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Biomedical subjects

C E Taylor

Publications and source records attributed to C E Taylor.

At least 109 records · Page 6Linked to original sources
PubMed1984

Immunoglobulin concentrations in nasopharyngeal secretions.

Sequential nasopharyngeal secretions were collected from 36 breast fed and 14 bottle fed babies followed from birth to 7 weeks of age. Secretions free of covert blood contamination were obtained from only 12 breast fed and 5 bottle fed infants aged less than 1 week. In secretions from all bottle fed babies negative for blood contamination and from 8 bottle fed babies positive for blood contamination no IgA was detected by enzyme-linked immunosorbent assay. All secretions contained IgG and four contained IgM. In contrast, IgA could be shown in the nasopharyngeal secretions of 6 of 12 breast fed babies. All breast fed babies had detectable concentrations of IgG and in two, IgM was detectable. By 7 weeks of age all babies had detectable nasal IgA, IgG, and IgM and there were no differences between breast fed and bottle fed babies. At this time IgG concentrations were low in both groups, having halved since birth. The origins of nasopharyngeal IgA and IgG in infant secretions and their possible role in protection against respiratory virus infection is discussed.

Body Fluids↗
PubMed1984

Automated detection of micro-organisms in blood cultures by means of the Malthus Microbiological Growth Analyser.

A prototype Malthus Microbiological Growth Analyser was compared with conventional methods for examining blood cultures in a trial of 651 cultures mostly from patients with haematological malignancy or undergoing haemodialysis or renal transplantation. Of 100 significantly positive cultures, organisms from 82 grew in the conventional aerobic (+ CO2) bottle, 78 in the conventional anaerobic bottle and 71 in the Malthus bottle. The differences were not statistically significant (p greater than 0.05). The Malthus system detected 83.6% of significantly positive cultures earlier than the comparable conventional bottles while 7.3% positive cultures were detected earlier by the conventional system. When use of the Malthus system was restricted to the hours of 09.00 to 17.30 daily 27.3% positive cultures were detected earlier by the Malthus system and 16.4% were detected earlier by the conventional system. One of the organisms which grew in the Malthus bottle, a contaminating Staphylococcus epidermidis, was not detected by the Malthus system. Instability of electrodes resulted in 26.9% false positive cultures with the prototype Malthus system. Contamination rates in both the Malthus and conventional anaerobic bottles were lower than in the aerobic bottles.

Bacteria↗
PubMed1984

Characteristics of amplifier T cells involved in the antibody response to the capsular polysaccharide of type III Streptococcus pneumoniae.

Amplifier T cell activity can be transferred by spleen cells harvested 72 hr after priming with type III pneumococcal polysaccharide (SSS-III) and can be abolished by treating the transferred cells with monoclonal anti-Lyt-1, or anti-Thy-1 antibodies in the presence of complement; thus, amplifier cells represent a distinct subpopulation of T cells. Amplifier T cells were found to be sensitive to irradiation but not to treatment with cyclophosphamide. When amplifier cells were transferred to athymic nude (nu/nu) mice, the enhancement obtained was much greater than that produced in thymus-bearing (nu/+) mice; this is presumably due to the lack of suppressor T cell activity in nu/nu mice that enables amplifier T cell activity to be expressed more fully. Amplifier T cells also were found to be present in peripheral blood; these amplifier T cells were Lyt-2- in phenotype. Although the induction and activation of amplifier T cells appear to be antigen-specific, the product made by amplifier T cells may not be antigen specific in its mode of action. Because amplifier T cells can be induced and activated by exposure to immune B cells, specificity is presumably due in whole or in part to the ability of amplifier T cells to recognize the idiotypic determinants of B cell-associated antibody specific for SSS-III.

Animals↗
PubMed1983

Activation of antigen-specific suppressor T cells by B cells from mice immunized with type III pneumococcal polysaccharide.

The transfer of B lymphocytes from mice immunized with type III pneumococcal polysaccharide (SSS-III) results in antigen-specific suppression of the antibody response of recipients immunized with SSS-III. Such suppression shares many features associated with low-dose paralysis, a phenomenon mediated by suppressor T cells; it reaches maximal levels 3 d after the transfer of viable or irradiated immune B cells and can be eliminated by the depletion of SSS-III-binding cells from spleen cell suspensions before transfer. In a two-step cell transfer experiment, purified T lymphocytes, isolated from recipients previously given immune B cells, caused suppression upon transfer to other mice immunized with SSS-III. Also, B-cell-induced suppression could be abrogated in a competitive manner by the infusion of amplifier T lymphocytes, as was previously demonstrated in the case of low-dose paralysis. These findings suggest that B cell surface components, presumably the idiotypic determinants of cell-associated antibody specific for SSS-III, are instrumental in activating suppressor T cells involved in regulating the magnitude of the antibody response to SSS-III.

Animals↗
PubMed1983

Cyclic expression of low-dose paralysis.

Prior treatment (priming) with a single injection of a subimmunogenic dose of Type III pneumococcal polysaccharide results in an antigen-specific T-cell-dependent form of unresponsiveness (low-dose paralysis) mediated by suppressor T cells. Although such unresponsiveness persists for several months after priming, it is expressed in a cyclic manner with a periodicity of about 3 days. This cyclic pattern is accompanied by concurrent periods of Velban sensitivity that also are cyclic. This suggests that the maintenance of low-dose paralysis in part requires some degree of cell proliferation which proceeds in an ordered manner in response to a "signal" generated after priming with antigen.

Animals↗
PubMed1983

Cell surface antigens and other characteristics of T cells regulating the antibody response to type III pneumococcal polysaccharide.

The administration of a subimmunogenic dose of type III pneumococcal polysaccharide (SSS-III) produces an antigen-specific T cell-dependent phenomenon termed low-dose paralysis (immunologic unresponsiveness). This form of unresponsiveness can be transferred by spleen cells obtained 5 to 24 hr after priming, and the suppressive activity of the transferred cells is abolished by prior treatment with monoclonal anti-Lyt-2 and anti-I-J antibody in the presence of complement, indicating that suppression is mediated by a distinct subset of T cells (suppressor T cells). If primed spleen cells are transferred 24 to 72 hr after immunization with SSS-III, however, the resulting antibody response of immunized recipients is enhanced. Greater enhancement is noted when transferred cells, pretreated with monoclonal anti-Lyt-2 antibody plus complement to remove suppressor T cells, are used; such enhancement is attributed to amplifier T cells. These findings indicate suppressor T cells regulate the antibody response to SSS-III by influencing the expansion of SSS-III-specific clones of B cells as well as the expression of amplifier T cell activity; the latter causes B cells to proliferate further in response to SSS-III.

Animals↗
PubMed1981

In vitro macrophage manifestation of cortisone-induced decrease in resistance to mouse hepatitis virus.

Genetically resistant G3H mice routinely yielded macrophages that were resistant when grown in 90% horse serum. These mice also routinely yielded macrophages that were susceptible to the same virus, MHV (PRI), in vitro after the mice had been treated with three intraperitoneal doses, of hydrocortisone. Dexamethasone and prednisolone when similarly administered also increased the susceptibility of C3H macrophages taken from the treated animal, but progesterone and testosterone did not. In addition, spleen cells from mice treated with cortisone made the resistant C3H macrophages 100 times more susceptible in vitro. Increased in vitro susceptibility induced in this way by hydrocortisone was reversed by exposure to supernatant fluid removed from cultures of concanavalin A-treated spleen cells.

Animals↗
PubMed1981

Hitchhiking and linkage disequilibrium between hemoglobin S and nearby restriction sites.

The association of the hemoglobin S mutation with an unusual 13 kb Hpa I restriction fragment has been reexamined using new data and a stochastic model for linkage disequilibrium. In agreement with earlier analyses with deterministic models, the present-day association of the beta S allele with the 13 kb fragment is lower than would be expected if all beta S alleles carried by American blacks were derived from a unique mutation that occurred in the ancestral Bantu population. However, from the stochastic model, if the effective population size was small for an appreciable period during the time that selection has been operating on HbS, then the confidence limits on the allelic association are very large and a unique West African beta S mutation cannot be ruled out from the two locus data alone.

Base Sequence↗
PubMed1979

Serological response of patients with non-gonococcal urethritis to causative organism of contagious equine metritis 1977.

The presence of allugtinins to the causative organism of contagious equine metritis (C.E.M.) in human serum has been confirmed. Agglutinins were found in the serum of 84 (37.6%) of 223 patients with non-gonococcal urethritis (N.G.U.), and in 12.5% of these patients there was a four-fold or greater rise in titre during the course of their illness. There was no evidence that these agglutinins were the result of infection by chlamydiae or ureaplasmas. Certain patients with these agglutinins seemed to respond better to therapy with antibiotics to which the C.E.M. bacterium is susceptible in vitro than did patients in whom these agglutinins were not found. The findings suggest that the C.E.M. bacterium or a microorganism related to it may be aetiologically involved in a proportion of patients with N.G.U. A search for such an organism in these patients is in progress.

Agglutination Tests↗