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Biomedical subjects

B S Handwerger

Publications and source records attributed to B S Handwerger.

71 records · Page 4Linked to original sources
PubMed1977

A comparative study of procedures for sheep erythrocyte-human-T-lymphocyte rosette formation.

A comparative study of several published methods for sheep red blood cell-T-lymphocyte rosette formation was performed. Maximum SRBC-rosette formation occurred with AET treated SRBC in medium supplemented with 20% FCS or with untreated SRBC in 100% FCS. Prolongation of the 4 degrees C incubation period from 4 to 18 h enchanced rosette formation. Fluorescein diacetate staining significantly increased calculated percentage of rosette formation. Fluorescein diacetate staining significantly increased calculated percentage of rosette-forming lyphocytes by allowing accurate indentification of the central lymphocytes in morulas.

Animals↗
PubMed1977

Evidence for the replication of bovine leukemia virus in the B lymphocytes.

Bovine peripheral blood lymphocytes from a cow with persistent lymphocytosis were separated on nylon wool columns into nylon-adherent and nonadherent populations. Nylon-adherent cells were highly enriched for surface immunoglobulin (SIg) bearing B lymphocytes (95.5%) and nonadherent cells for SIg negative non-B cells, presumably T lymphocytes (96.3%). The B lymphocytes were found to be the major producers for bovine leukemia virus. A total of 39% of the B-enriched cells, surviving after 72 hours in culture, produced bovine leukemia virus as compared with 0.5% of the non-B cells.

Animals↗
PubMed1976

The genetics of cell-mediated lympholysis.

The role of HLA antigens in the generation of cytotoxic cells in CML has been investigated. Cytotoxic effector cells were generated in MLC among HLA-A or HLA-A and HLA-B disparate, HLA-D identical siblings, and among HLA-A and HLA-B disparate, MLC identical (%RR less than or equal to 2 3.6) unrelated individual. The data indicate that HLA-D differences and poliferative MLC responses as measured by 3H-thymidine incorporation are not requisite for the in vitro generation of cytotoxic cells and suggest the existence of a CML-S locus (loci) distinct from HLA-A, HLA-B and HLA-D. The degree of cytotoxicity generated in a proliferative versus a "nonproliferative" MLC was comparable. In addition, these studies demonstrate that antigens other than the currently definable HLA-A, HLA-B, HLA-C, and HLA-D can serve as target determinants in cell-mediated lympholysis.

Chromosome Mapping↗
PubMed1975

Demonstration that monocytes rather than lymphocytes are the insulin-binding cells in preparations of humah peripheral blood mononuclear leukocytes: implications for studies of insulin-resistant states in man.

Insulin receptors have been demonstrated on mononuclear leukocytes prepared by centrifugation of buffy coats from normal blood donors on Ficoll-Hypaque gradients. The cell type that specifically binds insulin in this mixture of lymphocytes and monocytes has never been clearly identified, although it was assumed to be the lymphocyte since this cell constitutes about 80% of the population. In the present studies, insulin-binding assays were performed on the mononuclear leukocyte preparation before and after selective depletion or enrichment for monocytes using glass wool or Sephadex G-10 adherence columns. The amount of 125-I-labeled insulin specifically bound correlated significantly with the number of monocytes but not with the number of B or T lymphocytes. Approximately 90% of the specific insulin binding of this preparation could be accounted for by its content of monocytes. The amount of binding was unaffected by phagocytosis of latex particles or by metabolic inhibitors added to prevent endocytosis. Autoradiograms made on smears of whole peripheral blood and mononuclear leukocytes demonstrated that all of the cells that bound 125-I-labeled insulin were large mononulcear cells, 85-90% of which could be identified as monocytes by morphological criteria or by the functional criterion of latex particle ingestion. Since insulin receptor concentration may be altered in disease states in man, it is essential, when using this cell population for detecting such changes, to quantitate the number of monocytes in the preparation so that the insulin-binding data can be appropriately interpreted.

B-Lymphocytes↗
PubMed1975

Augmented antibody-dependent cell-mediated cytotoxicity following sensitization or nonspecific stimulation of human effector cells.

Human peripheral blood leukocytes were stimulated in vitro with mitogens (poke-weed mitogen, concanavalin A, and phytohemagglutinin) or allogeneic cells. Each form of stimulation augmented the cytotoxic effector cell activity of lymphoid cells in a 4-hr test for antibody-dependent cell-mediated cytotoxicity. This augmented activity did not involve release of detectable nonspecific toxins, nor did it require the presence of mitogen during the cytotoxicity test. Stimulated attacking cells appeared more cytotoxic either because of a more potent cytotoxic mechanism per individual cytotoxic cell or because of an increased percentage of cytotoxic cells.

Antibodies↗
PubMed1975

Identification of macrophage-like characteristics in a cultured murine tumor line.

A mouse tumor line P388D1 passaged in tissue culture for many years has been characterized morphologically and functionally as a macrophage like cell. P388D1 cells phagocytize latex particles and firmly adhere to glass and plastics. In addition they have been shown to carry cellbound receptors for immunoglobulin (Fc) and complement (C3). They fail to stain with fluorescent anti-mouse Ig or heterologous anti-mouse. Functionally, these cells exhibited high effector activity in an antibody-dependent, cell-mediated cytotoxic system. The accessibility of well characterized and pure macrophage-like cell lines, such as P388D1, will facilitate studies where cell purity is essential.

Animals↗
PubMed1975

Lack of B lymphocyte depletion from murine spleen cell populations by a human gamma-globulin, anti-human gamma-globulin column system.

It has been reported previously that enriched populations of mouse thymus-dependent (T) lymphocytes could be prepared by the use of a column procedure that is believed to remove selectively cells with receptors for antigen-antibody complexes. In our hands, this procedure does not selectively remove B lymphocytes but rather masks the surface immunoglobulin. Analysis of the column-passed cells revealed an apparent decrease in the percentage of immunoglobulin-bearing cells but little decrease in either the percentage of complement receptor lymphocytes or the mitogenic response to lipopolysaccharide. Furthermore, rabbit immunoglobulin could be detected on the surface of 35 to 45% of the cells emerging from the columns prepared with rabbit anti-human gamma-globulin (HGG). After overnight incubation, 30 to 40% of the emerging cells reexpressed mouse immunoglobulin on their surfaces. Adsorption of the antisera used to make the columns with mouse gamma-globulin (MGG) diminished the depleting capacity of the columns. We conclude from these observations that antibodies in the anti-HGG sera, cross-reactive with mouse immunoglobulin, account for the spacious depletion of B lymphocytes observed when cells are passed over these antigen-antibody complex columns.

Animals↗
PubMed1974

Synergy between subpopulations of mouse spleen cells in the in vitro generation of cell-mediated cytotoxicity: evidence for the involvement of a non-T cell.

Two subpopulations separated from normal spleen have been shown to synergize as responding cells in the in vitro induction of specific cell-mediated cytotoxicity during the mixed lymphocyte culture (MLC). The synergizing populations are a nylon wool column-adherent and a nylon wool column-nonadherent fraction, enriched for B lymphocytes and T lymphocytes, respectively. When a mixture of these fractions is used as the responding cell population in MLC, greater cytotoxicity is generated than would be expected from the sum of activities generated in the two subpopulations sensitized separately. The synergy appears to occur at the sensitization rather than the effector phase. The synergizing cell which is contained in the nylon-adherent subpopulation is distinct from the cytotoxic effector T lymphocyte, is resistant to lysis by rabbit antimouse brain serum, and is unresponsive to phytohemagglutinin; its synergizing function could not be replaced by either plastic-adherent spleen cells or peritoneal exudate cells. These results suggest a role of a non-T-cell nonmacrophage population in the generation of cytotoxic activity.

Animals↗
PubMed1972

Thyroid hormone binding by human serum prealbumin (TBPA). Electrophoretic studies of triiodothyronine-TBPA interaction.

Thyroxine-binding prealbumin (TBPA) in normal human serum has been shown in a polyacrylamide gel electrophoresis system to bind 7-9% of tracer level purified [(125)I]triiodothyronine (T3), and more than 30% of T3 in serum deficient in thyroxinebinding globulin (TBG). The T3-TBPA interaction has been confirmed at pH 9.0 and pH 7.4 in this electrophoretic demonstration of TBPA binding of T3 in serum. Purified human TBPA has also been shown to bind T3. Progressive additions of unlabeled thyroxine (T4) to serum containing tracer [(125)I]T3 displace T3 from TBG, its principal carrier, to TBPA and albumin; however, T4 loading does not lead to significant T3 displacement from TBPA even at T4 levels known to saturate TBPA. Loading of serum with unlabeled T3 results in displacement of more than 50% of [(125)I]T3 from TBPA, as well as from TBG, to albumin. Studies carried out with serum containing diphenylhydantoin (DPH) or MK-185, known inhibitors of T4 binding by TBG, also showed T3 displacement from TBG to TBPA and albumin. Although salicylate and tetraiodothyroacetic acid (TETRAC) displace T4 from sites on TBPA, they have only minimal effects on T3-TBPA interaction.

Acetamides↗
PubMedDate not supplied

Calcium channel blockers inhibit cellular uptake of thymidine, uridine and leucine: the incorporation of these molecules into DNA, RNA and protein in the presence of calcium channel blockers is not a valid measure of lymphocyte activation.

An important role of transmembrane flux of calcium in lymphocyte activation has been previously demonstrated. Herein, we demonstrate that the calcium channel blockers verapamil and isradipine are able to inhibit in a concentration-dependent manner 3H-thymidine incorporation into DNA in phytohemagglutinin (PHA)-stimulated human peripheral blood mononuclear cells (PBMC). However, verapamil and isradipine diminish PHA-stimulated thymidine incorporation into DNA to the same extent whether they are added at the beginning of culture or 4 h prior to completion of a 72-h culture. Thus, 3H-thymidine incorporation into DNA in the presence of verapamil or isradipine is not a valid measure of mitogen-induced lymphocyte proliferation. Similarly, verapamil and isradipine also inhibit PHA-stimulated incorporation of 3H-leucine into protein and 3H-uridine into RNA whether the drugs are added at the beginning of culture or 4 h prior to completion of 24-h cultures. There is no intracellular accumulation of 3H-thymidine, 3H-leucine, or 3H-uridine into 10% trichloroacetic acid-soluble molecules during inhibition with verapamil or isradipine, suggesting that these drugs impair the cellular uptake of these substances rather than directly inhibiting their incorporation into DNA, protein, or RNA, respectively. Since previous reports documenting the inhibitory effects of calcium channel blockers on lymphocyte proliferation have utilized 3H-thymidine incorporation into DNA to measure proliferation, we have re-examined the antiproliferative effects of these drugs by determining their effect on PHA-stimulated cell cycle progression, employing cytofluorometric analysis of propidium iodide-stained cells. When added at the initiation of culture, both verapamil and isradipine inhibited in a concentration-dependent manner PHA-stimulated cell cycle progression.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗
PubMedDate not supplied

The effect of calcitonin on food intake in diabetic mice.

The characteristic hyperphagia of the genetically obese diabetic (C57Bl/Ks-db+/db+) mouse (db/db) is thought to be due to defect in the satiety circuitry with a secondary overproduction of a circulating satiety factor to which they are insensitive. Recent studies have suggested that calcitonin may be a potent hormonal mediator of the satiety reflex. In this study it was shown that db/db mice were eight fold more sensitive to calcitonin than their heterozygote littermate controls. Mice with streptozotocin-induced diabetes were ten-fold more sensitive to calcitonin than their littermate controls. These results show that diabetes increases the sensitivity to the satiety effects of calcitonin.

Animals↗