PubMed Health⌕ Search

Biomedical subjects

A Grieder

Publications and source records attributed to A Grieder.

At least 19 recordsLinked to original sources
PubMed1990

Effect of salmon calcitonin on the infiltration of T lymphocytes in a synovium-like membrane of a rat inflammatory model.

The effect of salmon calcitonin (SCT) on the number of T lymphocytes accumulating in air pouch lining membranes produced on the back of Wistar rats was studied. SCT was given from day 0 through day seven following the air cavitation by daily injections of 2.5-20 micrograms/kg directly into the air cavity. Compared with saline controls, treatment with SCT caused a clear reduction in percentage of T lymphocytes, T helper cells and T non-helper subset in the synovial-like air pouch lining as revealed by FITC-labeled monoclonal antibodies and quantified by flow cytophotometric measurements. This effect may be due to a reduction in local vascular permeability caused by SCT.

Air↗
PubMed1989

The geriatric patient: one- or two-visit complete denture construction technique. Part 1.

The next two articles will discuss the construction of quality complete dentures in one- or two-patient appointments. Material and techniques are presented for controlling costs by reducing laboratory expenses and dentist chair time. A block unit of 12 to 14 attached flat plane acrylic teeth, light cured denture base materials and modified techniques which incorporate multiple procedures are introduced. The procedure will be divided into two segments and described in two articles. The initial article will carry the technique through the completion of the maxillo-mandibular relations and articulation for the casts. The second section, described in the second article, will encompass the set-up of the teeth, try-in of the set-up, processing of the dentures and insertion of the case.

Aged↗
PubMed1986

Microscopic and flow cytophotometric analysis of parasitemia in cultures of Plasmodium falciparum vitally stained with Hoechst 33342--application to studies of antimalarial agents.

Conditions for rapid vital staining of Plasmodium falciparum infected human erythrocytes were 1 microgram/ml of the dye Hoechst 33342 for 15 min in the standard culture medium at 37 degrees C. Fixed and stained cultures were analyzed by fluorescence microscopy and flow cytophotometry. The usefulness of this type of analysis for in vitro studies of antimalarial agents was demonstrated using three such agents--cyclosporin A, chloroquine, and pyrimethamine.

Antimalarials↗
PubMed1986

Prolactin as a modulator of lymphocyte responsiveness provides a possible mechanism of action for cyclosporine.

Lymphocyte responsiveness in rats was found to depend on serum prolactin levels. Blocking pituitary prolactin release with bromocriptine severely reduces lymphocyte reactivity in vitro (mixed lymphocyte reaction) as well as in vivo (graft-versus-host reaction). In addition, evidence for a prolactin/growth hormone-related mRNA species produced in mitogen- and antigen-stimulated lymphocytes has been obtained. Prolactin was shown to compete in a dose-dependent fashion with the immunosuppressant cyclosporine (cyclosporin A) for a common binding site on the surface of T lymphocytes. Further, stimulation of prolactin secretion reversed the immunosuppression induced by cyclosporine. We conclude that prolactin is involved in the maintenance of T-cell immunocompetence and that the immunosuppressive effects of cyclosporine may be mediated by the displacement of prolactin from binding sites on lymphocytes.

Animals↗
PubMed1985

Reciprocal biological activities of the cyclic tetrapeptides chlamydocin and HC-toxin.

Chlamydocin, a potent cytostatic agent against cultured mammalian cells, and HC-toxin, a host-specific phytotoxin, are cyclic tetrapeptides containing the same epoxide alpha-amino acid. We show here that these compounds have reciprocal biological activity; HC-toxin is cytostatic against cultured mastocytoma cells, and chlamydocin has host-specific toxin activity against maize. Chlamydocin and another related cyclic peptide, Cyl-2, are less host-specific than HC-toxin because maize tolerant to HC-toxin is more sensitive to chlamydocin and Cyl-2.

Animals↗
PubMed1985

Interference of cyclosporin with lymphocyte proliferation: effects on mitochondria and lysosomes of cyclosporin-sensitive or -resistant cell clones.

Cyclosporin was previously shown to interfere with--but not to abolish--the increased activities of lysosomes and mitochondria consequent to a mitogenic activation of normal mouse lymphocytes. This was evident from the fluorescence profiles of cell populations after vital staining with euchrysine (giving a lysosomal-specific red fluorescence) and rhodamine-123 (giving a mitochondrial-specific green fluorescence). Fluorescence profiles of the population of cells not exposed to a mitogen were also altered by cyclosporin, with lower lysosomal and mitochondrial fluorescence of these cell populations. In order to find out more precisely what could be the direct effects of cyclosporin on those cellular organelles, our cyclosporin-sensitive (BE7) and cyclosporin-resistant (LB7) lymphoblastoid cell lines were tested and showed clear-cut differences. Only minor effects could be detected for the lysosomal and mitochondrial activities of the resistant cells. On the contrary, cyclosporin caused, in the cells of the sensitive clone BE7, a clear decrease of mitochondrial activity together with an unexpected increase of the red fluorescence of euchrysine. The latter might not correspond to a real increase of the lysosomal activity of such cells. Indeed electron microscopy studies do not show higher numbers of lysosomes; rather they show that numerous vacuoles appear in the cytoplasm of the cyclosporin-treated BE7 cells (but not in the cells of the resistant clone and not in untreated cells of either types).

Animals↗
PubMed1984

Interference of cyclosporin with lymphocyte activation: blockage of the mitogen-induced increases of lysosomal and mitochondrial activities.

Mouse lymphocytes were activated by a mitogenic dose of concanavalin A and analysed by flow cytometry to monitor the increases of mitochondrial activity (using rhodamine 123 as probe) and of lysosomal activity (using euchrysin [acridine orange] as probe). Cyclosporin A-treated lymphocytes were not capable of responding to concanavalin A in the same way as untreated lymphocytes: both the increased uptakes of rhodamine 123 by mitochondria and of acridine orange by lysosomes were strongly diminished, though not abolished. Cyclosporin may thus interfere at a step of activation prior or concurrent to those early changes of lymphocyte physiology. It looks like that it allows mitogen-activated cells to go through part of the mitochondrial maturation which precedes initiation of nuclear DNA synthesis, after which the cells remain blocked at that incomplete maturation level.

Acridine Orange↗
PubMed1981

Involvement of cyclic AMP in the regulations of lymphokine induced glia cell stimulation.

T and B lymphocytes of human or murine origin were found to secrete a factor which increases the DNA and RNA synthesis of cultured glia cells. This factor, termed glia cell stimulating factor (GSF), is released upon stimulation of such immune cells by mitogen or antigen qualifying it as a lymphokine. In this communication we report on the role of cyclic AMP (cAMP) in regulating the effect of GSF on glia cells. Prostaglandin E1 (PGE1), isoproterenol and theophylline were effective in suppressing the GSF-induced increase of the glia cell proliferation. No inhibition of DNA synthesis and no decrease in cell number was observed when testing these substances on glia cells not being activated by GSF. The drugs were found to induce an increase in cAMP concentrations of glia cells. A partial desensitization of the glia cells to these drug induced elevations of cAMP was detected after pretreatment of the glia cell cultures with GSF. It is suggested that stimulated lymphocytes not only release GSF but also low molecular weight proteins such as PGE1 which regulate the effects of GSF on glia cells by activating their adenylate cyclase.

Alprostadil↗
PubMed1981

Glia cell response to bacterial lipopolysaccharide: effect on nucleotide synthesis, its genetic control and definition of the active principle.

Cell types sensitive to lipopolysaccharides (LPS) include macrophages, polymorphonuclear leukocytes, platelets, B-lymphocytes and fibroblasts. Earlier observations that during endotoxemia or intracerebral injection of LPS morphological and functional alterations of the central nervous system develop, suggest that LPS may also interact with brain cells. The effects of bacterial products on nucleotide synthesis of cultured murine glia cells are examined in this study. LPS extracted from the outer cell wall of gram-negative bacteria were found to cause an increased RNA synthesis and an inhibition of DNA synthesis in the cultured glia cells. The inhibitory effect of LPS on DNA synthesis is not due to an LPS-mediated increase of the cAMP content in the glia cells or contact inhibition of the monolayer culture. Within the structure of LPS lipid A was found to be the active part. On the basis of the LPS-induced increase of RNA synthesis, the glia cells of C3H/HeJ mice are low responders to low doses of LPS. We conclude that in the presence of fetal calf serum glia cells are sensitive to the lipid A part of LPS, the sensitivity being under genetic control.

Animals↗
PubMed1980

In vitro stimulation of glia cells by a lymphocyte-produced factor.

The factors responsible for the activation of astrocytes surrounding inflammatory brain tissues are unknown. The present study was designed to examine the ability of lymphocytes to produce astrocyte stimulating activity in cell culture. Normal rat lymphocytes stimulated with Concanavalin A, or sensitized lymphocytes, challenged with antigen in vitro, activate cultured rat glia cells by a soluble mediator which we have termed glia stimulating factor (GSF). In undifferentiated glioblasts both RNA synthesis, as measured by [5-3H]uridine uptake, and DNA synthesis, as measured by [6-3H]thymidine uptake, were stimulated by the presence of GSF. Preliminary characterisation showed the GSF to be non-dialysable and heat stable at 56 degrees C for 30 min, but not stable at 80 degrees C for 30 min. To study the effect of this factor on differentiated glia cells, brain cell cultures were treated with dibutyryl cyclic AMP (db-cAMP) which induces a morphologic transformation of glioblasts to multipolar cells that have a characteristic astrocytic appearance. After addition of GSF to db-cAMP treated astrocytes only an increase in RNA synthesis was observed. The significance of this in vitro phenomenon, mediated by a glia stimulating factor, to activation of astrocytes and astrocytic gliosis in human brain diseases is discussed.

Animals↗