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Biomedical subjects

A Gaur

Publications and source records attributed to A Gaur.

At least 55 records · Page 3Linked to original sources
PubMed1993

SEB induced anergy: modulation of immune response to T cell determinants of myoglobin and myelin basic protein.

Superantigens have the ability to stimulate a subset of T cells based upon their expressed TCR beta-chain. It has been demonstrated that the administration of staphylococcal enterotoxin B (SEB) in mice leads to unresponsiveness in V beta 8+ T cells in vivo which are the same T cells that could be stimulated in vitro by this enterotoxin. We present here data on the effect of SEB administration in DBA/2 and (PL/J x SJL)F1 mice on their T cell response to two different T cell determinants, the responses against which are dominated by the use of V beta 8+ T cells. Treatment of mice with SEB not only diminished their primary T cell proliferative response to these determinants, but also was able to effectively reduce the memory T cell response. SEB treatment, however, showed only a modest effect in preventing Ac 1-11-induced experimental autoimmune encephalomyelitis in H-2u mice.

Amino Acid Sequence↗
PubMed1993

B cell tolerance induction by cross-linking of membrane IgM, but not IgD, and synergy by cross-linking of both isotypes.

Previous studies in our laboratory demonstrated that overnight exposure of adult splenic B cells to anti-Ig resulted in an unresponsive state characterized by decreased antibody synthesis but normal mitogen-driven proliferation (i.e., energy). Because both anti-F(ab')2 and anti-mu were equally effective at inducing tolerance, it was important to determine whether cross-linking of IgD together with or separately from IgM influenced the induction of unresponsiveness. Although anti-mu induced significant unresponsiveness, treatment of adult splenic B cells with anti-delta alone generally failed to reduce the subsequent response to either LPS or fluoresceinated Brucella abortus. Interestingly, anti-delta synergized with suboptimal concentrations of anti-mu to induce tolerance. Synergy could be observed in this system when anti-delta was added either simultaneously with or before (but not after) anti-mu; moreover, anti-delta was effective in a pretreatment (wash-out) protocol. To investigate the role of protein tyrosine kinase (PTK) activity in tolerance induction, splenic B cells were treated with tyrphostin before treatment with either anti-mu or anti-delta. We found that pretreatment with tyrphostin for 2 h before the addition of anti-mu prevented the induction of unresponsiveness with this antibody, whereas this PTK inhibitor facilitated tolerance when used with anti-delta treatment only. We propose that cross-linking of surface IgM directly or indirectly invokes a tyrphostin-sensitive, PTK-dependent pathway leading to the early events in tolerance induction, which can be augmented under limiting conditions by anti-IgD. Because cross-linking of either receptor initiates several common pathways, simultaneous cross-linking can lead to synergy and a dominance of the IgM signal. In contrast, IgD alone may fail to elicit tolerance because this isotype may also be associated with different PTK that cause positive signaling.

Animals↗
PubMed1993

Requirement for CD8+ cells in T cell receptor peptide-induced clonal unresponsiveness.

T cell receptor (TCR) vaccination in rats prevents the development of experimental allergic encephalomyelitis (EAE), an animal model of multiple sclerosis. The mechanism of this potential immunotherapy was examined by vaccinating mice with an immunogenic peptide fragment of the variable region of the TCR V beta 8.2 gene. Another immunogen that usually induces an immune response mediated by V beta 8.2+ T cells was subsequently inhibited because specific clonal unresponsiveness (anergy) had been induced. Depletion of CD8+ cells before TCR peptide vaccination blocked such inhibition. Thus, the clonal anergy was dependent on CD8+ T cells, and such immunoregulatory T cells may participate in the normal course of EAE.

Animals↗
PubMed1993

Rectal nifedipine for the management of intraoperative hypertension.

The effect of rectal administration of nifedipine for the management of intraoperative hypertension was studied in 12 adult neurosurgical patients, physical status II and III. A rise in mean arterial pressure (MAP) of > 20 mm Hg over the preoperative value was taken as the point at which rectal nifedipine (150 micrograms kg-1) was administered. Onset of action of nifedipine was observed in 4.5 +/- 1.5 min (mean +/- SD) with a peak effect at 30.8 +/- 10.7 min. MAP decreased from 124 +/- 4.5 mm Hg to 97 +/- 2.4 mm Hg. Heart rate and central venous pressure were unchanged. Endoscopic examination of the rectal mucosa 48 h after administration of nifedipine did not show any abnormality. Rectal nifedipine was found to be effective and safe for the management of intraoperative increases in arterial blood pressure as well as being convenient to administer to patients undergoing neurosurgical procedures.

Administration, Rectal↗
PubMed1993

Bancroftian filarial pleural effusion.

This paper describes a case of filarial pleural effusion, the fifth such to be reported. Microfilariae of Wuchereria bancrofti were detected in the pleural fluid on cytological examination. There was a prompt and complete response to treatment with diethylcarbamazine. There were, however, no symptoms and signs of tropical pulmonary eosinophilia nor any peripheral eosinophilia.

Adolescent↗
PubMed1993

Changes in phospholipids, fatty acids, oxidative enzymes, phenolics and protein levels during growth of normal and habituated tissues of Cocculus pendulus.

Cultures of C. pendulus were maintained on hormone free and hormone supplemented (NAA 1.0 mg/l and kinetin 0.5 mg/l) Murashige and Skoog medium. During the growth period, hormone free cultures had higher phenolic content, polyphenol oxidase activity and less protein content, peroxidase and IAA oxidase activity. Activity of all the three oxidising enzymes and phenolic content were high at 16 days growth. Total lipid content was higher (2.7-folds at 15 days) in hormone free cultures. Phospholipid content of both cultures was not markedly dissimilar except PC and DGDG contents. Thus it is evidenced that both the tissues were similar metabolically.

Alkaloids↗
PubMed1992

Amelioration of autoimmune encephalomyelitis by myelin basic protein synthetic peptide-induced anergy.

Experimental autoimmune encephalomyelitis (EAE), a demyelinating disease of the central nervous system that can be induced in susceptible strains of mice by immunization with myelin basic protein (MBP) or its immunodominant T cell determinants, serves as a model of human multiple sclerosis. Tolerance to MBP in adult mice was induced by intraperitoneal injection of synthetic peptides of immunodominant determinants of MBP and prevented MBP-induced EAE. Furthermore, tolerance-inducing regimens of peptides administered to mice after the disease had begun (10 days after induction with MBP) blocked the progression and decreased the severity of EAE. Peptide-induced tolerance resulted from the induction of anergy in proliferative, antigen-specific T cells.

Animals↗
PubMed1992

Internalization of a major group human rhinovirus does not require cytoplasmic or transmembrane domains of ICAM-1.

Intercellular adhesion molecule-1 (CD54), a cell adhesion molecule and the receptor for the major group of rhinoviruses, is a class 1 membrane protein with five Ig-like domains in its extracellular region, a transmembrane domain, and a short cytoplasmic domain. The amino-terminal domains (D1 and D2) are sufficient for virus binding and the first is most important (1). We have investigated whether other extracellular domains, transmembrane or cytoplasmic domains are required for virus entry as determined by postinfection virion protein biosynthesis. We demonstrate that cytoplasmic, transmembrane, and Ig-like domains 3, 4, and 5 are not essential for rhinovirus entry into transfected COS cells. The efficiency of rhinovirus infection directly correlates with the efficiency of rhinovirus binding and a form of intercellular adhesion molecule-1 that is glycophosphatidyl-inositol anchored, and thus does not extend into the inner leaflet of the membrane bilayer or the cytoplasm efficiently supports virus entry.

Cell Adhesion Molecules↗
PubMed1992

Transferable antibiotic resistance among thermotolerant coliforms from rural drinking water in India.

A total of 231 thermotolerant coliforms was isolated from rural drinking water from four states of India. Of these, 220 isolates were resistant to ampicillin, chloramphemicol, streptomycin and tetracycline. Multiple (MAR), double and single antibiotic resistances were observed in 31.4, 48.6 and 13.7% of the isolates, respectively. Out of 177 antibiotic-resistant isolates examined for transmissibility, only 15.3% were able to transfer their resistances to Escherichia coli K-12 recipient. The resistances were transferred by 32.5% of MAR, 21.9% of double resistant and 7.6% of single resistant isolates. Ampicillin resistance was transferable in 14.69% strains while resistances for the rest of the antibiotics were transferable in less than 4% strains. MAR strains of E. coli and Klebsiella sp. showed highest levels of R-plasmid transfer.

Ampicillin Resistance↗
PubMed1992

Transient achalasia of esophagus in tetanus.

A case with tetanus presenting with progressive dysphagia due to lower esophageal dysfunction is described. A barium swallow at the onset of symptoms showed esophageal dilatation with a smooth tapering at the lower end suggestive of achalasia cardia. The patient recovered from tetanus over the ensuing three weeks; repeat barium swallow at this time was normal, suggesting that esophageal dysfunction was a manifestation of tetanus.

Deglutition Disorders↗
PubMed1992

Prevention of B cell clonal deletion and anergy by activated T cells and their lymphokines.

B cell tolerance is described as the absence of a measurable antibody forming response to an antigenic challenge. The establishment of antigen-specific tolerance requires, by definition, engagement of the B cell antigen-specific receptor. However, only in some circumstances does this engagement lead to tolerance, while in others it produces B cell activation and secretion of immunoglobulins. Several mechanisms occur naturally in vivo abrogating the expression of deleterious autoantibodies and contributing to the state of self-tolerance. In this review, we will examine different ways in which B cell tolerance can be broken, focusing on evidence showing that activated-T cells and/or their lymphokines can prevent B cell clonal deletion and thus have a potential role in the pathogenesis of autoimmune diseases. This approach is based on the well-known association of several lymphokines, such as IL-1, IL-2, IL-4, IL-5, and type I interferons, with autoimmune phenomena in vivo.

Animals↗
PubMed1992

Anti-immunoglobulin treatment of murine B-cell lymphomas induces active transforming growth factor beta but pRB hypophosphorylation is transforming growth factor beta independent.

Cross-linking of B-cell membrane immunoglobulin (Ig) receptors induces growth arrest at G1-S, leading to apoptosis and cell death in the immature lymphomas WEHI-231 and CH31, but not in the CH12 B-cell line. In this system, which has been used as a model for B-cell tolerance, we have established that these lymphomas produce active transforming growth factor beta (TGF-beta) when treated with anti-Ig and that their hierarchy of sensitivity to TGF-beta generally correlates with their growth inhibition by anti-Ig. TGF-beta, in turn, has been shown to interfere with the phosphorylation of the retinoblastoma gene product, pRB. Herein, we also demonstrate that in WEHI-231 B-lymphoma cells treated with anti-Ig for 24 h, the pRB protein is found to be predominantly in the underphosphorylated form, as previously reported for cells arrested by the exogenous addition of TGF-beta. However, neutralizing antibodies to TGF-beta failed to prevent growth inhibition by anti-Ig in WEHI-231 and CH31. When WEHI-231 lymphoma cells were selected for growth in TGF-beta, the majority of the TGF-beta-resistant clones remained sensitive to anti-Ig-mediated growth inhibition. In these clones, the retinoblastoma gene product was found to be in the underphosphorylated form after 24-h treatment with anti-Ig, but not with TGF-beta. These data show that anti-Ig treatment of murine B-cell lymphomas stimulates the production of active TGF-beta but that a TGF-beta-independent pathway may be responsible for the pRB underphosphorylation and cell cycle blockade.

Animals↗
PubMed1991

The T cell receptor repertoire influences V beta element usage in response to myoglobin.

T cell clones recognizing the sperm whale myoglobin (SpWMb) epitope 110-121 in association with H-2d major histocompatibility complex class II molecules display a very limited heterogeneity of T cell receptor (TCR) V beta usage in DBA/2 mice. All clones previously tested used the same V beta 8.2 gene segment and very restricted junctional regions. To investigate the significance of this observation in vivo, we immunized DBA/2 mice with the intact SpW Mb protein or peptide 110-121. Only the V beta 8+ T cells showed any significant response to the 110-121 epitope. The response to peptide 110-121 was then analyzed in mice which, either as a consequence of antibody depletion or through genetic deletion of TCR V beta genes, lacked V beta 8+ peripheral T cells. DBA/2 mice depleted of V beta 8+ T cells by antibody treatment responded poorly to the 110-121 peptide, and only at high antigen concentrations. In contrast, DBA/2V beta a mice (homozygous for a deletion of multiple V beta gene segments including the V beta 8 family) made a response at least as great as that made by DBA/2 mice, even though the DBA/2V beta a mice had a very restricted TCR V beta repertoire compared with DBA/2 mice. Mechanisms which might determine differences in the 110-121 specific response of DBA/2, DBA/2V beta a and F23.1-treated DBA/2 mice are discussed.

Animals↗
PubMed1991

A polyclonal model for B-cell tolerance. II. Linkage between signaling of B-cell egress from G0, class II upregulation and unresponsiveness.

Overnight exposure of adult splenic B cells to anti-Ig, a surrogate for antigen/tolerogen, can result in a hyporesponsive state in terms of antibody synthesis. Since B cells treated with either intact of F(ab')2 fragments of anti-Ig will exit the G0 phase of the cell cycle and enter G1 or S, respectively, we examined which steps in B-cell activation were required for this form of hyporesponsiveness. We found that B-cell hyporesponsiveness could be induced under conditions leading to either abortive or productive B-cell cycle progression, depending on the immunogenic challenge employed. Thus, PMA + ionomycin, concanavalin A, PMA alone, or ionomycin alone induced hyporesponsiveness. Each of these reagents is able to drive B-cell exit from G0 into G1 and cause class II hyperexpression. We next examined the effect of cyclosporin A (CSA), a reagent that blocks anti-Ig but not by PMA-induced class II hyperexpression. Interestingly, CSA only interfered with the induction of B-cell hyporesponsiveness with anti-Ig. These results suggest that upregulation of MHC class II may be coincident with a CSA-sensitive tolerance pathway in B cells stimulated by anti-Ig. Finally, IL-4 pretreatment was found to ablate hyporesponsiveness induced by either intact anti-Ig or PMA. These results parallel the Fc-dependent induction of hyporesponsiveness reported earlier (G. Warner and D. W. Scott, J. Immunol. 146, 2185, 1991). We propose that crosslinking of surface Ig, leading to cell cycle progression out of G0 as well as class II hyperexpression, in the absence of a cognate T cell signal, leads to B-cell hyporesponsiveness.

Animals↗
PubMed1990

Bypass by an alternate 'carrier' of acquired unresponsiveness to hCG upon repeated immunization with tetanus-conjugated vaccine.

We report here the use of an alternative carrier diphtheria toxoid (DT) in human subjects to overcome antigen-specific unresponsiveness upon immunization with a hapten/ligand-carrier conjugate. In the phase I clinical trial of a birth control vaccine using gonadotrophin subunits linked to tetanus toxoid, some of the subjects failed to evoke a booster antibody response to human chorionic gonadotrophin (hCG). Presentation of the ligand on DT instead in subsequent immunizations restored anti-hCG response.

Antibody Formation↗
PubMed1990

Antibiotic resistance of coliforms in drinking water in rural areas.

The antibiotic sensitivity of 197 coliform sp. isolated from drinking water in five rural areas was studied. Twelve strains (6.1%) showed multiple antibiotic resistance, three (1.5%) of which were able to transfer the resistances to an Escherichia coli K-12 recipient. It seems unlikely that the occurrence of transmissible multiple antibiotic resistance among coliforms in drinking water in the areas studied poses a significant public health risk.

Anti-Bacterial Agents↗