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Published: 4 June 2021
Last updated: 20 February 2023

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1

S, Authi Kalwant, Watson Steve P, Kakkar V. V, and International Symposium on Mechanisms of Platelet Activation and Control, (1992 : London, England), eds. Mechanisms of platelet activation and control. New York: Plenum Press, 1993.

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2

Histophysiology of the circulating platelet. Berlin: Springer-Verlag, 1990.

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3

Authi, Kalwant S., Steve P. Watson, and Vijay V. Kakkar, eds. Mechanisms of Platelet Activation and Control. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2994-1.

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4

Fondation IPSEN pour la recherche thérapeutique. Meeting. The role of platelet-activating factor in immune disorders: Proceedings of the Meeting of the "Fondation IPSEN pour la recherche thérapeutique", Paris, June 25-26, 1987 (part II). Edited by Braquet P. Basel: Karger, 1988.

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5

M, Winslow C., and Lee M. L, eds. New horizons in platelet activating factor research. Chichester [West Sussex]: Wiley, 1987.

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6

Fred, Snyder, ed. Platelet-activating factor and related lipid mediators. New York: Plenum Press, 1987.

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7

Snyder, Fred, ed. Platelet-Activating Factor and Related Lipid Mediators. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5284-6.

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8

1946-, Stute W., and Seminar on Empirical Processes (1985 : Düsseldorf, Germany), eds. Seminar on Empirical Processes. Basel: Birkhäuser Verlag, 1987.

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9

Pharmacy), Symposium on Problems on PAF (11th 1987 Tohoku College of. Trends in pharmacological research on platelet activating factor (PAF) in Japan: Proceedings of the Symposium on Problems on PAF held at the Tohoku College of Pharmacy, Sendai, Japan, September 19th, 1987. Tokyo: Ishiyaku EuroAmerica, 1988.

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10

Nigam, Santosh, Gert Kunkel, and Stephen M. Prescott, eds. Platelet-Activating Factor and Related Lipid Mediators 2. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0179-8.

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11

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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12

Kucey, Daryl Stanton. Modulation of macrophage procoagulant activity by platelet activating factor. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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13

Siegel, Andre Clifford. Biosynthetic pathways of platelet-activating factor in the nongolian gerbil model of cerebral ischemia. Ottawa: National Library of Canada, 1996.

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14

International Washington Spring Symposium (11th 1991 George Washington University). Prostaglandins, leukotrienes, lipoxins, and PAF. New York: Plenum, 1991.

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15

International Washington Spring Symposium (11th 1991 George Washington University). Prostaglandins, leukotrienes, lipoxins, and PAF: Mechanism of action, molecular biology, and clinical applications. New York: Plenum Press, 1991.

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16

Platelet activation. Tokyo: Academic Press, 1987.

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17

Authi, Kalwant S., Steven P. Watson, and Vijay V. Kakkar. Mechanisms of Platelet Activation and Control. Springer, 2012.

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18

Authi, Kalwant S., Steven P. Watson, and Vijay V. Kakkar. Mechanisms of Platelet Activation and Control. Springer London, Limited, 2012.

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19

A, FitzGerald G., Jennings Lisa K, Patrono Carlo 1944-, New York Academy of Sciences., and International Meeting on Platelets and Vascular Occlusion (3rd : 1993 : Santa Fe, N.M.), eds. Platelet-dependent vascular occlusion. New York: New York Academy of Sciences, 1994.

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20

P, Braquet, ed. CRC handbook of PAF and PAF antagonists. Boca Raton, Fla: CRC Press, 1991.

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21

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, which acts both to dilate the vessel wall and to inhibit platelet adhesion, activation, and aggregation. After trauma to the blood vessel wall, platelets are activated and, acting in concert with the endothelium and coagulation factors, form a stable clot. This chapter addresses platelet structure and function, and the response of platelets to vessel injury.
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22

Braquet, Pierre. Handbook of PAF and PAF Antagonist. CRC-Press, 1991.

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23

Pruthi, Rajiv K. Coagulation (Hemostasis and Thrombosis). Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0295.

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The coagulation system has 2 essential functions: to maintain hemostasis and to prevent and limit thrombosis. The procoagulant component of the hemostatic system prevents and controls hemorrhage. Vascular injury results in activation of hemostasis, which consists of vasospasm, platelet plug formation (platelet activation, adhesion, and aggregation), and fibrin clot formation (by activation of coagulation factors in the procoagulant system). The anticoagulant system prevents excessive formation of blood clots, and the fibrinolytic system breaks down and remodels blood clots. Quantitative abnormalities (deficiencies) and qualitative abnormalities of platelets and coagulation factors lead to bleeding disorders, whereas deficiencies of the anticoagulant system are risk factors for thrombosis. Common disorders of hemostasis and thrombosis are reviewed.
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24

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 ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
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25

Massa, Tania M. Platelet activation and fibrinogen presentation on polyetherurethane surfaces containing fluorinated surface-modifying macromolecules. 2006.

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26

Dawson, Dana, and Keith Fox. Anti-Platelet and Anti-Thrombotic Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0004.

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• Acute coronary syndromes (ACS) encompass a spectrum of presentations which include unstable angina, non-ST-elevation myocardial infarction (NSTEMI or NSTE-ACS), and ST-elevation myocardial infarction (STEMI or STE-ACS)• Anti-platelet and anti-thrombotic agents are administered as ancillary therapy to myocardial reperfusion in patients presenting with an acute coronary syndrome, to maintain the patency of the infarct-related coronary artery• More specific and potent inhibitors of platelet activation and of the coagulation cascade are emerging with the aim being to further improve clinical outcomes in patients presenting with an acute coronary syndrome, without increasing the risks of major bleeding.
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27

Kuiper, Gerhardus J. A. J. M., and Hugo ten Cate. Coagulation monitoring. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0266.

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Haemostasis is a dynamic process to stop bleeding after vessel wall damage. Platelets form a platelet plug via activation, adherence, and aggregation processes. The coagulation proteins are activated one-by-one, cascading towards fibrin polymerization, a process controlled by thrombin generation. Fibrinolysis is the process responsible for fibrin mesh degradation, which is also controlled by thrombin. Besides procoagulant proteins, anticoagulant proteins maintain a balance in the haemostatic system. Measuring platelet count and function can be done as part of the monitoring of haemostasis, while coagulation times are measured to assess the coagulation proteins. Degradation products of fibrin and lysis times give information about fibrinolysis. Point-of-care monitoring provides simple, rapid bedside testing for platelets and for whole blood using viscoelasticity properties. In trauma-induced coagulopathy (TIC) platelet counts and coagulation times are still common practice to evaluate haemostasis, but point-of-care measurements are being used more and more. Medication interfering with haemostasis is frequently used in intensive care unit patients. Each (group of) drug(s) has its own monitoring tests either based on classical or novel techniques.
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28

Geet, C. Van. Signal Transduction in Human Endothelial Cells and Endothelial Cell and Platelet Activation in Vivo in Man. Leuven University Press, 1990.

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29

Immunocytochemical Aspects of Platelet Membrane Glycoproteins and Adhesive Proteins During Activation (Progress in Histochemistry and Cytochemistry, Vol 30, No 1). Fischer Gustav Verlag GmbH & Co. KG, 1996.

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30

M, Winslow C., and Lee M. L, eds. New horizons in platelet activating factor research. Chichester: Wiley, 1987.

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31

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 the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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32

1946-, Barnes Peter J., Page C. P, and Henson P. M. 1940-, eds. Platelet activating factor and human disease. Oxford: Blackwell Scientific, 1989.

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33

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 further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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34

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Abstract:
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 further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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35

Shrivastava, Seema, Beverley J. Hunt, and Anthony Dorling. Coagulopathies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0135.

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Coagulation abnormalities are common in chronic kidney disease (CKD). Both haemorrhage and thrombosis are more common than in the general population. Haemorrhage, when it occurs, is associated with increased morbidity and mortality compared to that seen in non-uraemic patients. It is more likely spontaneously, but particularly in association with anti-platelet agents or anticoagulants. The increased risk of both arterial and venous thrombosis occurs in part because of the increase prevalence of traditional risk factors for thrombosis in CKD, in part because of the specific problems associated with nephrotic syndrome, and also because of specific putative prothrombotic factors associated with CKD, such as increased levels of coagulation factors and altered platelet function associated with uraemia. Two syndromes, both characterized by intravascular thrombosis can contribute to the development of CKD. The first is antiphospholipid syndrome, due to the presence of antibodies against negatively charged phospholipids, in which thrombosis of the renal vasculature is relatively common. The second is a group of conditions, the thrombotic microangiopathies, in which inherited or acquired deficiencies of ADAMTS13, antiphospholipid antibodies, or pathological endothelial cell activation in renal vessels, sometimes due to functional deficiencies of one or more proteins regulating coagulation or complement activation, leads to acute renal dysfunction associated with anaemia.
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36

1946-, Barnes P. J., Page Clive P, and Henson P. M. 1940-, eds. Plateletactivating factor and human disease. Blackwell Scientific, 1989.

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37

(Editor), C. P. Page, P. Barnes (Editor), and P. Henson (Editor), eds. Platelet Activating Factor & Human Disease, Frontiers in Pharmacology & Therapeutics. Blackwell Science, 1989.

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38

A, Dennis Edward, Hunter Tony 1943-, Berridge Michael J, and University of California, Los Angeles., eds. Cell activation and signal initiation: Receptor and phospholipase control of inositol phosphate, PAF, and eicosanoid production : proceedings of a UCLA symposium held in Keystone, Colorado, April 17-23, 1988. New York: A.R. Liss, 1989.

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39

Braquet. Platelet-activating Factor Cell Immuno. Karger, 1988.

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40

Platelet activating factor receptor: Signal mechanisms and molecular biology. Boca Raton, Fla: CRC Press, 1993.

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41

G, Holme, and Morley J. 1938-, eds. PAF in asthma. Academic Press, 1989.

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42

George, Holme, and Morley J, eds. PAF in asthma: Proceedings of a symposium held in Canada in June 1986. London: Academic Press, 1989.

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43

(Editor), J. Morley, ed. Paf in Asthma (Perspectives in Asthma Series, Vol 3). Academic Press, 1990.

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44

Platelet-Activating Factor Acetylhydrolases (PAF-AH). Elsevier, 2015. http://dx.doi.org/10.1016/s1874-6047(15)x0003-5.

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45

Tamanoi, Fuyuhiko, Diana Stafforini, and Keizo Inoue. Platelet-Activating Factor Acetylhydrolases (PAF-AH). Elsevier Science & Technology Books, 2015.

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46

K, Nigam S., Kunkel Gert, Prescott Stephen M, and International Congress on Platelet-Activating Factor and Related Lipid Mediators (1995 : Berlin, Germany), eds. Platelet-activating factor and related lipid mediators 2: Roles in health and disease. New York: Plenum Press, 1996.

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47

1952-, Schmitz-Schumann M., Menz G, and Page C. P, eds. PAF, platelets, and asthma. Basel: Birkhäuser, 1987.

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48

Snyder, F. Platelet-Activating Factor and Related Lipid Mediators. Springer, 2012.

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49

Snyder, F. Platelet-Activating Factor and Related Lipid Mediators. Springer London, Limited, 2013.

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50

(Editor), Santosh Nigam, Gert Kunkel (Editor), and Stephen M. Prescott (Editor), eds. Platelet-Activating Factor and Related Lipid Mediators 2: Roles in Health and Disease (Advances in Experimental Medicine and Biology). Springer, 1997.

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