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W Brooks

Publications and source records attributed to W Brooks.

33 records · Page 2Linked to original sources
PubMed1993

Inhibition of anti-CD3 monoclonal antibody-induced T-cell proliferation and interleukin-2 secretion by physiologic combinations of dexamethasone and prostaglandin E2.

1. The purpose of these studies was to characterize further previous observations from our laboratory indicating that physiologic concentrations of dexamethasone (DEX) and prostaglandin E2 (PGE2) added together result in synergistic inhibition of the proliferative response of T cells stimulated via the T-cell receptor CD3 signaling complex (TCR/CD3). 2. Various physiologic concentrations of DEX and PGE2 were added to T cells stimulated with immobilized anti-CD3 monoclonal antibody (mAb) and cultured at optimal and suboptimal cell densities. The results demonstrate that the proliferative response of anti-CD3 mAb-stimulated T cells cultured at a suboptimal cell density is more suppressed than that of T cells cultured at optimal concentrations. 3. The proliferative response of CD4+ T cells to immobilized anti-CD3 mAb was also determined in the presence of PGE2 and DEX. The data indicate that the CD4+ subset of T cells is more sensitive to the synergistic antiproliferative effects of DEX and PGE2 compared to whole T-cell populations. 4. Various concentrations of DEX and/or PGE2 were added to T cells stimulated with anti-CD3 mAb and the secretion of interleukin-2 (IL-2) was determined. The results demonstrate that concentrations of DEX and PGE2 which individually do not significantly suppress IL-2 synthesis act together to inhibit the synthesis of IL-2 synergistically. 5. The addition of an exogenous source of recombinant IL-2 (rIL-2) to T cells stimulated in the presence of DEX and PGE2 completely reversed the synergistic antiproliferative effect of these two compounds. This reversal was even more pronounced with T cells cultured at a suboptimal cell density. Additionally, PGE2 and DEX did not affect expression of the IL-2 receptor (IL-2R), as measured by upregulation of the alpha chain, on anti-CD3 mAb stimulated T cells. 6. Collectively these data indicate that physiologic concentrations of PGE2 and DEX, which alone have no effect on anti-CD3 mAb-induced T-cell proliferation, act synergistically to inhibit T-cell proliferation as well as IL-2 synthesis.

Antibodies, Monoclonal↗
PubMed1993

Blood flow measurement by Doppler ultrasound: a question of angles.

Ultrasound Doppler equipment is widely used to estimate blood velocity and volume flow. Recently there has been correspondence concerning the origin of the Doppler shift in blood vessels. The assumption that only the movement of the target need be considered is challenged by the observation that Doppler shifts occur where there is relative motion. In blood there is unlikely to be relative motion between a reflecting blood corpuscle and its supporting plasma. In the simple case of plug flow the relative movement takes place at the vessel wall. An investigation is described which uses a flow rig Doppler phantom to assess what effect, if any, this phenomenon would have on Doppler shift results obtained by insonating a vessel such as the aortic arch and range gating through a curved section where flow velocity gradients are encountered. It has been assumed that if the sample volume were to lie in that part of the vessel in which the blood velocity vector were directly towards the probe, then an angle of 0 degrees could be assumed for calculations using the Doppler equation. Our results indicate that the observed Doppler shifts lie midway between those expected if the shift were to occur solely at the first moving fluid boundary and those originating only from scatterers within the sample volume.

Blood Circulation↗
PubMed1992

Inhibition of anti-CD3 monoclonal antibody-induced T-cell proliferation by dexamethasone, isoproterenol, or prostaglandin E2 either alone or in combination.

1. The purpose of these studies was to investigate the modulation of the proliferation of human T cells obtained from peripheral blood by dexamethasone (DEX), isoproterenol (ISO), and prostaglandin E2 (PGE2). The former two substances interact with T cells via the glucocorticoid and beta-adrenergic receptors respectively. When occupied by their natural ligands, glucocorticosteroids and catecholamines, these receptors have a role in modulating T-cell function during stress. During the inflammatory response increased levels of PGE2 bind to their receptors on T cells and thus alter responsiveness. Proliferation of T cells was induced by immobilized anti-CD3 monoclonal antibody (mAb) in the presence or absence of an additional costimulatory signal delivered by anti-CD28 mAb. 2. Various physiologic concentrations of DEX, ISO, or PGE2 were added at the time of initiation of the cultures and subsequent proliferation of the unstimulated T cells was determined. The results demonstrate that physiologic concentrations of all three of these agents inhibit the anti-CD3 mAb-induced proliferation of T cells. 3. Although DEX and PGE2 were equipotent in suppressing T-cell proliferation, ISO was much less effective. 4. Because concomitant elevations in the peripheral levels of these substances may occur, experiments were performed to determine the T-cell inhibitory effects of DEX together with either PGE2 or ISO. Synergistic suppression of T-cell proliferation was observed when various concentrations of DEX and PGE2, but not DEX and ISO, were added to cultures. This synergistic suppression could not be explained by an increase in cAMP accumulation in T cells stimulated with DEX and PGE2. 5. Finally, the addition of anti-CD28 mAb to anti-CD3 mAb-stimulated T cells overcame much of the suppression of proliferation induced by PGE2 or ISO but less so than that induced by DEX.

Antibodies, Monoclonal↗
PubMed1991

Modulation of T-cell function by gliomas.

Patients with primary intracranial tumors (gliomas) exhibit a profound decrease in immunity, the mechanism of which has, until recently, remained obscure. Here Thomas Roszman, Lucinda Elliott and William Brooks reveal that T cells obtained from these patients exhibit defects in interleukin 2 secretion and in expression of the high-affinity IL-2 receptor and they discuss the role played by immunosuppressive factors produced by gliomas in inducing these defects.

Brain Neoplasms↗
PubMed1991

Ganciclovir.

Explore the source record for details and available documents.

Cytomegalovirus Infections↗
PubMed1991

Evaluation of an enzyme membrane immunoassay (Directigen RSV) for the rapid diagnosis of respiratory syncytial virus infections.

A rapid enzyme immunoassay (EIA) membrane test, the Directigen respiratory syncytial virus (Becton Dickinson), was compared with cell culture, an indirect immunofluorescence (IF) test, the Monofluokit respiratory syncytial virus (Diagnostics Pasteur), and a conventional enzyme immunoassay antigen test, the Abbott respiratory syncytial virus enzyme immunoassay in nasal aspirates specimens from children with suspected respiratory syncytial virus (RSV) bronchiolitis. The sensibility and specificity of the Directigen, respiratory syncytial virus were 91% and 98% respectively, as compared with those of culture, and of 93% and 86% as compared with the Monofluokit respiratory syncytial virus. In the comparison of the two enzyme immunoassays, Directigen respiratory syncytial virus detected more positive specimens: 68/127 than the other: 46/127. Directigen respiratory syncytial virus is a very rapid test, (15-min), sensitive and specific, which can be used as an alternative technique for detection of respiratory syncytial virus in nasal samples when viral isolation or immunofluorescence direct are not available.

Cells, Cultured↗
PubMed1987

Role of interleukin-2 (IL-2) and IL-2 receptor expression in the proliferative defect observed in mitogen-stimulated lymphocytes from patients with gliomas.

Patients with primary malignant brain tumors manifest, as previously demonstrated, a variety of abnormalities in cell-mediated and humoral immunity. Diminished lymphocyte reactivity has been recently shown in these patients to be linked to deficiencies in interleukin-2 (IL-2) production. In the present study, this observation was expanded by demonstrating that exogenous purified or recombinant IL-2 does not improve the mitogen responsiveness of lymphocytes obtained from these patients. Studies were also conducted to determine the percentage of IL-2-receptor-positive cells at various times after phytohemagglutinin stimulation with the use of anti-TAC monoclonal antibody. The results demonstrated that the number of lymphocytes induced to express receptors for IL-2 was reduced as compared to normal values. These cumulative data therefore suggest that the failure of mitogen to induce blastogenesis in lymphocytes from patients with malignant gliomas results from intrinsic deficiencies in potentially responsive cells, which are expressed in the early phase of the cell cycle.

Adolescent↗