Biomedical subjects

J B McLaughlin

Publications and source records attributed to J B McLaughlin.

5 recordsLinked to original sources

PubMed2004

Comments on "Bubble motion in aqueous surfactant solutions".

The numerical simulations of bubble motion in dilute surfactant solutions reported previously by two of the authors contained a serious numerical inaccuracy. In agreement with experiments, single bubbles released from rest were predicted to reach a maximum speed before slowing to a terminal speed. However, subsequent experiments demonstrated that, in the simulations, the bubbles reached their terminal speed too quickly. The source of the discrepancy is an inaccuracy associated with the numerical algorithm used to solve the surfactant transport equation on the bubble surface. After correcting the problem, the simulations agree much better with the experiments.

Letter↗

PubMed1988

Activation and proliferation signals in mouse B cells. IX. Protein kinase C activators synergize with non-mitogenic anti-immunoglobulin antibodies to drive B cells into G1.

Intact (IgG) rabbit anti-Ig antibodies, unlike F(ab')2 fragments, do not induce DNA synthesis in murine B cells. The F(ab')2 antibodies induce prolonged breakdown of phosphatidylinositol bisphosphate, and hence activation of protein kinase C (PKC) in B cells, whilst the non-mitogenic antibodies stimulate an abortive response. In order to investigate the role of PKC in B-cell activation, the cells were cultured with combinations of F(ab')2 or intact anti-Ig together with the PKC-activating phorbol esters PDB or PMA. Both these agents synergized with intact anti-Ig to drive resting B cells into the G1 phase of the cell cycle. This is in line with the concept that intact anti-Ig does not induce substantial cell cycle progression in B cells because it fails to cause sufficient activation of PKC. The Ca2+ signal generated by this ligand is apparently sufficient to synergize with PKC activation by phorbol esters to induce B cells to progress into G1. However, the combination of phorbol esters with either form of anti-Ig failed to stimulate B cells to synthesize DNA. This probably reflects the capacity of these agents to inhibit DNA synthesis stimulated by F(ab')2 anti-Ig.

Animals↗

PubMed1987

Effects of hyperthermia, irradiation, and cytotoxic drugs on fluorescein isothiocyanate staining intensity for flow cytofluorometry.

Measurement of fluorescein isothiocyanate (FITC) staining intensity of cultured lymphoblastoid cells following hyperthermia showed large increases without concomitant increases in nuclear protein. Similar measurements of cells following incubation with cytotoxic drugs showed fluorescent intensity increases that exceeded the increases in nuclear protein that were due to the cell cycle blocking action of the drug. The reverse, however, was true for cells following irradiation. In contrast, FITC staining intensity and nuclear protein measurements of cells proceeding through the cell cycle after removal of the cycle blocking agent showed nearly parallel changes, although there were reproducible minor differences, especially following blocking with hydroxyurea. These results suggest that FITC staining intensity is a function not only of nuclear protein content but also of stain access to the reaction sites of the protein constituents of the chromatin. Thus, it is possible that FITC staining may be used as a probe of changes in chromatin structure following experimental manipulation of cells in vitro or treatment of tumors in vivo.

Antineoplastic Agents↗

PubMed1987

B-cell-stimulatory factor 1 reverses Fc receptor-mediated inhibition of B-lymphocyte activation.

Intact (IgG class) rabbit anti-immunoglobulin antibodies are not mitogenic for mouse B cells but inhibit proliferation induced by F(ab')2 anti-Fab fragment antibodies (anti-Ig). In addition, cross-linkage of Fc and surface immunoglobulin receptors on B cells by intact anti-Ig inhibits inositol phospholipid breakdown (but not Ca2+ flux) resulting from ligation of antigen receptors. This system, therefore, provides a polyclonal model for B-cell inactivation by antigen-antibody complexes. T-cell-derived B-cell-stimulatory factor 1 acts synergistically with submitogenic concentrations of F(ab')2 anti-Ig to induce B-cell proliferation. We show here that B-cell-stimulatory factor 1 and intact anti-Ig also induce B cells to synthesize DNA. However, B-cell-stimulatory factor 1 does not induce inositol phospholipid breakdown, does not mobilize Ca2+ in B cells, nor does it influence the magnitude of these responses provoked by intact anti-Ig.

Animals↗

PubMed1984

Relationship between cell ploidy and glucocorticoid induced death in human lymphoid cell lines.

We have found a relationship between sensitivity to glucocorticoid induced cell death (at 10 microM glucocorticoid) and ploidy in the human lymphoid cell line CCRF/CEM-C7. Most sensitive clones are diploid, whilst resistant clones and the resistant parent line CCRF/CEM are tetraploid. Diploid sensitive clones have a tendency to become aneuploid within a few months of isolation, with alterations in their kinetic responses to glucocorticoids. This is followed by a doubling in DNA content which results in reversion to the tetraploid glucocorticoid resistant state of the parent line CCRF/CEM. A few sensitive clones have been found to be tetraploid but with different kinetic responses to glucocorticoids as compared to diploid clones. The principal difference being an extended lag period (48-72 h) prior to lethal response. The relationship between ploidy and glucocorticoid sensitivity does not appear to extend to other human lymphoid cell lines.

Cell Line↗