Relevant bibliographies by topics / Platelet aggregation

Academic literature on the topic 'Platelet aggregation'

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Published: 4 June 2021
Last updated: 22 February 2023

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Journal articles on the topic "Platelet aggregation"

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Sugiyama, T., M. Okuma, F. Ushikubi, S. Sensaki, K. Kanaji, and H. Uchino. "A novel platelet aggregating factor found in a patient with defective collagen-induced platelet aggregation and autoimmune thrombocytopenia." Blood 69, no. 6 (June 1, 1987): 1712–20. http://dx.doi.org/10.1182/blood.v69.6.1712.1712.

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Abstract We found a novel platelet aggregating factor in a patient with steroid- responsive immune thrombocytopenic purpura that is associated with defective collagen-induced platelet functions. The aggregating factor and platelet functions were analyzed. The patient, a 58-year-old female, had purpura and prolonged bleeding time despite adequate platelet counts (greater than 140,000/microL) after steroid therapy. The patient's platelets responded normally to all agonists except collagen. Platelet adhesion to collagen fibrils was decreased. The patient's plasma induced irreversible aggregation and ATP release in normal platelet-rich plasma (PRP). This platelet aggregating factor was found in F(ab')2 fragments of the patient's IgG, which caused thromboxane B2 synthesis, elevation of cytoplasmic Ca2+ levels, and phosphorylation of 40 kDa protein in normal platelets. Platelet aggregation by the patient's IgG was inhibited by prostacyclin, dibutyryl cAMP, diltiazem, disodium ethylenediaminetetraacetate, and antimycin A plus iodoacetate, but ADP scavengers, cyclo-oxygenase inhibitors, and heparin had little or no effect. The aggregating activity of the patient's IgG absorbed to and eluted from normal platelets. The patient's Fab fragments did not induce platelet aggregation in eight of ten normal PRP but specifically inhibited aggregation induced by collagen and by the patient's IgG. The major component of an immunoprecipitate made with the patient's IgG from radiolabeled membrane proteins of normal platelet extract had a 62 kDa mol wt, while no such precipitate appeared in extracts of the patient's platelets. These results indicated that platelet aggregation by the patient's IgG was induced by the reaction of an antibody with a specific antigen on the normal platelet membrane through stimulus- response coupling. This antigen may be a collagen receptor on the platelet, most likely a polypeptide of 62 kDa under reducing condition. The defect of collagen-induced aggregation of the patient's platelets seemed to be due to alteration of the membrane protein related to this putative collagen receptor.
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Sugiyama, T., M. Okuma, F. Ushikubi, S. Sensaki, K. Kanaji, and H. Uchino. "A novel platelet aggregating factor found in a patient with defective collagen-induced platelet aggregation and autoimmune thrombocytopenia." Blood 69, no. 6 (June 1, 1987): 1712–20. http://dx.doi.org/10.1182/blood.v69.6.1712.bloodjournal6961712.

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We found a novel platelet aggregating factor in a patient with steroid- responsive immune thrombocytopenic purpura that is associated with defective collagen-induced platelet functions. The aggregating factor and platelet functions were analyzed. The patient, a 58-year-old female, had purpura and prolonged bleeding time despite adequate platelet counts (greater than 140,000/microL) after steroid therapy. The patient's platelets responded normally to all agonists except collagen. Platelet adhesion to collagen fibrils was decreased. The patient's plasma induced irreversible aggregation and ATP release in normal platelet-rich plasma (PRP). This platelet aggregating factor was found in F(ab')2 fragments of the patient's IgG, which caused thromboxane B2 synthesis, elevation of cytoplasmic Ca2+ levels, and phosphorylation of 40 kDa protein in normal platelets. Platelet aggregation by the patient's IgG was inhibited by prostacyclin, dibutyryl cAMP, diltiazem, disodium ethylenediaminetetraacetate, and antimycin A plus iodoacetate, but ADP scavengers, cyclo-oxygenase inhibitors, and heparin had little or no effect. The aggregating activity of the patient's IgG absorbed to and eluted from normal platelets. The patient's Fab fragments did not induce platelet aggregation in eight of ten normal PRP but specifically inhibited aggregation induced by collagen and by the patient's IgG. The major component of an immunoprecipitate made with the patient's IgG from radiolabeled membrane proteins of normal platelet extract had a 62 kDa mol wt, while no such precipitate appeared in extracts of the patient's platelets. These results indicated that platelet aggregation by the patient's IgG was induced by the reaction of an antibody with a specific antigen on the normal platelet membrane through stimulus- response coupling. This antigen may be a collagen receptor on the platelet, most likely a polypeptide of 62 kDa under reducing condition. The defect of collagen-induced aggregation of the patient's platelets seemed to be due to alteration of the membrane protein related to this putative collagen receptor.
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Teng, Che-Ming, Ya-Fei Kang, Ya-Ling Chang, Feng-Nien Ko, Shu-Chen Yang, and Feng-Lin Hsu. "ADP-mimicking Platelet Aggregation Caused by Rugosin E, an Ellagitannin Isolated from Rosa rugosa Thunb." Thrombosis and Haemostasis 77, no. 03 (1997): 555–61. http://dx.doi.org/10.1055/s-0038-1656005.

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SummaryAmong the nine ellagitannins, rugosin E was the most potent platelet aggregating agent with an EC50 of 1.5 ± 0.1 µM in rabbit platelets and 3.2 ±0.1 µM in human platelets. The aggregations caused by rugosin E and ADP were inhibited by EGTA, PGE1, mepacrine, sodium nitroprusside and neomycin, but not by indomethacin, verapamil, TMB-8, BN52021 and GR32191B. Rugosin E-induced thromboxane formation was suppressed by indomethacin, EGTA, PGE,, verapamil, mepacrine, TMB-8 and neomycin. ADP-scavenging agents, such as CP/CPK and apyrase inhibited concentration-dependently ADP (20 εM)-, but not rugosin E (5 εM)-induced platelet aggregation. In thrombin (0.1 U/ml)-treated and degranulated platelets, rugosin E and ADP still caused 63.5 ± 3.0% and 61.2 ± 3.5% of platelet aggregation, respectively. Selective ADP receptor antagonists, ATP and FSBA inhibited rugosin E- and ADP-induced platelet aggregations in a concentration-dependent manner. Both rugosin E and ADP did not induce platelet aggregation in ADP (1 mM)-desensitized platelets. In contrast to ADP, rugosin E did not decrease cAMP formation in washed rabbit platelets. Both rugosin E and ADP did not cause phosphoinositide breakdown in [3H]myo-inositol-labeled rabbit platelets. In fura-2/AM- load platelets, both rugosin E and ADP induced increase in intracellular calcium concentration and these responses were inhibited by ATP and PGEj. All these data suggest that rugosin E may be an ADP receptor agonist in rabbit platelets.
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Higashihara, M., H. Maeda, Y. Shibata, S. Kume, and T. Ohashi. "A monoclonal anti-human platelet antibody: a new platelet aggregating substance." Blood 65, no. 2 (February 1, 1985): 382–91. http://dx.doi.org/10.1182/blood.v65.2.382.382.

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Abstract A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich plasma and with washed platelets, but not with formalin-fixed washed platelets. TP82- induced aggregation was completely inhibited by disodium ethylendiaminotetraacetate, diltiazem, W-7, PGE1, and several metabolic inhibitors. At a concentration of apyrase or CP/CPK, which inhibited adenosine 5-diphosphate-induced aggregation. TP82-induced aggregation was only partially affected. Thrombin was not required for the antibody- mediated effects, since two thrombin inhibitors failed to block the reaction. The antibody, at least at a high concentration, induced platelet aggregation by a mechanism almost independent of thromboxane A2 formation, since cyclooxygenase inhibitors had little inhibitory effect on aggregation. TP82 monoclonal antibody is a new platelet- aggregating substance that interacts with a low-molecular-weight binding site on the platelet membrane.
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Higashihara, M., H. Maeda, Y. Shibata, S. Kume, and T. Ohashi. "A monoclonal anti-human platelet antibody: a new platelet aggregating substance." Blood 65, no. 2 (February 1, 1985): 382–91. http://dx.doi.org/10.1182/blood.v65.2.382.bloodjournal652382.

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A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich plasma and with washed platelets, but not with formalin-fixed washed platelets. TP82- induced aggregation was completely inhibited by disodium ethylendiaminotetraacetate, diltiazem, W-7, PGE1, and several metabolic inhibitors. At a concentration of apyrase or CP/CPK, which inhibited adenosine 5-diphosphate-induced aggregation. TP82-induced aggregation was only partially affected. Thrombin was not required for the antibody- mediated effects, since two thrombin inhibitors failed to block the reaction. The antibody, at least at a high concentration, induced platelet aggregation by a mechanism almost independent of thromboxane A2 formation, since cyclooxygenase inhibitors had little inhibitory effect on aggregation. TP82 monoclonal antibody is a new platelet- aggregating substance that interacts with a low-molecular-weight binding site on the platelet membrane.
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Burgess-Wilson, ME, SR Cockbill, GI Johnston, and S. Heptinstall. "Platelet aggregation in whole blood from patients with Glanzmann's thrombasthenia." Blood 69, no. 1 (January 1, 1987): 38–42. http://dx.doi.org/10.1182/blood.v69.1.38.38.

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Abstract We examined platelet aggregation in platelet-rich plasma (PRP) and in whole blood from two patients with Glanzmann's thrombasthenia. In PRP, aggregation was measured by monitoring the changes in light absorbance that occurred in response to aggregating agents; to measure platelet aggregation in whole blood, we used a platelet counting technique. In PRP, the patients' platelets showed defective aggregation in response to ADP, adrenaline, arachidonic acid (AA), and collagen, but normal agglutination occurred in response to ristocetin. In whole blood, however, platelet aggregation in response to the aggregating agents appeared to be either very similar to that which occurred in blood from normal subjects or only slightly reduced. There was a reduced response to all concentrations of ADP and to low concentrations of collagen but a normal response to all concentrations of adrenaline, AA, and higher concentrations of collagen. Conversely, there seemed to be an increased agglutination response to ristocetin. The abnormality in our two patients with Glanzmann's thrombasthenia probably lies in the inability of their platelets to form large, macroscopic aggregates rather than in platelet aggregation per se.
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Burgess-Wilson, ME, SR Cockbill, GI Johnston, and S. Heptinstall. "Platelet aggregation in whole blood from patients with Glanzmann's thrombasthenia." Blood 69, no. 1 (January 1, 1987): 38–42. http://dx.doi.org/10.1182/blood.v69.1.38.bloodjournal69138.

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We examined platelet aggregation in platelet-rich plasma (PRP) and in whole blood from two patients with Glanzmann's thrombasthenia. In PRP, aggregation was measured by monitoring the changes in light absorbance that occurred in response to aggregating agents; to measure platelet aggregation in whole blood, we used a platelet counting technique. In PRP, the patients' platelets showed defective aggregation in response to ADP, adrenaline, arachidonic acid (AA), and collagen, but normal agglutination occurred in response to ristocetin. In whole blood, however, platelet aggregation in response to the aggregating agents appeared to be either very similar to that which occurred in blood from normal subjects or only slightly reduced. There was a reduced response to all concentrations of ADP and to low concentrations of collagen but a normal response to all concentrations of adrenaline, AA, and higher concentrations of collagen. Conversely, there seemed to be an increased agglutination response to ristocetin. The abnormality in our two patients with Glanzmann's thrombasthenia probably lies in the inability of their platelets to form large, macroscopic aggregates rather than in platelet aggregation per se.
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Refaai, Majed A., Kelly F. Henrichs, Sherry L. Spinelli, Richard P. Phipps, Edward Masel, Brian H. Smith, Charles W. Francis, and Neil Blumberg. "Platelet Activation Following Exposure to Anti-ABO Antibodies— An In Vitro Study." Oncology & Hematology Review (US) 07, no. 01 (2011): 72. http://dx.doi.org/10.17925/ohr.2011.07.1.72.

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Since platelets possess A and B antigen, mismatched ABO platelets could, theoretically, become activated or hypofunctional by exposure to anti-A or anti-B antibodies found in transfused or recipient plasma. Following normal baseline platelet aggregation to adenosine diphosphate (ADP), platelets from normal donors of different blood types were incubated at 37°C for 10 minutes with 50μl of normal saline (NS), O plasma, or AB plasma. Aggregation was then induced with ADP. No significant changes from baseline were seen in platelet aggregation studies following incubation with NS. However, platelet aggregations of type A and type B platelets were significantly inhibited when incubated with O plasma (mean of 41 and 22%, respectively). Our findings indicate that mediators in group O plasma, very likely anti-A and anti-B antibodies, cause impaired platelet aggregation of ABO non-identical platelets.
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Chiang, T. M., A. Jin, and A. H. Kang. "Platelet-collagen interaction. Inhibition by a monoclonal antibody raised against collagen receptor." Journal of Immunology 139, no. 3 (August 1, 1987): 887–92. http://dx.doi.org/10.4049/jimmunol.139.3.887.

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Abstract Monoclonal antibodies to the purified platelet type I collagen receptor were produced to study platelet receptor function. The antibody specifically reacted with the platelet receptor in immunoblot experiments. The IgG purified from the monoclonal antibodies and isolated Fab' fragments inhibited the binding of radiolabeled alpha 1(I) chain to washed platelets competitively. Soluble and fibrillar type I collagen-induced platelet aggregations were inhibited by purified IgG suggesting that soluble and fibrillar collagens shared a common receptor. The adhesion of platelets to an artificial collagen matrix was also inhibited by the monoclonal antibody. However, adenosine diphosphate-induced platelet aggregation was not inhibited by the same amount of IgG that inhibited collagen-induced platelet aggregation. The results suggest that collagen-induced platelet aggregation is mediated through the interaction of collagen with the platelet receptor.
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Cimminiello, C., M. Milani, T. Uberti, G. Arpaia, and G. Bonfardeci. "Effects of Ticlopidine and Indobufen on Platelet Aggregation Induced by A23187 and Adrenaline in the Presence of Different Anticoagulants." Journal of International Medical Research 17, no. 6 (November 1989): 514–20. http://dx.doi.org/10.1177/030006058901700603.

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As Ca2+ is known to play a fundamental role in platelet function, the effect of combining two platelet aggregating agents (adrenaline and the ionophore A23187) with different effects on Ca2+ was studied at levels subthreshold for aggregation using platelet-rich plasma from eight atherosclerotic patients. Adrenaline lowered the A23187 threshold required to induce aggregation. The effects of treating patients with the antiplatelet agents, indobufen and ticlopidine, on A23187 and adrenaline induced aggregation of platelets prepared in hirudin or sodium citrate was also evaluated. Aggregation was also studied using platelets resuspended in Ca2+-free and Ca2+-enriched Tyrode solution. Before treatment hirudin treated platelet-rich plasma, which has physiological extraplatelet Ca2+ levels, was more sensitive to A23187 and adrenaline than was citrated platelet-rich plasma, which has suppressed Ca2+ levels. Ticlopidine significantly raised the concentration of A23187 required to induce aggregation in citrated but not hirudin treated platelet-rich plasma. Indobufen did not significantly affect A23187 induced aggregation. Ticlopidine acts by inhibiting the glycoprotein IIb – IIIa complex on the platelet membranes. Low levels of extracellular Ca2+ and ticlopidine may act synergistically to reduce the aggregatory response of stimulated platelets.
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Dissertations / Theses on the topic "Platelet aggregation"

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Vanags, Daina M. "Adrenergic and serotonergic potentiation of platelet aggregation /." Title page, summary and contents only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phv217.pdf.

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Burgess-Wilson, Michael Edward. "Platelet aggregation in whole blood." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=7393.

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Wong, Truman. "Dynamics of platelet shape change and aggregation size-dependent platelet subpopulations." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61778.

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Riddell, David Ramsey. "Inhibition of platelet aggregation by apolipoprotein E." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287865.

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Meikle, Claire K. "Platelet-Leukocyte Aggregation in Lung Cancer Patients." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1555937904448281.

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Sato, Masami. "Effects of barbiturates on human platelet aggregation." Kyoto University, 2003. http://hdl.handle.net/2433/148488.

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Wilson, Andrew. "Ethnicity, coronary heart disease risk and platelet aggregation." Thesis, The University of Sydney, 1996. https://hdl.handle.net/2123/27600.

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Objectives: Part A. To analyse existing risk-factor studies in the population of Sydney for differences in established risk factors, particularly smoking, blood pressure and blood lipids, between Southern-European-born migrants and Australian-born subjects. Part B. To examine a sample of Southern-European and Australia-born men without current CHD, of similar socio-economic background to: i. Compare factors relating to haemostasis and coagulation which have been reported as predictive of CHD risk, especially platelet aggregability, fibrinogen and Factor VIIc levels. ii. Compare other measures of haemostasis and coagulation which have been reported as varying among ethnic groups. iii. Examine the determinants of platelet aggregability, especially the nutrient content of their usual diet. iv. Examine the relations among established risk factor for CHD and measures of platelet aggregability.
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Bunescu, Andreia. "Cellular markers indicating activation of the hemostatic system : studies on platelets and leukocytes in peripheral human blood /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-759-2/.

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Modica, Angelo. "Inflammation, platelet aggregation and prognosis in acute myocardial infarction." Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-32519.

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Para, Andrea N. "Preventing rapid platelet accumulation under very high shear stress." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/44726.

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Atherosclerosis is a major cause of mortality in industrialized nations. Atherosclerosis is characterized by plaque deposition which decreases the lumen diameter into a stenosis. The creation of a restriction increases shear rates pathologic levels exceeding 3,500/s. Following plaque cap rupture, thrombus may form from the accumulation of millions of platelets, occluding the vessel, leading to heart attack and stroke. Studies of high shear thrombosis show that platelet activation, GPIIb/IIIa and vWF are involved. However, some recent studies also suggest that high shear aggregation is not dependent on activation or GPIIb/IIIa. Several antiplatelet pharmaceuticals against activation and GPIIb/IIIa have been proposed, but their efficacy in patients remains mixed. The overall objective of this project is to determine the factors necessary for thrombosis to occlusion in very high shear regions seen in diseased arteries. Our central hypotheses are that platelet activation and the subsequent conformational change in GPIIb/IIIa are necessary for thrombosis, and that higher concentrations of vWF in the plasma will increase thrombosis. To this end, we developed a new high shear hemodynamic model utilizing 30mLs of whole blood and quantified thrombus thickness, volume accumulation and accumulation rates. We demonstrate that thrombosis to occlusion stems from a second phase of Rapid Platelet Accumulation (RPA). Thrombus accumulation is completely prevented by PGE1 inhibition of platelet activation. Similarly, GPIIb/IIIa blockade via abciximab prevented significant thrombus deposition and RPA. We also found that increasing plasma vWF levels in high shear regions increased thrombus thickness and suggestively increased RPA rates. The results clarify the need for activation of mural platelets for long term thrombus accumulation without the activation of circulating platelets.
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Books on the topic "Platelet aggregation"

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White, Melanie McCabe. Platelet protocols: Research and clinical laboratory procedures. San Diego: Academic Press, 1999.

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1951-, Parnham Michael J., and Prop Gerrit, eds. Cologne Atherosclerosis Conference, Nr. 3, platelets. Basel: Birkhäuser, 1986.

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El-Nageh, Nuria Mabrouk. Studies on the mechanism of inhibition of blood platelet aggregation by pyridoxal-5'-phosphate. Dublin: University College Dublin, 1996.

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1932-, Oates John A., Hawiger Jacek, and Ross Russell, eds. Interaction of platelets with the vessel wall. Bethesda, Md: American Physiological Society, 1985.

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Jacek, Hawiger, ed. Platelets: Receptors, adhesion, secretion. San Diego: Academic, 1989.

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D, Cohen Marc M., ed. Handbook of antiplatelet therapy. London: Martin Dunitz, 2003.

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D, Wiviott Stephen, and American Heart Association, eds. Antiplatelet therapy in ischemic heart disease. Chichester, West Sussex, UK: Wiley-Blackwell, 2009.

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Rhône-Poulenc Santé - INSERM Conference (1985 Menthon-Saint-Bernard). Biology and pathology of platelet-vessel wall interactions: Proceedings of the Rhône-Poulenc Santé - INSERM Conference, held at Menthon-Saint-Bernard (Annecy), France, September 30th to October 2nd, 1985. London: Academic Press, 1986.

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Rhône-Poulenc Round Table Conference (4th 1985 Menthon-Saint-Bernard, France). Biology and pathology of platelet-vessel wall interactions: Proceedings of the Rhône-Poulenc Santé-INSERM Conference, held at Menthon-Saint-Bernard (Annecy), France, September 30th to October 2nd, 1985. London: Academic Press, 1986.

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1943-, O'Flaherty Joseph T., Ramwell Peter W, and International Business Communications Inc, eds. PAF antagonists: New developments for clinical application. Woodlands, Tex: Portfolio Pub. Co., 1990.

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Book chapters on the topic "Platelet aggregation"

1

Hayward, Catherine P. M., and Karen A. Moffat. "Platelet Aggregation." In Platelets in Thrombotic and Non-Thrombotic Disorders, 619–35. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47462-5_41.

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Ruf, A., M. M. Frojmovic, and H. Patscheke. "Platelet Aggregation." In Platelets and Their Factors, 83–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60639-7_4.

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Born, G. V. R. "Platelet Aggregation Inhibitors." In Secondary Prevention in Coronary Artery Disease and Myocardial Infarction, 95–100. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5024-5_11.

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Lakin, K. M., and V. A. Makarov. "Inhibitors of Platelet Aggregation." In Thrombosis and Thrombolysis, 311–63. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1659-6_13.

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Gryglewski, R. J., J. Robak, and J. Swięs. "Flavonoids — Lipoxygenases — Platelet Aggregation." In Drugs Affecting Leukotrienes and Other Eicosanoid Pathways, 149–66. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-7841-9_13.

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Arulprakasam, Karthick Raja, and Dhanasekaran Dharumadurai. "Assessment of Platelet Aggregation." In Methods and Protocols in Food Science, 165–70. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2509-5_18.

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Metze, Dieter, Tam Nguyen, Birgit Haack, Alexander K. C. Leung, Noriko Miyake, Naomichi Matsumoto, A. J. Larner, et al. "Defects in Platelet Aggregation." In Encyclopedia of Molecular Mechanisms of Disease, 498. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9132.

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Douste-Blazy, L., G. Mauco, B. Perret, M. Plantavid, F. Laffont, M. F. Simon, and H. Chap. "Phospholipids and Platelet Aggregation." In Lipid Metabolism and Its Pathology, 61–66. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2445-4_7.

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Nachman, Ralph L., Lawrence L. K. Leung, and Margaret J. Polley. "Molecular Mechanisms of Platelet Adhesion and Platelet Aggregation." In Platelet Membrane Glycoproteins, 245–57. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4880-1_11.

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Clemetson, K. J., and J. Polgár. "Platelet Adhesion and Aggregation Receptors." In Platelets and Their Factors, 155–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60639-7_8.

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Conference papers on the topic "Platelet aggregation"

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Ikeda, Y., M. Murata, Y. Araki, M. Yamamoto, K. Watanabe, M. Ichitani, K. Sakai, I. Itagaki, and Y. Mori. "BINDING OF FIBRINOGEN TO PLATELET GLYCOPROTEIN (GP) IIb/IIIa IS CRUCIAL FOR SHEAR-INDUCED PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643527.

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It is well known that human platelets can aggregate in vitro under certain shear stress without adding aggregating inducers. However, the mechanism of this shear-induced platelet aggregation has not been clarified yet. In this paper, we have investigated the role of fibrinogen and GP IIb/IIIa in shear-induced platelet aggregation. Citrated human platelet-rich plasma (PRP) was subjected to controlled shear stress levels in a polycarbonate cone and plate viscometer at 37°C for 2 minutes. After shearing the particle count was measured by an electronic particle counter. Particles with sizes from 3 to 20 μ cum were considered as single platelets. In unsheared PRP most of the particles were single platelets, but platelet doublets and platelet fragments larger than 3 μ cum were also counted. After exposure to shear rate of 3,600 - 9,000 sec−1 , the particle counts were decreased in a shear rate dependent manner, while LDH leakage from platelets was not significantly increased and 3H-serotonin release was 2-7%. Scanning electronmicroscopy clearly showed the presence of large platelet aggregates when the particle counts were decreased. Platelets from two patients with thrombasthenia and one patient with afibrinogenemia, however, failed to aggregate at a shear rate of 9,000 sec−1. Shear-induced aggregation was inhibited by monoclonal antibody to GPIIb/IIIa (1 μg/ml) and synthetic peptide, Arg-Gly-Asp-Ser, (1 mM). When fibrinogen was added to PRP from a patient with afibrinogenemia, shear-induced aggregation became evident as seen in normal platelets. Apyrase and hirudin showed no effect on shear-induced aggregation. Indomethacin (100 μM) and TXA2 synthetase inhibitor, OKY-046 (100 μM) markedly inhibited aggregation, while TXA2 competitive inhibitor, ONO-3708 (100 μM) exhibited only partial inhibition.Our results indicate that binding of fibrinogen to GPIIb/lIIa is also crucial for shear-induced platelet aggregation and that the exposure of fibrinogen receptor on GPIIb/IIIa may partially depend upon TXA2 synthesis in platelets.
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2

Bryckaert, M. C., A. Wasteson, G. Tobelem, F. Rendu, and J. P. Caen. "PLATELET DERIVED GROWTH FACTOR (PDGF) BINDS TO HUMAN PLATELETS AND MODULATES PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643493.

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PDGF which is released during platelet activation like the other ∝ granule components (fibrinogen, F VIII/vWF, PF4) could bind to platelet membrane Following this hypothesis, we have studied the binding of 125I pure human PDGF to washed human platelets activated by collagen. This binding was specific and time dependent and reached a plateau with 20 μg/ml of collagen. With 200 fold excess of unlabeled PDGF, the binding of 125I-PDGF decreased progressively to 10 .whereas unlabeled Epidermal Growth Factor did not compete with 125I-PDGF. Saturation curve and scatchard analysis have shown one class of sites 3,000 sites/cell with an apparent Kd = 10-8 M. The demonstration of PDGF binding to platelets led us to investigate the effects of PDGF on platelet function. PDGF inhibited the aggregation and 14C serotonin release induced by thrombin or collagen. This inhibition was dose dependent and more effective with human PDGF. A total inhibition of collagen-induced platelet aggregation was obtained with 50 ng/ml of human PDGF and 200 ng/ml of porcine PDGF. The aggregation and 14C serotonin release induced by arachidonic acid were not inhibited by PDGF. The metabolism of phosphoinositide was also investigated on washed human platelets prelabeled with 32P orthophosphate. We found that PDGF (200 ng/ml) induced a decrease of 32P associated with phosphatidylinositol 4 biphosphate (72 %) after 3 min, with a parallel increase of 32P-phosphatidylinositol 4 Phosphate (120 %) and 32P-phosphatidylinositol (120 %).In conclusion i) PDGF binds to activated platelets, ii) PDGF inhibits platelet aggregation and secretion, iii) PDGF modifies phosphoinositide metabolism. These results are in favour of a role of PDGF in a negative feed back control of platelet activation.
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Jansen, J. W. C. M. "EFFECTS OF INHIBITORS ON COLLAGEN INDUCED PLATELET AGGREGATION IN SIX DIFFERENT SPECIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643445.

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One approach to the development of antithrombotics is inhibition of platelet aggregation. The pharmacological approach often used is to test compounds on collagen induced platelet aggregation measured in platelet rich plasma. Therefore we have compared inhibitors with different mechanism of action on aggregation of platelets from six different species commonly used in pharmacological studies. Aggregation was induced with submaximal amounts of collagen (Hormone Chemie).Inhibitors of the cyclooxygenase system, aspirin and indomethacin, were very potent in inhibiting aggregation of platelets from humans guinea pig and dog (IC50 20-60 and 1-3 ¼M resp.). Aggregation of pig and rat platelets was poorly inhibited by both of these compounds (IC5: 700-900 ¼M), whereas platelets from mice showed intermediate sensitivety (IC50 ca.100 ¼M).The combined lipoxygenase/cyclooxygenase inhibitor BW755C, was extremely active on platelets of guinea pig (IC50 1 ¼M) and was poorly active in mice platelets (IC50 300 ¼M). In the other species the inhibitory activity ranged from 20-80 ¼M.The phosphodiesterase inhibitors, papaverine and BL3459 inhibited aggregation in all species (IC50 50-100 and 1-5 ¼M resp.). Dipyridamole inhibited aggregation also in all species but with lower activity (IC50 > 100 ¼M).Conclusion: remarkable species differences are present with respect to inhibition of collagen induced platelet aggregation by the various compounds e.g. rat and porcine platelet aggregation was hardly inhibited by cyclooxygenase inhibitors. The effects of the compounds on human platelets are comparable to the effects on canine plateletes.
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4

Fogelson, Aaron, and Haoyu Yu. "Computational Modeling of Platelet Aggregation." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0389.

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Abstract Platelet aggregation is an essential component of normal hemostasis and pathological thrombosis. It involves complex, dynamic, often competitive, mechanical and chemical interactions among platelets, fluid, and vessel wall, the balance among which determines whether and to what extent aggregate growth occurs and persists. It is very difficult in a laboratory setting to measure more than a few quantities of interest, and usually only at a few spatial locations or a few times. From such measurements, it is very hard to piece together a coherent picture of the dynamics. Further it is very difficult to control more than a couple of the players involved. Mathematics, by contrast, is well suited for studying the evolution of a complex system, and for precisely controlling the inputs into the system. It can provide a wealth of temporal and spatial detail about the interactions taking place. It allows for extraction of ‘essential’ elements of the complex system, and through study of the behavior of the simplified system can provide insight into the workings of the true biological system. It thus complements more traditional experimental approaches. But the mathematical study of platelet aggregation presents its own substantial challenges, among them how to handle the mechanical interactions between fluid and platelets, platelets and other platelets, and platelets and vessels walls. This talk is addressed at ways to meet these challenges.
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Mannucci, L., R. Redaelli, and E. Tremoll. "EFFECTS OF BLOOD CELLS ON PLATELET AGGREGATION BY IMPEDANCE METHOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644870.

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To evaluate the effects of blood cells on the response of platelets to aggregating agents using whole blood impedance aggregometer, studies were carried out on whole blood (WB) of normal subjects and of patients with: polycythemia vera (PV), iatrogenic anemia (IA), primary thrombocytosis (PT), idiopathic thrombotic purpura (ITP), myeloid chronic leukemia (MCL), iatrogenic leukopenia (IL). The in vitro effects of red blood cells (RBC) and of white blood cells (WBC) on platelet rich plasma (PRP) aggregation were also evaluated. WB, PRP, WBC and RBC were prepared by conventional methods. Aggregation was performed using the impedance aggregometer (mod. 540, Chrono Log Corp). In normal subjects the concentration of collagen giving 50 % aggregation (AC50 ) found in PRP did not differ from that of WB, indicating that hematocrit values within the normal range did not appreciably affect platelet aggregation. The results obtained in WB of patients are summarized in the table: In vitro data showed that aggregation in prp in wb of normal subjects was related to the number of platelets present in the sample. RBC added to PRP significant reduced aggregation only when the RBC number was greater than 4.101 cells. No effect of WBC on collagen induced aggregation of PRP was observed, whereas significant inhibition was detected after ADP. It is concluded that the aggregation evaluated in WB with impedance method is dependent on the platelet number. Also, in vitro data and studies in WB of patients indicate that aggregation is significantly affected by the presence of cells other than platelets only in conditions of changes of the ratio between platelets and leukocytes and/or red cells.
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6

Okita, J. R., M. M. Frojmovic, S. Kristopeit, T. Wong, and T. J. Kunicki. "MONTREAL PLATELET SYNDROME: DECREASED ACTIVITY OF PLATELET CALPAINS ASSOCIATED WITH AGGREGATION ABNORMALITIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642822.

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The Montreal platelet syndrome (MPS) is an inherited disorder of platelet function characterized by a) severe thrombocytopenia, b) formation of "giant" platelets upon physical or biochemical stimulation, c) spontaneous aggregation (stir-induced microaggregate formation) and d) a lack of aggregation in response to thrombin. The Bernard-Soulier syndrome (BSS) is similar to MPS in that both syndromes are characterized by "giant" platelets and an abnormal aggregation response to thrombin. BSS patients have a deficiency of specific platelet glycoproteins (GPs). From our investigations we conclude MPS patients have apparently normal amounts of major platelet GPs. However, a defect in calpains (calcium-activated neutral proteinases) was detected in MPS platelets. The specific activity of calpains was decreased by 70% (p<0.001) in the cytosolic fraction of platelets from MPS patients as compared to that of platelets from normal control donors. The calpain activity of platelets from BSS patients was within the normal range.During the course of the biochemical studies, platelets from the MPS patients were shown to exhibit concurrent functional defects, i.e., stir-induced spontaneous aggregation and reduced to absent aggregation response to thrombin. It is concluded that MPS can be distinguished from BSS at the molecular level as follows: 1) MPS platelets contain normal amounts of GPs Ib, V and IX which are decreased or absent in BSS platelets; 2) The specific activity of calpains is reduced in MPS platelets but normal in BSS platelets. Supported by NIH (HL-33925, HL-32279), Amer. Heart Assoc. (85—GA—67, 83-186), Canadian Med. Res. Council (248-59) and Quebec Heart Fndn.
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7

Casonato, A., L. De Marco, M. G. Del Ben, M. Mazzucato, F. Fabris, Z. M. Ruggeri, and A. Girolami. "A NEW PLATELET DISFUNCTION CHARACTERIZED BY SPONTANEOUS PLATELET AGGREGATION AND ENHANCED von WILLEBRAND FACT0R-PLATELET INTERACTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644101.

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The proposita is a 48 years old woman who presents mild bleeding tendency and a bleeding time of 7 min. (n. 6 min ± 1.4). Her platelet count is within normal limits and has normal plasma Factor VIII coagulant activity, Ristocetin cofactor activity, von Willebrand Factor (vWF) antigen and vWF multimeric pattern. Spontaneous platelet aggregation (SPA) is observed when citrated PRP is stirred in an aggregometer cuvette. SPA is completely abolished by an anti glycoprotein IIb/IIIa monoclonal antibody and slightly affected by the addition of an anti GPIb monoclonal. The proposita shows an increased ristocetin-induced platelet aggregation although to a lesser extent than that observed in type I IB von Willebrand disease. The distinct feature of this patient, which is also present in two family members studied, is the strong platelet aggregation observed upon the addition of purified vWF at concentrations ranging from 60 to 120 μg/ml f.c. In several normal individuals the addition of vWF up to 300 μg/ml always failed to induce platelet aggregation. The vWF induced platelet aggregation is abolished by anti GPIb and anti GPIIb/IIIa monoclonal antibodies and by EDTA (5 mM). Apyrase (5 ATPase U/ml) inhibits the second wave of aggregation. Patient′s platelets in PRP are 6-6 times more reactive to asialo vWF (AS vWF) induced platelet aggregation than normal platelets. We were not able to demostrate any increased binding of vWF to the patient′s platelets in the presence or in the absence of ristocetin, while we have demonstrated enhanced binding of As vWF, compared to normal, to platelets in PRP. Patient′s platelets do not show an abnormality of GPIb as detected by SDS page and immunoblot analysis using antibody LJIb 10 which reacts with denaturated and reduced GPIb alfa chain. The number of GPIb molecules detected by monoclonal antibody is 17,870 (n. 19,796 ± 3,791). Unlike the previous reported patients with pseudo or platelet type von Willebrand disease, our patient has normal vWF parameters.
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Seigneur, M., J. Bonnet, B. Dorian, P. Hourdille, G. Gouverneur, J. Larrue, R. Crockett, M. Boisseau, P. Ribereau-Gayon, and H. Bricaud. "WINE CONSUMMATION AND PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644868.

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To compare the effects of ethanol and wine on factors inducing thrombosis, 16 healthy male volunteers had to drink3 kinds of beverage according to the following regimen :Ethanol reference is hydroethanolic solution at PH and ethanolic titre of wine.White wine is the reference of all wine cofactors excepting phenolics.Red wine is the reference all wine cofactors.At the beginning and at the end of each period, aggregation was measured with ADP 2 umole, Adrenaline 0,75 mg/1, Arachidonic Acid 0,5 mg/1.Results show statistically significant hyperaggregation with the 3 aggregation inductors during the ethanol period, no variation during white wine period and statistically significant hypoaggre-gation with adrenaline and ADP during red wine period.In contrast of ethanol, red wine seems to induce antiaggregant properties that could explain low incidency of CAD in countries of south of Europa.
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Modderman, P. W., J. G. Huisman, J. A. van Mourik, A. E. G. Kr, and v. d. Borne. "PLATELET ACTIVATION INDUCED BY A MONOCLONAL ANTIBODY AGAINST THE PLATELET GP Ilb/IIIa COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643514.

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A receptor for fibrinogen on the platelet GP Ila/lIIb complex is induced by ADP, thrombin and other agonists. To study functional domains on GP Ilb/IIIa, the effects of anti-GP Ilb/IIIa monoclonal antibodies (Mab’s) on platelet function were determined. One of these Mab’s, 6C9, induced platelet aggregation. The antibody binds to the intact GP Ilb/IIIa complex only, not to free GP lib or free GP Ilia. Its epitope is different from that of C17, a Mab that inhibits ADP-induced fibrinogen binding and platelet aggregation. 6C9 induces fibrinogen-mediated aggregation rather than agglutination since 6C9-induced platelet interactions were blocked by treatments that also inhibited the effects of ADP etc., without inhibiting binding of 6C9 itself. 6C9 induces binding of 125I-fibrinogen (35.000 ± 7.300 molecules/platelet, Kd = 1.3 ± 0.4 µM) to unstirred platelets. Binding of fibrinogen was 60 to 80% inhibited by apyrase, which indicates that 6C9-induced fibrinogen binding is largely mediated via ADP released from platelets. In addition, 6C9 induced aggregation of platelets in the absence of extracellular fibrinogen. Mediation of this process by platelet fibrinogen or other a-granule proteins, released upon activation by 6C9, was implicated by the finding that aggregation of washed platelets, but not of platelets to which fibrinogen was added, could be blocked by PGI2. Platelet release was also assessed directly by measuring β-thromboglobulin (α-granules) and (14C) serotonin (dense granules) in the medium of unstirred platelets incubated with 6C9. F(ab')2 fragments of 6C9 only aggregated platelets in the presence of fibrinogen and did not release (14C) serotonin. Moreover, release induced by intact 6C9 was inhibited by anti-GP Ilb/IIIa Mab C17 but not by C17 F(ab’)2, although the latter inhibited ADP-induced platelet aggregation. These data indicate that binding of antibodies to specific sites on GP Ilb/IIIa may induce Fc-dependent platelet activation.This study was supported by the Foundation for Medical Research MEDIGON (grant no. 900-526-057.
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Teng, C. M., and F. N. Ko. "COMPARISON OF THE PLATELET AGGREGATION INDUCED BY THREE THROMBIN-LIKE ENZYMES OF SNAKE VENOMS AND THROMBIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644535.

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Acutin was isolated from Agkistrodon acutus venom and batroxobin and thrombocytin were isolated from Bothrops atrox venom. These three thrombin-like enzymes had different specificity for platelet activation and fibrinogen clotting. The clotting activities were 700, 170 and 7 μ/mg for batroxobin, acutin and thrombocytin, respectively. They induced aggregation and ATP release of washed rabbit platelets. The aggregating activities were 102, 104 and 105 times less than that of thrombin for thrombocytin, acutin and batroxobin, respectively basing on the clotting unit. The platelet -activating potency was correlated with their effectiveness on the retractility and elasticity of the clots. Platelet aggregation induced by thrombin or thrombocytin could be inhibited by heparin with antithrombin III while that by acutin or batroxobin could not. The thrombin-like enzymes did not induce aggregation of thrombin-degranulated platelets even fibrinogen was added. Indomethacin showed weak inhibition on the aggregation while the ADP - scavenging system, creatine phosphate/creatine phosphokinase, or apyrase inhibited the aggregation induced by the three thrombin-like enzymes but not that by thrombin. In the presence of EGTA, only thrombin could induce ATP release from platelets. It is concluded that the aggregation induced by thrombin-like enzymes is different from that of thrombin and mainly due to ADP released from platelets.
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Reports on the topic "Platelet aggregation"

1

Dubick, M. A., A. F. Kilani, J. J. Summary, J. Y. Greene, and C. E. Wade. Further Evaluation of the Effects of 7.5% NaCl/6% Dextran-70 (HSD) administration on Coagulation and Platelet Aggregation in Hemorrhaged and Euvolemic Swine. Fort Belvoir, VA: Defense Technical Information Center, April 1993. http://dx.doi.org/10.21236/ada266477.

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