thermolabile and non-dialysable, and passed through a 450-nm filter. This SF was shown to be a low molecular weight substance, with an approximate MW of 18,000 daltons.
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The quantity of clofazimine absorbed from the gastrointestinal tract when administered to lepromatous leprosy patients at varying single doses of 600 mg., 400 mg., 300 mg., and 100 mg. has been worked out by determining the amount of clofazimine present in total faecal excreta. Except in 100 mg. dose where the percentage absorption was 62.5 +/- 17 in all other case the values were around 45%. The efficacy of daily administration of 100 mg. clofazimine is discussed in this first article.
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