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Relevant bibliographies by topics / Adhesion of platelets

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Academic literature on the topic 'Adhesion of platelets'

Author: Grafiati

Published: 3 June 2025

Last updated: 1 August 2025

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Journal articles on the topic "Adhesion of platelets"

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Adam, Frederic, Shilun Zheng, Aurelio V. Santos, John G. Kelton та Catherine P. M. Hayward. "Mechanisms of Static and Shear-Induced Platelet Adhesion: Differences in the Adhesion Supported by MMRN1 Comparisons with Other β3 Integrin Ligands." Blood 106, № 11 (2005): 2659. http://dx.doi.org/10.1182/blood.v106.11.2659.2659.

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Abstract Platelet adhesion and aggregation at the site of vascular injury are key events in hemostasis and thrombosis. These processes are supported by interactions between platelet glycoprotein (GP) receptors (including integrin αIIbβ3, GP Ib-IX-V and GPVI) and ligands that include von Willebrand factor (VWF), collagen, and fibrinogen (Fg). Recently, the polymeric protein multimerin 1 (MMRN1) was identified to bind β3 integrins. Normally, MMRN1 is sequestered within secretion granules of platelets, megakaryocytes, and endothelium until its release. In static adhesion assays, MMRN1 supports pl

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Bombeli, Thomas, Barbara R. Schwartz та John M. Harlan. "Adhesion of Activated Platelets to Endothelial Cells: Evidence for a GPIIbIIIa-dependent Bridging Mechanism and Novel Roles for Endothelial Intercellular Adhesion Molecule 1 (ICAM-1), αvβ3 Integrin, and GPIbα". Journal of Experimental Medicine 187, № 3 (1998): 329–39. http://dx.doi.org/10.1084/jem.187.3.329.

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Although it has been reported that activated platelets can adhere to intact endothelium, the receptors involved have not been fully characterized. Also, it is not clear whether activated platelets bind primarily to matrix proteins at sites of endothelial cell denudation or directly to endothelial cells. Thus, this study was designed to further clarify the mechanisms of activated platelet adhesion to endothelium. Unstimulated human umbilical vein endothelial cell (HUVEC) monolayers were incubated with washed, stained, and thrombin-activated human platelets. To exclude matrix involvement, HUVEC

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Canalli, Andreia A., Carla F. Franco-Penteado, Fabiola Traina, et al. "Altered Red Cell and Platelet Adhesion in the Hemolytic Diseases: Hereditary Spherocytosis, Paroxysmal Nocturnal Hemoglobinuria and Sickle Cell Anemia." Blood 108, no. 11 (2006): 1238. http://dx.doi.org/10.1182/blood.v108.11.1238.1238.

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Abstract Increasing evidence exists to suggest that intravascular hemolysis may have important pathophysiological consequences resulting from reduced vascular nitric oxide (NO) bioavailability due to hemoglobin-mediated NO scavenging; such consequences may include endothelial dysfunction and vasculopathy. Hemolytic diseases such as hereditary spherocytosis (HS), paroxysmal nocturnal hemoglobinuria (PNH) and sickle cell anemia (SCA), despite having diverse etiologies, share a number of complications that include pulmonary and systolic arterial hypertension, cutaneous leg ulcerations and, in PNH

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Kuwahara, Mitsuhiro, Mitsuhiko Sugimoto, Shizuko Tsuji, Shigeki Miyata, and Akira Yoshioka. "Cytosolic Calcium Changes in a Process of Platelet Adhesion and Cohesion on a von Willebrand Factor-Coated Surface Under Flow Conditions." Blood 94, no. 4 (1999): 1149–55. http://dx.doi.org/10.1182/blood.v94.4.1149.

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Abstract Recent flow studies indicated that platelets are transiently captured onto and then translocated along the surface through interaction of glycoprotein (GP) Ib with surface-immobilized von Willebrand factor (vWF). During translocation, platelets are assumed to be activated, thereafter becoming firmly adhered and cohered on the surface. In exploring the mechanisms by which platelets become activated during this process, we observed changes in platelet cytosolic calcium concentrations ([Ca2+]i) concomitantly with the real-time platelet adhesive and cohesive process on a vWF-coated surfac

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Kuwahara, Mitsuhiro, Mitsuhiko Sugimoto, Shizuko Tsuji, Shigeki Miyata, and Akira Yoshioka. "Cytosolic Calcium Changes in a Process of Platelet Adhesion and Cohesion on a von Willebrand Factor-Coated Surface Under Flow Conditions." Blood 94, no. 4 (1999): 1149–55. http://dx.doi.org/10.1182/blood.v94.4.1149.416k18_1149_1155.

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Recent flow studies indicated that platelets are transiently captured onto and then translocated along the surface through interaction of glycoprotein (GP) Ib with surface-immobilized von Willebrand factor (vWF). During translocation, platelets are assumed to be activated, thereafter becoming firmly adhered and cohered on the surface. In exploring the mechanisms by which platelets become activated during this process, we observed changes in platelet cytosolic calcium concentrations ([Ca2+]i) concomitantly with the real-time platelet adhesive and cohesive process on a vWF-coated surface under f

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Yamanouchi, Jun, Jun An, Hiroshi Fujiwara, Yoshihiro Yakushijin, Takaaki Hato та Masaki Yasukawa. "Activation of Integrin αIIbβ3 through Toll-Like Receptors in Platelets." Blood 110, № 11 (2007): 3892. http://dx.doi.org/10.1182/blood.v110.11.3892.3892.

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Abstract [Purpose] Toll-like receptors (TLRs) play a critical role in innate immunity by recognizing the great conserved structures on various bacteria, viruses, and fungi. Recently, several groups reported that TLRs are expressed in human platelets and that platelet TLR4 participates in the defense mechanism against bacteria. Although TLRs are known to activate intracellular signaling pathways leading to various immune responses, the platelet responses to TLR ligands are poorly characterized. In this study, we examined whether TLR lignads can induce activation of platelet major integrin, αllb

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Moroi, Masaaki, Stephanie M. Jung, Shosaku Nomura, Sadayoshi Sekiguchi, Antonio Ordinas, and Maribel Diaz-Ricart. "Analysis of the Involvement of the von Willebrand Factor–Glycoprotein Ib Interaction in Platelet Adhesion to a Collagen-Coated Surface Under Flow Conditions." Blood 90, no. 11 (1997): 4413–24. http://dx.doi.org/10.1182/blood.v90.11.4413.

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Abstract The requisite initial reaction for in vivo thrombus formation in flowing blood is platelet adhesion to the exposed surface of the extracellular matrix. The contribution of von Willebrand factor (vWF ) in plasma and glycoprotein (GP) Ib on the platelet membrane to platelet adhesion has been well-documented. We have recently developed a procedure (the “flow adhesion assay”) for measuring platelet adhesion under flow conditions that allowed us to characterize platelet adhesion to a collagen-coated surface. Here, we apply our method to analyze platelet adhesion to a vWF-coated surface to

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Moroi, Masaaki, Stephanie M. Jung, Shosaku Nomura, Sadayoshi Sekiguchi, Antonio Ordinas, and Maribel Diaz-Ricart. "Analysis of the Involvement of the von Willebrand Factor–Glycoprotein Ib Interaction in Platelet Adhesion to a Collagen-Coated Surface Under Flow Conditions." Blood 90, no. 11 (1997): 4413–24. http://dx.doi.org/10.1182/blood.v90.11.4413.4413_4413_4424.

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The requisite initial reaction for in vivo thrombus formation in flowing blood is platelet adhesion to the exposed surface of the extracellular matrix. The contribution of von Willebrand factor (vWF ) in plasma and glycoprotein (GP) Ib on the platelet membrane to platelet adhesion has been well-documented. We have recently developed a procedure (the “flow adhesion assay”) for measuring platelet adhesion under flow conditions that allowed us to characterize platelet adhesion to a collagen-coated surface. Here, we apply our method to analyze platelet adhesion to a vWF-coated surface to determine

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Zijenah, L. S., L. F. Morton, and M. J. Barnes. "Platelet adhesion to collagen. Factors affecting Mg2+-dependent and bivalent-cation-independent adhesion." Biochemical Journal 268, no. 2 (1990): 481–86. http://dx.doi.org/10.1042/bj2680481.

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Platelet adhesion to collagens immobilized on plastic has been measured, with the following results. (1) Human, but not rabbit, platelets adhered readily to pepsin-extracted monomeric collagens in an Mg2(+)-dependent manner. (2) Rabbit platelets adhered to a monomeric collagen extracted without pepsin by a process that was cation-independent; human platelet adhesion to this collagen exhibited a cation-independent element. (3) Human platelet adhesion to polymeric collagens, including intact native fibres and those reconstituted from pepsin-extracted monomeric collagens, exhibited appreciable ca

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Walker, Britta, Syeda T. Towhid, Evi Schmid, et al. "Dynamic adhesion of eryptotic erythrocytes to immobilized platelets via platelet phosphatidylserine receptors." American Journal of Physiology-Cell Physiology 306, no. 3 (2014): C291—C297. http://dx.doi.org/10.1152/ajpcell.00318.2013.

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Glucose depletion of erythrocytes triggers suicidal erythrocyte death or eryptosis, which leads to cell membrane scrambling with phosphatidylserine exposure at the cell surface. Eryptotic erythrocytes adhere to endothelial cells by a mechanism involving phosphatidylserine at the erythrocyte surface and CXCL16 as well as CD36 at the endothelial cell membrane. Nothing has hitherto been known about an interaction between eryptotic erythrocytes and platelets, the decisive cells in primary hemostasis and major players in thrombotic vascular occlusion. The present study thus explored whether and how

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Dissertations / Theses on the topic "Adhesion of platelets"

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Eriksson, Andreas. "Platelet Adhesion to Proteins in Microplates : Applications in Experimental and Clinical Research." Doctoral thesis, Linköping : Department of Medical and Health Sciences, Linköping University, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-11733.

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Cicmil, Milenko. "Platelet endothelial cell adhesion in molecule -1 (PECAM-1/CD31) signalling in platelets." Thesis, University of Reading, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270922.

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Grunkemeier, John M. "Effect of adhesion proteins and surface chemistry on the procoagulant state of adherent platelets /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8087.

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Plummer, Christopher. "Characterisation of the adhesion interaction between oral streptococci and human platelets." Thesis, University of Sheffield, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419277.

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Shrum, Jeff. "Platelet adhesion in an asymmetric stenosis flow model." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=100235.

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Platelets have been shown to be a main contributor to thrombus formation in stenotic arteries leading to acute coronary syndromes. It is thought that increased activation and adhesion of platelets under variable shear and complex flow conditions contribute to thrombosis. The objective of this work was to evaluate the relationship between asymmetric stenosis hemodynamics and platelet adhesion using in-vitro models developed to properly simulate physiological conditions. In this study, platelet rich plasma was circulated through stenotic and straight coronary artery models. Adhesion results were

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Giuliano, Simon 1975. "Calcium signalling regulating platelet adhesion and thrombus growth." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/7875.

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Travers, M. "In vitro and clinical investigation of blood-membrane interactions : Influence on platelets and the immune system of membrane structure and antithrombotic agents." Thesis, University of Strathclyde, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382445.

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Bark, David Lawrence Jr. "Mechanistic numerical study of trhombus growth." Thesis, Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/22550.

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Kim, Chang-Beom Wootton David Macmullen Kresh J. Yasha. "A novel microscopic assay of transient platelet - von Willebrand Factor adhesion, kinetics, margination, and blood rheology /." Philadelphia, Pa. : Drexel University, 2006. http://hdl.handle.net/1860/1159.

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Wellings, Peter John. "Mechanisms of platelet capture at very high shear." Thesis, Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/39582.

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Arterial thrombus forms from the capture and accumulation of circulating platelets on a stenosis. As the thrombus grows, the lumen becomes further stenotic producing very high shear rates as the blood velocities increase through the narrowed cross-section. This study explores the molecular binding conditions that may occur under these pathologic shear conditions where circulating platelets must adhere quickly and with strong bonds. Platelets binding in an arterial stenosis of >75% are subject to drag forces exceeding 10,000 pN. This force can be balanced by 100 simultaneous GPIb-vWFA1 bonds

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Books on the topic "Adhesion of platelets"

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

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Kirton, Christopher Michael. The ability of platelets to promote the adhesion of flowing neutrophils to confluent vascular endothelium. University of Birmingham, 1999.

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L, Gordon J., ed. Vascular endothelium: Interactions with circulating cells. Elsevier, 1991.

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Eriksson, Andreas. Platelet adhesion to proteins in microplates: Applications in experimental and clinical research. Department of Medical and Health Sciences, Linköping University, 2008.

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Platelets, receptors, adhesion, secretion. Academic, 1989.

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Abelson, John N., Melvin I. Simon, and Jacek J. Hawiger. Platelets: Receptors, Adhesion, Secretion, Part A. Elsevier Science & Technology Books, 1989.

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Platelets: Receptors, adhesion, secretion Part A. Elsevier, 1989. http://dx.doi.org/10.1016/s0076-6879(00)x0378-3.

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Abelson, John N., Melvin I. Simon, and Jacek J. Hawiger. Platelets: Receptors, Adhesion, Secretion, Part B. Elsevier Science & Technology Books, 1992.

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(Editor), John N. Abelson, Melvin I. Simon (Editor), and Jacek J. Hawiger (Editor), eds. Platelets: Receptors, Adhesion, Secretion, Part A, Volume 169: Volume 169: Platelets Part A (Methods in Enzymology). Academic Press, 1989.

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(Editor), John N. Abelson, Melvin I. Simon (Editor), and Jacek J. Hawiger (Editor), eds. Platelets: Receptors, Adhesion, Secretion, Part A, Volume 169: Volume 169: Platelets Part A (Methods in Enzymology). Academic Press, 1989.

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Book chapters on the topic "Adhesion of platelets"

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van Zanten, G. H., P. G. de Groot, and J. J. Sixma. "Platelet Adhesion." In Platelets and Their Factors. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60639-7_3.

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Gardiner, Elizabeth E., and Robert K. Andrews. "Platelet Adhesion." In Platelets in Thrombotic and Non-Thrombotic Disorders. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47462-5_23.

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

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Mulvihill, J. N., and J. P. Cazenave. "Platelet adhesion to surfaces." In The Role of Platelets in Blood-Biomaterial Interactions. Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1745-6_6.

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Schuster, Jonathan M., María L. Vera, Margarita E. Laczeski, Mario R. Rosenberger, and Carlos E. Schvezov. "Adhesion of Blood Platelets in TiO2Coatings." In TMS2015 Supplemental Proceedings. John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781119093466.ch80.

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Kasirer-Friede, Ana, and Sanford J. Shattil. "Regulation of Platelet Adhesion Receptors." In Platelets in Thrombotic and Non-Thrombotic Disorders. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47462-5_6.

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Schuster, Jonathan M., María L. Vera, Margarita E. Laczeski, Mario R. Rosenberger, and Carlos E. Schvezov. "Adhesion of Blood Platelets in TiO2 Coatings." In TMS 2015 144th Annual Meeting & Exhibition. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-48127-2_80.

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Tersteeg, Claudia, Simon F. De Meyer, and Hans Deckmyn. "Inhibitors of Platelet Adhesion to VWF and Collagen." In Platelets in Thrombotic and Non-Thrombotic Disorders. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47462-5_88.

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Richardson, Peter D., and Manfred Steiner. "Adhesion of Human Platelets Inhibited by Vitamin E." In Vitamin E in Health and Disease. CRC Press, 2023. http://dx.doi.org/10.1201/9781003418160-30.

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Ascari, Edoardo, Carlo L. Balduini, Fabiola Sinigaglia, and Cesare Balduini. "The Membrane Glycoproteins: Adhesion and Aggregation of Platelets." In Advances in Hemostasis and Thrombosis. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-9424-6_7.

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Conference papers on the topic "Adhesion of platelets"

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Ordinas, A., E. Bastida, M. Garrido, J. Monteagudo, L. de Marco, and R. Castillo. "ASIALO VON WILLEBRAND FACTOR ENHANCES PLATELET ADHESION TO VASCULAR SUBENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644098.

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Native Von Willebrand factor (NvWF) binds to platelets activated by thrombin, ADP or ristocetin, and also supports the adhesion of platelets to subendothelium at high shear rates. In contrast, asialo von Willebrand factor (AvWF) induces platelet aggregation in absence of platelet activators. We investigated the role of AvWF in supporting the adhesion of platelets to rabbit vessel subendothelium under flow conditions at a shear rate of 2000 sec-1 for 5 min using the Baumgartner perfusion system. We also studied the effects of blockage of platelet GPIb or GPIIb/IIIa on platelet adhesion using mo

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Tuszynski, George P., Vicki L. Rothman, Andrew Murphy, et al. "Thranbospondin Promotes Cell-and Platelet-Substratum Adhesion." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643820.

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Thrombospondin (TSP), isolated from human platelets, promotes the in vitro, calcium-specific adhesion of a variety of cells, including platelets, melanoma cells, muscle cells, endothelial cells, fibroblasts, and epithelial cells. The cell adhesion-promoting activity of TSP is species independent since human, bovine, pig, rat and mouse cells all adhered to TSP. Furthermore, the cell adhesion-promoting activity of TSP is specific and not due to a nonspecific protein effect or to contamination by fibronectin, vitronectin, or laminin. That is, neither bovine serum albumin nor TSP preparations trea

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Pintigny, D., L. J. Wautier, B. Andreassian, and P. J. Caen. "PLATELET ADHESION TO HUMAN AORTIC FRAGMENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643549.

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Due to the fact that the adhesion of platelet aggregates to microdamaged sites in the vascular endothelium holds a critical step in the pathogenesis of thrombotic and sclerotic plaques, we investigated the adhesion of platelets to arteritic vessel wall. Aortic samples were obtained from patients with peripheral vascular disease who required a prosthetic replacement in their aortic bifurcation. Aortic fragments were collected into buffer and tested within 24 hours after collection. The adhesion of normal platelets to the vessel fragment and the prostacyclin (PGI2) production were tested in 11 c

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Sakariassen, S. K., E. Fressinaud, D. Meyer, J. J. Sixma, and R. H. Baumgartner. "RHEOLOGY AND PLATELET-SURFACE ADHESION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643987.

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The process of platelet adhesion to sites of vascular injury is pivotal for the arrest of bleeding. The same process may, on the other hand, lead to formation of mural thrombi and may play a role in atherogenesis through the release of platelet-derived growth factor. The events of platelet-surface adhesion may be divided into initial attachment and the subsequent spreading on the surface. These interactions are mediated by a variety of factors, including glycoproteins (GP) in the platelet membrane, von Willebrand factor (vWF) in plasma, and the composition of the surface.However, in most insta

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Kantak, Ameya, Yuri Lvov, David K. Mills, James G. Spaulding, and Steven A. Jones. "Platelet Function Assessment in a Microfabricated Device." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33135.

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Although platelets are small and simple in shape, they are complicated in their physiologhy. Their alpha granules and dense bodies secrete a large number of agents that are involved in haemostasis, and the glycoproteins on their surfaces form the linkages with proteins like fibrinogen, fibronectin, collagen and von Willebrand factor that are necessary for adhesion and aggregation (Frojmovic, 1998). Diseases such as heart attack (Meade, 1992), stroke (Harker, 1998) and eclampsia (Schindler et al., 1990), can be the result of pathologies in platelets. Although devices have been recently develope

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Adams, G. A., and C. Hallée. "THROMBOSPONDIN ADSORPTION AND PLATELET ADHESION TO SURFACES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643589.

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Recent research into cell adhesion has focused on a tripeptide sequence arg-gly-asp (RGD) that is common to a number of cytoadhesive proteins such as von Willebrand factor, fibronectin and fibrinogen. We have previously reported that thrombospondin (TSP) inhibited platelet adhesion to RGD proteins. On further purification of TSP, the inhibitory activity separated away from the TSP. In this report, we demonstate that TSP adsorbs to surfaces and promotes platelet adhesion and thus may belong to this family of cytoadhesins. TSP was purified by heparin affinity chromatography, ammonium sulfate pre

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Nievelstein, P. F. E. M., M. Ottenhof-Rovers, M. D. Pierschbacher, and J. J. Sixma. "THE ARG-GLY-ASP(SER) SEQUENCE OF FIBRONECTIN, AND THE GLYCOPROTEIN IIB-IIIA COMPLEX ARE NOT INVOLVED IN FIBRONECTIN DEPENDENT PLATELET ADHESION IN FLOW." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643590.

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Activated blood platelets interact with fibronectin through it to the glycoprotein IIb-IIIa(GPIIb-IIIa)-complex. The cell attachment site of fibronectin with its crucial arg-gly-asp-(-ser) (RGD(S))sequence is involved in this binding. We have studied the importance of this interaction for the fibronectin dependence of platelet adhesion under flow conditions. An RGDS-containing hexapeptide (GRGDSP) was compared with a non-reactive control peptide (GRGESP). The GRGDSP-peptide inhibited thrombin induced aggregation and adhesion under static conditions at 0.1 mM. This concentration had no effect o

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van Breugel, Hans H. F. I., Philip G. de Groot, and Jan J. Sixma. "KINETIC BEHAVIOUR OF VON WILLEBRAND FACTOR AND FIBRONECTIN EXPLAINS DEPENDENCE OF PLATELET ADHESION ON PHYSICAL PARAMETERS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643632.

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To study the kinetics of the contribution of von Willebrand Factor (vWF) and fibronectin (FN) in platelet adhesion we developed a method with which we can perform binding studies of platelets to these purified proteins under static and flow conditions. Glass coverslips were incubated for one hour with vWF (50 (jg/ml) or FN (300 pg/ml) in saline and were perfused with washed platelets (resuspended in human albumin solution) in the flat perfusion chamber as developed by Sakariassen (J.Lab.Clin.Med. 102, 522-535, 1983). Static conditions were achieved by incubating the coated coverslips with the

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Hawiger, J. "PLATELET RECEPTOR RECOGNITION DOMAINS AND THEIR SYNTHETIC PEPTIDE ANALOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643726.

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Adhesive molecules and their receptorsplay an essential role in hemostasis and thrombosis. Platelet thrombi are formed through the interaction of cell adhesion molecules (CAMs) with intercellular adhesion molecules (IAMs)and substrate adhesion molecules (SAMs). Platelet CAMs encompass membrane glycoproteins lb, lib, Ilia,and possibly la and IV, which constitutemembrane receptors for IAMs(e.g., fibrinogen) and for SAMs encompassingvon Willebrand Factor (vWF), fibronectin, vitronectin, collagen, and thrcmbospondin. Receptorfunction of platelet CAMs can be specific,i.e., only one adhesive protein

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van Breugel, Hans H. F. I., Jan J. Sixma, and Robert M. Heethaar. "EFFECTS OF FLOW PULSATILITY ON PLATELET ADHESION TO SUBENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644218.

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Platelet adhesion studies in perfusion chambers are generally performed with constant flow rate or with pulsatile flow generated by a roller pump. No information is available about the effect of flow pulsatility in the physiological range. For this purpose we devised a system consisting of a eccentric rotating disc which forces a driver toward a flexible tube. This movement causes a sinusoidal laminar flow component. The effect of this sinusoidal pulse on platelet adhesion was studied with the annulai^perfusion chamber of Baumgartner using umbilical arteries and In-labeled platelets. Condition

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Reports on the topic "Adhesion of platelets"

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Harna, Bushu, Vinay Gupta, Shivali Arya, et al. Efficacy of Platelet-rich Plasma in Adhesive Capsulitis of Shoulder: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.11.0127.

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