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A Vazquez

Publications and source records attributed to A Vazquez.

At least 91 records · Page 5Linked to original sources
PubMed1987

Antigen-induced and polyclonal B-cell responses in human peripheral blood lymphocyte cultures.

This work was designed to delineate the anti-hapten antibody (Ab) response induced by trinitrophenol-polyacrylamide (TNP-PAA) beads from the nonspecific B-cell response which concomitantly occurs in human peripheral blood mononuclear cell (PBMC) cultures. Indeed human PBMC produce consistent amounts of immunoglobulins when cultured at high cell density in the presence of fetal bovine serum, regardless of the presence of antigen. In contrast, the stimulation of such cultures by TNP-PAA leads to an Ab response characterized by the following: cells secreting anti-hapten Ab at a high rate (detected by a plaque-forming cel (PFC) assay); a 10-30 times enhancement in the number of hapten-specific binding cells (detected by a rosette-forming cell (RFC) assay); the production of anti-TNP IgM Ab (detected by an ELISA assay). The anti-TNP response is specifically triggered by the particulate antigen, as shown by the following: The TNP-PAA antigen induces a clear-cut increase in the amount of anti-TNP Ab whereas it only marginally increases that of total IgM. The anti-TNP Ab response is specifically abolished when anti-TNP RFC are depleted from the PBMC preparation before the initiation of the cultures. The anti-TNP Ab response is specifically abolished when PBMC are triggered by TNP-PAA in the concomitant presence of a soluble TNP-protein conjugate. These results demonstrate the ability of polymeric antigens to specifically activate human peripheral blood B cells.

Acrylic Resins↗
PubMed1987

Functional effects of epidermal cell culture supernatants (ECCS) on human B-cell activation.

Epidermal cells (EC) were cultured without stimulation and the effect of these EC culture supernatants (ECCS) on human in vitro B-cell response was determined. Supernatants obtained between Days 5 and 7 were able to replace monocytes in the antibody response to the particulate antigen trinitrophenyl-polyacrylamide (TNP-PAA). These results were obtained when highly monocyte-depleted cultures (less than 0.5% peroxidase-positive cells) were used and were reproduced with supernatants from several different EC cultures. ECCS could not substitute for T cells in the T-dependent response to TNP-PAA. They contained an interleukin 1 (IL-1) activity but no interleukin 2 or B-cell growth factor (BCGF) activities. We tested the effect of ECCS on the proliferative response of highly monocyte-depleted B cells cultured at low cell density costimulated with anti-u antibody and BCGF. ECCS had no BCGF-like activity of its own but did potentiate the effect of BCGF. Thus EC cultures produce IL-1-like factor(s) which act directly on the early stages of B-cell activation.

Antibody Formation↗
PubMed1987

Prevention of adriamycin-induced cardiotoxicity by prenylamine: a pilot double blind study.

Adriamycin (ADM) is an effective antineoplastic drug. However, the amount of ADM that can be administered must be limited because of the risk of developing a severe dose-dependent myocardiopathy. Prenylamine (PNL), a calcium antagonistic drug, provided partial protection against ADM-induced cardiotoxicity in mice and in the rabbit. Thus, it was considered important to evaluate the cardioprotective potential of PNL in patients given ordinary doses of ADM. Twenty-six patients were selected and randomized in two groups, and a double-blind trial was begun. Group A (n = 13): patients received ADM, i.v. at standard oncological doses up to 550 mg/m2, plus placebo, orally. Group B (n = 13): ADM was administered as in Group A, but PNL 200 mg/day was given instead of placebo. Standard ECG and chest radiographs were performed at the beginning of treatment and every two months. Mode-M echocardiograms and 24-hour ambulatory ECGs were obtained previously to the beginning of the ADM treatment and two months after the administration of the last dose of the drug. In Group A, three patients died from oncological causes, total ADM dose was 359 +/- 100 mg/m2, and the mean age was 59.7 years. One patient in this group developed a congestive myocardiopathy while another patient developed a severe supraventricular arrhythmia. In Group B, four patients died from oncological causes, total ADM dose was 367 +/- 132 mg/m2, and the mean age was 63.8 years. No myocardiopathy was found in this group. These findings suggest that simultaneous administration of PNL may mitigate ADM cardiotoxicity, but larger trials are needed to draw definite conclusions.

Aged↗
PubMed1987

A new family with hereditary choreo-acanthocytosis.

We describe a new family with hereditary choreo-acanthocytosis. Two members of this family were affected; neither of them suffered from anaemia or signs of haemolysis. The acanthocytes showed an impaired deformability with an increase in whole blood viscosity. The composition of the plasma and erythrocyte membrane lipids was normal, as was the fatty acid composition of the erythrocyte ghost membranes. The only alteration found was a decrease in the fluidity of the erythrocytic membrane.

Acanthocytes↗
PubMed1987

Functional heterogeneity of B-CLL lymphocytes: dissociated responsiveness to growth factors and distinct requirements for a first activation signal.

We studied the effects of B cell directed growth factors on B lymphocytes from 11 patients with chronic lymphocytic leukemia (B-CLL). B-CLL lymphocytes were costimulated with anti-mu antibody (Ab) and with three growth factor preparations: recombinant IL2, B cell growth factor (BCGF) (20 kiloDalton (kD) BCGF) and a high molecular weight BCGF (50 kD BCGF). IL2 was the more active factor (in six of 11 patients). The effect of IL2 was dependent on a costimulation with anti-mu Ab or occurred independently of anti-mu Ab, according to the patients. This pattern of reactivity did not correlate with the presence or absence of the IL2 receptor (IL2-R) molecule on fresh B-CLL lymphocytes. Five patients responded to the 20 kD BCGF. Although four of them were also strong responders to IL2, one strongly responded to the 20 kD BCGF and did not respond to IL2. Only one patient responded to the 50 kD BCGF. When an anti-IL2-R Ab was introduced into the culture, only the responsiveness to IL2 was abolished: thus both 20 kD and 50 kD BCGFs activate B-CLL lymphocytes independently of the IL2-R. These results show that several B cell directed growth factors can act independently to support the proliferation of B-CLL lymphocytes.

Antigens, Surface↗
PubMed1987

Differential photoabsorption using argon laser radiation on atherosclerotic plaque in non-hemolyzed and hemolyzed blood.

Since argon laser radiation (488 to 514 nm) can vaporize human atherosclerotic plaque, we determined whether different blood media--hemolyzed versus non-hemolyzed blood--can alter photoabsorption of atherosclerotic plaque. Forty cadaveric aortic fibrous plaque samples were fitted onto small vials containing 0.02 ml of either non-hemolyzed blood or hemolyzed blood over the surface of the plaque. The distal end of a 400-mu core diameter quartz fiber was directed onto the surface of the plaque and the proximal end of the fiber was connected to an argon laser. The vaporized area and depth of plaque penetration were measured and the estimated volume of crater formation was derived. Following 2.5, 5, 10 and 20 J of laser energies, vaporized volumes were 0.12, 0.72, 0.97 and 4.09 mm3, respectively, for hemolyzed blood and were 0 (p less than 0.01), 0 (p less than 0.01), 0.92 (NS) and 4.39 mm3 (NS), respectively, for non-hemolyzed blood. Laser radiation destroys red blood cells; the higher the energies, the greater the hemolysis. Thus, different blood media such as hemolyzed and non-hemolyzed blood can alter photoabsorption of atherosclerotic plaque. Low level argon laser absorption upon plaque can occur under hemolyzed blood but not under non-hemolyzed blood. Since higher levels of argon laser energies cause greater lysis of red blood cells, comparable degrees of plaque ablation are observed under either blood medium.

Arteriosclerosis↗
PubMed1986

gp 140, the C3d/EBV receptor (CR2), is phosphorylated upon in vitro activation of human peripheral B lymphocytes.

gp 140, the C3d/EBV receptor (CR2), is a specific marker of human B lymphocytes. Very recent data suggest that CR2 is a membrane site involved in early B cell activation. These properties of CR2 led us to analyze the molecular events associated with gp 140. We analyzed whether in some conditions of B lymphocyte activation, CR2 could be phosphorylated. We have found that when highly enriched peripheral B cells were cultured for 48 h with anti-mu Ab and/or SAC, in order to provide an optimal activating signal, phosphorylation of the CR2 was induced.

B-Lymphocytes↗
PubMed1986

Human B cell activation: selective sensitivity of the early stages to calcium channel-blocking drugs.

The importance of Ca2+ in the early events of lymphocyte activation has been suggested by several studies. We examined the effect of calcium channel-blocking drugs (verapamil and nitrendipine) on the progression of human B cells through their activation cycle. Our results show that these drugs suppress the anti-mu-induced human B cell proliferation and interfere with the early events of the B cell activation in a dose-dependent fashion. This suppression correlates with a marked decrease in anti-mu-induced 45Ca2+ uptake. Calcium channel-blocking drugs inhibit the anti-mu-induced uridine incorporation and the appearance of the activation marker defined by the 4F2 monoclonal antibody. Calcium channel-blocking drugs also inhibit B cell proliferation induced by the costimulation with anti-mu antibody and B cell growth factor (BCGF). However, this inhibition takes place at the early (anti-mu-dependent) stage of B cell activation: the BCGF-dependent proliferation of in vitro anti-mu-activated B cells is only marginally inhibited. Finally the proliferation of Epstein-Barr virus-infected B cell lines is resistant to the effect of calcium channel-blocking drugs.

Antigens↗
PubMed1986

Differentiation factors for human specific B cell response.

Nonspecific T cell factors produced by lectin-activated human peripheral blood lymphocytes (PBL) were used to restore the T-dependent B cell response to trinitrophenyl-polyacrylamide (TNP-PAA). Preincubation experiments with the particulate antigen TNP-PAA and/or a soluble TNP-protein conjugate show that a first specific signal provided by the antigen and nonspecific lymphokines sequentially acts on B cells. By gel filtration the T cell-replacing factor (TRF) activity is present in the 30-15-kDa fraction of T cell supernatants and is associated to interleukin 2 (IL2). However, absorption of IL2 does not abolish the TRF activity. Moreover, chromatofocusing of this 30-15-kDa material allows the obtaining of an IL2-free fraction containing a differentiation factor (with an isoelectric point of 5.7 +/- 0.2). The ability of this fraction to restore the anti-TNP response is manifest in the presence of a 50-kDa B cell growth factor. This latter, prepared by a combination of absorption on concanavalin A-Sepharose and gel filtration, was IL2 free and unable to support the anti-TNP response. We thus directly demonstrate that in the absence of IL2 three separate signals (the antigen, T cell-derived growth and differentiation factors) are involved in human-specific B cell response.

B-Lymphocytes↗
PubMed1986

B cell hyperactivity in systemic lupus erythematosus: selectively enhanced responsiveness to a high molecular weight B cell growth factor.

To characterize B cell hyperactivity in systemic lupus erythematosus (SLE) patients we studied the early events of B cell activation in 14 patients and controls. We measured B cell proliferation induced by three interleukin (IL) preparations (20-kDa B cell growth factor, BCGF, recombinant IL2 and 50-kDa BCGF) in the absence and in the presence of an anti-mu antibody (Ab). SLE B cells exhibited a markedly enhanced proliferative response to the 50-kDa BCGF in the absence of an anti-mu Ab, while responding normally in the presence of a first signal. This pattern of hyperactivity was observed in 11 out of 14 patients tested, and was absent in control patients. In contrast, SLE B cells behaved like normal B cells for the response to the other two IL tested, and to the anti-mu Ab alone. It should be pointed out that SLE B cells responded normally to recombinant IL2 whereas T cells from the same patients exhibited a decreased response to this IL. The selectively enhanced responsiveness of SLE B cells to the 50-kDa BCGF suggests that the events leading to B cell hyperactivity in this disease affect the early stages of B cell activation.

Adult↗
PubMed1986

Different human B cell subsets respond to interleukin 2 and to a high molecular weight B cell growth factor (BCGF).

After activation by anti-mu antibody human B cells acquire the ability to proliferate in the presence of recombinant interleukin 2 (IL 2), a 20-kDa mol. mass B cell growth factor (BCGF) and a high mol. mass BCGF (50-kDa BCGF). An anti-IL 2 receptor (IL 2R) monoclonal antibody inhibits the IL 2-dependent proliferation without affecting that induced by BCGF. B cells expressing the IL 2R after anti-mu antibody activation (IL 2R+ cells) were separated from those not expressing IL 2R (IL 2R- cells). IL 2 stimulated the proliferation of only IL 2R+ cells whereas the 20-kDa BCGF acted on both IL 2R+ and IL 2R- cells. Importantly, the 50-kDa BCGF supported the proliferation of IL 2R- cells whereas it was inactive on IL 2R+ cells. Thus, the B cell subset responding to the 50-kDa BCGF after anti-mu antibody activation is distinct from that responding to IL 2.

Antibodies, Monoclonal↗
PubMed1986

Early events in human B cell activation: metabolic pathways vary according to the first signal used.

The effects of the calcium channel blocking drug Verapamil and of palmitoyl-carnitine (PTC), an inhibitor of protein-kinase C activity, on human B cell activation were measured. Both Verapamil and PTC inhibited the B cell proliferation induced by costimulation with anti-mu antibody and with 3 different growth factors: interleukin 2, 20-kDa B cell growth factor and 50-kDa B cell growth factor. Both uridine and thymidine incorporation induced by costimulation with ionomycin and phorbol 12-myristate 13-acetate (PMA) were inhibited by Verapamil and PTC. In contrast, B cell proliferation was resistant to Verapamil (while being still inhibited by PTC) in two situations: when B cells were costimulated with PMA and growth factors and when B cells previously activated in vitro (by anti-mu antibody or PMA) were stimulated with growth factors. These results confirm that the late stage (G1----S transition) of B cell activation is independent of Ca2+ entry. More importantly, they show that the initial events induced by anti-mu antibody and by PMA are based on different biochemical pathways: PMA would act on a subpopulation of B cells which has already received an early signal of activation in vivo. This emphasizes the functional and biochemical heterogeneity of the G0 stage among circulating B cells.

B-Lymphocytes↗
PubMed1986

Characteristics of monoclonal antibody measurements in human peripheral blood.

Three areas of monoclonal antibody measurements using flow cytometry have been presented. These include a description of a dual immunofluorescent method for measuring two antibodies simultaneously, the effects of blood storage on enumeration of helper (H) and suppressor (S) cells, and the relationship between absolute lymphocyte count and H/S ratio in both control and AIDS patients. These studies reveal that a dual immunofluorescent labeling method is useful for enumerating lymphocytes from peripheral blood which bear the helper, suppressor and/or thymus-derived (T) cell receptors. Fluorescein (FL)-conjugated Leu-3a + 3b antibodies were used to enumerate helper T-lymphocytes, while the B-phycoerythrin (B-PE)-conjugated Leu-2a antibodies were utilized for enumerating suppressor T-lymphocytes. Dual immunofluorescently stained lymphocytes, prepared from whole blood, were analyzed by flow cytometry. Two light scatter parameters, (forward and 90 degree scatter) were used to define the lysed erythrocyte, lymphocyte, monocyte, and granulocyte populations. Only the lymphocytes were analyzed for dual immunofluorescence activity. The helper and suppressor distributions from 167 control patients were as follows: The average percentage +/- SD of the helper and suppressor cells were 42.8 +/- 7.5 and 21.6 +/- 6.4, respectively. The H/S ratio was 2.17 +/- .75. These studies show that the H/S ratio can be determined in a single preparative sample and analyzed by dual immunofluorescence in a single flow cytometric analysis even though the H/S ratio may vary from normal during a disease condition. The dual immunofluorescent assay enables one to correlate the activities of two antibodies against cell surface receptors and allows the measurement of a large number of samples in a minimal time. This study also compared the effects of anticoagulant, storage time, and temperature on the phenotypic determination of the percentages of helper and suppressor T-lymphocytes in human peripheral blood. Blood was drawn in ACD, heparin, and EDTA and stored for up to 4 days at room temperature or 4 degrees C. Phenotypic determination of helper/suppressor lymphocytes was most stable for ACD or heparinized blood at room temperature. Marked changes were observed in the percentages of helper cells at 4 degrees C, whereas the percentages of suppressor cells did not change appreciably regardless of the anticoagulant storage time or temperature. Finally, the relationship between ALC and the H/S ratio in control and AIDS patients was determined. The ALC varied considerably in both control and patient populations as a function of time. Conversely, the H/S ratio remained constant.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1985

Argon laser radiation of human clots: differential photoabsorption in red cell rich and red cell poor clots.

Since argon laser radiation (454-514 nm) can vaporize human clots, we determined whether the absorption of laser energies can differ among different types of blood clots. Thus we performed spectrophotometric studies and examined the ability of this laser to penetrate red cell rich and red cell poor clots. Fifty-four red cell rich and red cell poor clot samples, varying in depth from 1.8 to 5.0 mm, were subjected to 3, 5 and 7 watts from an argon laser beam. At a given power intensity, the deeper the red cell rich clot, the longer was the time needed to penetrate the clot. The higher the power used, the shorter was the red clot penetration time. In contrast, all power levels used up to 5 minutes did not penetrate any of the varying depths of red cell poor clots. Spectrophotometrically, the red cell rich clot had an absorption curve typical of hemoglobin pigment while the red cell poor clot, in the absence of hemoglobin, had poor absorption between 350 and 600 nm and was unable to absorb argon laser energies. Thus, the argon laser provides a therapeutic modality for human red cell rich clot dissolution but the present approach does not appear to be effective against red cell poor clots.

Blood Coagulation↗
PubMed1985

Enhancement of human B cell proliferation by an antibody to the C3d receptor, the gp 140 molecule.

The C3d receptor is a specific marker of B lymphocytes. Recently we have shown that C3d receptor activity is carried by a gp 140 membrane antigen. A polyclonal antibody has been prepared by immunizing a rabbit with highly purified gp 140 molecule isolated from membranes of the human B lymphoblastoid cell line Raji and its high specificity was previously demonstrated. We tested the effect of this antibody to the C3d receptor on the B cell proliferative response. Purified B cells from human blood were induced to proliferate by a B cell growth factor (BCGF)-containing partially purified supernatant from activated T cells. The anti-C3d receptor F(ab')2 enhanced the BCGF-dependent B cell proliferation. This effect was dose dependent, was observed in the presence of different concentrations of BCGF and did not correspond to a change in the time course of the response. The anti-C3d receptor F(ab')2 had no mitogenic effect in the absence of T cell supernatant. In contrast the undigested anti-C3d receptor IgG suppressed the BCGF-dependent B cell proliferation. These results emphasize the potentialities of anti-gp 140 F(ab')2 to explore the involvement of the C3d receptor in the regulation of B cell response to T cell products.

Adjuvants, Immunologic↗
PubMed1985

Suppressor T cell induction by soluble OKT3 antibody does not require cross-linking of the T3 molecule.

The monoclonal antibody OKT3 can induce T suppressor cells of the in vitro antibody response when used at concentrations as low as 10 ng/ml and in cultures containing as few as 4% OKT3-pretreated T cells. These suppressor cells are radioresistant, cyclosporin sensitive and belong to the T4 as well as the T8 subpopulations. In contrast with the mitogenic effect of OKT3 the suppressor activity can be induced and expressed in highly monocyte-depleted cultures. Moreover F(ab')2 fragments of OKT3, although not mitogenic, are able to induce suppressor cells. Thus cross-linking of the T3 molecule (such as that realized when intact OKT3 IgG and monocytes are present) is not required to induce suppressor cells among resting normal T cells.

Antibodies, Monoclonal↗
PubMed1985

Molsidomine in the treatment of acute heart failure.

In this report we present the results of hemodynamic monitoring with a Swan-Ganz balloon catheter in 14 patients with heart failure associated with acute myocardial infarction, before and during 8 hours after a single oral dose of molsidomine (6 mg). Molsidomine induced the following changes: heart rate was reduced between 1.6% and 4.7% (significant at 4 hours, p less than 0.05); systolic blood pressure decreased 8.4% at 1 hour (p less than 0.05); pulmonary capillary pressure decreased approximately 30% (significant and lasting until 8 hours after administration, p less than 0.002); cardiac index did not change significantly, although individual analysis showed an increase in 6 of 12 cases; stroke volume index increased by 6% (significant at 1 hour, p less than 0.025); and left ventricular stroke work index increased from 9.8% to 24.5% (significant at 1 and 4 hours, p less than 0.01 and 0.025). These findings show the beneficial hemodynamic effects of molsidomine in patients with heart failure complicating acute myocardial infarction.

Aged↗