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Biomedical subjects

A Mathur

Publications and source records attributed to A Mathur.

At least 19 recordsLinked to original sources
PubMed1992

Primary immunodeficiencies: genetic risk factors for lymphoma.

It has been estimated that up to 25% of patients with certain genetically determined immunodeficiencies will develop tumors, primarily B-cell lymphomas, during their lifetime. Epstein-Barr virus appears to be an important cofactor in the development of lymphoproliferative disorders in patients with primary immunodeficiencies, as well as acquired immunodeficiencies. Additionally, host defects in immunoregulation and/or gene rearrangement, which are features of certain primary immunodeficiencies, probably contribute to the risk of lymphomagenesis in patients at risk.

Adolescent↗
PubMed1992

Use of the computed tomographic scan in Japanese encephalitis.

Fourteen children with laboratory-confirmed Japanese encephalitis were given cranial computed tomographic (CT) scans six to 30 days after the onset of illness. The findings were variable; there was a generalized decrease in attenuation values, three patients showed features of cerebral atrophy, and four others had normal scans. The findings appeared to relate to both the severity and the stage of the illness at the time the scans were made. CT would appear to be of little use in making a specific diagnosis of Japanese encephalitis.

Brain↗
PubMed1992

Breakdown of blood-brain barrier by virus-induced cytokine during Japanese encephalitis virus infection.

In this study we have shown, for the first time, that Japanese encephalitis virus (JEV) and a low molecular weight (10 kDa) macrophage-derived neutrophil chemotactic factor (MDF) produced following JEV infection in mice could cause an alteration in the permeability of the blood-brain barrier resulting in leakage of plasma protein bound Evans blue dye and radiolabelled erythrocytes in brain. The maximum leakage occurred at day 6 after intracerebral (i.c.) JEV infection and was sensitive to anti-JEV antisera. Further, MDF caused peak leakage of dye and radiolabelled erythrocytes at 1 h post inoculation with a decline thereafter. Complete restoration of the integrity of the blood-brain barrier occurred by the 4th hour. The extent of leakage was dose dependent and showed a direct correlation between the level of MDF, clinical sickness and virus titre in brain. Anti-MDF antisera protected the mice against the effects of MDF. These findings show that JEV-induced cytokine, MDF, alters the integrity of the blood-brain barrier and thus controls the cellular and plasma leakage into the CNS.

Animals↗
PubMed1992

Characterization of the dengue virus-induced helper cytokine.

Dengue type 2 virus (DV) induces a subpopulation of T lymphocytes of mouse spleen to secrete a soluble helper cytokine (HF) which enhances the DV-specific IgM antibody plaque forming cells (PFC). The present study undertaken to purify and characterize HF shows that it can be purified by low pressure liquid chromatography (LPLC) using Sephacryl S-200 column. HF consisted of two subunits, having a M(r) of 65-68 kDa on SDS-PAGE, and both had similar activity. The isoelectric point of HF was 6.5. HF-specific antisera (HFAS) raised in mice neutralized the activity of HF in mice, reacted with it in a Western blot assay, and bound HF in an immunosorbent column. HF bound to DV-antigen in an immunosorbent column and enhanced only the DV-specific PFC. HF had no effect on PFC against heterologous antigens such as Japanese encephalitis virus, Coxsackie B4 virus or sheep red blood cells. HF generated in mice of H-2k haplotype, enhanced DV-specific PFC in the same strain of mice but had no effect on that in the H-2d or H-2q haplotype strains of mice. Thus, DV-induced HF with a M(r) of 65-68 kDa, antigen-specificity and genetic-restriction differs from most of the similarly acting cytokines but appears similar to the cell-free form of T cell receptor alpha beta dimer.

Animals↗
PubMed1992

Comparison of immediate hemodynamic response to closed mitral commissurotomy, single-balloon, and double-balloon mitral valvuloplasty in rheumatic mitral stenosis.

The hemodynamic response to closed mitral commissurotomy, single-balloon, and double-balloon mitral valvuloplasty was compared using 20 patients in each group. All patients had symptomatic rheumatic mitral stenosis with a mitral valve area < 1 cm2, without any left atrial clot, mitral valve calcification, or mitral regurgitation. There was a significant improvement in hemodynamics following intervention in all three groups. The mean pulmonary artery pressure decreased from 49.1 +/- 17.5 to 28.6 +/- 8.3 mm Hg (p < 0.001), 48.8 +/- 12.3 to 34.0 +/- 13.9 mm Hg (p < 0.001), and 46.7 +/- 18.0 to 26.3 +/- 13.7 mm Hg (p < 0.001) in the closed mitral commissurotomy, single-balloon, and double-balloon mitral valvuloplasty groups, respectively. The mitral valve area increased from 0.62 +/- 0.27 to 1.5 +/- 0.5 cm2 (p < 0.001), 0.68 +/- 0.24 to 1.5 +/- 0.4 cm2 (p < 0.001), and 0.68 +/- 0.25 to 1.9 +/- 0.8 cm2 (p < 0.001) in the closed mitral commissurotomy, single-balloon, and double-balloon mitral valvuloplasty groups, respectively. The increase in the mitral valve area was maximum in the group with double-balloon mitral valvuloplasty. In the closed mitral commissurotomy group there was a significant rise in left ventricular end-diastolic pressure, from 6.8 +/- 3.9 to 9.3 +/- 3.1 mm Hg (p < 0.001), but this remained unchanged in the single-balloon and double-balloon mitral valvuloplasty groups. Our study shows that single-balloon and double-balloon mitral valvuloplasty are comparable to closed mitral commissurotomy in the immediate hemodynamic response, with a larger valve area in the double-balloon mitral valvuloplasty group.

Adolescent↗
PubMed1992

Immunopathology, rheumatic features, and therapy of sarcoidosis.

A spectrum of immune alterations underlies the clinical syndrome of sarcoidosis. There is an increase in the number of helper T lymphocytes at sites of disease activity. Both macrophages and T cells are in a state of activation. Inflammation in sarcoidosis probably attracts specific T lymphocytes, as has been shown by the preferential usage of the C beta 1 elements of the T-cell antigen receptor. Acute sarcoid arthritis is distinctly different in its HLA association and clinical outcome than chronic sarcoid arthritis. Muscle and osseous lesions are well described but are usually asymptomatic. Childhood sarcoidosis may be confused with juvenile rheumatoid arthritis because of the similarity of eye and articular involvement. Nonsteroidal anti-inflammatory drugs and corticosteroids are effective for most patients. Hydroxychloroquine, methotrexate, and cyclosporine have been tried with success in patients with refractory sarcoidosis.

Adrenal Cortex Hormones↗
PubMed1991

Enhancer mediated suppression of epsilon heavy-chain gene expression in a murine IgE-producing hybridoma.

In vitro co-culture of IgE-secreting hybridoma cells (B53) with spleen cells harvested from mice with established B53 tumours results in a specific, T cell-dependent suppression of epsilon-chain expression in the B53 cells. The role of immunoglobulin enhancers in the suppression of IgE synthesis in B53 cells was examined by transfecting B53 cells with CAT expression vectors containing the immunoglobulin heavy- or kappa light-chain intron enhancers or a Rous sarcoma virus (RSV) LTR. When epsilon-chain expression of transfected cells was suppressed in vitro. CAT expression was also suppressed in cells transfected with vectors containing the immunoglobulin heavy-chain gene enhancer, but not in cells transfected with vectors containing the kappa enhancer or RSV LTR. Thus, the T cell-dependent suppression of IgE synthesis in B53 cells correlates with a specific inactivation of the immunoglobulin heavy chain enhancer, strongly suggesting that T cell-mediated suppression of Ig synthesis can normally occur through specific repression of Ig enhancer function. This represents a new regulatory pathway involved in the control of IgE synthesis and is the first indication that the enhancer mediated expression of Ig genes in B cells can be modulated through T cell-dependent processes.

Animals↗
PubMed1991

A teratogenic study of carbaryl in Swiss albino mice.

To study the teratogenicity of carbaryl, groups of 10 pregnant mice were dosed, by gavage, with 0, 100, 150 or 200 mg carbaryl/kg body weight, in corn oil, on day 8 or day 12 of pregnancy or daily (as daily doses) from day 6 to day 15. The two higher doses were toxic to both dams and foetuses regardless of the timing of treatment. Treated dams generally showed reduced weight gains but total weight gain was significantly reduced only for dams given 200 mg carbaryl on day 8 or day 12 of gestation. Maternal mortality was increased in most groups given 150 or 200 mg carbaryl. Carbaryl treatment tended to reduce litter size, to increase the percentage of resorbed foetuses, and to reduce foetal weight. There were increased incidences of open eye, of certain visceral abnormalities, and of reduced ossification in virtually all treated groups. The variety of abnormalities in treated foetuses reflected the dysmorphogenic potential of the pesticide. More aberrations were seen in foetuses from dams treated throughout organogenesis than in those from dams given a single dose.

Abnormalities, Drug-Induced↗
PubMed1991

Breakdown of the blood-brain barrier during dengue virus infection of mice.

A breakdown of the blood-brain barrier occurred in mice inoculated intracerebrally (i.c.) or intraperitoneally (i.p.) with dengue virus type 2 (DEN2). This resulted in leakage of protein-bound Evans blue dye and 51Cr-labelled erythrocytes into the brain tissue. The leakage increased with time after infection and coincided with an increase of a DEN2-induced cytokine, the cytotoxic factor (CF), in the spleens of such mice. The titres of virus in the brain increased exponentially in i.c. inoculated mice but the virus was not detected in brains of mice given DEN2 by the i.p. route. Similar breakdown of the blood-brain barrier also occurred in mice inoculated intravenously with CF; the damage was dose-dependent and the vascular integrity was restored during the 3 h period after inoculation. Treatment of mice with antihistamine drugs, blocking H1 or H2 receptors, decreased the DEN2-induced protein leakage by up to 50% in i.c. inoculated mice and up to 92% in those inoculated i.p. Indomethacin, a prostaglandin synthetase inhibitor, had no effect. In i.c. inoculated mice protein leakage was inhibited by about 60% by treatment with CF-specific (CFA) or DEN2-specific antisera (DEN2A) whereas protection was complete with the combined treatment with both antisera. On the other hand, in i.p. inoculated mice the inhibition of protein leakage was 80 to 89% with CFA. These findings show a breakdown of the blood-brain barrier leading to cerebral oedema during DEN2 infection which is mediated via the release of histamine by a virus-induced cytokine.

Animals↗
PubMed1991

An Indian hospital study of viral causes of acute respiratory infection in children.

From Sept. 1986 to Jan. 1989, a hospital-based study was conducted on 736 children, under 5 years of age, with acute respiratory infection. Nasopharyngeal secretions were examined for viruses by culture and by immunofluorescence. Viruses were detected in 22% of specimens: respiratory syncytial (5%), parainfluenza (5%), influenza A (4%), influenza B (2%), adenovirus (3%), measles (3%). The highest rates of detection were with patients diagnosed clinically as pneumonia or upper respiratory tract infection. The case fatality rate was very high (43%) in children with measles virus infection.

Child, Preschool↗
PubMed1991

Effect of macrophage-derived factor on hypoferraemia induced by Japanese encephalitis virus in mice.

Depression of serum iron following Japanese encephalitis virus (JEV) infection was observed in mice. The hypoferraemia was associated with the accumulation of iron in reticulo-endothelial cells in the spleen. Splenectomy (compared with sham-operation) prevented the depression in serum iron concentration after JEV infection. It also prevented the rise in levels of liver iron. The effect of JEV-stimulated, splenic macrophage-derived factor (MDF) was evaluated in causing hypoferraemia. MDF produced a rapid reduction in the serum iron levels with accumulation of iron in spleen. These observations suggest that MDF plays a key role in the regulation of iron metabolism during JEV infection.

Animals↗
PubMed1991

Japanese encephalitis virus latency in peripheral blood lymphocytes and recurrence of infection in children.

In a study group of 40 children who had been admitted to hospital with acute encephalitis, the disease was due to infection with Japanese encephalitis virus (JEV). Three children developed recurrence of disease 8-9 months later. No virus had been isolated from these three patients during the acute stage of their illness, but virus was recovered from all during the recurrence phase by co-cultivation of their peripheral blood mononuclear cells in primary mouse embryo fibroblast cultures. Virus was also recovered by co-cultivation of peripheral blood mononuclear cells collected 8 months after their acute disease from three out of eight randomly selected asymptomatic children within the study group but not from similar cultures set up from JEV-seronegative children used as controls. Virus was also isolated by co-cultivation of T lymphocytes of asymptomatic children as detected by indirect immunofluorescence or by inoculation in mice.

Cells, Cultured↗
PubMed1991

Neutrophil chemotactic factor produced by Japanese encephalitis virus stimulated macrophages.

The mechanism of neutrophil leucocytosis in cases of Japanese encephalitis is not known. We here report that during Japanese encephalitis virus (JEV) infection in mice the splenic macrophages secrete a chemotactic factor that attracts the neutrophils. The peak activity of macrophage derived factor (MDF) was observed on day 7 following infection. The MDF acted in a dose-dependent manner. This chemoattractant was purified by low pressure liquid chromatography and gave a single band of 10 kD on silver stained polyacrylamide gel. The MDF was found to be heat resistant and sensitive to prolonged incubation with proteases.

Animals↗
PubMed1991

Obligatory role of Ca2+ in the cytotoxic activity of dengue virus-induced cytotoxin.

The role of calcium ions (Ca2+) in the cytotoxic activity of the dengue type 2 virus (DV)-induced macrophage (M phi) cytotoxin (CF2) was investigated in the present study. The findings show that CF2 prepared in Ca(2+)-free medium had no cytotoxic activity on normal mouse spleen cells suspended in Ca(2+)-free medium but killed the cells suspended in the medium with Ca2+. Substitution with calcium chloride restored the cytotoxic activity of CF2 the optimal dose being 10(-4) M concentration. CF2 induced an influx of Ca2+, as assayed by uptake of radiolabelled calcium chloride (45Ca), in the susceptible target cells, viz. M phi and T lymphocytes. The cytotoxic activity of CF2 as well as the CF2-induced influx of 45Ca was inhibited by treatment of the target cell with the calcium channel blocking drugs verapamil and nifedipine. Thus, the presence of Ca2+ is obligatory for the cytotoxic activity of CF2 and cell death is associated with increased intracellular Ca2+.

Animals↗