Clinico-virological study of the recurrence of dengue epidemic with haemorrhagic manifestations at Kanpur during 1969.
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Biomedical subjects
Publications and source records attributed to A Mathur.
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An epidemic of febrile illness associated with haemorrhagic manifestations and shock occurred at Kanpur, India, during 1968. The epidemic was widespread in the city, involving about one-tenth of the population; cases were more frequent in thickly populated localities with poor sanitary conditions. Those affected were mainly adolescents and adults of both sexes and multiple cases occurred in families. The disease was characterized by the sudden onset of fever, associated with severe headache and low backache. A number of patients had bradycardia, vomiting and diarrhoea and macular skin rashes associated with itching. A small percentage of the patients had haemorrhagic manifestations in the form of haematemesis, haemoptysis, melaena, haematuria and bleeding per vaginum. The mortality was very low. Dengue type 4 virus has been implicated in the epidemic.
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Several epidemics of febrile illnesses associated with haemorrhagic manifestations occurred in India during 1963 and 1964. These epidemics were restricted to the eastern coastal areas. However, in northern India, for the first time, a widespread epidemic of febrile illness associated with haemorrhagic manifestations occurred at Kanpur in 1968. In the present study, the virological findings of the epidemic are reported.The role of dengue type 4 virus in the epidemic is demonstrated by the isolation of the virus from a number of cases, including one with haematemesis, and conversion of antibody titres with dengue type 4 virus in the paired sera.
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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.
Stem-cell therapy provides the prospect of an exciting and powerful treatment to repair the heart. Although research has been undertaken in animals to analyse the safety and efficacy of this new approach, results have been inconclusive. The mechanism by which stem cells could improve cardiac function remains unclear. We describe the background to the concept of natural repair and the work that has been done to establish the role of stem cells in cardiac repair. Controversies have arisen in interpretation of experimental data. The important issues surrounding the application of stem-cell therapy to man are discussed critically. We discuss the future of this pioneering work in the setting of growing concerns about clinical studies in man without understanding the biological mechanisms involved, with the difficulties in funding this type of research.
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.