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Biomedical subjects

F Albert

Publications and source records attributed to F Albert.

At least 55 records · Page 3Linked to original sources

Lipid peroxidation is a consequence of elicitor activity.

Elicitor-active preparations from the fungal pathogen of bean Colletotrichum lindemuthianum stimulated the accumulation of products characteristic of lipid peroxidation in treated bean tissues. Bean suspension cells treated with crude and purified elicitors accumulated ;lipofuscin-like pigment' (LEP) and malondialdehyde. The accumulation of LFP after about 6 h of treatment coincided with the onset of visible browning and production of the bean phytoalexins kievitone, phaseollin, and phaseollinisoflavan. The induction of phytoalexins and accumulation of LFP were also triggered by treatments with generators of activated oxygen species, xanthine:xanthine oxidase and Fe:ethylenediaminedi-o-hydroxyphenylacetic acid. These data suggest that generation of active oxygen species may be involved in lipid peroxidation triggered by elicitors.

Journal Article↗

[Serum sickness after fibrinolysis using intravenous streptokinase in myocardial infarction].

A case of serum sickness was observed 7 days after administration of intravenous streptokinase in the acute phase of myocardial infarction. The clinical presentation was the sudden development of fever, a papuloerythematous skin rash, myalgia and polyarthritis accompanied by a severe biological inflammatory syndrome without any signs of bacterial or viral infection. Spontaneous regression was observed within 72 hours. Although this complication of streptokinase fibrinolysis seems to be rare, clinicians should be aware of it and not confuse the allergic reaction with that of another drug, the withdrawal of which could be prejudicial for the patient.

Humans↗

The Effect of Pseudomonas putida Colonization on Root Surface Peroxidase.

Increased activities of peroxidase and indole 3-acetic acid (IAA) oxidase were detected on root surfaces of bean (Phaseolus vulgaris) seedlings colonized with a soil saprophytic bacterium, Pseudomonas putida. IAA oxidase activity increased over 250-fold and peroxidase 8-fold. Enhancement was greater for 6-day-old than for 4- or 8-day-old inoculated plants No IAA oxidase or peroxidase activities were associated with the bacterial cells. Native polyacrylamide gel electrophoresis demonstrated that washes of P. putida-inoculated roots contained two zones of peroxidase activity. Only the more anodic bands were detected in washes from noninoculated roots. Ion exchange and molecular sizing gel chromatography of washes from P. putida-colonized roots separated two fractions of peroxidase activity. One fraction corresponded to the anodic bands detected in washes of P. putida inoculated and in noninoculated roots. A second fraction corresponded to the less anodic zone of peroxidase, which was characteristic of P. putida-inoculated plants. This peroxidase had a higher IAA oxidase to peroxidase ratio than the more anodic, common enzyme. The changes in root surface peroxidases caused by colonization by a saprophytic bacterium are discussed with reference to plant-pathogen interactions.

Journal Article↗

Analysis of T cell activation requirements with the use of alloantigens or an anti-clonotypic monoclonal antibody.

H-2Kb-specific alloreactive cytotoxic T lymphocyte (CTL) clones, which secrete macrophage-activating factor (MAF) in response to antigen, were used to study the antigenic and physiologic parameters for T cell-antigen receptor (Ti)-mediated activation. When H-2Kb was presented on untreated, formaldehyde (FOR)-fixed cells, or liposomes, optimal stimulation in the absence of co-factors was obtained only with the untreated cells. FOR cells, which were efficient inhibitors of CTL-target cell interactions for the CTL clones studied, had a greatly reduced activating capacity. Phorbol myristic acetate (PMA), which alone had no activating effect on the CTL clones, acted in synergy with FOR cells, restoring an unimpaired H-2Kb-dependent activation for some CTL clones. H-2Kb-liposomes were not stimulatory even in the presence of PMA and/or splenic feeder cells. For one H-2Kb-specific CTL clone (KB5-C20), activation was studied with the use of an anti-clonotypic (anti-Ti) monoclonal antibody (mAb), Désiré-1. By using this immunoglobulin (Ig) G2a mAb or its F(ab')2 or Fab fragments, it was observed that the association constant of the IgG2a (4.7 X 10(9) M-1) for KB5-C20 was 30-fold higher than that of the Fab fragment, whereas the molar concentration of mAb required to inhibit 50% of the H-2Kb-specific CTL activity of clone KB5-C20 was 70-fold to 90-fold higher for the Fab fragment than for the IgG2a (1 to 5 X 10(-10) M). It was also observed that activation as measured by MAF secretion of clone KB5-C20 was obtained by using the divalent IgG2a mAb or its F(ab')2 fragment at 10(-9) M to 10(-8) M in the absence of any added co-factor or feeder cells, whereas a 500-fold higher molar concentration of the Fab fragment only induced very low levels of MAF secretion. Also, in the presence of PMA, the mAb-mediated activation of MAF secretion by clone KB5-C20 was increased, but Fab-induced activation never resulted in high titers of MAF. We conclude that the intrinsic "affinity" of the H-2Kb-Ti interaction is probably so low for the Ti of clone KB5-C20 that efficient activation by H-2Kb is obtained only when multivalency is achieved on H-2Kb-expressing cells, and possibly when molecules on the T cells such as Lyt-2 and LFA-1 stabilize the interactions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Calcium ionophore plus phorbol ester can substitute for antigen in the induction of cytolytic T lymphocytes from specifically primed precursors.

Previous studies indicated that Ca++ ionophores and phorbol esters in synergy could substitute for the initial activation step of normal T lymphocytes or T cell clones leading to increased expression of receptors for the growth factor interleukin 2 (IL 2) and secretion of interleukins, with the mitogenic signal for T cell proliferation being dependent on the presence of IL 2. In this study, the question was addressed as to whether T lymphocytes activated through the Ca++ ionophore ionomycin and the phorbol ester 12-o-tetradecanoyl phorbol 3-acetate (TPA) also acquired the competence to kill relevant target cells. The results indicate that T lymphocytes from primed mice proliferate and lyse the relevant allogeneic target cells after in vitro stimulation with ionomycin plus TPA, and that T lymphocyte preparations enriched for a subpopulation bearing the Lyt-2 marker are dependent on exogeneous sources of IL 2 to proliferate and become competent killer cells, whereas preparations enriched for subpopulations bearing the L3T4 marker grow independently of exogenous IL 2.

Animals↗

Distinction between antigen receptor and IL 2 receptor triggering events in the activation of alloreactive T cell clones with calcium ionophore and phorbol ester.

A previous study indicated that Ca++ ionophores in conjunction with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) could induce normal T lymphocytes to express receptors for the T cell growth factor, interleukin 2 (IL 2), to secrete IL 2, and to proliferate (1). Here we used long-term alloreactive Lyt-2+ cytotoxic or T4+ "helper" T cell clones. In response to their specific alloantigen, all of the clones secreted IFN-gamma but only the T4+ clone secreted IL 2 and proliferated in response to the appropriate alloantigen in the absence of exogenous IL 2. The Ca++ ionophore ionomycin and TPA, used in conjunction, mimicked the effect of specific alloantigen on these T cell clones, i.e., they induced the secretion of IFN-gamma in all clones and the secretion of IL 2 in the T4+ clone. In the absence of exogenous IL 2, a proliferative response was induced only for the IL 2 secreting clone. Increased sensitivity to exogenous IL 2 for some T cell clones was also observed after either alloantigen or ionomycin and TPA treatment; this could be correlated with an increase in the expression of IL 2 receptors 6 hr after a pulse with ionomycin and TPA. These results suggest that, for a given T cell clone, activation of the Ca++ -dependent protein kinase c can replace the antigen-receptor triggering events leading to interleukin secretion and increased expression of IL 2 receptors but cannot substitute for the IL 2 dependent triggering of the IL 2 receptor.

Animals↗

[Diffusion of tetroxoprim and sulfadiazine in the cerebrospinal fluid of neurosurgery patients].

Two studies were conducted in neurosurgical patients to establish cerebrospinal fluid (CSF) and plasma levels of tetroxoprim (TXP) and sulphadiazine (SDZ) following the oral administration of co-tetroxazin in a standard dosage regimen. Both TXP (0,62-0,42 micrograms/ml) and SDZ (2,5-4,5 micrograms/ml) adequately penetrated into the CSF, resulting in concentrations above the MICs for most relevant pathogens. In relation to the respective plasma levels and under steady state conditions, CSF-availability is 37,5% for TXP and 31,8% for SDZ.

Adolescent↗

Interaction between MHC-encoded products and cloned T cells. II. Analyses of physiological requirements indicate two different pathways of stimulation by class I alloantigens.

The interaction between class I major histocompatibility complex (MHC) products and T cells was studied using H-2Kb-specific alloreactive T-cell lines and clones obtained by repeated in vitro stimulation with allogeneic cells. Induction of proliferation of these T cells appeared to involve two signals: the H-2Kb alloantigen and interleukins. Immunopurified liposome-inserted H-2Kb, which stimulates specific secondary in vitro cytotoxic T lymphocyte (CTL) responses, could not replace cell-associated H-2Kb in the stimulation of these T-cell lines, even in the presence of feeder cells and interleukins. When T-cell lines were initiated in vitro and repeatedly stimulated with H-2Kb liposomes and feeder cells, it was possible to obtain T cells that could proliferate in response to H-2Kb liposomes in the presence of feeder cells and interleukin-2-containing supernatants or on H-2Kb-expressing cells. Only stimulation with cells permitted maintenance of these T cells in culture for more than 12 weeks. Analyses of cell surface markers and of patterns of inhibition of proliferation by monoclonal antibodies (mAb) of T-cell lines induced in vitro with cell- or liposome-associated H-2Kb indicated that T-cell stimulation by class I antigen can occur in at least two ways. In the first, the H-2Kb-induced proliferation of Lyt-1- Lyt-2+ T4- T cells is inhibited by H-2Kb- and by Lyt-2-specific mAb, but not by Ia or T4-specific mAb. In the second, both Lyt-2+ and T4+ T cells are involved and the H-2Kb-induced proliferation is inhibited by H-2Kb- and Lyt-2-specific mAb and by Ia- and T4-specific mAb.

Animals↗

Immunopurification and insertion into liposomes of native and mutant H-2Kb: quantification by solid phase radioimmunoassay.

To study the interaction between T cells and isolated H-2Kb, we developed protocols for the immunopurification of the molecule from monoclonal anti-H-2Kb immunoadsorbent columns and for its insertion in lipid vesicles. Patterns of reactivity of two anti-H-2Kb monoclonal antibodies (mAb) (20-8-4 and Y3) on H-2 recombinant and H-2Kb mutant mice indicated that mAb Y3 reacted with all six mutant forms of H-2Kb tested. Binding competition studies indicated that Y3 and 20-8-4 recognized distinct epitopes of H-2Kb. A solid phase radioimmunoassay was established using these two mAb to monitor H-2Kb activity in detergent containing cell lysates, after immunopurification, and after insertion into liposomes. About 70% of H-2Kb activity could be eluted from anti-H-2Kb-immunoadsorbents in the presence of 3 M NH4SCN and octyl glucoside (pH 7.4). A procedure of liposome formation combining gel dilution and dialysis yielded liposomes bearing H-2Kb molecules which could inhibit antibody plus complement cytolysis and could stimulate in vivo primed T cells to generate cytotoxic T lymphocytes in vitro. The present protocol can be extended to immunopurify and obtain H-2Kbm1 bearing liposomes.

Animals↗

I region-restricted T cell line stimulated with hapten-treated syngeneic cells: selection of clones with reactivity for both allogeneic Ia determinants and self-I-A plus hapten.

The apparent switch in proliferative T cell reactivity which occurred in a B10 T cell line (B10(T4)) repeatedly stimulated with trinitrobenzene sulfonic acid (hapten)-treated syngeneic cells is described. This functionally heterogenous T cell population, apparently depleted of alloreactivity and strictly dependent on cells expressing syngeneic I-A and the hapten for its propagation, lost, after its 10th restimulation, the previously detected T cell functions, and expressed a new pattern of proliferative reactivity; this pattern included reactivity to self-I-A plus hapten as well as to untreated stimulating cells expressing certain allogeneic determinants. Analysis of reactivity of B10(T4) cells grown under limiting dilution conditions and of five clones of cells derived from B10(T4) indicated that the same T cells were reactive to both self-I-A plus hapten, and to a public I-A-mapped alloantigen possibly related to the serologically defined Ia.5 specificity.

Animals↗

Interactions between MHC-encoded products and cloned T-cells. I. Fine specificity of induction of proliferation and lysis.

To study the interactions between T cells and class I MHC products, we developed in vitro a T-cell line reactive to H-2Kb stimulating cells and derived T-cell clones from it. Although the T-cell line could proliferate in the absence of exogeneous T-cell growth factors when stimulated with H-2Kb spleen cells, each of the derived T-cell clones required both H-2Kb stimulating cells and an external source of T-cell growth factor for its propagation. Each of the T-cell clones was also cytolytic for H-2Kb target cells. Such T-cell clones allowed the comparison of the antigenic requirements for proliferation and cytolysis. By using H-2Kb mutant mice, we found that while the original anti-H-2Kb T-cell line reacted with each of the six mutants tested, the individual T-cell clones could be distinguished in terms of their reactivity pattern. Similar fine specificity patterns were found when H-2Kb mutant cells were used as stimulating or target cells for any given T-cell clone. Each of the three monoclonal H-2Kb-specific antibodies reacting with different epitopes of the H-2Kb molecule totally inhibited H-2Kb-induced proliferation and lysis by the T-cell clones. Further blocking studies involved use of Fab antibody fragments and definition of their reactivity on cells from the H-2Kb mutants. We concluded that: (1) blocking with a monoclonal antibody does not prove identity of alloantigens recognized by the T-cells and the antibody; (2) a monoclonal antibody could either block or not block H-2Kb-CTL interactions depending on structural variations of the H-2Kb molecule not affecting the CTL-H-2Kb functional interaction; (3) blocking one type of H-2Kb-T-cell interaction (induction of proliferation) always affects the other type (cytolysis).

Animals↗

[CT findings in cerebellar hemangioblastomas (author's transl)].

The computed tomographic (CT) findings in 16 personal cases of cerebellar hemangioblastomas are presented. According to other reports in the literature, three-quarters of the tumours were cystic, containing a small mural nodule, whereas the others were predominantly solid. By CT scan the cystic tumours were always identified as roundish or oval space-occupying lesions, sharply demarcated from the surrounding tissue. The solid portion of these tumours, projecting into the cystic part, was delineated more precisely by contrast enhancement, but sometimes escaped identification. On the contrary, even after contrast enhancement the predominantly solid tumours could not be clearly identified as hemangioblastomas. Calcification could not be demonstrated. Additional angiographic investigations were imperative in order to establish the diagnosis, besides visualizing further hypervascular nodules of hemangioblastoma, which CT scanning failed to reveal.

Cerebellar Neoplasms↗

Antigenic and genetic parameters in the stimulation and in the lytic phases of anti-hapten + self cytotoxic T cells and their derived clones: role of the T helper cell.

Requirements for stimulation of cytotoxic T cells (CTL) and for their lytic recognition have been compared in T cell lines repeatedly stimulated with trinitrobenzene sulfonate-treated syngeneic murine spleen cells. Differences were observed between the requirements for cells to stimulate or to be lysed by the CTL, which included: (a) the expression of major histocompatibility complex (MHC = H-2) encoded allelic products, and (b) the hapten density. Propagation of the CTL within the line required I-A intra-H-2 homology between hapten-treated stimulation cells and the line cells, whereas the lytic interaction required H-2K region homology between hapten-treated target cells and CTL. The hapten density requirement was analyzed for a responder (H-2k) and a non-responder (H-2b) strain to low hapten density modified syngeneic cells. This property was found to be a characteristic of the lytic phase rather than of the stimulation of CTL. CTL clones could be derived by growing the line cells under conditions of limiting dilution in the presence ot T cell growth factors. Such CTL clones were unable to be stimulated by their target antigens and were dependent on T cell growth factors for their propagation. These results are discussed in terms of the dependence of the development and growth of CTL on T helper cells.

Animals↗