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Dissertations / Theses on the topic 'Blood – Coagulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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1

Gray, E. "Lipoproteins, blood coagulation and thrombosis." Thesis, Open University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372834.

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The main aim of this study was to investigate the involvement of plasma lipoproteins in the blood coagulation system and the implications of this relationship in the pathogenesis of thrombosis. This study has shown that lipid peroxide-induced thrombin generation is caused by a two-fold mechanism: direct interaction of lipid peroxides with lipoprotein phospholipids and inhibition of anti-thrombin III via its heparin-binding site. Experiments using purified lipoproteins have shown that triglyceride-rich lipoproteins, i.e. chylomicra and very low density lipoproteins, are sources of procoagulant activity, whereas low density and high density lipoproteins have little effect. Further work with phospholipids extracted from chylomicra has demonstrated that lipid peroxides interact with the phospholipid component of the lipoprotein molecule and, possibly through an increase in overall negative charge, provide a suitable surface for the binding of clotting factors. Subcutaneous injection of potent lipase releasers, which are weak in vitro anticoagulants, reduce the ex vivo thrombin-generating activity of post-infusion plasma. This reduction in procoagulant activity is caused by the phospholipase action of the hepatic tri-glyceride lipase (HTGL) released. Human HTGL also enhances plasma anti-Xa activity, due to direct inhibition of Xa clotting activity, but the amidolytic activity of Xa is unaffected, thus implying that the serine site of Xa is not preferentially targeted. The phospholipid binding site of Xa appears to be involved, but this anti-Xa effect is not due to the phospholipase action of HTGL. The antithrombotic effects of heparin and heparin analogues may thus be partly due to the release of HTGL, which can reduce pro-coagulant activity via inhibition of lipid peroxide-induced thrombin generation and enhancement of plasma anti-Xa activity.

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2

Sowedan, Ahmed M. "Rheometrical study of blood coagulation." Thesis, Swansea University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678535.

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3

Perdomo, Joana L. "Mathematical Modeling of Blood Coagulation." Scholarship @ Claremont, 2016. https://scholarship.claremont.edu/hmc_theses/71.

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Blood coagulation is a series of biochemical reactions that take place to form a blood clot. Abnormalities in coagulation, such as under-clotting or over- clotting, can lead to significant blood loss, cardiac arrest, damage to vital organs, or even death. Thus, understanding quantitatively how blood coagulation works is important in informing clinical decisions about treating deficiencies and disorders. Quantifying blood coagulation is possible through mathematical modeling. This review presents different mathematical models that have been developed in the past 30 years to describe the biochemistry, biophysics, and clinical applications of blood coagulation research. This review includes the strengths and limitations of models, as well as suggestions for future work.

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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

Tate, Geoffrey Michael. "The blood coagulation mechanism and hypercoagulability." Thesis, University of Leeds, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281131.

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6

Tosenberger, Alen. "Blood flow modelling and applications to blood coagulation and atherosclerosis." Doctoral thesis, Institut Camille Jordan, CNRS UMR 5208, Université Claude Bernard Lyon 1, Université Claude Bernard Lyon 1, France, 2014. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/244806.

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7

Fung, Marion R. "Molecular genetics of blood coagulation factor X." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28783.

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Thirty thousand colonies of a bovine liver cDNA library were screened with a mixture of synthetic oligodeoxyribonucleotides coding for bovine factor X. Five positive colonies were identified, and plasmid DNA was isolated. Cleavage with restriction endonucleases showed that these plasmids (designated pBXl-5) contained inserts of 1530 bp, 770 bp, 700 bp, 1100 bp and 930 bp. DNA sequence analysis of the plasmid with the largest insert (pBXl) confirmed that bovine factor X cDNAs had been cloned. The cDNA sequence predicts that factor X is synthesized as a single chain precursor in which the light and heavy chains of plasma factor X are linked by the dipeptide Arg-Arg. The cDNA sequence also predicts that factor X is synthesized with a preproleader peptide. It is proposed that at least five specific proteolytic events occur during the conversion of preprofactor X to plasma factor Xa. A human liver cDNA library was screened by colony hybridization with a bovine factor X cDNA probe. Three of the positive plasmids contained overlapping DNA that coded for most of human factor X mRNA. A second human liver cDNA library was screened by in situ hybridization with 32P-labeled human factor X cDNA clones obtained from the first screen. Several clones were isolated that contained longer inserts. DNA sequence analysis of these clones allowed the prediction of the amino acid sequence of the precursor form of human plasma factor X. From these studies, it is predicted that human factor X is synthesized as a single polypeptide chain precursor in which the light and heavy chains of plasma factor X are linked by the tripeptide Arg-Lys-Arg. The cDNA sequence also predicts that human factor X is synthesized as a preproprotein having an aminoterminal leader peptide of 40 amino acid residues. A comparison of the amino acid sequences of human and bovine factor X shows high sequence identity around the calcium- binding regions and catalytic regions but low sequence identity around the nonfunctional regions. A human genomic phage library was screened with a human factor X cDNA as a hybridization probe. Thirty-two overlapping phage clones were isolated. Characterization of six of these clones indicates that over 32 Kbp of contiguous sequence is represented. DNA sequence and restriction map analysis shows that the factor X gene is comprised of at least 8 exons and 7 introns. No clones representing the 5' untranslated region and the prepeptide of the leader sequence were identified. Two further genomic phage libraries and two libraries specific for the 5' region of the factor X gene were screened, but no 5' end clones were obtained. Restriction enzyme mapping and Southern blot analysis indicate that thus far, the human factor X gene maps to 24 Kbp of the human genome. Comparison of the factor X gene with other vitamin K-dependent blood coagulation factor genes reveals homologous exon organization. Within the blood coagulation serine proteases factor X, factor IX, factor VII, and protein C form a closely related gene family.
Medicine, Faculty of
Biochemistry and Molecular Biology, Department of
Graduate

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8

Sarphie, Anna Frances. "Changes in blood coagulation associated with hyperlipidaemia." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319009.

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9

Smith, Brian. "Protein models in blood coagulation and fibrinolysis." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239327.

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10

Head, Denise Marie. "Pharmacological modulation of the blood coagulation cascade." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298832.

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11

Hobby, Deanna Jeanne. "A COMPARISON OF ACTIVATED PARTIAL THROMBOPLASTIN TIME OBTAINED BY TWO TECHNIQUES IN PATIENTS FOLLOWING PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/291339.

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A descriptive study was conducted to test the null hypothesis: There will be no statistically significant difference between serum activated partial thromboplastin time (aPTT) obtained by two methods; venipuncture and large bore femoral arterial catheter. The convenience sample consisted of seventeen adults who had undergone percutaneous transluminal coronary angioplasty (PTCA) for the treatment of coronary artery disease. After the PTCA procedure, patients returned to an intensive care unit with a femoral intra-arterial catheter in place. Seventeen pairs of serum samples were obtained; one by venipuncture and one through the femoral intra-arterial catheter. Prior to obtaining the sample from the femoral intra-arterial catheter, 6.0 milliliters (3 times the deadspace of the catheter) of blood was withdrawn and discarded. aPTT samples were analyzed. T-tests were used to compare the results. Findings revealed that there was no statistically significant difference in the aPTT value when drawn from venipuncture versus the femoral intra-arterial catheter.

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12

He, Shu. "Hypercoagulation in preeclampsia : implications for maternal health and foetal growth /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3647-1/.

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13

Eriksson-Berg, Margita. "Hemostasis in middle-aged women with coronary heart disease /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-978-1/.

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14

Lindoff, Claes. "Haemostasis during pregnancy and perimenopausal age studies of fibrinolytic components and coagulation factors involved in vascular disease /." Lund : Dept. of Obstetrics and Gynaecology, Lund University, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39750405.html.

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15

Soons, Johannes Wilhelmus Pieter Hubertus. "Studies on the inhibition of blood coagulation factor XIa." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1987. http://arno.unimaas.nl/show.cgi?fid=5391.

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16

Nguyen, Vina, and Vina Nguyen. "Microfluidic Paper Analytic Device for Assessment of Blood Coagulation." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/624139.

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Monitoring blood coagulation while a patient is on cardiopulmonary bypass (CPB) is critical in preventing clots from arising in the bypass machine and consequently being sent into the patient’s bloodstream. Current methods used to monitor blood coagulation such as Activated Clotting Time (ACT) yield results that do not correlate coagulation time to heparin or protamine dosage and will typically take at least 400 s to yield a result that is safe to initiate bypass. Microfluidic paper-based analytical devices (μPAD) are advanced sensors based on a wide range of recently developed techniques for complex analytical methods. In this research, a point-of-care (POC) sensor was developed based on techniques adapted from lateral flow and µPAD. The effects of varied dosages of heparin and protamine were observed using this POC µPAD and an accompanying Raspberry pi-based monitoring device. Paper microfluidic channels were printed on nitrocellulose paper with a wax pattern. Human whole blood was added to an absorbent fiber glass sample pad preloaded with known amount of heparin or protamine. By having this absorbent pad on the inlet of the channel, the blood sample is able to travel through the channel via capillary flow. Significantly different (p < 0.05) rates of flow between blood samples with different doses of heparin and protamine show that the device can monitor the extent of coagulation and patient-specific responses to each drug. Thus a low-cost device was built that monitors the extent of blood coagulation and allows for individualized dosing of heparin and protamine in as little at 20 s and no more than 180 s.

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17

Ruttmann, Thomas Gotthard. "The effect of in vitro haemodilution on coagulation." Master's thesis, University of Cape Town, 1996. http://hdl.handle.net/11427/26986.

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18

Goldenberg, Neil A. "Development of the clot formation and lysis (CloFAL) global assay and its application to the investigation of bleeding disorders in children and adults /." Connect to abstract via ProQuest. Full text is not available online, 2008. http://proquest.umi.com/pqdweb?did=1545571881&sid=1&Fmt=2&clientId=18952&RQT=309&VName=PQD.

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Thesis (Ph.D. in Clinical Science) -- University of Colorado Denver, 2008.
Typescript. Includes bibliographical references (leaves 136-146). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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19

Davidson, Colin John. "Molecular evolution of haemostasis." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368908.

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20

Jones, D. W. "Factor XII and antiphospholipid antibodies." Thesis, University of Kent, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311229.

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21

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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22

Thomas, Stephen. "Antithrombotic agents under flow conditions." Thesis, Open University, 2003. http://oro.open.ac.uk/54153/.

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Haemostasis is the result of a fine balance of interactions between the endothelium, plasma proteins and blood cells under a wide range of flow rates. To mimic these conditions in vitro, a parallel plate flow chamber with human umbilical vein endothelial cells (HUVEC) or extracellular matrix (ECM) has been developed. A method to investigate thrombin generation (TG) in platelet rich defibrinated plasma was validated and used to investigate inhibition by two distinct classes of antithrombotic agents: anti-platelet antibodies and anticoagulants, including unfractionated heparin (UFH), low molecular weight heparin (LMWH) and hirudin. Increasing flow rates increased TG, which was higher in the presence of ECM than in the presence of HUVEC. All anti thrombotic agents investigated were less effective in the presence of ECM. The monoclonal anti-platelet glycoprotein (GP) lIb/IlIa antibody, RFGP56, partially inhibited TG under static or arterial flow conditions and was less effective under venous flow conditions. The monoclonal anti-platelet GP Iba antibody, RFGP37, did not inhibit TG under flow or static conditions. A combination of the two antibodies showed no further activity than RFGP56 alone. UFH, which has equal anti-factor Xa and anti-thrombin activity, was able to inhibit TG under static and flow conditions. On an anti-Xa unit basis, comparatively more LMWH (with a 10: 1 ratio of anti-factor Xa to anti-thrombin activity) was required to inhibit TG under static and venous conditions, but under arterial conditions LMWH was as effective as UFH. Hirudin, a thrombin specific inhibitor, was totally effective under static conditions, but was only able to inhibit up to 40 % ofTG under flow. This study shows that some anti-platelet agents can inhibit coagulation and this may contribute to their antithrombotic efficacy under certain flow conditions. Although both the anti-factor Xa and anti-thrombin activities of anticoagulants are effective, anti-factor Xa activity may play a more important inhibitory role under flow conditions.

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23

Ungerstedt, Johanna S. "Coagulation and inflammation in experimental endotoxemia in vitro and in vivo : monitoring method and effects of nicotinamide /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-477-1/.

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24

Jesting, Amalie. "Evaluation of prolonged surface activated coagulation time." Thesis, Malmö universitet, Fakulteten för hälsa och samhälle (HS), 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-27144.

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Background: Blood coagulation is an essential defense mechanism to prevent bleeding. Disorders in the coagulation system can be severe and blood tests measuring the blood’s ability to coagulate are important. Activated partial thromboplastin time (APTT) is a blood test that measures blood coagulation time. An abnormal prolonged APTT can both be associated with a bleeding tendency or a risk of thrombosis. Additional blood tests are needed to discover the cause of a prolonged APTT. One potential test is the APTT mixing study, which can separate samples with and without inhibitors. The aim of this project is to investigate how the cause of a prolonged APTT is evaluated today and to examine if it is possible to indicate the cause of a prolonged APTT using the APTT mixing study performed on routine samples. The goal is to be able to indicate the cause of a prolonged APTT immediately when is it ﬁrst discovered. This will save time and help guide the physicians in their work with the patient. Methods: Retrospective data is used to examine how the cause of a prolonged APTT is evaluated today. Samples with known cause of prolonged APTT are used to establish a cut-oﬀ value for the APTT mixing study to indicate the cause of a prolonged APTT. The cut-oﬀ values are then tested using routine APTT samples. Pre-analytical variables relevant to APTT are also investigated. Results: Today, specialized departments request most special coagulation blood tests. The APTT mixing study can separate samples with and without inhibitors with 90% speciﬁcity and sensitivity using index of circulating anticoagulants cut-oﬀ value of 16.0. In regard to pre-analytical variables, the centrifugation force aﬀects the plasma platelet count but not APTT and sample storage has an aﬀect on APTT. Conclusion: The APTT mixing study can be implemented as an additional test to indicate the cause of a prolonged APTT on routine samples.

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25

Matata, Bashir Mnene. "Blood response to biomaterials : in vitro and clinical investigation of the contact phase of blood coagulation." Thesis, University of Strathclyde, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297340.

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26

Rathete, Sello Athlone. "A comparative study on the effects of stress on some aspects of in vitro blood coagulation in two freshwater fish species." Thesis, University of Limpopo, 1993. http://hdl.handle.net/10386/2092.

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27

Carlsson, Karin. "Tissue Factor in Complex : Studies of interactions between blood coagulation proteins." Doctoral thesis, Linköpings universitet, Biokemi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-63688.

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Many biological processes rely on specific protein-protein interactions, for example immune responses, cell signaling, transcription, and blood coagulation. Blood coagulation is initiated when a vessel wall is damaged, exposing tissue factor (TF) to the circulating factor VII/factor VIIa (FVII/FVIIa) which results in the formation of the TF:FVIIa complex and thereby the initiation of blood coagulation. One of the substrates for the TF:FVIIa complex is factor X (FX), which is activated to factor Xa (FXa), subsequently leading to a series of reactions resulting in clot formation. Tissue factor pathway inhibitor (TFPI) is the major physiological inhibitor of the sTF:FVIIa complex, involved in regulation of coagulation by forming the TF:FVIIa:FXa:TFPI complex. Occasionally, the blood coagulation mechanism malfunctions, resulting in conditions such as the inability to stop bleeding or thrombosis. The fact that TF is the main initiator of the coagulation makes this an interesting protein to study, in the hunt for means to interfere with players involved in the blood clotting process. Throughout the studies included in this thesis the site-directed labeling technique is utilized to attach spectroscopic probes to cysteines, introduced at specific positions by mutagenesis, in the protein of interest. These fluorescent or spin-probes are sensitive for changes in their immediate environment and can thus, for example be used to monitor protein-protein complex formation and conformational changes. No complete structure has been obtained as yet for the large complex involving sTF, FVIIa, FXa, and TFPI. Therefore, we introduced a fluorescent probe at specific positions in soluble tissue factor (sTF) and the changes in fluorescence emission were detected upon sTF:FVIIa:FXa:TFPI complex formation. From these measurements it was concluded that not only parts of the C-terminal domain of sTF (TF2), but also residues in the N-terminal domain (TF1) are involved in binding to FXa in the quaternary complex. In order to investigate conformational changes occurring in the extended interface between sTF and FVIIa upon binding of different inhibitors spectroscopic probes were introduced in sTF, in the vicinity of the interaction region. From the obtained data it was concluded that the exosite-binding inhibitor E-76 induces equivalent structural changes at the interface of sTF and the protease domain (PD) of FVIIa, as do the active-site inhibitors FFR and TFPI, i.e. makes the region around the active-site more compact. Binding of these inhibitors shows similar effects despite their differences in size, binding site, and inhibitory mechanism. In addition, the Ca2+ dependence of the formation of the sTF:FVIIa complex was studied. Association between sTF and FVIIa during Ca2+ titration begins by Ca2+ binding to the first EGF-like domain of FVIIa. However, Ca2+ saturation of the γ-carboxyglutamic acid-rich (Gla) domain of FVIIa is required for complete sTF:FVIIa complex formation, and we were also able to detect that a Gla domain with vacant Ca2+ sites hinders the docking to sTF. Finally, we investigated the structural changes of free inhibited FVIIa upon sTF and Ca2+ binding by FRET and quenching measurements. From this it was concluded that inhibited FVIIa does not seem to undergo large global structural changes upon binding to sTF, when taking the dynamics of free FVIIa into account. However, Ca2+ binding induces minor local conformational changes in the active-site region of the PD of inhibited FVIIa and subsequent binding of sTF causesfurther structural rearrangements in this area.

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28

Ariëns, Robert Anton Sybrand. "The tissue factor pathway of blood coagulation in health and disease." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5931.

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29

Bakker, Harm Marten. "Accelerin the activated form(s) of human blood coagulation factor V /." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6954.

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30

Humphries, Petro. "Effects of aspartame on the blood coagulation system of the rabbit." Thesis, University of Pretoria, 2007. http://upetd.up.ac.za/thesis/available/etd-05162008-162042.

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31

Brown, Anthony James Moginie. "Studies of the molecular structures of the blood coagulation fibrinolytic proteins." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294268.

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32

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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33

Li, Hua. "Qualitative Blood Coagulation Test Using Paper-Based Microfluidic Lateral Flow Device." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406810864.

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34

Barton, Jennifer Kehlet. "Predicting dosimetry for laser coagulation of in vivo cutaneous blood vessels /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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35

Boys, C. W. G. "X-ray studies on bovine prothrombin : The structure of bovine prothrombin fragment 1." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382485.

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36

Thiemermann, Christoph. "Endothelium-derived mediators and the control of the vascular system." Thesis, Open University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293312.

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37

Evington, J. R. N. "Protein-polysaccaride interactions and the catalysis of the thrombin/antithrombin reaction." Thesis, University of Bristol, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370826.

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38

Apap-Bologna, Angela. "Conformational studies of fibrinogen and its derivatives." Thesis, University of St Andrews, 1988. http://hdl.handle.net/10023/14957.

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There is much controversy regarding the conformation of fibrinogen. Several models have been proposed ranging from a trinodular arrangement to a globular conformation. It has also been suggested that fibrinogen has a flexible structure where the shape of the molecule is influenced by its environment, one major factor being calcium concentration, In addition, although the importance of tightly bound calcium ions (kd 1M) to the fibrinogen molecule is well established, the role of the larger number of low affinity sites (kd 1mM) is still a matter of some debate. In this study, the two techniques of photosensitized radioactive surface labelling and photosensitized cross-linking were selected for development and assessment. This was done with a view to examining the conformation of fibrinogen in its native state and under different solvent conditions, with particular reference to the influence of calcium. The two techniques have been shown to have definite applications in their use as probes into the conformation of fibrinogen. Results derived using these methods support the view put forward by various authors that fibrinogen is a dynamic molecule having a flexible conformation and that the conformation adopted is dependent on solvent composition. Calcium concentration in the millimolar range is particularly significant and consequently so is the saturation of the low affinity binding sites which may well have a regulatory function. Experimentally two extreme conformations have been demonstrated, - a closed, compact structure at low calcium concentrations compared to a more open one at higher calcium concentrations. More importantly, the techniques used also show the subtle changes which occur within the molecule as the calcium concentration is raised, changes which may be more significant physiologically. The most important of these are the effect of calcium on the C-terminal parts of the Aa-chains and the D domains of the molecule.

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39

Kajs, Marylyn. "A COMPARISON OF COAGULATION VALUES OBTAINED BY TRADITIONAL VENIPUNCTURE AND INTRA-ARTERIAL LINE METHODS IN ADULT PATIENTS." Thesis, The University of Arizona, 1985. http://hdl.handle.net/10150/275285.

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40

Fall, Lewis. "Redox regulation of haemostasis : modulation by inspiratory hypoxia and physical exercise." Thesis, University of South Wales, 2012. https://pure.southwales.ac.uk/en/studentthesis/redox-regulation-of-haemostasis-modulation-by-inspiratory-hypoxia-and-physical-exercise(712686ec-639c-4d2f-b779-47e1b3b21da1).html.

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Introduction: Haemostasis is the arrest of bleeding. In recent years, in-vitro studies have suggested that secondary haemostasis (blood coagulation) is subject to activation by reactive oxygen species (ROS). It is known that patients who suffer from vascular disease are typically hypoxaemic and in the case of peripheral occlusive artery disease (POAD), physical exercise is used to improve symptom free mobility in the affected limbs. Hypoxia and physical exercise are two potent independent and synergistic initiators of ROS. We identified a clear need for in-vivo analysis of this novel area of research. Aims: There were two main aims of this research. 1. To explore the in-vivo influences of inspiratory hypoxia and physical exercise on biomarkers of haemostasis; and in doing so and subsequently carry out a randomised double blind placebo control trial to explore the interaction between oxidative stress (ROS accumulation) and haemostasis. Hypothesis: It was hypothesised that hypoxia and exercise would be independently and synergistically associated with an increase in oxidative stress, resulting in coagulation activation. We hypothesised that intervention with free radical reaction-chain breaking antioxidant vitamins would attenuate oxidative stress and thus attenuate the activation of coagulation. Methods: study 1 - Healthy males were subjected to six hours of normobaric hypoxia (12% inspired oxygen) and then a physical exercise challenge to exhaustion (cycling ramp-test). Citrated plasma was collected pre hypoxic exposure, post six hours of exposure, then immediately post exercise and analysed for routine clinical markers of coagulation (aPTT, PT, TT and fibrinogen) and analysed with and without correction for plasma volume shift. Data were analysed using a one-factor repeated measures ANOVA incorporating one within (condition: time point) subjects factor. Following a significant main effect and interaction, paired samples t-tests were employed to make post hoc comparisons at each level of the within-subjects factor. Study! - Healthy males were subjected to a double blind, randomised, placebo controlled intervention with vitamin C (a water soluble) and vitamin E (a lipid soluble), two ROS-scavenging, chain breaking antioxidants. The intervention lasted eight weeks to insure membrane enrichment with antioxidants. The methods of study one were repeated but with a pre-intervention time point added and the addition of two extra markers of thrombin generation (PF1+2 and T-AT). Data were analysed using a two-factor mixed ANOVA incorporating one between (group: antioxidant intervention vs. placebo control) and one within (condition: time point) subjects factor. Following a significant main effect and interaction, a paired samples t-test was used to make post hoc comparisons at each level of the within-subjects factor, with the alpha level Bonferroni corrected for multiple comparisons Between-group comparisons were assessed using independent samples t-tcsts applied to each level of the between-subjects factor. Results: Study 1 - Hypoxia was not associated with activation of coagulation. Physical exercise increased the activity of contact factor coagulation pathway activation. Study 2 - The intervention increased thrombin generation in the antioxidant group. This was met with an antagonistic antithrombin activation. Hypoxia did not impact the placebo group, but normalised the thrombin generation of the antioxidant group. Physical exercise increased contact factor pathway (CFP) as per study 1, but thrombin generation was unaltered. Hypoxia suppressed fibrinolysis post exercise, which is known to be activated in normoxic exercise. Discussion: hi study one, hypoxia alone did not activate coagulation. We hypothesised that this could be tentative evidence of a ROS concentration threshold for activation since once exercise was superimposed the accumulation of ROS activated the CFP. Correction for changes in plasma volume nullified the increased activity of the CFP. Corrections for shifts in plasma volume are routinely ignored in the literature and this was a novel finding. Study 2 was the first intervention of its kind. The increase in thrombin generation pre-post intervention with antioxidants suggests compelling evidence of in-vivo regulation of coagulation by ROS. But the direction of change was completely contrary to the original hypothesis. The confirmation that hypoxia does not activate coagulation is important, especially given the controversy surrounding long-haul flight deep vein thrombosis. Interestingly, exercise did not increase thrombin generation, despite the increase in the CFP. These findings suggest haemostasis is indeed subject to control by the body's redox state invivo via an as of yet, unknown mechanism.

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41

Sweeney, Robin Emily, and Robin Emily Sweeney. "Biosensors for Blood and Infection Analysis." Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/626360.

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Three major topics will be discussed in this dissertation. The first is an optical biosensor for specific diagnosis of bacterial skin and wound infection, followed by a paper microfluidic assay and accompanying monitoring device for monitoring blood coagulation and determining patient-specific heparin and protamine dosing. The final work to be discussed is ongoing work involving the detection of circulating tumor cells (CTCs) using a paper microfluidic detection platform. All of these works involve the development of biosensors for the simultaneous advancement and simplification of diagnosis and analysis of blood and bacterial infection. The aims of each of these projects included significantly decreasing the time to diagnosis and decreasing the reagents, laboratory space, personnel, and other resources needed for detection and diagnosis. The first works are focused on the design, development, and testing of an optical biosensor for the immediate detection of bacterial skin and wound infection, including diagnosing the specific species of bacteria responsible for the infection. The optical biosensor developed allows for diagnosis of a bacterial infection on skin or in a wound in as little as three seconds, in a contact-free, reagent-free manner. The second work focused on the design, development, and testing of a paper microfluidic assay and accompanying Raspberry Pi-based monitoring device for use before, during, and after surgeries requiring the use of cardiopulmonary bypass. The assay monitors the extent of blood coagulation of a whole blood sample and determines patient-specific dose response curves of an anticoagulant and its reversal agent. The final work discussed focuses on developing a paper microfluidic assay for the detection of CTCs from whole blood samples. The goal of this work is to detect multiple morphologies of CTCs from whole blood samples to provide insight on patient prognosis in a rapid, low resource manner.

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Alnsour, Hamza Mohammad Khaleel. "Role of the blood clot stabilization in early bone regeneration and osseointegration." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46960399.

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Background: Blood clot formation is one of the first events in bone regeneration and osseointegration. The blood clot adheres to dental implants with hydrophilic surfaces more favorably than to those with hydrophobic surfaces. This appears to result in better bone healing and bone fill of defects around dental implants. Objective: To assess the impact of blood clot stabilization at modSLA titanium implants on bone formation in chronic-type defects in a dog model. Material & methods: Ten modSLA implants were installed in 5 dogs after creation of saddle-type buccal-lingual bony defects. In 5 implants (test sites), the blood clot was removed by sterile saline irrigation, while the clot was left undisturbed on the other 5 implants (control sites). After 8 weeks of healing, the animals were sacrificed and sections were prepared for histomorphometric analysis. The following measurements were performed: The residual defect length (DL), the buccal and lingual most coronal level of bone in contact with the implant (CBI-b and CPI-l), the new bone height (NBH), the percentage of bone to implant contact (BIC), the area of new bone fill (BF), the difference in buccal and lingual dimensions of CBI (D-CBI), and percentage of linear bone fill (PLF). Results: the mean values of DL were similar in both groups (3.4 mm). All parameters assessed were consistently more favorable in control sites: CBI-b: 1.3 vs. 1.5, CBI-l: 1.3 vs. 0.8, D-CBI: -0.2 vs -0.5, NBH: 1.9 mm vs. 2.1 mm, PLF: 57.1% vs. 64.5% and BF: 4.4 mm? vs. 6.0 mm?. However, these differences were not statistically significant. Conclusion: In the light of consistently more favorable parameters assessed for the healing of saddle-shaped bony defects around implants, it is assumed that a stabilized blood clot contributed to early bone regeneration and osseointegration. Undisturbed blood clot formation may, indeed, be a prerequisite for optimal treatment outcomes. However, owing to the small sample size in the present study, these tendencies ought to be explored in further studies.
published_or_final_version
Dental Surgery
Master
Master of Dental Surgery

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43

Hornsey, Valerie Scott. "Studies on monoclonal antibodies to Von Willebrand factor and coagulation factor VIII." Thesis, Heriot-Watt University, 1988. http://hdl.handle.net/10399/972.

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CAMPOS, LUCELIA de A. "Isolamento e caracterização da delta toxina do veneno de Crotalus durissus terrificus." reponame:Repositório Institucional do IPEN, 2006. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11452.

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Made available in DSpace on 2014-10-09T12:52:03Z (GMT). No. of bitstreams: 0
Made available in DSpace on 2014-10-09T13:57:51Z (GMT). No. of bitstreams: 0
Dissertação (Mestrado)
IPEN/D
Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP

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45

Ansari, Mohammed Toseef. "Changes in coagulation, fibrinolysis, and endothelial perturbation markers in the lower limb venous blood associated with prolonged cramped sitting in healthy adult male volunteers in a simulation of prolonged travel." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31556991.

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46

Holland, Susan Katrina. "X-ray studies of proteins of medical and biological interest." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236327.

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47

Martin, David Michael Alan. "Structure function studies on the tissue factor/factor VIIa complex." Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321656.

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48

Krailadsiri, Pranee. "Microvesicles in platelet concentrates for transfusion." Thesis, Open University, 2000. http://oro.open.ac.uk/58061/.

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The key objective of this study was to examine whether leucocyte depletion generated or removed platelet-derived microvesicles in platelet concentrates for transfusion. Three in-process leucocyte removal filters for pooled buffy coat derived platelet concentrates, i. e. negative charged polyester, positively charged polyester, and non-charged polyurethane, were compared. The effects of three major leucocyte depletion technologies currently in use in the UK, i. e. Cobe LRS and Haemonetics MCS+ LD apheresis, and filtration of pooled buffy coat derive platelets, on platelet microvesiculation were also examined. Furthermore, the effects of various leucocyte filters and leucocyte depletion technologies on platelet activation and the activation of coagulation/complement systems were investigated. The procoagulant and anticoagulant properties of microvesicles isolated from platelet concentrates were explored. Leucocyte filtration of pooled bully coat derived platelet concentrates by all three filters did not have a net effect on the level of microvesicles. All three leucocyte depletion technologies gave similar values of microvesicles on day 1, but on day 5 MCS+ LD apheresis showed the lowest value, whilst Cobe LRS apheresis and buffy coat methods were equivalent. Among the three filters, the negatively charged filter activated the coagulation system as measured by kallikrein-like and thrombin-like activities, but removed some activated complement C3a, whereas the positively charged filter generated C3a. Among the three leucocyte depletion technologies, platelets prepared by Cobe LRS showed the lowest degree of activation of the coagulation system. However, both Cobe LRS and MCS apheresis showed higher levels of C3a than filtered buffy coat derived platelets. The microvesicles isolated from day 1 platelet concentrates could act as a catalytic surface for both the coagulant and anticoagulant reactions as measured by the formation of prothrombinase complex and the inactivation of FVa by activated protein C. The microvesicles isolated from day 5 platelets showed an increased procoagulant activity, whereas the anticoagulant activity substantially diminished.

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Hirbawi, Jamila. "Cofactor control of a vital enzymatic reaction the effect of factor Va on thrombin formation during blood coagulation /." Cleveland, Ohio : Cleveland State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=csu1260910688.

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Thesis (Ph.D.)--Cleveland State University, 2009.
Abstract. Title from PDF t.p. (viewed on Jan. 13, 2010). Includes bibliographical references (p. 124-131). Available online via the OhioLINK ETD Center and available in print.

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Thorelli, Elisabeth. "Pro- and anticoagulant activities of factor V." Lund : Dept. of Clinical Chemistry, Malmö University Hospital, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/68945027.html.

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