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D A Terle

Publications and source records attributed to D A Terle.

8 recordsLinked to original sources
PubMed1998

Hemoglobin A0 and alpha-crosslinked hemoglobin (alpha-DBBF) potentiate agonist-induced platelet aggregation through the platelet thromboxane receptor.

Chemically modified hemoglobins are potential oxygen-carrying blood substitutes, but their in vivo administration has been associated with a variety of unexpected side events, including increased platelet reactivity. We studied the effects of hemoglobin A0 (HbA0) and alpha-crosslinked hemoglobin (alpha-DBBF) on platelets in vitro. Neither hemoglobin A0 nor alpha-DBBF activated platelets when added alone, but both proteins potentiated submaximal agonist-induced platelet aggregation without increasing other markers of platelet activation such as serotonin secretion. Only agonists that are known to cause release of platelet arachidonic acid (AA) were potentiated while aggregation induced by ADP, which does not release AA, was not potentiated. Blockade of the thromboxane receptor with SQ-29,548 prevented the HbA0-induced and the alpha-DBBF-induced potentiation suggesting that the AA/thromboxane signaling pathway mediates the interaction of platelets with hemoglobin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Effects of gamma-IFN and NGF on subpopulations in a human neuroblastoma cell line: flow cytometric and morphological analysis.

Neuroblastomas are neural crest-derived tumors that contain neuronal, melanocyte, and Schwann cell precursors. We examined the effects of treatment with gamma-interferon (gamma-IFN) and nerve growth factor (NGF), alone, and in combination, on these progenitor subpopulations in the human neuroblastoma cell line, SH-SY5Y. Using fluorescence-activated flow cytometry (FACS), changes in expression of three differentiation-specific or -associated marker proteins, the 200 kD neurofilament protein, the myelin basic protein, and the S-100 protein, were analyzed. Growth rates and morphological changes associated with each treatment over the 2-wk incubation period were noted. The greatest effects were observed with combined IFN + NGF treatment. These were significant increases in expression of all three proteins, distinctive morphological signs of differentiation, and extensive inhibition of proliferation compared to control cultures. Treatment with NGF alone resulted in increased neurofilament protein expression and in the length and number of neurite extensions, but there was no effect on the growth rate. IFN induced striking morphological changes, significant inhibition of growth, and changes in protein expression that correlated with neuronal to non-neuronal subpopulation shifts due to the death of differentiated cells. When treatment was discontinued after 15 d, the morphological changes induced by NGF were reversed within 2-3 d, while those induced by IFN +/- NGF were present up to 4 wk post-treatment. Small, neuroblastic colonies were observed throughout the treatment period and within 4-6 wk after the cessation of treatment this cell-type fully reconstituted the cultures suggesting the presence of a stem cell. Our results indicate that treatment with gamma-IFN +/- NGF can regulate growth and induce, either stem cells or progenitor neuronal, Schwann and melanocyte subpopulations in the SH-SY5Y cell line to irreversibly differentiate.

Cell Division↗
PubMed1996

Adhesion of platelets to chemotactically responsive and non-responsive neutrophils.

Aims-To investigate the heterotypic adhesion of unactivated platelets to chemotactically responsive (migrated) and non-responsive (non-migrated) polymorphonuclear neutrophils (PMN).Methods-Platelets and PMN were isolated from autologous, normal blood. Migrated and non-migrated PMN were separated after N-formylmethionyl-leucylphenylalanine (FMLP) stimulation. Platelets were labelled with a fluorescent monoclonal antibody directed against CD41 (GPIIb-IIIa). Platelets (3 x 10(8)/ml) and PMN (3 x 10(6)/ml) were incubated together. Heterotypic cell adhesion was measured in isolated PMN and PMN co-incubated with platelets by flow cytometric analysis of platelet marker fluorescence in PMN gated events. Platelet-PMN adhesion was also visualised by fluorescence microscopy.Results-In studies of isolated PMN, contaminating platelets were bound to 16-34% of unstimulated PMN, 7-22% of stimulated PMN, 2-4% of migrated PMN, and 17-24% of non-migrated PMN. When platelets were co-incubated with migrated or non-migrated PMN, 15-78% of PMN bound one or two platelets.Conclusions-Unactivated platelets adhere to isolated PMN in vitro. Fewer unactivated platelets were adhered to migrated PMN than to non-migrated PMN in isolated PMN preparations. These results indicate that platelets adhering to PMN are removed during PMN migration.

Journal Article↗
PubMed1996

Amphotericin B induced abnormalities in human platelets.

Aims-To investigate in vitro the effect of amphotericin B on platelets in order to understand poor platelet recovery in patients receiving platelet transfusions and amphotericin B simultaneously.Methods-Washed platelets were isolated from platelet concentrates and exposed to amphotericin B (4 mug/ml) for one hour. Platelet function was assessed by aggregation response to thrombin (0-0.6 U/ml), serotonin release, response to hypotonic stress, and mean platelet volume. The expression of surface membrane glycoprotein (GP) Ib-IX complex, GPIIb-IIIa complex and CD62P (P-selectin) was examined by flow cytometry using fluorescence labelled monoclonal antibodies. Heterotypic cell adhesion was measured in amphotericin B treated platelets coincubated with isolated, autologous polymorphonuclear leucocytes (PMN) by flow cytometric analysis.Results-Amphotericin B induced platelet dysfunction. The rate of aggregation by thrombin, serotonin uptake and thrombin induced release of serotonin, and the response of platelets to hypotonic stress were inhibited. There was up to a two-fold increase in the mean platelet volume. The expression of platelet surface GPIb-IX and GPIIb-IIIa was not affected. P-selectin, normally expressed only on the surface of activated platelets, was also expressed on unactivated platelets. Amphotericin B increased platelet adherence to PMN and the number of platelets bound per PMN.Conclusions-In vitro, amphotericin B induces P-selectin expression on the surface of unactivated platelets and increases platelet adhesion to PMN, which is exacerbated by storage. Platelet dysfunction resulting from exposure to amphotericin B may contribute to poor platelet recovery in vivo when amphotericin B is administered concomitantly with platelet transfusion.

Journal Article↗