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Dissertations / Theses on the topic 'Blood platelets'

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Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Law, Robert. "PDE3A signalling in blood platelets." Thesis, University of Hull, 2016. http://hydra.hull.ac.uk/resources/hull:13761.

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Cyclic 3’, 5’ adenosine monophosphate (cAMP) signalling downstream of prostacyclin (PGI₂) is a key inhibitory pathway in blood platelets. This pathway is dynamically regulated by phosphodiesterase 3A (PDE3A), which hydrolyses cAMP into metabolically inactive AMP. Although PDE3A is an established drug target in anti-platelet therapies, the molecular mechanisms that underlie its function in platelets remain unclear. Therefore, the major aim of this study was to further explore PDE3A signalling in human platelets. Using a combination of cell fractionation and immunoblotting we identified two PDE3A splice variants in platelets, PDE3A1 and PDE3A2, that were differentially localised within the cell. PDE3A1 was located in the membrane fraction, whereas PDE3A2 was primarily located in the cytosolic fraction. Treatment of platelets with PGI2 induced a transient phosphorylation of PDE3A2 at Ser³¹² in a PKA dependent manner. In contrast, no phosphorylation of PDE3A1 was detected. The phosphorylation of PDE3A2 was associated with increased PDE3A enzymatic activity, which suggested that cAMP signalling activated only the cytosolic form of the enzyme. In many cells, A-kinase anchoring proteins (AKAPs) orchestrate a coordinated response between PKA and its effector proteins. The phosphorylation and activation of PDE3A2 in response to PGI2 was blunted by a cell permeable peptide inhibitor of PKA-AKAP interactions suggesting that PKA-mediated activation of PDE3A2 was dependent on an AKAP. Using a cAMP-pull down approach to enrich cAMP binding proteins combined with immunoblotting, we confirmed the presence of two AKAP7 isoforms (δ and γ) in platelets. Additionally, we found that AKAP7δ co-precipitated with PDE3A2 and possessed associated PDE3A activity. Furthermore, AKAP7 also possessed PKA activity, which was a result of its constitutive association with PKA-II. Critically, immunoprecipitated PDE3A was found to be co-associated with both PKA-II and AKAP7δ. The findings in this thesis suggest that blood platelets express multiple differentially-regulated PDE3A splice variants, of which PDE3A2 is regulated by PKA-II within a novel cytosolic AKAP7δ facilitated signalling complex. The selective inhibition of PDE3A splice variants and/or pharmacological disruption of PDE3A signalosomes may provide safer and more specific ways of controlling pathological platelet activation.

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2

Stott, Andrew James. "Studies on human blood platelets." Thesis, University of Warwick, 1990. http://wrap.warwick.ac.uk/57766/.

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This project was undertaken to increase the understanding of platelet function, with paticular emphasis on abnormal platelets in diabetes mellitus, and improving the quality of platelet concentrates for transfusion. {1} Potential platelet antagonists, including PGE1, verapamil, insulin and hirudin, were added to platelet concentrates in an attempt to improve the recovery and shelf-life of the concentrate. Each "preservative" caused some improvement in platelet concentrate quality, as measured by functional tests, and radio-immunoassay for the platelet activation marker, B- thromboglobulin. The best results were obtained with the addition of PGE1, which facilitated recovery of all samples to which it was added, suggesting a cheap way of ensuring consistently good platelet concentrates. {2} Various investigations were carried out regarding abnormal platelet function in diabetes mellitus. No significant differences were found in the responses of platelets from diabetics and age-matched controls to the calcium-channel blocking drug, Verapamil, in vitro. Similarly, the capacity of diabetic platelets to produce malondialdehyde, a by-product of thromboxane A2 synthesis, was not significantly different from control platelets. The use of insulin in aggregometry studies showed, surprisingly, that insulin could have a pro-aggregatory effect on platelets from diabetics, but not those from healthy controls. In addition, evidence for the existence of a platelet aggregation-enhancing factor in the plasma of diabetics and older controls was obtained. {3} Extensive tests to investigate the nature of spontaneous platelet aggregation (SPA) in whole blood have established the existence of two types of SPA, (i) ADP-dependent, and (ii) ADP-independent. The results obtained suggest a major role for erythrocytes in the development of inappropriate platelet aggregation.

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3

Kremer, Hovinga Johanna Anna. "Malondialdehyd fomation by blood platelets /." Bern, 1990. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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4

Ramström, Sofia. "The role of platelets in whole blood coagulation /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med776s.pdf.

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5

Carter, A. J. "Thromboxane synthesis in human blood platelets and blood vessels." Thesis, University of Nottingham, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355288.

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6

Ledent-Semple, Elisabeth. "A study of factors influencing the quality of blood products during preparation, storage and filtration /." Linköping : Univ, 2001. http://www.bibl.liu.se/liupubl/disp/disp2001/med667s.pdf.

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7

Taha, Mariam. "Bacterial Contamination of Platelet Concentrates: Role of Biofilm Formation and Manufacturing Process." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35192.

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Bacterial contamination of platelet concentrates (PCs) poses the highest transfusion-associated infectious risk with skin flora, such as Staphylococcus epidermidis and Staphylococcus capitis, being the predominant contaminants. These bacteria are able to form surface-attached aggregates or biofilms, which are present in the skin of healthy blood donors and can subsequently be isolated from contaminated PCs. Disinfection of the venipuncture area before donation with a combination of 2% chlorhexidine-gluconate and 70% isopropanol is used at Canadian Blood Services. However, not all bacteria are eliminated during skin disinfection since contaminated PCs are still captured during routine PC screening. In this thesis, the ability of biofilm-forming S. epidermidis and S. capitis to resist the currently used disinfectants was explored. It was demonstrated that although a combination of chlorhexidine and isopropanol has a bactericidal effect, it is unable to completely eradicate skin flora biofilms. Several countries have implemented Pathogen Inactivation Technologies (PITs) as a measure to help control transfusing bacterially-contaminated PCs by exposing PC units to ultra violet light. However, no investigations have been done to evaluate the ability of PITs against bacterial biofilms, which was one of the objectives of this thesis. Data revealed that the efficacy of a currently used PIT, the Mirasol® system, is similar for S. epidermidis present in PCs produced from whole blood inoculated with biofilm or non-biofilm cells. However, treatment effectiveness was strain dependent. In conclusion, further investigation to improve donor skin disinfection and PITs should be considered. Surveillance at Canadian Blood Services shows that contamination rates in single-donor apheresis PCs (Aph-PCs) is generally higher than in four-donor buffy coat platelet pools (BC-PCs). This study investigated whether the BC-PC production method contributes to this observation as BC-PCs are derived from WB that is left to rest overnight while Aph-PCs are collected directly from the donor. Data showed that WB hold during BC-PC production does not have a broad-spectrum bactericidal effect and therefore other factors contribute to low rates of contamination in BC-PCs. The work presented in this thesis provides an insight to bacterial residence and persistence during blood product manufacturing and makes suggestions for PC safety improvements.

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8

Lisiak, Karolina. "The role of platelets in the activation of TAFI in model thrombi." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24805.

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9

Bateson, E. A. J. "Cryopreservation of platelets : investigation of factors affecting recovery and function of frozen and thawed platelets." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233520.

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10

Sage, Stewart O. "Stimulus-response coupling in human blood platelets." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236016.

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11

Geberhiwot, Tarekegn. "Laminin of platelets and leukocytes : molecular characterization, integrin receptors and functional roles /." Stockholm, 2000. http://diss.kib.ki.se/2000/20001212gebe/.

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12

VISMARA, MAURO. "Blood platelets and cancer: the involvement of platelet-derived extracellular vesicles in tumour progression." Doctoral thesis, Università degli studi di Pavia, 2021. http://hdl.handle.net/11571/1425254.

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In addition to their roles in haemostasis and thrombosis, blood platelets have been extensively implicated in the progression of cancer. During metastasis, circulating tumour cells (CTCs) induce platelet activation and aggregation, that are exploited to increase cancer dissemination though multiple mechanisms [1, 2]. Platelet-derived extracellular vesicles (PEVs) are shed from platelet membrane in response to extracellular stimuli and carry important biological signals to recipient cells. In vitro, cancer cells induce the release of PEVs and, accordingly, cancer patients display increased levels of circulating PEVs [3, 4]. PEVs are known mediators of cell-to-cell communication and gaining growing attention as potential mediators of the platelet-cancer interplay [5]. Nevertheless, PEVs ability to regulate target cancer cells is largely unexplored. This study aims to investigate the effects of PEVs on breast cancer cells in vitro. Four breast cancer cell lines MDA-MB-231, SKBR3, MCF-7, and BT474, characterized by different metastatic potential, were used. PEVs were purified by differential centrifugation from thrombin-stimulated platelets. Breast cancer cells were co-cultured with PEVs and different aspects were analysed. PEVs specifically bind to different breast cancer cells and elicit cell-specific functional responses. We found that PEVs massively interact with the metastatic cell lines MDA-MB-231 and SKBR3 and the ductal carcinoma cell line BT474, but not with MCF-7 cell line. Confocal microscopy analysis demonstrated that PEVs are internalized by the three cell lines, although with different efficiency. PEVs internalization was associated to the acquisition of the specific platelet marker integrin αIIb, as demonstrated by several approaches, such as immunofluorescence microscopy and immunoblotting analyses. Within 48 hours, in SKBR3 and BT474 cell lines, PEVs induced minor alteration in the different phases of the cell cycle without affecting cell viability. Conversely, PEVs potently stimulated migration and invasion of MDA-MB-231, without affecting the progression of cell cycle. PEVs triggered a sustained increase of intracellular Ca2+ concentration in MDA-MB-231, SKBR3 and BT474 cells, indicating that these microvesicles activate signalling responses that may influence the behaviour of recipient cells. Although in all the analysed breast cancer cells PEVs evoked intracellular Ca2+ mobilization, only in MDA-MB-231 cells the event was associated to the stimulation of selected signalling proteins implicated in migration, including p38MAPK and myosin light chain 2 (MLC2). Importantly, the inhibition of myosin light chain phosphorylation by a Rho kinase inhibitor prevented PEVs-stimulated migration of MDA-MB-231 cells. Our results indicate that different breast cancer cells can interact and internalize PEVs, which induce intercellular calcium movements. Moreover, PEVs are versatile regulators of cancer cell behaviour and elicit a variety of different responses depending on the specific breast cancer cell subtype. References 1. Gay, L.J. and B. Felding-Habermann, Contribution of platelets to tumour metastasis. Nat Rev Cancer, 2011. 11(2): p. 123-34. 2. Bambace, N.M., J.E. Levis, and C.E. Holmes, The effect of P2Y-mediated platelet activation on the release of VEGF and endostatin from platelets. Platelets, 2010. 21(2): p. 85-93. 3. Zarà, M., et al., Release of Prometastatic Platelet-Derived Microparticles Induced by Breast Cancer Cells: A Novel Positive Feedback Mechanism for Metastasis. TH Open, 2017. 1(2): p. e155-e163. 4. Chaari, M., et al., Impact of breast cancer stage, time from diagnosis and chemotherapy on plasma and cellular biomarkers of hypercoagulability. BMC Cancer, 2014. 14: p. 991. 5. Mezouar, S., et al., Involvement of platelet-derived microparticles in tumor progression and thrombosis. Semin Oncol, 2014. 41(3): p. 346-58.

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13

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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14

Kelly, Anne Margaret. "Platelets : relating functional phenotypes to transfusion outcomes." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708623.

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15

Hurley, Bridget Anne. "Design of an acoustic device to measure platelet adherence and aggregation." Thesis, Georgia Institute of Technology, 1998. http://hdl.handle.net/1853/16379.

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16

Bunescu, Andreia. "Cellular markers indicating activation of the hemostatic system : studies on platelets and leukocytes in peripheral human blood /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-759-2/.

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17

Bienz, Denise Edith. "Human blood platelets : the role of glycoproteins in the platelet interaction with thrombin and collagen /." [S.l.] : [s.n.], 1988. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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18

Sink, Carolyn A. "Canine Platelet Concentrates: An In Vitro Study to Effectively Provide a Source of Functional Platelets." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/31620.

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This study monitored the storage lesion of 15 units of canine platelet concentrates harvested by differential centrifugation. Canine platelet concentrates were stored at 20-24Â° C in a platelet rotator for a total of 9 days; the storage lesion of three second generation platelet storage containers was compared. The battery of in vitro tests used to monitor the storage lesion were selected from previous studies performed with human platelet concentrates separated by differential centrifugation. Based on these tests, canine platelet concentrates exhibited a storage lesion similar to human platelet concentrates. Metabolic analytes demonstrated decreasing pH, carbon dioxide, bicarbonate and glucose concentrations concurrent with increasing oxygen and lactate dehydrogenase activity over the 9-day period. Platelet structural changes were monitored by mean platelet volume, which began to increase on Day-5. Platelet function appeared to be compromised, as indicated by aggregation studies using collagen and adenosine diphosphate as agonists. Product sterility was maintained. There was no consensus of data supporting superior performance of one platelet storage container. This study indicates that canine platelet concentrates may be harvested by differential centrifugation of whole blood. In vitro studies utilizing three second-generation platelet storage bags support a previous study and concurs that canine platelet concentrates stored at 20-24Â° C using continuous agitation are viable for at least 5 days.
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19

Robertson, D. N. "A study of blood platelets in experimental myocardial ischaemia." Thesis, Robert Gordon University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377585.

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20

Appleby, Jackie A. "Role of platelets in the procoagulant environment in blood." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/29886.

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The project investigated the mechanisms whereby platelets expose a procoagulant surface and induce tissue factor (TF) in monocytes. A whole blood flow cytometric assay to measure phosphatidylserine (PS) exposure on platelets was established and validated. Using this assay, it was demonstrated that collagen is the primary agonist in eliciting platelet PS exposure, individuals' platelets vary in their response to collagen, and not all express PS despite maximal activation. Collagen-induced PS exposure was independent of other aspects of platelet activation. ADP enhanced the procoagulant effect of collagen, but could not induce PS exposure on its own. The potentiating effect of ADP was mediated mainly through P2Y12 and was required for the formation of microparticles. Procoagulant microparticles were enriched in CD42b and P-selectin, but had reduced ability to bind fibrinogen. Thrombin could instigate PS exposure only where there was platelet-platelet contact. These data suggest that at a wound site, platelet PS exposure is stimulated by subendothelial collagen at the same time as coagulation is initiated by TF. It is not dependent on initial thrombin generation but thrombin and ADP perpetuate thrombin generation by promoting PS exposure where there is platelet-platelet contact within a thrombus. Activated platelets caused upregulation of gene expression of monocyte TF within 2 hours, and, at a later stage, of its inhibitor, tissue factor pathway inhibitor. These effects were primarily mediated via soluble factors. Analysis of TF antigen on monocytes and monocyte-platelet aggregates by flow cytometry suggested that TF might be platelet-associated.

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21

Webb, Rachel J. "Characterisation of P2-receptors on human platelets." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342989.

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22

Sjölinder, Mikael. "Leukotriene C₄ synthesis and export in human platelets and leukocytes : LTC₄ synthase expression in normal and leukemic myeloid cells /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3730-3/.

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23

Anani, Sarab Gholamreza. "Construction, expression and antigenic characterisation of recombinant human platelet antigen-1 (HPA-1)." Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=158493.

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Previously it has been shown that sequences containing both Trp²⁵ and Leu³³ are the most effective at inducing Th cell proliferation in HLA-DRB3*0101 positive women, alloimmunised with anti-HPA-1a. The Leu³³/Pro³³ polymorphism is embedded in the N-terminal plexin/semaphorin/integrin (PSI) domain of GPIIIa. In the present study, amino acids 1-62 of the GPIIIa (Leu³³ or Pro³³) PSI domain were cloned into the vector pGEX-6p-1. The recombinant proteins were expressed and tested by ELISA, Luminex and Absorption Assays. The presence of the HPA-1a/-1b epitope was confirmed by the ability of PSI-Leu³³/-Pro³³ recombinant fragments to specifically capture its corresponding HPA-1 antibody. Cells from a human B cell line (HHKB), homozygous for HLA-DRB3*0101, were pulsed with the recombinant PSI domain fragment of GPIIIa expressing the HPA-1a antigen. MHC class II/peptide complexes were isolated from the pulsed cells using an immunoaffinity column. A nested set of naturally processed and presented HPA-1a derived peptides, each containing the residues Trp²⁵ – Leu³³ core epitope was identified. For the first time a naturally processed and presented HPA-1a peptide that spans the HPA-1a polymorphism has been identified, bound to the class II molecule encoded by HLA-DRB3*0101. The efficient processing and presentation of this peptide, which includes the putative dominant Th epitope, is likely to be an important contributory factor in the immunogenicity of HPA-1a. Such peptides may also provide the basis for novel treatments to tolerise the corresponding Th response in HPA-1b1b women at risk of NAIT with an HPA-1a-positive fetus.

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24

Ives, Julie A. "The role of thromboxane in platelet activation." Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358392.

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25

Sargeant, Paul. "Calcium signalling in human platelets : stored-regulated calcium entry." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318268.

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26

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

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27

Morrow, Gael Beverley. "Platelets harbour pro- and anti-fibrinolytic proteins on their activated membrane surface that regulate fibrinolysis of thrombi formed under flow." Thesis, University of Aberdeen, 2018. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=237022.

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Platelets play an essential role in haemostasis by adhering to the damaged vessel wall and forming a platelet plug to arrest bleeding. Although platelets are traditionally thought of as pro-coagulant, they possess the ability to harbour functional proteins that are key to fibrinolysis, the breakdown of the blood clot, on their surface. They are therefore substantially well equipped to regulate local fibrinolysis. This thesis aims to further define the role of platelets in fibrinolysis, in particular platelet-derived plasminogen activator inhibitor 1 (PAI-1) and plasminogen. PAI-1 is the principal physiological inhibitor of tissue-type plasminogen activator (tPA), and plasminogen is the zymogen for plasmin. In Chapter 3, we show that platelet-derived PAI-1 is released from platelet α-granules by an αIIbβ3 and fibrin dependent mechanism. We found that a significant portion of α-granular PAI1 is retained on the surface of highly activated PS-positive platelets, and activity analysis revealed the majority of PAI-1 on the platelet surface was in its active form. The functional role of platelet PAI-1 was investigated by analysis of tPA-mediated lysis of Chandler model thrombi. Our data revealed a striking dependence for platelet PAI-1 in stabilising platelet-rich thrombi against degradation. Chapter 4 characterises the expression of a novel transmembrane receptor, Plg-RKT, on the surface of human and mouse platelets. This revealed that plasminogen and Plg-RKT augment one another's binding to the platelet surface. Furthermore, analysis of plasminogen binding to the platelet surface revealed two distinct binding sites: 1) via Plg-RKT and 2) via a fibrin and αIIbβ3 dependent mechanism. Finally, Chapter 5 of this thesis discusses the optimisation of a system that monitors thrombus formation and fibrinolysis under flow. Use of this model will help to further elucidate the complex role that platelets play in controlling the balance between coagulation and fibrinolysis.

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28

Zagai, Ulrika. "Platelets and eosinophils in lung tissue remodelling /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-841-X/.

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29

Poole, Alastair W. "Responses of equine blood platelets induced by adenosine 5'-diphosphate." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260575.

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30

Dillon, Anne M. R. "An investigation of protein tyrosine phosphorylation in equine blood platelets." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390250.

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31

Wicki, Andreas Niklaus. "The membran glycoprotein Ib, complex from the human blood platelets /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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32

Holland, Errol Anthony. "The platelet laminin receptor : discovery of a 67kDA receptor for laminin on the membranes of human platelets : characterisation and isolation." Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27034.

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Previous work on the binding of resting platelets to the basement membrane glycoprotein, laminin, has identified the Ic/IIa integrin c01aplex (CD49f/CD29), also known as VLA-6, as the receptor. There exists however, another protein with a molecular weight of 67kDa, that mediates this function on other cells. It is abundantly expressed on the membranes of breast cancer cells, where it plays a key role in both the localisation at, and penetration of vascular beds, by metastases. The objectives of this study were: * The development of a micro-titre assay similar to those used in previous studies, standardised and calibrated to characterize the adhesion of unstimulated normal human platelets to laminin-coated surfaces. * To determine the effect on adhesion of platelet activation, enzymatic surface-glycoprotein removal, antibodies to specific receptors and interaction with other adhesive proteins known to bind to platelet membranes. * To establish the in vivo relevance of the experimental findings, by the assay of adhesion of glycoprotein IIb/IIIa-deficient platelets of two patients with Glanzmann's Thrombasthenia. These studies serve d to distinguish specific binding sites for laminin from the known surface receptors of platelets. The methodology used to isolate laminin receptors from the membranes of breast carcinoma cells was then applied to platelet concentrates. Membranes were obtained by centrifuging the ultrasonic lysate of a unit of platelets. These were solubilized and passed over a laminin-Sepharose column. The bound components were eluted and identified by means of SDS-gel electrophoresis, after which a concentrate was tested for laminin binding by means of dot-blot methodology. The principle contribution of this work is the finding of a 67kDa receptor for laminin on the surface membranes of platelets. The combination of the various approaches applied to characterise the adhesion of platelets to laminin, show that this is a specific, Mg²⁺-dependent process, inhibited by Ca²⁺ and not enhanced by platelet activation. Adhesion was decreased by proteolysis with trypsin and chymotrypsin, showing that the adhesion is mediated by a surface glycoprotein. Proteolysis with the Serratia marcescens metalloprotease, which cleaves off glycoprotein lb, did not affect adhesion, proving that this well-known receptor for platelet adhesion is not involved in the adhesion. The receptors GPIV and glycocalicin were also excluded, as the presence of antibodies to these receptors had no effect. Prior incubation with fibrinogen or von Willebrand factor, which binds to specific receptors on the platelet membrane, inhibited adhesion, most likely due to spatial interference with the receptor site for laminin. The presence of the tetrapeptide recognised by the membrane receptors for many adhesive proteins, RGDS, at concentrations of up to 1mM, had no effect. The platelets of the two subjects with Glanzmann's Thrombasthenia adhered normally, definitively ruling out the involvement of GPIIb/IIIa, which is absent from these platelets. The isolation process recovered a membrane component from the laminin-Sepharose column with an elution pattern identical to that for the well characterised 67kDa receptor for laminin on the surface of breast carcinoma cells. They have the same molecular weights in both the reduced (67kDa) and non-reduced (53kDa) states. Blot identification demonstrated laminin binding by the eluate. In the last part of the work, collaborative studies using more sophisticated methodology have confirmed that platelet receptors for laminin play a role in their adhesion to living tissue. Anti-laminin Fab antibodies significantly decreased the adhesion when whole blood was perfused over isolated rabbit aortic segments. That these receptors are identical to the 67kDa receptor of breast carcinoma cells was shown by the specific, high affinity binding of antibodies directed at the carcinoma receptors to the surface of platelets when examined by flow cytometry. In addition, they inhibit platelet adhesion by 50-60% in the micro-titre assay. It is proposed that both the VLA-6 and the 67kDa receptors are required for platelet adhesion to laminin, possibly as a two-stage process, similar to the systems for adhesion to von Willebrand factor, where binding is initially to GPIb, followed by binding to GPIIb/IIIa. The possible relevance of this receptor in the pathophysiology of the metastatic process is discussed.

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33

Le, Blanc Katarina. "Platelet function in polycythemia vera : studies of agonist and cytokine induced platelet activation /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3442-8/.

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34

Reasor, Daniel Archer. "Numerical simulation of cellular blood flow." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/42760.

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In order to simulate cellular blood, a coarse-grained spectrin-link (SL) red blood cell (RBC) membrane model is coupled with a lattice-Boltzmann (LB) based suspension solver. The LB method resolves the hydrodynamics governed by the Navier--Stokes equations while the SL method accurately models the deformation of RBCs under numerous configurations. This method has been parallelized using Message Passing Interface (MPI) protocols for the simulation of dense suspensions of RBCs characteristic of whole blood on world-class computing resources. Simulations were performed to study rheological effects in unbounded shear using the Lees-Edwards boundary condition with good agreement with rotational viscometer results from literature. The particle-phase normal-stress tensor was analyzed and demonstrated a change in sign of the particle-phase pressure from low to high shear rates due to RBCs transitioning from a compressive state to a tensile state in the flow direction. Non-Newtonian effects such as viscosity shear thinning were observed for shear rates ranging from 14-440 inverse seconds as well as the strong dependence on hematocrit at low shear rates. An increase in membrane bending energy was shown to be an important factor for determining the average orientation of RBCs, which ultimately affects the suspension viscosity. The shear stress on platelets was observed to be higher than the average shear stress in blood, which emphasizes the importance of modeling platelets as finite particles. Hagen-Poiseuille flow simulations were performed in rigid vessels for investigating the change in cell-depleted layer thickness with shear rate, the Fåhraeus-Linqvist effect, and the process of platelet margination. The process of platelet margination was shown to be sensitive to platelet shape. Specifically, it is shown that lower aspect ratio particles migrate more rapidly than thin disks. Margination rate is shown to increase with hematocrit, due to the larger number of RBC-platelet interactions, and with the increase in suspending fluid viscosity.

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35

Albert, Johanna. "Effects of nitric oxide on hemostasis with special attention to platelet function /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3783-4/.

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36

英志麟 and Chee-lun Aaron Ying. "Hypothermia and platelet dysfunction: monitoring and effects of desmopressin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40722168.

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37

Al-Subaie, Abeer. "Genetic studies on surface expression of platelet glycoproteins." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648804.

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38

Ying, Chee-lun Aaron. "Hypothermia and platelet dysfunction monitoring and effects of desmopressin /." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40722168.

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39

Chen, Kan. "Prothrombotic platelet signaling by the scavenger receptor CD₃6." Cleveland, Ohio : Case Western Reserve University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1226608419.

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40

Zhang, Yi. "Studies on the functions of pleckstrin in blood platelets : interactions of pleckstrin with phospholipids and soluble platelet proteins /." [Hamilton, Ont.] : McMaster University, 2005.

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41

Magwenzi, Simbarashe G. "Roles of coagulation factor XIII in the functions of blood platelets." Thesis, University of Hull, 2011. http://hydra.hull.ac.uk/resources/hull:5785.

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Activated blood coagulation factor XIII (FXIIIa) is a transglutaminase that stabilises fibrin clots and associates with platelets. In the present study, the role of factor XIII (FXIII) in modulating physiological platelet functional responses including adhesion, signal transduction and spreading were examined. Under static conditions, platelets adhered to surface-immobilised plasma-purified and recombinant human FXIII leading to the formation of filopodia and lamellipodia. Adhesion to FXIIIa was mediated through integrin-dependent mechanisms, since it was abolished by treatment with RGDS. Moreover, platelet adhesion to FXIIIa was reduced partially, but significantly by either the specific integrin dnbPs antagonist tirofiban or the selective avp3-blocking antibody LM609, and abolished when used in combination. However, spreading was exclusively mediated by OubPs since it was ablated by tirofiban, but unaffected by LM609. Importantly, FXIIIa-mediated platelet accrual was preserved under venous and arterial flow conditions where both integrins played essential roles. Under these conditions, platelet adhesion to immobilised activated FXIII (FXIIIa) was apparent at a shear rate of 300s"1, significantly reduced at 800s"1, but absent above 1000s"1. These platelet-FXIII interactions occurred independently of FXIII transglutaminase and protein disulfide isomerase activities. However, platelet adhesion and spreading were abolished by the Src family inhibitor PP1 indicating a tyrosine kinase-dependent mechanism. Consistent with this, FXIIIa stimulated tyrosine-phosphorylation of several proteins including Syk, SLP-76 and PLCv2 but not LAT, in adherent platelets. FXIIIa immobilised rapidly on collagen, and enhanced collagen-induced thrombus formation at a shear rate of 800s"1 . When co-immobilised with fibrinogen and vWF, the coagulation factor also accentuated platelet accrual by these key platelet adhesive proteins also at arterial shear. These data provide evidence that FXIIIa supports platelet adhesion under flow and potentiates the thrombogenic effects of established platelet ligands, suggesting a novel role for FXIIIa in enhancing platelet-dependent haemostasis.

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42

Sincock, Paul Martin. "Characterisation of human PETA-3 : a member of the transmembrane 4 superfamily." Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phs6159.pdf.

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Copy of author's previously published article in pocket on back end-paper. Includes bibliography (leaves 135-185). Aims to characterise the expression of PETA-3 (Platelet Endothelial Tetraspan Antigen-3), CD9, CD63 and ?gb?s1 integrins in normal human tissue ; to determine the subcellular localisation in endothilial cells and platelets ; to investigate protein-protein interactions involving PETA-3 ; and to examine the effects of anti-PETA-3 monoclonial antibodies on platelet and endothilial cell function.

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43

Gray, S. J. "Studies of cyclic AMP in relation to human blood platelet behaviour." Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235383.

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44

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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45

Rumjantseva, Viktoria. "Dual roles for hepatic lectin receptors in the clearence of chilled platelets /." Göteborg : Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine, The Sahlgrenska Academy, University of Gothenburg, Department of Translational Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, Göteborg and Boston, 2009. http://hdl.handle.net/2077/21173.

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46

Blamey, Chad Joseph. "Calcium- and integrin-binding protein 1 structure and function /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 3.06 Mb., p, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3220732.

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Thesis (Ph.D.)--University of Delaware, 2006.
Principal faculty advisors: Ulhas P. Naik, Dept. of Biological Sciences and Brian J. Bahnson, Dept. of Chemistry and Biochemistry. Includes bibliographical references.

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47

Willoughby, Scott R. "Inhibition of human platelet aggregation by perhexiline maleate : mechanisms and therapeutic implications /." Title page, contents and summary only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phw739.pdf.

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48

Abeysinghe, Rajeewa Dhammika. "The use of metal chelators in radiolabelling blood cells and their effects on cell function." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339138.

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49

Harrold, Marc W. "Part 1, synthesis of trimetoquinol analogs as potential thromboxane A2 receptor antagonists ; Part 2, synthesis of permanently charged and permanently uncharged dopamine antagonists /." The Ohio State University, 1987. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487584612165271.

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50

Poliachik, Sandra Louise. "An investigaton of the mechanisms of high intensity focused ultrasound induced platelet activity /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8011.

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