Gotowe bibliografie tematyczne / Platelet response

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  3. Książki
  4. Części książek
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Gotowa bibliografia na temat „Platelet response”

Autor: Grafiati
Data publikacji: 2 czerwca 2025
Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Platelet response"

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DeHelian, Daniel, Shuchi Gupta, Jie Wu, et al. "RGS10 and RGS18 differentially limit platelet activation, promote platelet production, and prolong platelet survival." Blood 136, no. 15 (2020): 1773–82. http://dx.doi.org/10.1182/blood.2019003251.

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Abstract G protein–coupled receptors are critical mediators of platelet activation whose signaling can be modulated by members of the regulator of G protein signaling (RGS) family. The 2 most abundant RGS proteins in human and mouse platelets are RGS10 and RGS18. While each has been studied individually, critical questions remain about the overall impact of this mode of regulation in platelets. Here, we report that mice missing both proteins show reduced platelet survival and a 40% decrease in platelet count that can be partially reversed with aspirin and a P2Y12 antagonist. Their platelets ha
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Kim, Soochong, and Satya P. Kunapuli. "Negative Regulation of Gq-Mediated Pathways in Platelets by G12/13 Pathways through Fyn Kinase." Blood 112, no. 11 (2008): 2854. http://dx.doi.org/10.1182/blood.v112.11.2854.2854.

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Abstract Platelets contain high levels of Src family kinases (SFKs) suggesting an important role for these enzymes in platelet function. In this study, we have investigated the regulation of platelet function by SFKs downstream of G12/13 pathways. Calcium-independent platelet shape change induced by selective G12/13 stimulation with YFLLRNP was potentiated with a small mobilization of intracellular calcium in the presence of SFK inhibitors PP1 or PP2, which was abolished by the chelation of intracellular calcium, suggesting that SFKs downstream of G12/13 negatively regulate calcium mobilizatio
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Naylor-Adamson, Leigh, Zoe Booth, Simon Hart та ін. "Bruton's Tyrosine Kinase Inhibitors Impair Fcγriia-Mediated Responses of Healthy Donor Platelets and Chronic Lymphocytic Leukaemia Derived Platelets to Bacteria". Blood 136, Supplement 1 (2020): 1. http://dx.doi.org/10.1182/blood-2020-142624.

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Platelets play a key role in innate immunity and can interact with bacteria through multiple molecular mechanisms. One key receptor for platelet-bacteria interactions is FcγRIIa, a low affinity IgG immune receptor found on the surface of platelets, which is associated with platelet aggregation, phagocytosis and the release of bactericidal substances and cytokines from alpha and dense granules. The signalling pathways that regulate FcγRIIa mediated platelet responses to bacteria are not fully understood. Downstream of the FcγRIIa receptor is the protein Bruton's tyrosine kinase (Btk) and potent
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Auger, Jocelyn, Imke Munnix, Judith Cosemans, and Johan Heemskerk. "Platelet response heterogeneity in thrombus formation." Thrombosis and Haemostasis 102, no. 12 (2009): 1149–56. http://dx.doi.org/10.1160/th09-05-0289.

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SummaryVascular injury leads to formation of a structured thrombus as a consequence of platelet activation and aggregation, thrombin and fibrin formation, and trapping of leukocytes and red cells. This review summarises current evidence for heterogeneity of platelet responses and functions in the thrombus-forming process. Environmental factors contribute to response heterogeneity, as the platelets in a thrombus adhere to different substrates, and sense specific (ant)agonists and rheological conditions. Contraction of platelets and interaction with fibrin and other blood cells cause further res
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Norol, Françoise, Philippe Bierling, Françoise Roudot-Thoraval, et al. "Platelet Transfusion: A Dose-Response Study." Blood 92, no. 4 (1998): 1448–53. http://dx.doi.org/10.1182/blood.v92.4.1448.

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Abstract Early recommendations on prophylactic transfusion of thrombocytopenic patients involved a standard platelet dose of about 0.5 × 1011/10 kg body weight. Given the lack of data supporting this dose, we prospectively studied the dose response to platelet transfusions in adults and children with hematologic malignancies. Each patient received, in similar clinical conditions, a medium, high, and very high dose of fresh (< 24 hours old) ABO-compatible platelets, in the form of apheresis platelet concentrates (APC). For the adults, the medium dose was defined as APC containing between
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Norol, Françoise, Philippe Bierling, Françoise Roudot-Thoraval, et al. "Platelet Transfusion: A Dose-Response Study." Blood 92, no. 4 (1998): 1448–53. http://dx.doi.org/10.1182/blood.v92.4.1448.416k10_1448_1453.

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Early recommendations on prophylactic transfusion of thrombocytopenic patients involved a standard platelet dose of about 0.5 × 1011/10 kg body weight. Given the lack of data supporting this dose, we prospectively studied the dose response to platelet transfusions in adults and children with hematologic malignancies. Each patient received, in similar clinical conditions, a medium, high, and very high dose of fresh (< 24 hours old) ABO-compatible platelets, in the form of apheresis platelet concentrates (APC). For the adults, the medium dose was defined as APC containing between 4 and 6 × 10
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Chouchane, Osoul, Valentine Léopold, Christine C. A. van Linge, et al. "Role of Liver Kinase 1B in Platelet Activation and Host Defense During Klebsiella pneumoniae-Induced Pneumosepsis." International Journal of Molecular Sciences 26, no. 8 (2025): 3714. https://doi.org/10.3390/ijms26083714.

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Pneumonia is the most common cause of sepsis, with Klebsiella pneumoniae frequently implicated as a causative pathogen. Platelets play a crucial role in host defense during sepsis, and their activation is essential for effective immune responses, which is at least in part induced through activation of the collagen receptor glycoprotein (GP)VI. Platelets require energy for their activation, and Liver kinase B1 (LKB1) is a key regulator of energy metabolism. We sought to determine the role of LKB1 in platelet function and host response during K. pneumoniae-induced pneumosepsis. Platelet-specific
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Cloutier, Nathalie, Isabelle Allaeys, Genevieve Marcoux, et al. "Platelets release pathogenic serotonin and return to circulation after immune complex-mediated sequestration." Proceedings of the National Academy of Sciences 115, no. 7 (2018): E1550—E1559. http://dx.doi.org/10.1073/pnas.1720553115.

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There is a growing appreciation for the contribution of platelets to immunity; however, our knowledge mostly relies on platelet functions associated with vascular injury and the prevention of bleeding. Circulating immune complexes (ICs) contribute to both chronic and acute inflammation in a multitude of clinical conditions. Herein, we scrutinized platelet responses to systemic ICs in the absence of tissue and endothelial wall injury. Platelet activation by circulating ICs through a mechanism requiring expression of platelet Fcγ receptor IIA resulted in the induction of systemic shock. IC-drive
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Page, Martin J., and Etheresia Pretorius. "A Champion of Host Defense: A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection." Seminars in Thrombosis and Hemostasis 46, no. 03 (2020): 302–19. http://dx.doi.org/10.1055/s-0040-1708827.

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AbstractThrombocytopenia is commonly associated with sepsis and infections, which in turn are characterized by a profound immune reaction to the invading pathogen. Platelets are one of the cellular entities that exert considerable immune, antibacterial, and antiviral actions, and are therefore active participants in the host response. Platelets are sensitive to surrounding inflammatory stimuli and contribute to the immune response by multiple mechanisms, including endowing the endothelium with a proinflammatory phenotype, enhancing and amplifying leukocyte recruitment and inflammation, promoti
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Stalker, Timothy J. "Platelet Activation Gradients During Thrombus Formation." Blood 126, no. 23 (2015): SCI—13—SCI—13. http://dx.doi.org/10.1182/blood.v126.23.sci-13.sci-13.

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The hemostatic response requires the tightly regulated interaction of the coagulation system, platelets, other blood cells and components of the vessel wall at a site of vascular injury. The dysregulation of this response may result in excessive bleeding if the response is impaired, and pathologic thrombosis with vessel occlusion and tissue ischemia if the response is overly robust. Extensive studies over the past decades have sought to unravel the regulatory mechanisms that coordinate the multiple biochemical and cellular responses in time and space to ensure that an optimal response to vascu
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Rozprawy doktorskie na temat "Platelet response"

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Murphy, Christine Therese. "Mechanisms of stimulus-response coupling in platelet-activating factor stimulated platelets." Thesis, University of Bath, 1992. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304999.

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Rattray, Andrew. "Platelet response to haemodynamic shear forces." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367819.

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Muller, Michael John. "Modulation of the response to cutaneous injury /." [St. Lucia, Qld.], 2000. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16146.pdf.

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Navaratnam, K. "Platelet function and response to low-dose aspirin in pregnancy." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3009774/.

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Pre-eclampsia is a serious multisystem disorder unique to pregnant women and associated with significant maternal and perinatal morbidity and mortality worldwide. Despite the investment of decades of basic science and clinical research, the pathophysiology of pre-eclampsia has been incompletely illustrated. In low doses, the cyclooxygenase inhibitor and antiplatelet, aspirin, can redress the thromboxane/prostacyclin imbalance observed in pregnancies affected by pre-eclampsia. Low-dose aspirin is currently recommended for high risk pregnancies in many countries, despite affording only modest ov
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Allen, David L. "A study of the Human Platelet Antigen 1a (HPA-1a) antibody response in neonatal alloimmune thrombocytopenia (NAIT)." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:44a10539-de5d-44dc-9c51-5f43cf3c3a82.

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Neonatal alloimmune thrombocytopenia (NAIT) is caused by maternal alloantibodies against fetal platelet antigens inherited from the father and which are absent from maternal platelets. In Caucasians, antibodies against the Leu33 (HPA-1a) polymorphism of integrin β3 (part of the platelet αIIbβ3 complex) account for >70% of cases. Antenatal screening for these antibodies does not currently take place in the UK, partly because of the absence of sensitive, predictive tests. We hypothesized that the poor sensitivity and predictive abilities of current assays are due to the use of β3 in an inappropr
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Järemo, Petter. "Platelets and the inflammatory response in coronary heart disease /." Linköping, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med816s.pdf.

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Barbosa, Alzira Maria de Castro. "Chronic immune thrombocytopenic purpura and infection Helicobacter pylori: platelet response to the bacteria elimination of treatment." Universidade Federal do CearÃ, 2015. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=16378.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico<br>The Chronic Immune Thrombocytopenic Purpura (ITPc) is a condition caused by autoimmune response resulting awareness of platelets by self antiplatelet antibodies, causing lysis of platelets. Infection with H. pylori has been shown to likely factor for the development of PTIc, with possible platelet response relationship in PTIc after treatment of bacterial eradication. The objective was to evaluate possible effects of eradication of Helicobacter pylori in the number of platelets of patients with PTIC patients at the University Hos
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Narayanan, Padmini. "Interleukin 1 Receptor1 signaling in Platelet Inflammatory responses Interleukin-1ß processing and secretion." Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1425911007.

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Nijm, Johnny. "Inflammation and cortisol response in coronary artery disease /." Linköping : Univ, 2007. http://www.bibl.liu.se/liupubl/disp/disp2007/med1037s.pdf.

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Balasubramaniam, Karthik. "Platelet dependent thrombosis, blood thrombogenicity and response to antiplatelet therapy in health, ageing and type 2 diabetes mellitus." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3499.

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Elderly and type 2 diabetes mellitus (T2DM) patients with stable coronary artery disease (CAD) have increased risk of atherothrombotic events despite recommended secondary prevention therapy. High platelet reactivity drives this risk. Novel approaches to antiplatelet therapy are needed. Objectives: To:  determine the effect of age and T2DM on blood thrombogenicity and response to dual antiplatelet therapy in stable CAD  assess the effect of changes in platelet count on thrombus quantity and quality with Rafigrelide Methods: Study 1: Patients with stable CAD, 4 groups: age < 75 non-DM, age≥75
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Książki na temat "Platelet response"

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J, Westwick, ed. Mechanisms of stimulus-response coupling in platelets. Plenum Press, 1985.

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Holm, Holmsen, ed. Platelet responses and metabolism. CRC Press, 1986.

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Holm, Holmsen, ed. Platelet responses and metabolism. CRC Press, 1987.

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Westwick, J., M. F. Scully, D. E. MacIntyre, and V. V. Kakkar, eds. Mechanisms of Stimulus—Response Coupling in Platelets. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-9442-0.

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Curry, Nicola, and Raza Alikhan. Normal platelet function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0281.

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The platelet is a small (2–4 µm in diameter), discoid, anucleate cell that circulates in the blood. In health, it plays a vital role in haemostasis, and in disease it contributes to disorders of bleeding and thrombosis. Platelets are produced from the surface of megakaryocytes in the bone marrow, under tight homeostatic control regulated by the cytokine thrombopoietin. Platelets have a lifespan of approximately 7–10 days, and usually circulate in the blood stream in a quiescent state. Intact, undamaged vessel walls help to maintain platelets in this inactive state by releasing nitric oxide, wh
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Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its a
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Platelet Responses and Metabolism. Not Avail, 1987.

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Levi, Marcel, and Tom van der Poll. Coagulation and the endothelium in acute injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0307.

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Vascular endothelial cells play a pivotal mediatory role in many responses to systemic inflammation, including the cross-talk between coagulation and inflammation in sepsis. Endothelial cells respond to the cytokines expressed and released by activated leukocytes, but can also release cytokines themselves. Furthermore, endothelial cells are able to express adhesion molecules and growth factors that may not only promote the inflammatory response further, but also affect a myriad of downstream responses. It has recently become clear that, in addition to these mostly indirect effects of the endot
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and
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Części książek na temat "Platelet response"

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Lüscher, Ernst F. "Plasma Membrane Receptors and Platelet Response." In Platelet Membrane Glycoproteins. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4880-1_1.

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Sternberg, David, and Joshua Sonett. "Platelet Activation After Lung Transplantation." In Inflammatory Response in Cardiovascular Surgery. Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4429-8_46.

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Wainwright, Cherry L., and James R. Parratt. "Platelet-derived Substances in Acute Myocardial Injury." In Myocardial Response to Acute Injury. Macmillan Education UK, 1992. http://dx.doi.org/10.1007/978-1-349-12522-7_9.

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Bevers, Edouard M., Paul Comfurius, and Robert F. A. Zwaal. "Mechanisms Involved in Platelet Procoagulant Response." In Advances in Experimental Medicine and Biology. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2994-1_15.

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Detwiler, Thomas C., Bernice M. Martin, and Richard D. Feinman. "Stimulus-Response Coupling in the Thrombin-Platelet Interaction." In Novartis Foundation Symposia. John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720172.ch5.

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Shannon, Oonagh. "Determining Platelet Activation and Aggregation in Response to Bacteria." In Methods in Molecular Biology. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6673-8_17.

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Braquet, P., M. Paubert-Braquet, and M. Rola-Pleszczynski. "The Role of Platelet Activating Factor in the Immune Response." In Lipid Mediators in the Immunology of Shock. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0919-2_49.

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Kurachi, Michio, Kayoko Hongoh, Akiko Watanabe, and Hironaka Aihara. "Suppression of Bronchial Response to Platelet Activating Factor Following Taurine Administration." In Advances in Experimental Medicine and Biology. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-0405-8_20.

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Smith, J. Bryan, Carol Dangelmaier, and Gerard Mauco. "Quantitation of Arachidonate Released during the Platelet Phosphatidylinositol Response to Thrombin." In Prostaglandins, Leukotrienes, and Lipoxins. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4946-4_20.

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Lapetina, Eduardo G., and Wolfgang Siess. "Platelet Response in Relation to Metabolism of Inositides and Protein Phosphorylation." In Calcium in Biological Systems. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2377-8_5.

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Streszczenia konferencji na temat "Platelet response"

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Labow, R. S., E. Meek, G. A. Adams, and G. Rock. "AGGREGATION RESPONSE OF PLATELETS DURING INHIBITION OF PHOSPHOLIPASE A2." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644542.

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Arachidonic acid (AA) is liberated from platelet membrane phospholipids during stimulation and promotes cellular aggregation through the synthesis of thromboxane A2. Two pathways; phospholipase A2 (PLA2) or phospholipase C (PLC) followed by the action of acylglycerolipases, are thought to be activated during platelet stimulation and supply the necessary AA. We have reported that mono (2-ethylhexyl)phthalate (MEHP), a physiological metabolite of the plasticizer di(2-ethylhexyl)-phthalate (DEHP), commonly used in a variety of medical devices and storage containers, inhibits PLA2, but not PLC in
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Gentry, P. A., and G. S. Bondy. "The aggregation of bovine platelets is not dependent on thromboxane B2 production." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644500.

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Bovine and human platelets appear to be equally sensitive to inhibition by several environmental toxins even though the bovine is not generally recognised as a species prone to thromboembolic and hemorrhagic disease. During the examination of the mechanism of action of the toxins it became necessary to establish parameters for normal bovine platelet function.Bovine platelets suspended in homologous plasma demonstrate various responses to different agonists. Bovine platelets aggregate effectively and irreversibly to fibrillar form collagen and adenosine-diphosphate (ADP), undergo reversible agg
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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 M
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Van Nueten, J. M., W. J. Janssens, and F. De Clerck. "VASOCONSTRICTION IN RESPONSE TO HUMAN PLATELET-VESSEL WALL INTERACTIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644598.

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Human blood platelets, stimulated with thrombin, induced contractions of isolated basilar artery segments of the dog. These platelet-mediated vascular contractions were inhibited in a concentration-dependent way by flunarizine, a Ca2+-entry blocker, selective for vascular tissues. This inhibition increased gradually as a function of time after contact with flunarizine to reach its maximum after 60-90 min. Biochemical and pharmacological analyses, using the 5-HT2-serotonergic antagonist ritanserin, the thromboxane A2/prostaglandin endo-peroxide antagonist BM 13.177 and the fatty acid cyclo-oxyg
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Ware, J. A., B. A. Clark, M. Smith, and E. W. Salzman. "ABNORMALITIES OF CYTOPLASMIC [Ca++] IN PLATELETS FROM UREMIC PATIENTS STUDIED WITH AEQU0RIN AND INDO-1." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644748.

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Uremic patients have a hemorrhagic tendency, often with prolonged bleeding times and abnormalities of platelet function in vitro. Whether these defects result from plasma factors, abnormalities in platelet surface receptors, or intracellular mediators is unknown. Accordingly, blood was obtained from 16 patients with severe uremia (BUN &gt;90), and platelets were washed, loaded with aequorin or indo-1, gel-filtered, and resuspended in either plasma or buffer. Of the 16 patients, 4 had template bleeding times greater than 12 minutes, but platelet aggregation in plasma was not consistently impair
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Joist, J. H., J. E. Bauman, and S. P. Sutera. "PLATELET ALTERATIONS IN RESPONSE TO REPETITIVE, SHORT-DURATION LAMINAR SHEAR STRESS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642843.

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We examined platelet aggregation (PAG = loss of single platelets), platelet dense granule release, and platelet injury (LDH loss) in normal human citrated platelet-rich plasma subjected to biologically more relevant repetitive, laminar shear stress of 25 and 50 dyn/cm2 in a computer-controlled cone-plate viscometer. Shear pulse duration (1-3 sec), shear pulse ramp function (rate of shear stress increase and decrease per pulse, 0.6-4 sec), number of shear pulses (1-20) and pauses between shear pulses (0-5 sec) were varied in different combinations to assess the effects of each variable on plate
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Wyler, B., and K. J. Clemetson. "THE ROLE OF GPIb IN PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642922.

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Platelet membrane glycoprotein lb (GPIb) is known to contain a receptor for von Willebrand factor (vWf) and for thrombin. The role of GPIb in platelet activation was investigated by comparing the effect of removal of the binding sites by specific proteolysis with that of blocking them using specific antibodies. Specific removal of the 45 kDa outer part of GPIb by treatment of platelets with human leukocyte elastase caused loss of platelet agglutination response to von Willebrand factor (vWf) but also a weaker activation by thrombin similar to that found with Bernard-Soulier syndrome platelets
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Gool, R. Van, C. P. M. Reutelingsperger, G. Hornstra, and H. C. Hemkera. "PLATELET FUNCTION IN PLASMA AT PHYSIOLOGICAL CALCIUM CONCENTRATION. THE USE OF VAC AS AN ANTICOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643764.

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We have purified from human placenta an anticoagulatory protein (VAC, Mr= 32,000), which inhibits phospholipid dependent procoagulant reactions through a calcium dependent high affinity binding to procoagulant phospholipids..When tested in citrated platelet rich plasma (cPRP), VAC does not affect platelet aggregation and secretion in reponse to ADP, collagen and thrombin. Purified VAC (0.05 μM, final concentration; f.c.) was used as an anticoagulant to prepare PRP (VAC-PRP). Platelet aggregation (optical density method) and release of newly absorbed 14C-sero-tonin (5HT) in response to adenosin
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Melki, Imene, Nathalie Cloutier, Isabelle Allaeys, et al. "AI-05 Platelet response to immune complexes." In LUPUS 21ST CENTURY 2018 CONFERENCE, Abstracts of the Fourth Biannual Scientific Meeting of the North and South American and Caribbean Lupus Community, Armonk, New York, USA, September 13 – 15, 2018. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-lsm.5.

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SANJAR, S., D. SMITH, J. MORLEY, L. MAZZONI, and C. TAPPARELLI. "PAF ANTAGONISM AND THE RESPONSE TO ALLERGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644865.

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Intravenous infusion of platelet activating factor (PAF) causes platelets to aggregate and accumulate within the lung. A similar effect is observed when allergen is injected into sensitised animals. Since PAF is released in allergic reactions, it might be considered to be a mediator of this phenomenon. Intrathoracic accumulation of 111-Indium labelled platelets was detected by use of collimated sodium iodide crystal detectors as a part of an automated isotope monitoring system (AIMS 8000, Mumed ltd.). Intravenous infusion of PAF (600 ng/kg/h) caused progressive increase of the intrathoracic pl
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Raporty organizacyjne na temat "Platelet response"

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Thorbecke, G. J., and Zoltan Ovary. Effect of Adjuvants on Response to Pneumococcal Polysaccharide Injected Intraperitoneally. Platelet-Derived Immunoregulatory Activity. Defense Technical Information Center, 1985. http://dx.doi.org/10.21236/ada162996.

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