Relevant bibliographies by topics / GP IIb

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  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'GP IIb'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "GP IIb"

1

Kleiman, Neal S. "GP IIb/IIIa Antagonists." Drugs in R & D 1, no. 5 (January 1999): 361–70. http://dx.doi.org/10.2165/00126839-199901050-00001.

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2

Coleman, Stephen G., and Rosemary Duff. "GP IIb/IIIa Antagonists." Drugs in R & D 1, no. 5 (January 1999): 371–73. http://dx.doi.org/10.2165/00126839-199901050-00002.

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3

Parise, L. V., B. Steiner, L. Nannizzi, A. B. Criss, and D. R. Phillips. "Evidence for novel binding sites on the platelet glycoprotein IIb and IIIa subunits and immobilized fibrinogen." Biochemical Journal 289, no. 2 (January 15, 1993): 445–51. http://dx.doi.org/10.1042/bj2890445.

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The present study was designed to examine the interaction of the purified platelet glycoprotein IIb-IIIa complex (GP IIb-IIIa or integrin alpha IIb beta 3) and the individual subunits of the complex with immobilized fibrinogen. Although 125I-GP IIb-IIIa binding to fibrinogen immobilized on Sepharose was specific, this interaction exhibited properties distinct from those of reversible fibrinogen binding to platelets: 125I-GP IIb-IIIa binding appeared irreversible, but non-covalent, Ca(2+)-independent, and was inhibited only weakly, or not at all, by the anti-(GP IIb-IIIa) monoclonal antibodies 10E5 and 7E3 and synthetic peptides from known platelet-binding domains of fibrinogen. Reversibly dissociated GP IIb or GP IIIa subunits inhibited 125I-GP IIb-IIIa binding to immobilized fibrinogen and bound directly to the fibrinogen. However, these subunits did not bind to peptides derived from known platelet-binding domains within the fibrinogen alpha- and gamma-chains, although the GP IIb-IIIa complex did. These results show that the complexed form of full-length GP IIb and GP IIIa is required for binding to these synthetic peptides, but not necessarily for binding to immobilized fibrinogen. Thus GP IIb-IIIa can bind to immobilized fibrinogen by a distinct mechanism that appears to involve novel binding sites on each subunit of the GP IIb-IIIa complex and on fibrinogen.
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Kieffer, N., JL Wautier, L. Coulombel, M. Titeux, MP Wautier, W. Vainchenker, C. Ruan, and J. Breton-Gorius. "Uncoupling in the expression of platelet GP IIb/IIIa in human endothelial cells and K562 cells: absence of immunologic crossreactivity between platelet GP IIb and the vitronectin receptor alpha chain [see comments]." Blood 72, no. 4 (October 1, 1988): 1209–15. http://dx.doi.org/10.1182/blood.v72.4.1209.1209.

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Abstract Platelet glycoproteins (GP) IIb and IIIa exist as noncovalently associated Ca++-dependent heterodimer complexes within the platelet membrane and express the major platelet alloantigens Leka (Baka) and PIA1 (Zwa), which are genetic markers of GP IIb and GP IIIa, respectively. Since heterodimers immunologically related to platelet GP IIb/IIIa have been identified in a number of nucleated cell types, we tested anti-Leka and anti-PIA1 antiserum, polyclonal anti-platelet GP IIb/IIIa IgG, as well as a panel of 28 monoclonal anti-GP IIb, GP IIIa, or complex dependent anti-GP IIb/IIIa antibodies on endothelial cells, peripheral blood mononuclear cells, and the erythroleukemic cells HEL and K562 in order to determine whether nucleated cell GP IIb/IIIa related proteins and platelet GP IIb/IIIa are immunologically related. Using immunofluorescence, immunoblotting, and immunoprecipitation experiments, evidence is presented that (1) the alloantigen Leka is not expressed in endothelial cells of an individual whose platelets are of the Leka/PIA1 phenotype, whereas the PIA1 alloantigen is readily detectable in these cells, (2) that in contrast to HEL cells, which express platelet GP IIb/IIIa and are of the Leka/PIA1 phenotype, platelet GP IIb is immunologically undetectable in 12-O-tetradecanoyl- phorbol-13-acetate (TPA)-treated K562 cells despite the presence of platelet GP IIIa, and (3) that peripheral blood mononuclear cells do not express platelet GP IIb or GP IIIa on their cell surface.
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Kieffer, N., JL Wautier, L. Coulombel, M. Titeux, MP Wautier, W. Vainchenker, C. Ruan, and J. Breton-Gorius. "Uncoupling in the expression of platelet GP IIb/IIIa in human endothelial cells and K562 cells: absence of immunologic crossreactivity between platelet GP IIb and the vitronectin receptor alpha chain [see comments]." Blood 72, no. 4 (October 1, 1988): 1209–15. http://dx.doi.org/10.1182/blood.v72.4.1209.bloodjournal7241209.

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Platelet glycoproteins (GP) IIb and IIIa exist as noncovalently associated Ca++-dependent heterodimer complexes within the platelet membrane and express the major platelet alloantigens Leka (Baka) and PIA1 (Zwa), which are genetic markers of GP IIb and GP IIIa, respectively. Since heterodimers immunologically related to platelet GP IIb/IIIa have been identified in a number of nucleated cell types, we tested anti-Leka and anti-PIA1 antiserum, polyclonal anti-platelet GP IIb/IIIa IgG, as well as a panel of 28 monoclonal anti-GP IIb, GP IIIa, or complex dependent anti-GP IIb/IIIa antibodies on endothelial cells, peripheral blood mononuclear cells, and the erythroleukemic cells HEL and K562 in order to determine whether nucleated cell GP IIb/IIIa related proteins and platelet GP IIb/IIIa are immunologically related. Using immunofluorescence, immunoblotting, and immunoprecipitation experiments, evidence is presented that (1) the alloantigen Leka is not expressed in endothelial cells of an individual whose platelets are of the Leka/PIA1 phenotype, whereas the PIA1 alloantigen is readily detectable in these cells, (2) that in contrast to HEL cells, which express platelet GP IIb/IIIa and are of the Leka/PIA1 phenotype, platelet GP IIb is immunologically undetectable in 12-O-tetradecanoyl- phorbol-13-acetate (TPA)-treated K562 cells despite the presence of platelet GP IIIa, and (3) that peripheral blood mononuclear cells do not express platelet GP IIb or GP IIIa on their cell surface.
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Nurden, AT, D. Didry, N. Kieffer, and RP McEver. "Residual amounts of glycoproteins IIb and IIIa may be present in the platelets of most patients with Glanzmann's thrombasthenia." Blood 65, no. 4 (April 1, 1985): 1021–24. http://dx.doi.org/10.1182/blood.v65.4.1021.1021.

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Abstract Glanzmann's thrombasthenia is an inherited bleeding disorder characterized by abnormalities of platelet membrane glycoproteins (GP) IIb and IIIa. Most patients, usually designated as type I, have been reported to have undetectable levels of GP IIb and GP IIIa with the assay used. We have used polyclonal rabbit antibodies against GP IIb and GP IIIa in a sensitive immunoblot procedure capable of revealing trace amounts of these glycoproteins. Platelets from nine thrombasthenic patients, including seven with type I disease, were studied. GP IIIa, although decreased, was clearly detectable in platelets of eight patients and GP IIb was identified in five. Our findings suggest that residual quantities of GP IIb and GP IIIa are present in most patients with thrombasthenia and therefore that major deletions in the gene or genes encoding these proteins are uncommon.
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Nurden, AT, D. Didry, N. Kieffer, and RP McEver. "Residual amounts of glycoproteins IIb and IIIa may be present in the platelets of most patients with Glanzmann's thrombasthenia." Blood 65, no. 4 (April 1, 1985): 1021–24. http://dx.doi.org/10.1182/blood.v65.4.1021.bloodjournal6541021.

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Glanzmann's thrombasthenia is an inherited bleeding disorder characterized by abnormalities of platelet membrane glycoproteins (GP) IIb and IIIa. Most patients, usually designated as type I, have been reported to have undetectable levels of GP IIb and GP IIIa with the assay used. We have used polyclonal rabbit antibodies against GP IIb and GP IIIa in a sensitive immunoblot procedure capable of revealing trace amounts of these glycoproteins. Platelets from nine thrombasthenic patients, including seven with type I disease, were studied. GP IIIa, although decreased, was clearly detectable in platelets of eight patients and GP IIb was identified in five. Our findings suggest that residual quantities of GP IIb and GP IIIa are present in most patients with thrombasthenia and therefore that major deletions in the gene or genes encoding these proteins are uncommon.
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Peter, Karlheinz, Meike Schwarz, Jari Ylänne, Benedikt Kohler, Martin Moser, Thomas Nordt, Peter Salbach, Wolfgang Kübler, and Christoph Bode. "Induction of Fibrinogen Binding and Platelet Aggregation as a Potential Intrinsic Property of Various Glycoprotein IIb/IIIa (IIbβ3) Inhibitors." Blood 92, no. 9 (November 1, 1998): 3240–49. http://dx.doi.org/10.1182/blood.v92.9.3240.

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Abstract The blockade of platelet integrin glycoprotein (GP) IIb/IIIa is a promising new antiplatelet strategy. The binding of ligands or of the ligand-mimetic peptide RGD causes a conformational change of GP IIb/IIIa from the nonactivated to the activated state. Because several blocking agents/inhibitors are ligand-mimetics, the current study evaluates whether these agents have the intrinsic property to activate GP IIb/IIIa. Fibrinogen binding to GP IIb/IIIa on platelets or on CHO cells expressing recombinant GP IIb/IIIa was evaluated by flow cytometry or 125I-labeled fibrinogen. Incubation with the monoclonal antibody (MoAb) fragment c7E3 (abciximab) results in fibrinogen binding to GP IIb/IIIa and in the access of ligand-induced binding sites. At low concentrations (0.01 to 0.1 μg/mL), this intrinsic activating property of c7E3 can result in platelet aggregation. The disintegrin flavorodin and the RGD analogue fradafiban also induce fibrinogen binding, whereas the blocking MoAbs 2G12 and P2 and the activation-specific MoAb PAC-1 do not. Aspirin and indomethacin cannot block c7E3-induced fibrinogen binding to GP IIb/IIIa, but can inhibit c7E3-induced platelet aggregation. Thus, we conclude that GP IIb/IIIa inhibitors can demonstrate an intrinsic activating property, which can result in fibrinogen binding to GP IIb/IIIa and consequently in platelet aggregation. Cyclooxygenase inhibitors can inhibit platelet aggregation caused by GP IIb/IIIa inhibitors. Further studies will have to evaluate the clinical relevance of the potential intrinsic activating property of GP IIb/IIIa inhibitors and define consequences for the future drug development and evaluation of these potent antiplatelet agents. © 1998 by The American Society of Hematology.
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Peter, Karlheinz, Meike Schwarz, Jari Ylänne, Benedikt Kohler, Martin Moser, Thomas Nordt, Peter Salbach, Wolfgang Kübler, and Christoph Bode. "Induction of Fibrinogen Binding and Platelet Aggregation as a Potential Intrinsic Property of Various Glycoprotein IIb/IIIa (IIbβ3) Inhibitors." Blood 92, no. 9 (November 1, 1998): 3240–49. http://dx.doi.org/10.1182/blood.v92.9.3240.421k21_3240_3249.

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The blockade of platelet integrin glycoprotein (GP) IIb/IIIa is a promising new antiplatelet strategy. The binding of ligands or of the ligand-mimetic peptide RGD causes a conformational change of GP IIb/IIIa from the nonactivated to the activated state. Because several blocking agents/inhibitors are ligand-mimetics, the current study evaluates whether these agents have the intrinsic property to activate GP IIb/IIIa. Fibrinogen binding to GP IIb/IIIa on platelets or on CHO cells expressing recombinant GP IIb/IIIa was evaluated by flow cytometry or 125I-labeled fibrinogen. Incubation with the monoclonal antibody (MoAb) fragment c7E3 (abciximab) results in fibrinogen binding to GP IIb/IIIa and in the access of ligand-induced binding sites. At low concentrations (0.01 to 0.1 μg/mL), this intrinsic activating property of c7E3 can result in platelet aggregation. The disintegrin flavorodin and the RGD analogue fradafiban also induce fibrinogen binding, whereas the blocking MoAbs 2G12 and P2 and the activation-specific MoAb PAC-1 do not. Aspirin and indomethacin cannot block c7E3-induced fibrinogen binding to GP IIb/IIIa, but can inhibit c7E3-induced platelet aggregation. Thus, we conclude that GP IIb/IIIa inhibitors can demonstrate an intrinsic activating property, which can result in fibrinogen binding to GP IIb/IIIa and consequently in platelet aggregation. Cyclooxygenase inhibitors can inhibit platelet aggregation caused by GP IIb/IIIa inhibitors. Further studies will have to evaluate the clinical relevance of the potential intrinsic activating property of GP IIb/IIIa inhibitors and define consequences for the future drug development and evaluation of these potent antiplatelet agents.© 1998 by The American Society of Hematology.
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Royo, Teresa, Matilde Vidal, and Lina Badimon. "Purification of the Porcine Platelet GP IIb-IIIa Complex and the Propolypeptide of von Willebrand Factor." Thrombosis and Haemostasis 80, no. 08 (1998): 302–9. http://dx.doi.org/10.1055/s-0037-1615192.

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SummaryPlatelet membrane glycoproteins (GP) are involved in platelet adhesion and aggregation. The glycoprotein IIb-IIIa complex (GP IIbIIIa) is a Ca2+-dependent heterodimer that binds fibrinogen and other adhesive proteins, thereby mediating platelet aggregation and adhesion. We have purified two major glycoproteins from pig platelets by Concanavalin A-Sepharose, Heparin-Sepharose and Sephacryl S-300 HR chromatography (Fitzgerald et al. Anal Biochem, 1985): i) the GP IIb-IIIa complex, GP IIb Mr = 140,000 and GP IIIa a single chain of Mr = 95,000-100,000; and ii) a predominant glycoprotein of high molecular weight, the propolypeptide of von Willebrand factor (Mr = 80,000-100,000). Western-blot analysis of the purified GP IIb-IIIa showed that only certain monoclonal antibodies against the human receptor specifically recognize the porcine complex. Differences between the porcine and human GP IIb-IIIa glycoproteins could partially explain the decreased inhibitory effects of GP IIb/IIIa-antagonists (against the human receptor) in porcine platelets.
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Dissertations / Theses on the topic "GP IIb"

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McCaslin, James. "Platelet function in patients with polymorphisms of GP IIb/IIIa and cyclooxygenase." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493079.

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Platelets contribute to the progression of atherosclerotic disease by adhering to the subendothelial matrix at sites of shear-induced mechanical injury to the vessel. The understanding that genetic factors play a role in the development of atheroma led to recent interest in polymorphisms of platelet receptors as a possible basis for this. Furthermore, there is a growing body of evidence to link these polymorphisms with resistance to antiplatelet agents, the implications of which are not yet fully appreciated.
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MOREL-KOPP, MARIE-CHRISTINE. "Anticorps monoclonaux anti-complexe gp iib/iiia : outils pour l'etude de thrombopathies." Paris 6, 1991. http://www.theses.fr/1991PA066247.

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Les anticorps monoclonaux murins (moabs) sont devenus un outil indispensable pour l'etude structurale et fonctionnelle des proteines et glycoproteines. Nous avons produit des moabs diriges contre le complexe glycoproteique (gp) iib/iiia plaquettaire afin d'une part d'etudier certains aspects de la regulation de l'activation plaquettaire et d'autre part de caracteriser differentes thrombopathies dont la thrombasthenie de glanzmann. Parmi les moabs obtenus, nous avons selectionne un moab inducteur de l'activation et de l'agregation plaquettaire: le pl2-49 (anti-gp iib) et deux inhibiteurs: le pl1-64 (anti-gp iib) et le pl2-73 (anti-gp iib/iiia). L'activation, suivie d'une agregation, induite par le pl2-49 est ca++ et fc dependante. En presence de chelateur de ca++ (edta 5 mm) le pl2-49 ne se fixe plus sur la gp iib. En presence de ca++ extracellulaire, cette activation ne depend que partiellement de la synthese de thromboxane et de la secretion de l'adp des granules denses. L'agregation induite par le pl2-49 ne requiert ni complement ni fibrinogene exogene. Quant aux moabs inhibiteurs de l'agregation plaquettaire, leur fixation sur le complexe doit interferer avec le site recepteur du fg. A l'aide de ces moabs, nous avons etudie les aspects biochimiques et fonctionnels de thrombopathies liees a une anomalie quantitative et/ou qualitative du complexe gp iib/iiia: 26 gt de type i (absence des gp iib et iiia), 1 thrombasthenie de type ii (10 a 25% de gp iib et iiia residuelles) et 2 gt variants (anomalie qualitative associee a un defaut quantitatif) dont 1 est unique: les plaquettes de mme l. Presentent une nouvelle gp interferant fonctionnellement avec le complexe gp iib/iiia et induisant une absence virtuelle d'agregation a l'adp. L'etude analytique des gt de type i met en evidence une heterogeneite selon le taux de fibrinogene intraplaquettaire et les quantites de gp iib et iiia residuelles. Une etude systematique des sujets heterozygotes pourrait apporter une information sur l'origine genetique de l'anomalie
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Kulle, Konrad. "Thrombozyteninhibition und Glykoprotein-IIb/IIIa- Rezeptorbesetzung bei intrakoronarer versus intravenöser Bolusgabe von Abciximab bei Patienten mit ST-Hebungs- Infarkt." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-160129.

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Bei Patienten mit ST-Strecken-Elevations-Myokardinfarkt (STEMI) ist die direkte intrakoronare Bolusverabreichung des Glykoprotein-IIb/IIIa-Rezeptorantagonist Abciximab, im Gegensatz zur periphervenösen Bolusinjektion, mit einer Reduktion von Infarktgröße und mikrovaskulärer Obstruktion sowie mit einem höheren Anteil geretteten Myokards assoziiert, vermutlich ausgelöst durch eine höhere lokale Arzneimittelkonzentration und der dadurch gesteigerten Hemmung der Plättcheninhibition. Ziel der Arbeit war es herauszufinden, ob es Unterschiede gibt bezüglich der GP-IIb/IIIa Rezeptorbesetzung und der Thrombozyteninhibition im venösen Koronarblut, welches kurz nach intrakoronarer oder periphervenöser Abciximab-Bolusinjektion entnommen wurde. Dafür wurden bei 16 Patienten mit akutem STEMI vor und unmittelbar nach der Gabe eines Abciximab-Bolus sowie nach 30 Minuten Blutproben aus dem Korornarsinus entnommen. Jeweils 8 Patienten erhielten entweder den Bolus intrakoronar oder peripher venös verabreicht. Sofort nach der Bolusapplikation war die Rezeptorbesetzung im venösem Koronarblut signifikant höher bei Patienten, die einen direkten intrakoronaren Bolus erhalten hatten, im Vergleich mit Patienten mit peripherer Bolusadministration (intrakorornarer Bolus: 93.5% [IQR 92.7–95.4], intravenöser Bolus: 74.0% [IQR 17.6–94.0], p = 0.04). Das Ausmaß der Plättcheninhibition war früh nach Bolusgabe ebenso deutlich höher bei intrakoronarer anstatt intravenöser Bolusapplikation. In der späten Blutentnahme 30 Minuten nach der Bolusapplikation konnten keine signifikanten Unterschiede zwischen beiden untersuchten Gruppen, weder bezüglich der GP-IIb/IIIa Rezeptorbesetzung noch der Thrombozytenaggregationshemmung, gefunden werden. Zusammenfassend kann man sagen, dass die direkte intrakoronare Bolusapplikation akut in eine höhere lokale Inhibition der Thrombozytenfunktion und einem größeren Anteil an geblockten GP-IIb/IIIa Rezeptoren im Vergleich zur peripher venösen Bolusinjektion resultiert. Limitierend muss die geringe Fallzahl erwähnt werden. Die Ergebnisse sollten deshalb zurückhaltend interpretiert werden.
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Croizet, François. "Modélisation et conception d'antagonistes du récepteur plaquettaire du fibrinogène (αIIb/ß3 - GP IIb/IIIa)." Bordeaux 2, 1997. http://www.theses.fr/1997BOR2B006.

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Vetter, Christian. "Langzeitresultate nach PTCA mit - ohne Stentimplantation in Abhängigkeit vom Genotyp des Gp-IIb-IIIa-Rezeptors." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/122/index.html.

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Thon, Jonathan Noah. "Application of proteomics to the study of protein translation in stored platelet units." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2346.

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Platelet products have a short shelf life (5 to 7 days) owing in part to the deterioration of the quality of platelets stored at 22°C. This creates significant inventory challenges, and blood banks may suffer shortages and high wastage as a result. Proteomics offers a global quantitative approach to investigate changes occurring in stored blood products. These data sets can identify processes leading to storage-associated losses of blood component quality such as the platelet storage lesion (PSL). Changes to the platelet proteome between days 1 and 7 of storage were analysed with 3 complementary proteomic approaches with final mass spectrometric (MS) analysis: 2-dimensional (2D) gel electrophoresis/differential gel electrophoresis (DIGE), isobaric tagging for relative and absolute quantification (iTRAQ), and isotope-coded affinity tagging (ICAT). Although proteomics analyses identified many storage-associated protein changes, these varied significantly by method suggesting that a combination of protein-centric (2D gel or DIGE) and peptide-centric (iTRAQ or ICAT) approaches is necessary to acquire the most informative data. Validation of the proteomics results by western blotting, flow cytometry, quantitative real-time polymerase chain reaction (qRT PCR) and ³ٰ⁵S-methionine incorporation confirmed that platelets are capable of synthesising biologically relevant proteins ex vivo throughout a 10-day storage period with particularly long-lived mRNA (half-life of approximately 2.4 days), and has provided the first evidence for one of the mechanisms of the PSL. The development of an ³ٰ⁵Smethionine assay has since shown that stored human blood platelets incorporate ³ٰ⁵S-methionine at a rate that is proportional to time and substrate concentration, and is slower for freshly drawn platelets than those stored in pooled buffy coat derived units for 10 days. More interesting still are the observations that the overall ³ٰ⁵S-methionine incorporation rate was higher in pooled buffy coat platelet units versus freshly drawn platelets, that this rate increased upon agonist exposure in both, and that day 8 platelets showed significantly greater total protein translation than on days 2,3,7 and 10 of storage. This may be indicative of translational regulation of the platelet proteome during storage and upon activation. Translational control is a consequence of remarkable cellular specialisation and precise biochemical pathways which, in the case of platelets, may lead to storage-associated losses of blood component quality and must be understood if platelet storage times are to be extended.
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Carteaux, Jean-Philippe. "Circulation extra-corporelle, thrombose artérielle : modèles expérimentaux : rôle de l'inhibition des récepteurs plaquettaires GP IIb-IIIa." Nancy 1, 1996. http://www.theses.fr/1996NAN10340.

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La thrombose artérielle et les troubles de l'hémostase induits par la circulation extra corporelle (C. E. C. ) sont des préoccupations majeures du chirurgien cardio-vasculaire. Les plaquettes sanguines ont un rôle déterminant dans l'intrication des facteurs impliqués dans la physiopathologie des désordres cardio-vasculaires d'origine thrombotique ainsi que dans. La survenue des troubles hémobiologiques associés à la circulation extra-corporelle. La liaison du récepteur plaquettaire, la glycoprotéine IIb-IIIa (GP IIb-IIIa) au facteur Willebrand participe aux phénomènes d'adhésion plaquettaire ; la liaison de GP IIb-IIIa au fibrinogène supporte les phénomènes d’agrégation plaquettaire. Le blocage du récepteur GP IIb-IlIa est donc une cible thérapeutique qui permet d'inhiber à la fois les phénomènes d'adhésion et d'agrégation plaquettaires. Le but de ce travail à été d’étudier dans des conditions expérimentales la thrombose artérielle et les troubles de l'hémostase induits par la C. E. C. : Thrombose artérielle. Nous décrivons un modèle expérimental original de thrombose carotidienne chez le cochon d'Inde. Ce modèle permet de générer des phénomènes reproductibles de thrombose artérielle dans des conditions de force de cisaillement similaires à celles rencontrées dans les phénomènes de thrombose d'artères sténosées humaines. Grâce à ce modèle, nous montrons : i) L'efficacité thérapeutique de l'inhibition du récepteur GPIIb-IIIa, supérieure à celle de l'inhibition de la voie de la cyclooxygènase ou à celle de l'inhibition de la génération de thrombine; ii) L'importance de la mesure du temps de coagulation activé pour comparer l'activité antithrombotique des inhibiteurs direct et indirect de la thrombine. Circulation extracorporelle. L'inhibition du récepteur GP IIb-IIIa a été utilisée dans deux modèles expérimentaux: i) Un modèle original de C. E. C. Développé chez le cochon d'Inde, a permis de montrer que l'inhibition du récepteur GP IIb-IIIa prévient de façon dose dépendante la diminution du nombre de plaquettes circulantes observée durant la C. E. C. ; ii) Ces résultats ont été confirmés par une étude chez le chien, lors de la réalisation d'une C. E. C. Dans des conditions techniques et chirurgicales comparables à celles rencontrées en clinique. Par ailleurs dans ce travail, l'inhibition du récepteur GP IIb-IIIa a généré une perturbation des tests d'agrégation plaquettaire et un allongement du temps de saignement durant la C. E. C. Sans induire une augmentation des pertes sanguines post opératoires. Conclusion: - Le temps de coagulation activé doit être utilisé pour comparer l'activité antithrombotique des inhibiteurs direct et indirect de la thrombine. - Dans deux situations d'activation plaquettaire intense, la thrombose artérielle et la circulation extracorporelle, l'inhibition du récepteur plaquettaire GP lIb-IlIa se montre efficace dans la prévention des' phénomènes thrombotiques et dans la prévention des phénomènes de consommation plaquettaire. L'inhibition du récepteur plaquettaire GP lIb-IlIa apparaît comme une stratégie thérapeutique prometteuse.
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Jallu, Vincent. "Contribution à l'étude de l'immunologie du complexe GP IIb-IIIa : caractérisation d'anticorps humains et de la souris." Bordeaux 2, 1993. http://www.theses.fr/1993BOR28268.

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Troesch, Alain. "Biosynthèse et maturation de la glycoprotéine plaquettaire IIb/IIIa, récepteur du fibrinogène." Université Joseph Fourier (Grenoble), 1990. http://www.theses.fr/1990GRE10120.

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Les intégrines constituent une famille de récepteurs membranaires présents a la surface de nombreux types cellulaires et qui interviennent dans un grand nombre de phénomènes biologiques nécessitant des réactions d'adhérence (embryogénèse, prolifération et différenciation cellulaire, réponse hémostatique, angiogénèse, réponse immunitaire. . . ). Ces récepteurs sont des hétérodimères non covalents de type alpha-beta. La glycoprotéine plaquettaire IIb/IIIa (GPIIb/IIIa) et le récepteur de la vitronectine (VNR) sont deux intégrines qui possèdent la même sous unité beta et font partie du groupe des adhésines. La GPIIb/IIIa sert de récepteur au fibrinogène, a la surface de la plaquette activée et permet l'agrégation des plaquettes au cours de l'hémotase. Le travail présente dans cette thèse concerne les étapes essentielles de la biosynthèse de la GPIIb/IIIa, dans le mégacaryote humain, précurseur des plaquettes. La première partie est consacrée au transit intracellulaire de la GPIIb/IIIa. Cette étude a été réalisée dans le mégacaryocyte et dans une lignée leucémique myéloide continue a caractère mégacaryocytaire, lama-84. La seconde partie décrit la maturation et la glycosylation de la GPIIb/IIIa dans le mégacaryocyte et celle du récepteur de la vitronéctine (VNR) dans la cellule endothéliale. L'ensemble de ces résultats a permis de proposer un schéma de biosynthèse général pour les adhésines GPIIb/IIIa et VNR qui est applicable dans sa quasi-totalité aux récepteurs de la famille des intégrines
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Jaminet, Patrick. "Bifunktionale Fusionsproteine Kombination hochselektiver, direkter Faktor-Xa-Inhibition mit aktivationsspezifischer GP IIb/IIIa-Blockade einerseits, und zielgerichtetem Fibrin-Targeting andererseits /." [S.l.] : [s.n.], 2006. http://www.freidok.uni-freiburg.de/volltexte/2466/index.html.

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Books on the topic "GP IIb"

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DeMaria, Rusel, and Zach Meston. Sega Genesis Secrets, Volume 2. Rocklin, CA: Prima Publishing, 1991.

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Prima. Official Sega Genesis: Power Tips Book. Rocklin, CA: Prima Publishing, 1992.

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Awesome Super Nintendo Secrets 2. Lahaina, USA: Sandwich Islands Publishing, 1993.

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Arnold, J. Douglas, and Zach Metson. Awesome Sega Genesis Secrets 4. Lahaina, HI: Sandwich Islands Publishing, 1994.

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Tom, Badgett, ed. Official Sega Genesis and Game Gear strategies, 2ND Edition. Toronto: Bantam Books, 1991.

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Sandler, Corey. Official Sega Genesis and Game Gear strategies, 3RD Edition. New York: Bantam Books, 1992.

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Arnold, J. Douglas, and Zach Meston. Awesome Sega Genesis Secrets 3. Lahaina, HI: Sandwich Islands Publishing, 1993.

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Sega Genesis Secrets, Volume 4. Rocklin, CA: Prima Publishing, 1993.

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Eddy, Andrew, and Donn Nauert. Sega Genesis Secrets, Volume 4 (Prima's Secrets of the Games). Prima Games, 1993.

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Awesome Super Nintendo Secrets II. Bournermouth, U.K.: Paragon Publishing, Limited, 1993.

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Book chapters on the topic "GP IIb"

1

Timson, David J., Richard J. Reece, James B. Thoden, Hazel M. Holden, Andrea L. Utz, Beverly M. K. Biller, Eugen-Matthias Strehle, et al. "GT Platelet Glycoprotein IIb–IIIa Deficiency GP IIb–IIIa Complex." In Encyclopedia of Molecular Mechanisms of Disease, 760. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8590.

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Ranjan, Shraddha, and Gagandeep Singh Wander. "Intravenous anti-platelet therapy—GP IIb/IIIa blockers and cangrelor." In Acute Coronary Syndromes, 131–35. First edition. | Boca Raton : CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9780429025396-19.

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Cazenave, J. P., C. Gachet, and F. Lanza. "Pharmacological Inhibition of the ADP-GP IIb/IIIa-Fibrinogen Pathway of Platelet Aggregation." In Developments in Cardiovascular Medicine, 83–97. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3484-2_5.

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Berliner, Shlomo A., Richard A. Houghten, James R. Roberts, and Zaverio M. Ruggeri. "Multiple Epitope Specificity of Monoclonal Antibodies to a Single Synthetic Peptide: Use in the Characterization of the GP IIb-IIIa Binding Domain of Von Willebrand Factor." In Advances in Experimental Medicine and Biology, 133–44. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3806-6_13.

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Marie, Jean-Pierre, and Ollivier Legrand. "MDR1/P-GP Expression as A Prognostic Factor in Acute Leukemias." In Drug Resistance in Leukemia and Lymphoma III, 1–9. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4811-9_1.

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Dhooge, Catharina, and Barbara De Moerloose. "Clinical Significance of P-Glycoprotein (P-gp) Expression in Childhood Acute Lymphoblastic Leukemia." In Drug Resistance in Leukemia and Lymphoma III, 11–19. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4811-9_2.

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Karakaş, Z., L. Ağaoğlu, S. Erdem, G. Yanikkaya Demirel, M. Arasa, F. Süzergöz, G. Deniz, S. Anak, and G. Gedikoğlu. "Prognostic Value of P-gp Expression and Related Function in Childhood Acute Leukemia." In Drug Resistance in Leukemia and Lymphoma III, 21–28. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4811-9_3.

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Ahmadi, Shahram, Ali Shokuhfar, and Arash Rezaei. "Investigation of the Effects of GP Zones Formation on the Properties of AA2090 Alloy." In Diffusion in Solids and Liquids III, 18–21. Stafa: Trans Tech Publications Ltd., 2008. http://dx.doi.org/10.4028/3-908451-51-5.18.

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Niu, Xiaoshuang, and Yungan Tao. "New Developments in the Management of Nasopharyngeal Carcinoma." In Critical Issues in Head and Neck Oncology, 327–35. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_22.

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AbstractNasopharyngeal carcinomas (NPC) have unique characteristics with a specific geographic distribution and radiotherapy (RT) is the cornerstone of initial treatment due to its radiosensitive behaviour and deep-seated location. Intensity modulated radiotherapy (IMRT) has become the standard RT technique compared with 2D/3D and could reduce the late toxicities such as xerostomia. We established the international guideline for the delineation of clinical target volumes (CTV) and dose prioritization and constraint guideline for a better implementation of IMRT for NPC. The role of RT in addition to systemic therapy for the initially diagnosed metastatic NPC has recently been investigated in a randomized trial. The meta-analysis MAC-NPC confirmed the role of chemotherapy in addition to RT for NPC and established concomitant chemoradiotherapy (CCRT) as a standard of care in locally advanced (LA) NPC. In the recent actualization of MAC-NPC and network meta-analysis, more chemotherapy (adjuvant or induction) has been suggested to further improve treatment efficacy. However, a randomized trial did not shown survival benefit of adjuvant chemotherapy in addition to CCRT in LA-NPC. More recently, several phase III trials (French GORTEC trial and Chinese trials) showed benefit of induction chemotherapy (PF/TPF/GP) when added to cisplatin-based chemoradiotherapy. Preliminary study has failed to show benefit of adjuvant chemotherapy for the patients with detectable plasma Epstein Barr virus (EBV) DNA after chemoradiotherapy. The presentation will also focus on the ongoing trials with association of immune checkpoint inhibitors with chemoradiotherapy and the role of EBV DNA during or after treatment among others.
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"GP IIb/IIIa receptor antagonists." In Drug Therapy in Cardiology, 164–69. CRC Press, 2001. http://dx.doi.org/10.3109/9780203213476-35.

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Conference papers on the topic "GP IIb"

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Phillips, David R., Laurence A. Fitzgerald, Leslie V. Parise, and Israel F. Charo. "The Platelet Membrane Glycoprotein IIb-III a Complex: Member of a Superfamily of Adhesive Protein Receptors." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643727.

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The glycoprotein (GP) IIb-IIIa complex isthe receptor for fibrinogen,fibronectin and von Willebrand factor on the surface of activated platelets that mediates platelet aggregation.The GP IIb-IIIa complex contains two subunits; an a subunit, GP IIb, and a smaller 8 subunit, GP IIIa. To identify the subunits of GP IIb-IIIa responsible for fibrinogen binding, we examined the ability of purified subunitsto bind to immobilized fibrinogen. Both the GP IIb and the GP III a subunits have fibrinogen binding activity, suggesting that fibrinogen binds to multiple sites onthe GP I Ib-IIIa complex.A GP Ilb-IIIa-like complex has been identified on endothelial cells which is immunoreactive with antibodies raised against platelet GP IIb-III a. This complex binds a similar broadspectrum of adhesive proteins as plateletGP IIb-IIIa and appears to mediate the attachment of endothelial cells to the extracellular matrix. We have established, however, that while GP Ilia in endothelial cells is the same primary translation product as platelet GP Ilia, the endothelialcell "GP lib" is a different, but closely related, protein from platelet GP lib. This close relationship of the receptors on these two cells is reflective of recent observations in several laboratories which have shown that a wide variety of cells contain surface glycoproteins which have structural and functionalsimilarities to the GP IIb-IIIa complexinplatelets and the "GP IIb-IIIa-like" complex in endothelial cells.These glycoproteins, which have been termed "integrins" or "cytoadhesins", are complexes of highly homologous a and 8 subunits, mediate cell-cell or cel 1-substrata interactions, and may also bind the RGD sequence on adhesive proteins. Although in vertebrates this family includes at least ten receptor complexes, there are only three known 8 subunits, each of which defines a subset of receptors. One is GP IIIa, the 8 subunit for GP IIb-IIIa and the vitronectin receptor; another is the 8 subunit for the fibronectin receptors and the very late antigens on lymphocytes; the third is the 8subunit of the Mac-1, LFA-1, and P150/95 antigens on leukocytes. These three 6 subunits have been cloned and sequenced. Each contains 746-777 amino acids, a singletransmembrane domain near the carboxy terminus, 56 cysteines in identical positionsof the proteins, 31 of which are clustered into four repeats, and an overall identity in 45-47% of their amino acids. The asubunits are more diverse in size but appear to have a similar degree of homology.The available sequence information indicates that they contain a single transmembrane domain near their carbody terminii and four tandem repeats near their amino terminii which include sequences indicativeof four Ca2+-binding sites. These may account for the known Ca2+-binding properties of GP IIb. GP I Ib-IIIa and the other adhesive protein receptors therefore appear to have two membrane insertion sites, one on each subunit,with short cytoplasmic domains derived from the carboxy terminii of the two subunits. The amino terminii along with most ofthe mass of these proteins is extracellular. It can be anticipated that the highlyhomologous sequences between GP IIb-IIIa and the other adhesive protein receptors will help identify the functional domainswhich have been conserved since their evolutionary divergences.
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Tanoue, K., and H. Yamazaki. "DIFFERENT INTEGRITIES OF GP Ilb/Ilia COMPLEX ARE REQUIRED FOR ADP- OR THROMBIN-INDUCED AGGREGATIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644882.

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A relation between the integrity of platelet GP IIb/IIIa complex and aggregability by ADP or thrombin was studied on intact platelets with EDTA-induced irreversibly dissociated GP IIb/IIIa complex. Human platelets were washed once and suspended in Ca-, Mg-free HEPES-Tyrode's solution (pH 7d). Aliquots of the suspensions were incubated with 2mM EDTA at 37°C for 2 to 60 min. Control platelets were incubated at 22°C. Then, kwM CaCl2 were added to the samples, which were incubated for another 30 min at 37°C. The platelets were washed twice with HEPES-Tyrode1s solution (pH 6.7). For the measurement of amounts of GP IIb/IIIa complex, the platelets were solubilized with 1% Triton X-100 to 1+ X 10 /yl, five yl of which were subjected to crossed immunoelectrophoresis using constant volumes of anti-platelet antibody. The areas under the immunbprecipitates of GP IIb/IIIa complexes were measured as the amounts of GP Ilb/IIIa complex. For the aggregation studies, the platelets were suspended in HEPES- Tyrode's solution (pH 7d). ADP-aggregations were measured in the presence of added 1mg/ml fibrinogen and 2mM Ca. Platelets incubated with EDTA or CaCl2 at 22°C showed the same amounts of GP IIb/IIIa complex.ADP-aggregability declined more rapidly than the decrease GP Ilb/IIIa complex. In contrast, thrombin-aggregation were much better maintained than ADP-Aggregation during the incubation with 2mM EDTA. These results suggest either that the integrity of GP Ilb/IIIa complex required for ADP-aggregation is more strict than for thrombin-aggregation, or that thrombin-aggreagtion can be caused by an alternative mechanism which does not require the integrity of GP Ilb/IIIa complex.
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Parise, L. V., B. Steiner, L. Nannizzi, and D. A. Phillips. "PEPTIDES FROM FIBRINOGENAND FIBRONECTIN CHANGE THE CONFORMATIONOF PURIFIED PLATELET GLYCOPROTEIN IIb-IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643697.

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Specific amino acid sequences in fibrinogen and fibronectin appear to mediate the binding of these ligands to the glycoprotein (GP) IIb-IIIacomplex in platelets. Thesesequences include LGGAKQAGDV from the y chain of fibrinogen, and RGD(S) from the a chain of fibrinogenand the cell-binding domain of fibronectin. Several recent reports suggest thatfibrinogen and/or peptides with these sequences cause clustering of GPIIb-IIIa on the platelet surface and Na+/H+ exchange in epinephrine-stimulated platelets. Thus, it is possible that occupancy of specific sites on GP Ilb-IIIa affects its conformation, initiating such events. In this study,we determined whether LGGAKQAGDV, RGDS, and related peptides affect the conformation of purified platelet GP IIb-IIIa. Conformational changes in GP IIb-IIIa were evaluated bychanges in proteolytic susceptibility and hydrodynamic properties. Thepurified GP IIb-IIIa complex was fund to be resistant to proteolysis bythrombin. However, pretreatment of GP IIb-IIIa with various peptidesincreased the susceptibility ofGP libα to thrombin-induced proteolysis,as quantitated onpolyacryfamide gels.The order of potency of these peptides was RGDS<LGGAKQAGDV < KGDS < RGES. This order of potency agrees with that for the abilityof these peptides to inhibit 125I-fibrinogen binding to platelets. The effect of the peptides on proteolysis was time-, temperature-, and concentration-dependent; RGDS Induced a half-maximal effect at ˜60μM. Evaluation of the hydrodynamic properties of GP IIb-IIIa showed that LGGAKQAGDV orRGDS, but not RGES, decreased thesedimentation coefficient of GP IIb-IIIa from 8.5S to 7.7 S or7.4, S,respectively. This changewas accompanied by an increase in theStoke’s radius from 73 A to 84 A. These results suggestthat LGGAKQAGDV andRGDS alterthe conformationof the purified GPIIb-IIIa heterodimer complex by causing it to unfold.This change in conformation may be related to changesin the distribution and function of GP IIb-IIIaon the platelet surface that occurwith occupancy ofligand binding sites.
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Steiner, B., and D. R. Phillips. "CA2+-INDUCED STRUCTURAL TRANSITIONS OF THE PLATELET GP IIb-IIIa COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643956.

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Previous studies have shown that the membrane glycoprotein (GP) IIb-IIIa complex can be reversibly dissociated by incubating platelets for 5 min at 37°C in an EDTA-containing buffer. Prolonged incubations (30 min) with EDTA, however, result in the formation of high molecular weight aggregates of GP IIb and GP IIIa. These aggregates of individual GP's neither bind fibrinogen nor support platelet aggregation, indicating that chelation of Ca2+ can affect the functional activity of GP IIb-IIIa. The present study was designed to identify conditions for the generation of functionally active GP IIb and GP IIIa. Functionally active subunits were defined as those which reformed GP IIb-IIIa complexes. The complexes were quantified by sucrose gradient sedimentation (complexed, dissociated and aggregated GP’s have different sedimentation coefficients) and thrombin hydrolysis (dissociated and aggregated GP lib are susceptible to hydrolysis by thrombin while GP lib in the GP IIb-IIIa complex is thrombin resistant). Purified GP IIb-IIIa could be dissociated by a 5 min incubation at 37°C with ≤ 10−5 M Ca2+. When the complexes were dissociated in the presence of Ca2+ concentrations below 10−6 m, the monomeric GP IIIa was converted to a slower sedimenting form; this change in structure caused it to become functionally inactive. In the presence of very low Ca2+ concentrations 10−6 M) both dissociated subunits subsequently formed high molecular weight aggregates. However, these changes in structure and loss in function could be prevented by dissociating the complexes in 10−6 M Ca2+ and immediately readding raM Ca2+ at 4°C. When this solution was warmed to 20°C, almost 70% of the dissociated subunits reformed heterodimeric complexes. Storage at 4°C for as long as 6 h did not alter the functional activity of these subunits. Octylglucoside, but not Triton X-100, completely inhibited reassociation. Experiments performed in the presence of various H+ and salt concentrations showed that the interactive forces between GP IIb and GP IIIa are both electrostatic and hydrophobic. Thus, conditions have been obtained for the preparation of functionally active GP IIb and GP IIIa which can reform the native heterodimeric complex. Various Ca2+ concentrations can have multiple effects on the structure of the dissociated subunits.
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Charo, I. F., L. A. Fitzgerald, D. Meyer, L. S. Bekeart, and D. R. Phillips. "PLATELET GLYCOPROTEIN IIb-IIIa-LIKE PROTEINS MEDIATE ENDOTHELIAL CELL ATTACHMENT TO ADHESIVE MATRIX PROTEINS AND ARE UP-REGULATED BY PHORBOL ESTERS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642816.

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Human endothelial cells (EC) express glycoproteins that are similar to the platelet glycoprotein IIb-IIIa complex (GP IIb-IIIa), the platelet receptor for adhesive proteins. Although GP IIb—IIIa is abundant in both platelets and EC, its only known function is to mediate platelet aggregation. The present study tests the hypotheses that EC attachment to adhesive proteins in the extracellular matrix is mediated by the GP IIb-IIIa-1ike proteins. Endothelial cells attached well to glass slides that were previously coated with adhesive proteins, but not albumin. To determine whether GP IIb-IIIa was involved, EC adherence was measured in the presence and absence of a GP IIb-IIIa monoclonal antibody (7E3) which inhibits fibrinogen (Fg) binding to platelets. The attachment of EC to Fg and von Willebrand factor (vWf), but not fibronectin (Fn) coated slides, was completely inhibited by 7E3. Attachment to vitronectin was partially inhibited. In contrast, EC attachment to Fn was specifically inhibited by a Fn-receptor antibody. Endothelial cell adherence to vWf was also inhibited by a monoclonal antibody (Mab9) against the GP IIb-IIIa binding domain of vWf, but not by antibodies agains.t other portions of vWf. We have further found that 7E3 disrupts monolayers of endothelial cells by detaching the cells from their extracellular matrix. EC incubated in phorbol myris-tate.acetate (PMA) increase in size and appear more tightly adherent to their extracellular matrix. To determine if PMA increases synthesis of cellular receptors for matrix proteins, we have used cDNA probes to measure the mRNA levels of the large subunit of the Fn-receptor (FnRα) and GP IIIa in EC. After a 4 hour incubation in the presence of PMA (10 nM), there was a 2-fold increase in the mRNA levels of both FnRα and GP IIIa, as well as increased cell spreading on the matrix. We conclude: i) the GP Ilb-IIIa complex in EC is a surface receptor for specific adhesive proteins, and is distinct from the FnR, and ii) both GP IIIa and FnRα synthesis are increased by PMA, which causes a concomittant change in cell morphology.
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Nakajima, T., T. Koyama, Y. Nishida, H. Tanaka, E. Kakishita, and K. Nagai. "INHIBITORY EFFECTS OF ITP SERA ON BINDING OF ANTIPLATELET GLYCOPROTEIN (GP) IIb/IIIa MONOCLONAL ANTIBODIES TO HUMAN UMBILICAL VASCULAR ENDOTHELIAL CELLS (HUVE)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643363.

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Some ITP patients have specific autoantibodies to platelet GP IIb/IIIa. On the other hand, HUVE were shown to synthesize platelet GP IIb/IIIa like substances. Therefore, we studied the binding of ITP sera to HUVE by showing the inhibitory effect of ITP sera on the binding of anti-platelet GP IIb/IIIa monoclonal antibodies to HUVE. HUVE were cultured according to the method of Jaffe et al. 125-I-anti-platelet GP IIb/IIIa monoclonal antibody (125-I-Anti-GP) (40.3 mCi/mg), 40 yl, was added to a cell suspension of HUVE (1.5 × 104/500 μl) in a plastic RIA tube. After incubation for 30 min. at 4°C and centrifugation of 10,000 xg for 3 min., the radioactivity of the cell pellet was measured. Specific binding was determined by determining the difference between cell-bound radioactivity in the absence and presence of an excess amount of unlabelled ligand at 100 x concentrations. Scatchard analysis using 125-I-Anti-GP showed that the maximum binding capacity was 8 × 104/cell and Kd was 40.2 nM. The binding rate of 125-I-Anti-GP to HUVE treated with ITP (high PAIgG) sera (n=6) was 15.2±3.3% compared with 24.0±7.5%, observed for HUVE treated with normal sera (n=10). Treatment of ITP sera to HUVE significantly lowered the binding of 125-I-Anti-GP to HUVE (P<0.05). A combined analysis of SDS-PAGE and Western blotting of washed platelet and endothelial cell lysates shows that two proteins from each cells had similar or identical molecular masses to GP IIb/IIIa.These findings show that there are GP IIb/IIIa on the HUVE, ITP sera from our patients may have antibodies to HUVE GP IIb/IIIa and that anti-platelet GP IIb/IIIa antibodies in the ITP sera may bound not only to some platelets, but also to the HUVE
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Altieri, Dario C., Rossella Bader, and Pier M. Mannucci. "CHARACTERIZATION OF THE FUNCTIONAL ADHESION PROPERTY OF THE MONOCYTE FIBRINOGEN RECEPTOR WITH A MONOCLONAL ANTIBODY (Mab) DIRECTED TO THE ACTIVATED STATE OF THE PLATELET GLYCOPROTEIN (GP) IIb/IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643849.

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We recently showed that human blood monocytes bind fibrinogen through a genuine surface antigen only in part similar to the platelet GP Ilb/IIIa. Moreover, some anti-GP IIb/IIIa Mabs cross-react with monocytes. In this study we used the 7E3 Mab which preferentially binds to the activated conformation of the platelet GP IIb/IIIa to characterize the dynamic mechanism of "exposure" of the monocyte fibrinogen receptor. 7E3 Mab (25 μg/ml) completely suppressed the binding of i25I-fibrinogen to ADP (10μM)-stimulated monocytes. However, differently from the platelet GP IIb/IIIa, 125I-7E3 binding to unstimulated monocytes was a non-specific and non-saturable reaction. In contrast, after stimulation with ADP (10 μM), suspensions of human monocytes bound 125I-7E3 with saturation of 25-30 μg/ml of added Mab. Scatchard plot analysis was a single-affinity straight line revealing 97,400 binding sites/monocyte with a dissociation constant of 5.2×10−8 M. The monocyte surface antigen uniquely expressed after ADP-activation recognized by 7E3 was visualized by immunoprecipitation studies. Surface iodinated platelet lysate subjected to immunoprecipitation with 7E3 revealed a single band with molecular weight (Mr) of 116,000 corresponding to the platelet GP IIb/IIIa. In contrast, monocytes showed a dimeric surface antigen precipitated by 7E3 in two subunits with Mr=l55,000 and 95,000 respectively. These data indicate that the adhesion properties of the monocyte fibrinogen receptor defined by an anti-platelet GP IIb/IIIa cross-reacting Mab are structurally and functionally distinct from those of the platelet receptor.
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Giltay, J. C., O. C. Leeksma, C. Breederveld, and J. A. van Mourik. "NORMAL SYNTHESIS AND EXPRESSION OF ENDOTHELIAL GP IIb/IIIa IN GLANZMANN'S THROMBASTENIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642817.

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In Glanzmann’s thrombastenia (GT), an autosomal recessive inherited hemorrhagic disease, the platelet membrane glycoprotein (GP) IIb/IIIa complex is absent or reduced. Recently we and others demonstrated that cultured human umbilical vein endothelial cells synthesize a membrane protein complex that is structurally closely related to GP IIb/IIIa. Endothelial cells of thrombasthénie patients could, therefore be deficient in GP IIb/IIIa. We had the opportunity to culture endothelial cells isolated from the umbilical cord of a newborn with GT and to examine the plasma membrane composition of these cells. Employing a variety of immunochemical techniques, including immunoprecipitation, immunofluorescence staining and crossed immunoelectrophoresis, we demonstrated that the endothelial cells of the patient were indistinguishable from normal endothelial cells in their ability to synthesize and express GP IIb/IIIa. Our results indicate that GT is not accompanied by and "endotheliopathy".Zwa (P1A1) is an alloantigen, located on platelet GP IIIa, and, consequently, Zwa is absent on GT platelet. Data will he presented which show that not only normal endothelial IIIa carries the Zwa antigen, hut also GT endothelial cells normally express Zwa. This finding supports our view that GT endothelial GP IIb/IIIa is indistinguishable from normal endothelial GP IIb/IIIa. Moreover, this finding directly shows that the thrombastenic glycoprotein abnormality and the inheritance of Zwa antigen are controlled by different genes.
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Pidard, D., A. Fischer, C. Bouillot, F. Ledeist, and A. T. Nurden. "INHERITED DEFICIENCIESCAN AFFECT SEPARATELY THE PLATELET MEMBRANE GLYCOPROTEIN Ilb-IIIa COMPLEX AND THE LEUKOCYTE LFA-1, Mac-1 and pl50,95 COMPLEXES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643704.

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The human platelet membrane glycoprotein (GP) IIb-IIIa complex and a family of functional leukocyte cell membrane antigens, LFA-1 (L), Mac-1 (M) andpl50,95 (X), possess knownstructural analogies. Similaritiesinclude a heterodimeric structure with a high mol. wt. αsubunit (Mr∽ 145-180 kDa) , associated nonconvalently with a lower mol. wt.β-subunit (Mr ∽ 90-95 kDa),anda partial amino acid sequence hommology between GP lib and αL or CKM. Furthermore, GP lib, α L and αM were reported to be co-expressed in murine cells transfected with a 20 kilobase human DNA fragment.To address the question of a possible genomic linkage between these related glycoproteins of different cells, we have examined patients with either ‘LFA-1 immunodeficiency disease’ or with Glanzmann's thrombasthenia (GT). S.Bo. and P.Ce. are children affected by recurrent bacterial infections since birth. Cytofluorimetric analysis using monoclonal antibodies (MAbs) for the αL, αM,αX and β subunits demonstrated that the surface expression of LFA-1, Mac-1 and pl50,95 intheir leukocytes was ≤1% of the normal values. Platelets from both patients aggregated normally and readily bound the MAbs AP-2 (anti-GP IIb-IIIa) or Tab (anti-GP IIb). Crossed immunoelectrophoresis confirmed the presenceof GP IIb-IIIa complexes, whileSDS-polyacrylamide gel electrophoresis showed a normal migration of GP IIb and GP IIIa. Patients C. Bl. and M.Ca.are typical of the type I subgroupofGT. Their platelets are unable toaggregate and contain < 1% of the normal platelet content of GP liband GP Ilia.Cytofluoro-graphy showed a normal expression of LFA-1, Mac-1 and 150,95 on the surface of lymphocytes, polymorphonuclear cells and/or monocytes of both patients. Our data thus show that despite sequence homologies and a potential genomic linkage, the cellular expression of the platelet GP IIb-IIIa complex and of the LFA-1 related leukocyte antigens may be dissociated in genetic disorders where anabnormal glycoprotein distribution may be restricted to one type of cell.
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10

Thorsen, L. I., B. Hessel, F. Brosstad, G. Gogstad, and N. O. Solum. "THE N-DSK γ-CHAIN BINDS TO IMMUNOPRECIPITATED GP IIBIIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643774.

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We have previously demonstrated binding of the CNBr-split N-terminal disulphide knot of the fibrinogen molecule (N-DSK) to blood platelets and to their immunoprecipitated fibrinogen receptor, the glycoprotein IIb-IIIa complex. To further investigate which part of the N-DSK molecule that is responsible for its binding to GP IIb-IIIa, this fragment was split into its separate Aα (1-51), Bβ (1-118) and γ- (1-78) chains and carboxymethylated. GP IIb-IIIa was immunoprecipitated by crossed immunoelectrophoresis (CIE) of Triton X-100 extracts of platelets against rabbit antibodies to whole platelet proteins. The CIE plates were incubated with 125-I-radiolabelled N-DSK chains, and investigated for binding by autoradiography. The γ-chain but not the Aβ or Bβchains demonstrated binding to the GP IIb-IIIa. These results demonstrate that the fibrinogen molecule contains a third sequence of amino acids which is capable of binding to the fibrinogen receptor of the blood platelets, in addition to the two previously reported sequences C-terminally in the Aα-and γ-chains. Fragment E derived from fibrinogen (E fg) does not interact with the fibrinogen receptor. Thus, the γ-chain interaction site can not be present in the E fg-γ-chain (1-53). However, fragment E derived from fibrin (E1) with the γ-chain of residues 1-62, does react. The residues of N-DSK and E1 which are involved in binding to GP IIb-IIIa therefore appear to be present in the γ-chain sequences 54-62.
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Reports on the topic "GP IIb"

1

PEELER, DAVID. The Impact of the Proposed delta Gp Limits on Glass Formulation Efforts: Part II. Experimental Results. Office of Scientific and Technical Information (OSTI), July 2004. http://dx.doi.org/10.2172/835580.

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2

Holland, Darren, and Nazmina Mahmoudzadeh. Foodborne Disease Estimates for the United Kingdom in 2018. Food Standards Agency, January 2020. http://dx.doi.org/10.46756/sci.fsa.squ824.

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In February 2020 the FSA published two reports which produced new estimates of foodborne norovirus cases. These were the ‘Norovirus Attribution Study’ (NoVAS study) (O’Brien et al., 2020) and the accompanying internal FSA technical review ‘Technical Report: Review of Quantitative Risk Assessment of foodborne norovirus transmission’ (NoVAS model review), (Food Standards Agency, 2020). The NoVAS study produced a Quantitative Microbiological Risk Assessment model (QMRA) to estimate foodborne norovirus. The NoVAS model review considered the impact of using alternative assumptions and other data sources on these estimates. From these two pieces of work, a revised estimate of foodborne norovirus was produced. The FSA has therefore updated its estimates of annual foodborne disease to include these new results and also to take account of more recent data related to other pathogens. The estimates produced include: •Estimates of GP presentations and hospital admissions for foodbornenorovirus based on the new estimates of cases. The NoVAS study onlyproduced estimates for cases. •Estimates of foodborne cases, GP presentations and hospital admissions for12 other pathogens •Estimates of unattributed cases of foodborne disease •Estimates of total foodborne disease from all pathogens Previous estimates An FSA funded research project ‘The second study of infectious intestinal disease in the community’, published in 2012 and referred to as the IID2 study (Tam et al., 2012), estimated that there were 17 million cases of infectious intestinal disease (IID) in 2009. These include illness caused by all sources, not just food. Of these 17 million cases, around 40% (around 7 million) could be attributed to 13 known pathogens. These pathogens included norovirus. The remaining 60% of cases (equivalent to 10 million cases) were unattributed cases. These are cases where the causal pathogen is unknown. Reasons for this include the causal pathogen was not tested for, the test was not sensitive enough to detect the causal pathogen or the pathogen is unknown to science. A second project ‘Costed extension to the second study of infectious intestinal disease in the community’, published in 2014 and known as IID2 extension (Tam, Larose and O’Brien, 2014), estimated that there were 566,000 cases of foodborne disease per year caused by the same 13 known pathogens. Although a proportion of the unattributed cases would also be due to food, no estimate was provided for this in the IID2 extension. New estimates We estimate that there were 2.4 million cases of foodborne disease in the UK in 2018 (95% credible intervals 1.8 million to 3.1 million), with 222,000 GP presentations (95% Cred. Int. 150,000 to 322,000) and 16,400 hospital admissions (95% Cred. Int. 11,200 to 26,000). Of the estimated 2.4 million cases, 0.9 million (95% Cred. Int. 0.7 million to 1.2 million) were from the 13 known pathogens included in the IID2 extension and 1.4 million1 (95% Cred. Int. 1.0 million to 2.0 million) for unattributed cases. Norovirus was the pathogen with the largest estimate with 383,000 cases a year. However, this estimate is within the 95% credible interval for Campylobacter of 127,000 to 571,000. The pathogen with the next highest number of cases was Clostridium perfringens with 85,000 (95% Cred. Int. 32,000 to 225,000). While the methodology used in the NoVAS study does not lend itself to producing credible intervals for cases of norovirus, this does not mean that there is no uncertainty in these estimates. There were a number of parameters used in the NoVAS study which, while based on the best science currently available, were acknowledged to have uncertain values. Sensitivity analysis undertaken as part of the study showed that changes to the values of these parameters could make big differences to the overall estimates. Campylobacter was estimated to have the most GP presentations with 43,000 (95% Cred. Int. 19,000 to 76,000) followed by norovirus with 17,000 (95% Cred. Int. 11,000 to 26,000) and Clostridium perfringens with 13,000 (95% Cred. Int. 6,000 to 29,000). For hospital admissions Campylobacter was estimated to have 3,500 (95% Cred. Int. 1,400 to 7,600), followed by norovirus 2,200 (95% Cred. Int. 1,500 to 3,100) and Salmonella with 2,100 admissions (95% Cred. Int. 400 to 9,900). As many of these credible intervals overlap, any ranking needs to be undertaken with caution. While the estimates provided in this report are for 2018 the methodology described can be applied to future years.
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