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Books on the topic 'Blood platelets – Activation'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

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

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2

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

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3

Platelet activation. Academic Press, 1987.

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4

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. Plenum Press, 1993.

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5

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 Academy of Sciences, 1994.

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6

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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7

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 abnorm

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8

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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9

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, whi

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10

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

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11

(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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12

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

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13

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

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14

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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15

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

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16

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

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17

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

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18

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

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19

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

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20

S, Authi Kalwant, Bruchhausen F. von 1929-, and Walter U. 1949-, eds. Platelets and their factors. Springer, 1997.

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21

Multiple organ dysfunction syndrome: Examining the role of eicosanoids and procoagulants. Chapman & Hall, 1996.

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22

Williams, J. G. Multiple Organ Dysfunction Syndrome: Examining the Role of Eicosanoids and Procoagulants (Medical Intelligence Unit). Springer, 1996.

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23

Multiple Organ Dysfunction Syndrome: Examining the Role of Eicosanoids and Procoagulants (Medical Intelligence Unit). Landes Bioscience, 1996.

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