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Biomedical subjects

S L Gupta

Publications and source records attributed to S L Gupta.

At least 37 records · Page 2Linked to original sources
PubMed1986

Experimental Sarcocystis levinei infection in buffalo calves.

Six buffalo calves were orally inoculated with 3 graded doses of sporocysts of Sarcocystis levinei (0.5, 1.0 and 2.0 million sporocysts; 2 calves for each dose) while two more calves were kept as uninoculated controls. One calf from each group was killed at 30 days post infection (DPI) and the other at 80 DPI. Inoculated calves showed a dose dependent response. The calves inoculated with 0.5 and 1.0 million sporocysts did not manifest any clinical signs of disease up to 80 DPI. One of the two calves inoculated with 2.0 million sporocysts showed clinical signs of weakness, emaciation and anaemia during the 5th week post infection. The other calf remained healthy until it was killed at 30 DPI. Pale liver tissue, gelatinization of fat and haemorrhages in the heart were observed in one calf inoculated with 2.0 million sporocysts; only microscopic lesions were seen in other calves. Schizonts and merozoites were not observed in any calf. Mature sarcocysts were observed in cardiac and skeletal muscle of calves killed at 80 DPI whereas no sarcocysts were seen in calves killed at 30 DPI.

Animals↗
PubMed1985

Cholesterol monohydrate dissolution rate studies in aqueous micellar solutions of alpha-(nonylphenyl)-omega-hydroxydeca(oxyethylene), n-alkylamines, and fatty acids.

The influences of electrical and nonelectrical factors in the interfacially controlled dissolution of cholesterol monohydrate by mixed micelles of alpha-(nonylphenyl)-omega-hydroxydeca(oxyethylene) (polyoxyethylene [10]-nonylphenol ether; POEPE; 1) in combination with long-chain n-alkylamines or fatty acids were investigated and quantified under pH conditions where the amines and fatty acids exist in their charged and uncharged forms. The experimental findings were generally consistent with a mechanism involving micelle collision with the cholesterol surface. A significant interfacial barrier was found with neutral micelles; however, the magnitude of the barrier was smaller with uncharged mixed micelles than with the simple micelles of 1. With charged micelles, the interfacial mass transfer resistance decreased with the addition of sodium chloride to the extent that the interfacial barrier was essentially abolished and the dissolution kinetics became convective/diffusion controlled. The results are consistent with the phenomena of diffusion of charged micelles toward a charged surface, following the classical collision kinetic theory of colloids. The ease in the transfer of cholesterol monohydrate molecules from the crystal surface and into the micelles during the collision step was examined by considering factors affecting the crystal surface as well as those associated with the hydrophobic-hydrophilic structure of the micelle of 1 and the distribution of charged and uncharged amphipathic additives within the basic micelle structure of 1.

Amines↗
PubMed1985

Cholesterol monohydrate dissolution rate studies in aqueous micellar sodium chenodeoxycholate solutions.

The dissolution rate of cholesterol monohydrate in various concentrations of sodium chenodeoxycholate (1) was significantly influenced by the addition of strong electrolytes. The mass transfer resistances decreased with increasing electrolyte concentrations and attained an asymptotic minimum value predicted and experimentally established for the convective/diffusion-controlled situation. Reduction of the interfacial barrier to dissolution was many times more sensitive to Mg2+ than to Na+ at equimolar concentrations. Cholesterol monohydrate solubilities increased nonlinearly with increasing 1 in 0.01 M phosphate buffer at pH 8.0 and was not influenced by the presence of strong electrolytes. Measured diffusion coefficients gave supporting evidence that the effective micellar size remained the same within the various experimental systems up to 116 mM chenodeoxycholate. The experimental findings indicated that the interfacial barrier is electrostatic in character. They are consistent with the phenomenon of diffusion of negatively charged micelles toward a negatively charged cholesterol monohydrate surface and the subsequent collision complex transfer of cholesterol molecules at the crystal surface. The results and mechanistic interpretations are also in accord with the previous model studies on cholesterol monohydrate dissolution in the presence of mixed micelles composed of nonionic and ionic surfactants.

Benzalkonium Compounds↗
PubMed1985

Toxoplasma seroprevalence in animals in northern India.

In a serological survey of latent Toxoplasma prevalence on 3761 animals in northern India by the microtitre indirect haemagglutination test, 23.7 per cent were found to have antibody titres ranging from 1:4 to 1:1024. Seropositivity was recorded in 25.3 per cent of 1227 sheep, 30.3 per cent of 961 goats, 11.8 per cent of 603 horses, 19.3 per cent of 243 cattle, 15.7 per cent of 108 water buffaloes, 31.5 per cent of 178 pigs, 30.9 per cent of 175 dogs, 33.7 per cent of 80 cats and in 9.7 per cent of 186 bandicoot rats. Relevant epidemiological data has been furnished. High seropositivity in food animals and frequent isolations of Toxoplasma highlight the likely public health implications of the findings.

Age Factors↗
PubMed1985

Toxoplasma prevalence and human occupational groups.

Toxoplasma antibody prevalence was studied in four specialized groups of human population at Hissar, Haryana to study the influence, if any, of the degree of animal contact. While seropositivity among 64 persons of general population was 28.1 per cent, that in livestock and pet owners was found to be higher (35.0 per cent). Among other groups the overall positivity was similar to that in the general population, but there was greater concentration of higher serotitres among the laboratory animal handlers and postmortem attendants. It appears that the intimacy of animal contact is more important than the duration.

Animals↗
PubMed1984

Interferon receptor interaction. Internalization of interferon alpha 2 and modulation of its receptor on human cells.

Studies reported earlier [ Joshi et al. (1982) J. Biol. Chem. 257, 13884-13887] have indicated that human interferon-alpha 2 (HuIFN-alpha 2) binds to a specific macromolecular receptor on human cells as identified by cross-linking with bifunctional cross-linking reagents and analysis by polyacrylamide gel electrophoresis. We have carried out experiments to investigate the fate of the interferon-receptor complex on the cell surface under conditions which lead to cellular response. As analyzed by cross-linking and gel electrophoresis, the interferon-receptor complex, formed on incubation with 125I-IFN-alpha 2 at 4 degrees C, persisted at the cell surface for several hours at 4 degrees C; however, if the cells were switched to 37 degrees C, there was a rapid decline in the complex, apparently due to a loss of the interferon receptors from the cell surface. This was associated with an internalization of the 125I-interferon as indicated by the fact that, on incubation at 37 degrees C, an appreciable fraction of the cell-associated interferon (approximately equal to 50%) became resistant to trypsin digestion, or dissociation on incubation in growth medium or low-pH buffer. A large fraction of the trypsin-resistant (internalized) 125I-labeled material migrated as intact interferon in polyacrylamide gels, and it was immunoprecipitated by anti-(HuIFN-alpha)antibodies but not by anti-(HuIFN-beta)antibodies. The bulk of the internalized 125I-interferon was recovered in a particulate fraction and, on cross-linking with disuccinimidyl suberate, a 150000-Mr complex could be detected. The results suggest that interferon may be internalized as a complex with the receptor, which may account for the loss of the interferon-receptors on the cell surface. This modulation of the IFN-alpha/beta receptors was induced by HuIFN-alpha and HuIFN-beta but not by HuIFN-gamma. The recovery of the IFN-alpha/beta receptors, lost upon incubation with HuIFN-alpha, took several hours and required protein synthesis. The significance of the results is discussed.

Burkitt Lymphoma↗
PubMed1984

Receptors for human gamma interferon: binding and crosslinking of 125I-labeled recombinant human gamma interferon to receptors on WISH cells.

Purified recombinant human gamma interferon (HuIFN-gamma), labeled with 125I (125I-HuIFN-gamma), was used to study receptors for HuIFN-gamma on human WISH cells. 125I-HuIFN-gamma was bound to WISH cells, and this binding was displaced by unlabeled HuIFN-gamma but not by unlabeled recombinant HuIFN-alpha 2 or [Ser17]HuIFN-beta (HuIFN-beta with serine substituted for cysteine at position 17), indicating the presence of specific binding sites for HuIFN-gamma. The cell-bound 125I-HuIFN-gamma was crosslinked with disuccinimidyl suberate or ethylene glycol bis(succinimidyl succinate), which yielded a complex of Mr approximately 105,000 +/- 5000 as analyzed by NaDodSO4/PAGE. The formation of this complex was prevented by preincubation of cells with unlabeled HuIFN-gamma but not with HuIFN-alpha 2 or [Ser17]HuIFN-beta, indicating that HuIFN-gamma binds to a specific receptor molecule and that HuIFN-alpha 2 or HuIFN-beta do not interact with this receptor. Experiments were carried out with 125I-labeled recombinant [Ser17]HuIFN-beta (125I-[Ser17]HuIFN-beta) to verify this conclusion. Binding and crosslinking of 125I-[Ser17]HuIFN-beta to human WISH cells and Daudi cells yielded a complex of Mr approximately 150,000 similar to that obtained with 125I-HuIFN-alpha 2 as described earlier. The formation of this Mr 150,000 complex with 125I-[Ser17]HuIFN-beta was displaced by unlabeled [Ser17]HuIFN-beta and by HuIFN-alpha 2 but not by HuIFN-gamma, indicating that [Ser17]HuIFN-beta binds to the same receptor as does HuIFN-alpha 2, identified earlier, and that HuIFN-gamma does not compete with 125I-[Ser17]HuIFN-beta for this receptor. We conclude that HuIFN-gamma interacts with specific receptors that are distinctly different from the receptors recognized by HuIFN-alpha and HuIFN-beta.

Amnion↗
PubMed1984

Receptors for human alpha and beta interferon but not for gamma interferon are specified by human chromosome 21.

We examined the proposed role of human chromosome 21 in determining the cellular sensitivity to human alpha, beta, and gamma interferons (HuIFN-alpha, -beta, and -gamma) and the expression of the receptors for the HuIFNs with the use of mouse-human hybrid cells containing human chromosome 21. Hybrid cells (WA17) containing three copies of human chromosome 21 showed specific displaceable binding of 125I-labeled HuIFN-alpha 2 (125I-HuIFN-alpha 2), which was not observed with mouse parent (A9) cells. Crosslinking of 125I-HuIFN-alpha 2 bound to WA17 cells with disuccinimidyl suberate yielded a complex of Mr approximately equal to 150,000 similar to the 125I-HuIFN-alpha 2-receptor complex obtained with human cells as described earlier. Such a complex was not obtained with mouse parent (A9) cells or with hybrid cells containing certain other human chromosomes but not chromosome 21. Mice inoculated with mouse-human hybrid cells containing human chromosome 21 produce antibodies that block the antiviral action of HuIFN-alpha and -beta on human cells. Such antibodies could immunoprecipitate the 125I-HuIFN-alpha 2-receptor complex obtained from human cells but not free 125I-HuIFN-alpha 2, indicating that these antibodies were directed against the receptor. WA17 hybrid cells were highly sensitive to the antiviral action of HuIFN-alpha 2, -alpha (Le) and -beta but were completely insensitive to HuIFN-gamma. Furthermore, 125I-HuIFN-gamma showed specific binding to human WISH cells but not to WA17 hybrid cells or A9 mouse cells. The results indicate that the receptors for HuIFN-alpha and -beta but not for HuIFN-gamma are specified by human chromosome 21. Hybrid cells containing one, two, or three copies of human chromosome 21 were found to be increasingly sensitive to HuIFN-alpha 2, indicating that a chromosome 21-specified component (possibly the HuIFN-alpha receptor) may be a limiting factor in the cellular sensitivity to HuIFN-alpha.

Animals↗
PubMed1984

Receptors for human alpha interferon: are gangliosides involved?

Interferon (IFN) action on cells must begin with an interaction with cellular receptors. Binding and cross-linking experiments reported earlier with purified 125I-labeled recombinant human (Hu) IFN-alpha 2 have revealed that IFN-alpha 2 binds to a specific macromolecular receptor on human cells (Joshi et al., J. Biol. Chem. 257, 13884-13887, 1982). Based on indirect evidence such as neutralization of the antiviral action of IFN preparations by gangliosides and binding of IFNs to gangliosides coupled to solid supports, it has been suggested by various investigators that gangliosides may be a part of the IFN-alpha/beta receptors. Experiments presented here indicate that gangliosides could block the antiviral activity of HuIFN-beta, but not of HuIFN-alpha, although both species of IFN bound strongly to gangliosides coupled to poly-L-lysine-agarose. Furthermore, gangliosides did not inhibit the binding of 125I-labeled HuIFN-alpha 2 to specific receptors on human cells, and this binding was competed out by unlabeled HuIFN-alpha 2 and HuIFN-alpha(LE) which were preincubated with gangliosides. However, the capacity of HuIFN-beta to compete for the receptors was abolished by preincubation with gangliosides. These results were confirmed by cross-linking experiments to identify the IFN-receptor complex by gel electrophoresis. The results indicate that at least in the case of HuIFN-alpha species, the ganglioside binding is apparently not at the active site of the IFN molecules required for interaction with the receptors on the cell surface.

Binding Sites↗
PubMed1982

Interferon action in human fibroblasts: induction of 2', 5'-oligoadenylate synthetase in the absence of detectable protein kinase activity.

In several strains of human fibroblasts, treatment with human alpha- or beta-interferon (IFN) resulted in an induction of 2', 5'-oligoadenylate synthetase but no protein kinase activity. The antiviral and anticellular effects of IFN are elicited in these cells in the absence of detectable IFN-induced protein kinase activity.

2',5'-Oligoadenylate Synthetase↗
PubMed1982

Inhibition of interferon secretion in human fibroblast by vinblastine.

Vinblastine treatment of superinduced human fibroblast (FS-4) cultures strongly inhibited interferon (IFN) secretion and resulted in intracellular accumulation of IFN activity. The cell-associated IFN migrated slower than secreted IFN in sodium dodecyl sulfate-polyacrylamide gel electrophoresis, indicating a larger size. The results suggest the presence of a possible precursor form of mature HuIFN-beta with biological activity.

Cell Line↗