Dissertations / Theses: 'Coagulation'

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Huang, David Da-Teh. "Aerosol coagulation and nucleation." Diss., Pasadena, Calif. : California Institute of Technology, 1991. http://resolver.caltech.edu/CaltechETD:etd-06222005-162441.

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Cueto, Camejo Carlos [Verfasser], and Gerald [Akademischer Betreuer] Warnecke. "The singular coagulation and coagulation-fragmentation equations / Carlos Cueto Camejo. Betreuer: Gerald Warnecke." Magdeburg : Universitätsbibliothek, 2013. http://d-nb.info/1054420378/34.

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Fuentes-Prior, Pablo. "Structural investigations of coagulation factors." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=962013986.

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Sutherland, Michael R. "Initiation of coagulation on herpesviruses." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/29067.

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Herpesviruses are highly prevalent human pathogens that have the ability to form life-long latent infection in host cells. The persistent reinjury of vessels upon virus reactivation has been suggested to link infection to vascular disease. The goal of this study was to determine the mechanism and role of early initiating events in virus-mediated vasculopathy. We now report that these events are mediated through the expression of tissue factor (TF) and a previously unknown mechanism, that both function in the acceleration of factor VIIa (FVIIa)-dependent activation of factor X (FX) to FXa. The current study identifies herpes simplex virus type 1 (HSV1)-encoded glycoprotein C (gC) as a novel second independent FX activating pathway on the virus surface. Using specific chromogenic assays, an HSV1 gC-deficient virus invariably generated 5 fold less FXa per particle than either wild type or gC-rescued strains. The direct involvement of gC was confirmed using purified recombinant gC, which enhanced FXa production, and like TF, was dependent on FVIIa, Ca 2+ and anionic phospholipid. Differential inhibition of gC-competent and -deficient strains by an anti-TF antibody confirmed simultaneous and independent TF- and gC-dependent FX activating mechanisms on the virus. Hypothesizing that cell signaling by thrombin, the final coagulation protease, may be advantageous to the virus, the effect on Herpesvirus infection was assessed. Using plaque formation assays, a thrombin specific inhibitor, hirudin, was shown to attenuate the serum-dependent increase in infection, demonstrating the importance of virus initiated thrombin production. In agreement, the addition of purified thrombin resulted in an approximate 60--80% increase in infectious events. The same enhancement was facilitated by incubation with a protease activated receptor 1 (PAR1) agonist, TRAP, indicating the effect is mediated through at least PAR1 on the cell surface. Using western blot analysis and chromogenic assays, individual variations in thrombogenic potential associated with each Herpesvirus was also determined and correlated with well-documented clinical observations. Cumulatively, these observations illustrate that Herpesviruses have evolved strategies to mimic and exploit host proteins to generate haemostatic cell signaling enzymes that may ultimately lead to the increased susceptibility of cells to infection and perturbation of the vasculature.

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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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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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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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Chowdhury, Zaid Kabir. "Coagulation of submicron colloids in water treatment." Diss., The University of Arizona, 1988. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu_e9791_1988_35_sip1_w.pdf&type=application/pdf.

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Manna, Rosa. "Crystallographic studies of coagulation factor XII." Thesis, University of Nottingham, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.716467.

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Coagulation Factor XII (FXII) is an important protein involved in the initiation of the intrinsic pathway of the coagulation cascade. Recent studies suggested that FXII may play a role in pathological thrombosis without compromising physiological hemostasis. For this reason, the inhibition of FXII could represent a new and selective strategy for preventing stroke and other thromboembolic diseases. Since there is no structure available for the protease domain of FXII, the knowledge of the overall domain structure can be significantly helpful in the development of inhibitors with specific selectivity for the target. Three different constructs were made: pFXIIa, PFXIIG570R, a missense mutations that causes a reduced activity of FXIIa, and PFXIIa fused with Maltose Binding Protein (MBP) at the N-terminus. An expression and purification protocol was established for all the proteins. In order to assess the activity of the recombinant protein, the hydrolysis of chromogenic substrate S2302 was measured and a comparison with commercial aFXIIa and PFXIIa was performed. The kinetic parameters (&cat, Km , kcat/^M, Vmax) indicated that the catalytic behaviour of recombinant MBP-pFXIIa and PFXIIa is essentially identical to that of commercial PFXIIa purified from plasma. Therefore, the protein expressed and purified from insect cell system is catalytically competent. Large efforts were devoted to the identification of possible crystallization conditions for the expressed and purified constructs, in complex with different inhibitors, both small molecules and macromolecular inhibitors. Diffracting crystals were obtained for MBP-pFXIIa in complex with D-Phe-Pro-Arg-chloromethylketone (PPACK). A complete data set was collected at 4 A. Notwithstanding the low resolution of the data, the structural analysis of key elements and the comparison with the zymogen confirmed that recombinant protein is in the active conformation. Moreover, a first analysis of the structure and of the lattice packing enabled to understand some key differences between the interactions that PPACK forms when in complex to FXIIa and with thrombin, thus possible explaining the lower affinity of PPACK for FXIIa. This is the first crystallographic structure of FXIIa and it represents a first step in the study of protein-inhibitor interactions from structural consideration. (3FXII construct was also cloned in a different vector for the expression in E. coli. The cleavage of TF tag was performed using three different enzymes (HRV-3C protease, FXa and thrombin). The best results were obtained, using the thrombin and setting the reaction overnight at room temperature. However, it was not possible to continue the process, since the protein was lost after the cleavage. This could be due to a poor stability of the protein. For that reason, a different strategy was developed, consisting of co-purification of PFXII with Ecotin. The presence of the inhibitor was thought to stabilize the protein during the cleavage. However, the gel filtration revealed that the complex was not formed. The possibility to investigate at atomic level the interactions of the inhibitors with FXII could allow an understanding as to how the substrate-inhibitor recognition mechanism work. This could therefore represent a good starting point for the development of new inhibitors that have higher specificity for FXII.

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Song, Jina. "Coagulation factor V : pathology and biochemistry." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/5595.

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ROLE OF GLU96, ASP1O2 AND ASP111 IN FACTOR V Coagulation factor V activity is unmasked by thrombin-mediated excision of the central B domain resulting in a noncovalent heterodimer, factor Va. To understand the role of individual amino acids in maintaining the Ca²⁺-depenadent subunit interaction, G1u96 (E96A), Asp1O2 (D1O2A) or Asp111 (D111A) were mutated because of known effects on chelator sensitivity. The primary clotting activity of each mutant was reduced by “40%. Demonstrating at least two distinct inhibition mechanisms, only D111A was further inhibited by thrombin pre-treatment consistent with spontaneous subunit dissociation and severely inhibited Ca²⁺ binding. The parental factor V construct used here has a truncated B domain that does not require excision for activity. Therefore inhibition of D111A by thrombin-cleavage reveals a new B domain function that maintains factor V in a factor Va-like configuration independent of Ca²⁺ binding. In addition to Ca²⁺, factor V binds Cu²⁺, but with unknown function. Unexpectedly, D111A also lost detectable Cu²⁺. Finding that a single amino acid substitution simultaneously alters Ca²⁺ and Cu²⁺ suggests an interdependent metal ion binding site. Unlike D111A, the thrombin-mediated factor Va derived from E96A and D1O2A was stable, had only moderately faster subunit dissociation upon chelation and had normal metal ion binding. Thus, the current study defines the highly conserved acidic segment spanning G1u96-Asp112 in factor V as multifunctional. Of the three amino acids I evaluated, Asp111 is essential and likely functions through direct and indirect metal ion interactions. G1u96 and Asp102 individually influence factor V/Va function by more subtle effects at the metal ion-dependent subunit interface. FACTOR V-DEFICIENT PATIENT A factor V-deficient patient due to Y1702C mutation has been studied. The patient however did not suffer from severe bleeding despite of undetectable levels of plasma and platelet factor V. A close inspection of the patient’s blood coagulation cascade showed that the lack of available factor V was compensated by other factors that influence the intrinsic pathway. This finding suggests that the commonly observed phenotypic differences shown among factor V-deficient patients with the same genotypes may be due to existing hypercoagulant factors that influence the outcome of the disease.

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Pestana, da Costa Fernando M. "Studies in discrete coagulation-fragmentation equations." Thesis, Heriot-Watt University, 1993. http://hdl.handle.net/10399/1469.

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Soheili, Ali Reza. "Numerical analysis of coagulation-fragmentation equations." Thesis, Heriot-Watt University, 1997. http://hdl.handle.net/10399/692.

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Davies, Susan C. "Mathematical modelling of coagulation and gelation." Thesis, University of Nottingham, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287230.

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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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Lui, Wing. "Characterisation of miR-494 in coagulation." Thesis, Lui, Wing (2016) Characterisation of miR-494 in coagulation. Honours thesis, Murdoch University, 2016. https://researchrepository.murdoch.edu.au/id/eprint/30510/.

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Micro-ribonucleic acids (miRNAs) are non-coding RNAs that, in the majority of cases, regulate gene expression by binding to the 3’ untranslated region (UTR) sequence of target mRNAs to cause decreased mRNA levels. Recently, several studies showed that selected miRNAs also target important genes in coagulation and haemostasis. The miRNA, miR-494, downregulates Protein S (PS) mRNA levels by binding to the 3’UTR sequence of PROS1 mRNA transcript. Further study demonstrated that some coagulation factors without predicted miR-494 binding sites in their 3’UTR sequences showed significant changes in their mRNA levels, including plasminogen (PLG), tissue factor (F3) and C4BPα (C4BPA). It is possible that miR-494 directly targets transcriptional activators or repressors to indirectly regulate the expression of those coagulation factors lacking predicted miR-494 binding sites. This current study hypothesised that miR-494 has an important role in regulating coagulation pathways and haemostasis by targeting multiple coagulation factor genes via direct and indirect mechanisms. HuH-7 cells were transfected with miR-494 for 48h and 72h followed by mRNA and protein analysis. Direct interaction between miR-494 and transcription factor 3’UTRs (JUN, SP1 and STAT5B 3’UTRs) was determined using dual-luciferase reporter assays. The mRNA and protein levels of PS and PLG was significantly downregulated, and the C4BPA mRNA and protein levels were upregulated with the presence of miR-494. Moreover, the protein level of tissue factor (TF) was decreased at 72h post-transfection but no changes were found in its mRNA levels. Computational analyses showed that predicted miR-494 binding sites were found in the JUN, SP1 and STAT5B 3’UTRs. Dual luciferase reporter assay confirmed the presence of functional miR-494 binding sites in the 3’UTR sequence of SP1 and STAT5B. The SP1 and STAT5B mRNA levels were significantly downregulated with the presence of miR-494 but no change was observed for the JUN mRNA levels. Computational analysis showed that a predicted Sp1 binding site was found in the promoter region of human PLG gene. A report by Gutierrez-Fernandez et. al. (2007) suggested that Sp1 acts as a transcriptional activator in the murine PLG promoter. These suggested that miR-494 may indirectly downregulate PLG expression by targeting Sp1. Taken together, miR-494 directly downregulates PS expression, and indirectly downregulates PLG expression through Sp1 repression and upregulates C4BPA expression. These results suggested that miR-494 has a prothrombotic effect.

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Oommen, Bonney S. "Casein Supramolecules: Structure and Coagulation Properties." DigitalCommons@USU, 2004. https://digitalcommons.usu.edu/etd/5518.

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The changes in quaternary structure of casein supramolecules with various physical and chemical treatments were studied using transmission electron microscopy, and a model to account for the changes is put forth. The effects of casein structure on coagulation properties were also studied. The sample preparation for transmission electron microscopy involved physical methods of fixation and flash freeing to preserve the structure of caseins in the sample. The structure of caseins in sodium and calcium caseinate varied with sodium caseinate not exhibiting any spherical structure as opposed to the spherical structure seen in calcium caseinate, non-fat dried milk and native milk. This difference in structure was carried over to rennet coagulum made from those sources of casein. Addition of calcium and phosphate to sodium and calcium caseinate, respectively, improved their coagulation properties. Hydration parameters such as time and shear of hydration affected the extent of hydration. High shear (733 s-1) or approximately 10 hr of hydration was required to disperse and hydrate the dried milk protein powders. Acidification and treatment with excess EDT A resulted in dissociation of casein supramolecules into various sizes and shapes. Heat treatment of milk in the presence of ethanol also resulted in its dissociation. High heat treatment of milk at various pH levels induced different types of whey protein casein interactions. All these changes can be explained using an irregular supramolecular structure of caseins based on a node and strand network of proteins and calcium phosphate nanoclusters. Such a filigreed sponge-like appearance is seen in native bovine milk and in milk of other species.

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KOUCHOUK, ALAIN. "La coagulation post-morten : revue bibliographique." Lille 2, 1989. http://www.theses.fr/1989LIL2M284.

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Jourdain, Mercé. "Inhibiteurs de la coagulation et équilibre protéases-antiprotéases au cours des états septiques graves avec coagulation intravasculaire disséminée." Lille 2, 1993. http://www.theses.fr/1993LIL2M251.

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Kong, Kong Hang. "Chemical aspects of coagulation in water treatment." Thesis, University of Macau, 2000. http://umaclib3.umac.mo/record=b1445036.

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Teichmann, Jakob. "Stochastic modeling of Brownian and turbulent coagulation." Doctoral thesis, Technische Universitaet Bergakademie Freiberg Universitaetsbibliothek "Georgius Agricola", 2017. http://nbn-resolving.de/urn:nbn:de:bsz:105-qucosa-220625.

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Als Beitrag zu einer verbesserten Filtration von Metallschmelzen werden stochastische Modelle für den essentiellen Mechanismus der Koagulation von Brownschen Partikeln und Partikeln in turbulenten Strömungen entwickelt und untersucht. Formeln für die zeitliche Entwicklung der Partikelkonzentration in diesen Systemen erlauben die Bestimmung von physikalischen Parametern, welche die Koagulation und somit die Filtration begünstigen. Um wichtige Resultate im Zusammenhang mit der traditionellen Herangehensweise für Brownsche Partikel zu berichtigen und zu erweitern, wird ein neuer Ansatz in Form zweier Modelle entwickelt. Für beide werden Formeln für die Partikelkonzentration, auf Basis einer neuartigen Verallgemeinerung der Matérn Hard-Core-Punktprozesse, abgeleitet. Um im Hinblick auf die Koagulationsgleichung der fraktalartigen Gestalt der Agglomerate besser Rechnung zu tragen, wird deren Morphologie anhand zweier neuer Modelle quantifiziert. Die Arbeit wird durch Anwendung der Modelle und numerische Simulationen von Koagulation und Abscheidung in turbulenten Strömungen abgerundet.

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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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Bechor, Elan. "Two Models of Coagulation with Instantaneous Gelation." Thesis, University of California, Berkeley, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10621138.

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Two models of coagulation are presented: one, a system of coupled partial differential equations and the other microscopic Brownian particles. Both models feature a parameter that represents the tendency of two particles to coagulate at sufficiently close distances. Both models have a phase transition, viewed as the mass clumping together as a gel. Previous work has shown the models are connected, and in here we show that their phase transition to instantaneous gelation is connected as well.

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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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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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Smith, Ann Louise. "Mathematical analysis of discrete coagulation-fragmentation equations." Thesis, University of Strathclyde, 2011. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=15582.

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Atiomo, William Usinode. "Polycystic ovary syndrome coagulation and metabolic studies." Thesis, University of Plymouth, 1998. http://hdl.handle.net/10026.1/2828.

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The polycystic ovary syndrome (PCOS) is a heterogeneous disorder in women characterised by chronic ovulatory failure, hyperandrogenaemia, and insulin resistance. Some women are completely asymptomatic and others present with extreme menstrual disturbance, severe hirsutism, infertility and recurrent miscarriage. The pathophysiology of PCOS is not completely understood, but it is thought that insulin resistance plays a central role. In normal subjects, non-diabetic obese patients and patients with non-insulin dependent diabetes, insulin resistance is associated with elevated plasminogen activator inhibitor-1 (PAI-1) levels. PAI-1 is a glycoprotein, which inhibits the formation of plasmin (a proteolytic enzyme). Plasmin aids fibrinolysis and extracellular proteolysis. High PAI-1 and low plasmin levels increase the risk of thrombosis and impair extracellular proteolysis required in ovarian follicle growth, ovulation and embryo implantation. This study was designed to determine whether elevated plasminogen activator inhibitor-1 (PAI-1) was associated with the insulin resistance present in PCOS, investigate its possible role in the causation of anovulation and recurrent pregnancy loss in these women and ascertain whether it was an additional thrombotic risk factor so that clinicians and patients could take appropriate measures to reduce this risk In a pilot study, systemic PAI-1 activity was significantly elevated in oligomenorrhoiec women with PCOS. A larger study supported these findings, but demonstrated that obesity was a significant confounding factor, as the increase in PAI-1activity disappeared when standardised for weight. Activated Protein-C (APC) resistance was subsequently tested in these women because of the unexpected finding of an increased prevalence of a positive family history of thrombosis in women with PCOS compared with controls, but there was no increase in the prevalence of APC-resistance in PCOS. In another project, the cellular distribution of PAI-1 protein in human ovaries was described for the first time using immunohistochemistry. It was localised to the granulosa and theca cell compartments in both polycystic and normal ovaries, however there was no significant difference in the intensity of PAI-l staining between both groups on image analysis. PAI-1 messenger RNA expression was also evaluated in these biopsies by in-situ hybridisation, but no signal was detected suggesting that there was either a low overall RNA preservation in the tissues, or an insufficient sensitivity of the cocktail of oligonucleotide probes used. This study did not support the hypothesis that elevated PAI-1 was a feature of PCOS, however the in-situ location of PAI-1 protein was demonstrated for the first time in the human ovary and consistent with a previously suspected role in ovulation. The results did not support a role for PAI-1 in anovulation, recurrent miscarriage or increased thrombosis in PCOS.

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McDermott, A. "In-situ coagulation moulding of ceramic suspensions." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287181.

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McCulloch, Peter George. "Interactions between cancer and the coagulation system." Thesis, University of Aberdeen, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327905.

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Both aspects of the two way interaction between cancer and the haemostatic system were investigated. In a prospective study, Fibrinogen, Fibrinopeptide A (FPA), Fragment Bβ 15-42, Fibrin Plate Lysis Assay and Fibrin(ogen) Degradation Products (FDPs) were measured in patients with operable breast cancer (BC) patients with benign breast disease (BBD) and healthy subjects. Preoperatively, FPA and FDPs were highest in BC patients, but were also significantly elevated in BBD patients. Bβ 15-42 was elevated equally in these two groups. Neither pre nor postoperative haemostatic measurements were of any value in predicting early recurrent disease. Elevated FPA values persisted in BC patients 3 & 9 months postoperatively, whilst Bβ 15-42 rose further during this time. An association between oestrogen receptor result and Bβ 15-42 values was found. These findings suggest that much of the activation of haemostasis in cancer patients arises from non-specific causes, and that haemostatic changes do not correlate with prognosis. They suggest that a primary tumour may cause relative suppression of the fibrinolytic response. The inhibition of metastasis by warfarin was studied in an animal model. Warfarin was not cytotoxic for Mtln3 tumour cells, but inhibited metastasis. Deposition of fibrin within tumours was apparently not altered by warfarin treatment, and injection of fibrin or FDPs with tumour cells had no effect on metastasis or growth of the tumour. Pre-injection warfarin treatment of the host inhibited metastasis of Mtln3 cells, whilst pretreatment of tumour cells had no effect. Injection of factors II, VII, IX and X reversed this effect of warfarin, if given within 12 hours of tumour cells. Further studies demonstrated that factors II, IX and X together enhanced metastasis in non-anticoagulated rats. Finally, Arvin defibrination did not abolish this effect, and did not itself affect metastasis. It was concluded that the factor II, IX, X complex can enhance metastasis, and that the antimetastatic effect of warfarin appeared to be due to inhibition of these proteins. Since enhancement was not affected by defibrination, it may occur via mechanisms other than fibrin formation.

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McLaughlin, Donna Josephine. "Coagulation and fragmentation models : a semigroup approach." Thesis, University of Strathclyde, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249776.

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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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Hietala, N. (Noora). "Removal of perfluorinated compounds by coagulation-flocculation." Bachelor's thesis, University of Oulu, 2016. http://urn.fi/URN:NBN:fi:oulu-201607262611.

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Perfluorinated compounds are chemical compounds with carbon-fluorine bond, they are used in commercial products. The goal of this thesis was to find out how coagulation-flocculation method remove perfluorinated compounds from water. Occurrence of perfluorinated compounds in waters and soil were researched and methods of observing these concentrations in the nature. Different concentrations on different points of waste water treatment plants and drinking water treatment plants were also researched. Main focus was to study different coagulation methods. Research methods used in this thesis included research of previous studies, focusing on most recent studies. Findings were that perfluorinated compounds can be found worldwide, both soil and water. Perfluorinated compounds can be removed from water by coagulation-flocculation process. It was also found that the removal efficiency by using different coagulant methods varied. Using conventional coagulants did not reach as good removal efficiency as when enhanced coagulation was being used. The best removal rate was achieved when natural M.oleifera or CBHyC was used as a coagulant
Perfluoratut yhdisteet ovat kemiallisia yhdisteitä, joissa on hiili-fluorisidos. Perfluorattuja yhdisteitä käytetään useissa kuluttujatuotteissa. Työn tavoitteena oli selvittää kirjallisuuden pohjalta kuinka hyvin koagulaatio-flokkulaatiomenetelmä poistaa perfluorattuja yhdisteitä vedestä. Haluttiin myös selvittää kirjallisuuden avulla perfluorattujen yhdisteiden esiintymistä luonnossa. Työssä pyrittiin selvittämään yhdisteiden pitoisuusmääriä maaperässä, luonnonvesissä, jäteveden puhdistuslaitoksissa ja juomaveden puhdistuslaitoksissa. Työn tutkimusmenetelmänä käytettiin kirjallisuustutkimusta, keskittyen alan uusimpiin mahdollisiin julkaisuihin. Perfluorattuja yhdisteitä esiintyy maailmanlaajuisesti maaperässä, luonnonvesissä, sekä jäteveden puhdistuslaitoksissa että juomaveden puhdistuslaitoksissa. Koagulaatio-flokkulaatiomenetelmällä pystytään poistamaan perfluorattuja yhdisteitä vedestä, Poistumistehon hyötysuhde tavallisella koagulanteilla ei ole yhtä tehokas kuin uusilla koagulanteilla, kuten esimerkiksi luonnonmukaisilla koagulanteilla

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35

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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Boothello, Rio. "Studies on rationally designed, allosteric, coagulation inhibitors." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/622.

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Heparin is a natural allosteric modulator, with numerous structural and conformational variations leading to many reports of bleeding complications and variations in anticoagulant effects. A flurry of research has been directed towards understanding this puzzle. This work entails the utilization of three unique strategies to further our understanding of this complex issue. Traditional synthetic, biosynthetic and biophysical approaches have failed to conquer the GAG-protein complexity. Computational analysis however could serve as a powerful approach to decipher this dilemma. A dual filter algorithm was incorporated to identify unique hexasaccharide sequences for HCII and AT. Our experimental studies exhibit a good correlation with our computational findings in addition, to the discovery of the first reported heparin based hexasaccharide sequence (HX1) as a potent activator of HCII and AT. In contrast to the enormity of GAG sequences, there appears to be a pattern where rare sequences have been identified to modulate characteristic functions in proteins. Our search led us to a biosynthetically rare GAG residue 2-O-sulfated glucuronic acid (GlcAp2S). Our computational studies indicated elements of selective recognition with coagulation enzymes propelling us towards synthesizing a polymer, HS2S2S enriched in GlcAp2S and GlcNp2S saccharides. Our biological studies indicate its potential in activating AT and HCII in addition to a previously unobserved inhibition of thrombin but not FXa, which is corroborated by our computational studies. These studies therefore showcase the importance of studying rare sequences to further our understanding of differential recognition of proteins of the coagulation cascade. An alternate anticoagulant strategy involves utilization of upstream enzymes like FXIa. Consequently, we devised a rational strategy, which targets the differential hydrophobic domain near the heparin binding sites of proteins through the design of molecules termed as sulfated allosteric modulators. Our endeavor led to the discovery of a library of quinazolin4-(3H)ones) dimers as selective inhibitors of FXIa. We recognized the linker length and geometry to be an important element affecting potency and selectivity. We therefore synthesized a library of 18 dimers using simple reaction schemes. Our inhibition studies do highlight a 9-fold improvement in potency.

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Sharief, L. A. T. "Reproduction and coagulation factor XIII in women." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1414996/.

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Factor XIII (FXIII) deficiency is a rare bleeding disorder associated with pregnancy loss and severe bleeding diathesis. However, there are limited data on the borderline level of FXIII that is needed to avoid obstetric complications. The aim of this study is to obtain a better understanding about the clinical course and outcome of FXIII deficiency among women. A systematic review of literature was performed for congenital FXIII deficiency among women and its associated reproductive outcomes using an electronic search on databases. A total of 116 women were identified from 34 articles. It was concluded that women with congenital FXIII deficiency suffer significant bleeding complications. Menorrhagia and ovulation bleeding are common gynaecological problems and possibly more prevalent than reported. A cross sectional study of 376 healthy pregnant women measured FXIII activity during first (weeks 0-12, n=116), second (weeks13-28, n=132) third trimester (weeks 29-42, n=128) and postnatal period (day0-3; n=30) and a control group (n=25). A significant reduction in FXIII activity during second and third trimester compared to first trimester of pregnancy (p<0.0001). Mean FXIII level during second and third trimester and postnatal period were significantly lower compared to control group. A second study involved 32 women aimed to examine changes in plasma FXIII activity during the normal menstrual cycle. FXIII level was significantly higher during periovulatory and secretory phases of the cycle compared to the menstrual phase (p=0.036). The third study evaluates FXIII level among 68 women with recurrent miscarriage, compared to 62 women with no history of pregnancy loss and at least one living child. Even though women with miscarriages had lower FXIII activity compare to control group, such difference did not reach a statistical significant level (p=0.142). However, women with history of miscarriage had significantly more cases with FXIII activity <70 IU/dL compared to control group (p=0.034). In conclusion, women with congenital FXIII deficiency suffer significant obstetrics and gynaecological complications. Pregnancy is associated with a significant decrease in FXIII activity, reaching the lowest level during the third trimester of pregnancy. FXIII activity was also found to be lowest during menstrual and preovulatory phase of the cycle. Women with history of recurrent miscarriage are more likely to have low FXIII (<70 IU/dL) levels.

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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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39

Machenbach, Ingo. "Drinking Water Production by Coagulation and Membrane Filtration." Doctoral thesis, Norwegian University of Science and Technology, Department of Hydraulic and Environmental Engineering, 2007. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-2142.

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Drinking water production with low-pressure hollow-fibre membranes is becoming increasingly more widespread as replacement for conventional separation technology. Upstream coagulation can mitigate fouling layer formation on membranes and allows removal of colloidal and soluble compounds smaller than the membrane pores. However, integrating membrane systems with coagulation bears the risk of impaired system performance due to unfavourable aggregate characteristics. This is of particular importance when treating humic substances due to their strong dependence on the solution environment.

The experimental work in this study aimed at finding optimal coagulation, flocculation, and membrane operating conditions for treating a typically Nordic surface water with high humic content. Commercial aluminium-based coagulants and chitosan were applied in the pre-treatment step. Short, controlled flocculation was achieved by using a pipe, jet-mix, or packed-bed flocculator. An outside-in operated ultrafiltration system based on a polymeric hollow-fibre was used as separation unit.

The study showed that optimized coagulation conditions are crucial to successful operation of the membrane unit. For the applied raw water (colour 50 mg Pt/L), a specific aluminium dosage of 3 mg Al/L and a coagulation pH in the range of 6–6.5 were found optimal with respect to permeate quality, membrane operation, and metal residuals. Coagulant dosages exceeding the optimal dosage and a pH drop increased hydraulically not-reversible fouling significantly. Chitosan neither met the expectations for NOM removal for the investigated raw water nor did its use seem favourable in combination with a polymeric membrane. Controlling floc aggregation can reduce pressure increase rates on the hollowfibre membrane provided that flocculators are designed for low velocity gradients (G<30 ^s−1). The packed-bed flocculator outperformed the other flocculators. However, flocculation times longer than 5 minutes should be applied to avoid rapid backwash pressure increases on the membrane.

The membrane system was operated with fluxes in the range of 45–75 LMH during filtration and a 1.5 times higher value during backwashes. Forward filtration without air scouring proved feasible. To improve detachment of fouling layers, vigorous air scouring was used during backwashes. A filtration cycle of 30–60 minutes followed by a backwash interval of about 30 seconds gave good results. Increasing coagulant dosage and flux were the two most significant contributors to hydraulically non-reversible fouling. Water recovery only had a minor effect on the pressure development of the membrane. However, the results suggest that efficient sludge removal from the immersion tank is of importance. Operation at lower NOM concentrations left pressure increase rates unchanged, rendering the application potential of the system highest for NOM-rich surface waters.

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40

Wang, Zhi. "Functional study of hemolymph coagulation in Drosophila larvae." Doctoral thesis, Stockholms universitet, Institutionen för molekylärbiologi och funktionsgenomik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-75179.

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Many pathogen infections in nature are accompanied by injury and subsequent coagulation. Despite the contribution of hemolymph coagulation to wound sealing, little is known about its immune function. Based on the molecular knowledge of Drosophila innate immunity, this thesis investigated the immune function of clot both in vitro and in vivo, the immune relevant genes involved in a natural infection model, involving entomopathgenic nematodes (EPN) and the factors leading to crystal cell activation. Transglutaminase (TG) and its substrate Fondue (Fon) have been identified as bona fide clot components in Drosophila larvae. By knocking down TG or Fon via RNAi, we observed an increased susceptibility to EPN in larvae. In addition, this increased susceptibility was associated with an impaired ability of hemolymph clots to entrap bacteria. Immunostaining revealed that both clot components (Fon and TG) were able to target microbial surfaces. All these data suggest an immune function for the Drosophila hemolymph clot. Strikingly, similar results were obtained when we ran parallel experiments with human FXIIIa, an ortholog of Drosophila TG, indicating a functional conservation. We also found evidence for the regulation on both clot and immunity by eicosanoids in Drosophila larvae. The combination of EPN infection with the Drosophila model system allowed us to discover an immune function for TEP3 and Glutactin. However the molecular mechanism underlying the involvement of these two proteins in this particular host-pathogen interaction remains to be elucidated. Prophenoloxidase, the proform of enzyme involved in hardening the clot matrix, has been shown to be released by rupture of crystal cells. This cell rupture is dependent on activation of the JNK pathway, Rho GTPases and Eiger. Our work further identified the cytoskeletal component, Moesin, and the cytoskeletal regulator Rac2 as mediators of cell rupture. Despite the possible role of caspases in crystal cell activation, such cell rupture was turned out to be different from apoptosis. The implication of Rab5 in this process indicated that proper endocytosis is required for cell activation and subsequent melanization. Our findings furthered not only our understanding of the release of proPO via cell rupture but also our knowledge on different paths of immune cell activation.

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: In press. Paper 4: Manuscript.

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Clark, Vesna Dimitric. "Microscopic characterization of hydrocarbon-polyelectrolyte interactions during coagulation." FIU Digital Commons, 1999. http://digitalcommons.fiu.edu/etd/2375.

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The purpose of this study was to investigate effectiveness of polyelectrolyte in removal of different hydrocarbons and to obtain information on settling velocity, size and density of the floe. Image analysis technique provided multilevel data concerning interactions between hydrocarbons and polyelectrolyte. Captured images were digitized, enhanced by numerous filtering techniques and examined. Additional, video-monitoring system was used to provide information on settling velocity of the floes. Results indicated that polyelectrolyte Cat-Floc 2953, in comparison to EB-5000, was more efficient in removal of all hydrocarbons, which was supported with turbidity measurements, GS analysis and microscopic analysis.

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Ong, Kelly C. "The expression of coagulation factors during murine development." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34062.pdf.

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43

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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44

Gershom, Edwin S. "Herpesvirus mediated activation of coagulation and fibrinolytic proteins." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/38099.

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Vascular disease, a leading cause of death worldwide, is associated with multiple risk factors that include age, diet, lifestyle and genetics. Herpesviruses, highly prevalent in the general population, have also been linked to vascular disease. To investigate the molecular basis of this relationship, the interactions between virus surface proteins and host hemostatic plasma proteins, comprising both clot forming (coagulation) and clot dissolving (fibrinolytic) proteases, which can both contribute to vascular disease, were studied. Previously, our laboratory demonstrated that purified herpes simplex virus type-1 (HSV1) and -2 (HSV2) and cytomegalovirus (CMV) contain cell-derived tissue factor (TF) and anionic phospholipids (aPL). Independent of cells, TF and aPL with factor (F) VIIa (FVIIa) initiate the extrinsic pathway of coagulation, activate FX to FXa, and lead to thrombin generation. This thesis identified additional herpesvirus-mediated coagulation pathway(s) and also demonstrated herpesvirus-mediated fibrinolysis. In addition to TF, FVIII amplified HSV1-initiated coagulation through the intrinsic pathway. Alternatively, independent of TF, HSV1 initiated coagulation through the contact pathway, via FXII activation. The ability to exploit the extrinsic, intrinsic and contact pathway of coagulation should make herpesvirus infection a strong prothrombotic risk yet the clinical correlation to vascular disease is relatively weak. To explain the in vitro versus clinical discrepancy, virus-mediated fibrinolysis was evaluated. Purified herpesviruses accelerated tissue plasminogen activator (tPA)-dependent plasminogen (Pg) activation to plasmin (Pn), the primary fibrinolytic protease responsible for fibrin clot dissolution. This Pn generation was independent of the physiological cofactor fibrin. Cell-derived annexin 2 (A2), previously identified on the surface of CMV, is a known accelerator of tPA-dependent Pn generation. Although A2 was identified among several Pg binding partners associated with each herpesvirus, it was dispensable for Pn generation. Herpesvirus-mediated plasminogen activation enhanced fibrinolysis independent of exogenous tPA. The enhanced fibrinolysis may attenuate the prothrombotic risk of herpesviruses, as an independent predictor of vascular disease. Plasmin enhanced cell susceptibility to infection, a virus-survival advantage also known for thrombin, FVIIa and FXa. Overall, for herpesviruses and other enveloped viruses, a mechanism is suggested where the envelope constituents initiate the activation of both pro-coagulation and pro-fibrinolytic proteins, modulating host cell susceptibility to infection and contributing to vascular disease.

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45

Cardigan, Rebecca Anne. "An investigation into coagulation activation during extracorporeal circulation." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286275.

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46

Boij, Roland. "Aspects of inflammation, angiogenesis and coagulation in preeclampsia." Doctoral thesis, Linköpings universitet, Avdelningen för neuro- och inflammationsvetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-132446.

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Preeclampsia is a major challenge to obstetricians, due to its impact on maternal and fetal morbidity and mortality and the lack of preventive and treatment strategies. The overall aim of this thesis is to increase the knowledge of the pathogenesis of preeclampsia including the role of inflammation, angiogenesis and coagulation, both locally at the fetomaternal interface and in the maternal circulation. Uncompensated maternal endothelial inflammatory responses to factors from stressed trophoblasts seem to be a major contributor to the syndrome, together with an imbalance in angiogenesis and an activated coagulation system. An increasing amount of data indicates an involvement of the immune system with defect tolerance to the conceptus as an integral part of the pathogenesis, at least in early-onset preeclampsia (EOP). We showed that a single administration of human preeclampsia serum in pregnant IL-10−/− mice induced the full spectrum of preeclampsia-like symptoms including hypoxic injury in uteroplacental tissues and endotheliosis in maternal kidneys. Importantly, preeclampsia serum, as early as 12 to 14 weeks of gestation, disrupted cross talk between trophoblasts and endothelial cells in an in vitro model of endovascular activity (Tube formation test). These results indicate that preeclamptic sera can be used to better understand the pathophysiology and to predict the disorder. Preeclampsia has been associated with increased inflammation, aberrant angiogenesis and activated coagulation, but their correlation and relative contribution are unknown. We found that markers for all these mechanisms were independently associated with preeclampsia. Cytokines, chemokines, and complement factors seem all to be part of a Th1-associated inflammatory reaction in preeclampsia, more pronounced in EOP than in late-onset preeclampsia (LOP), in line with a more homogeneous pathogenesis in EOP as based on placental pathology. In women with intrauterine growth restriction (IUGR), with an anticipated pathologic placentation, only differences in levels for sFlt-1 and PlGF were found in comparison with mothers without IUGR. Thus, sFlt-1 and PlGF seem to be indicators of placental pathology, while other biomarkers might also reflect maternal endothelial pathology. Chemokines, in contrast to cytokines, may prove to be useful markers in preeclampsia. A deficiency in regulatory T (Treg) cells causing reduced immune regulatory capacity has been proposed in preeclampsia. Utilizing recent advances in flow cytometry phenotyping, we found no major alterations in circulating Treg numbers in preeclamptic women compared with normal pregnant and non-pregnant women. However, preeclampsia was associated with increased fractions of CTLA-4+ and CCR4+ cells within Treg subpopulations, which is in line with a migratory defect of Treg cells, and potentially associated with a reduced number of suppressive Treg cells at the fetomaternal interface. As we found that corticosteroid treatment affected the results, it should be accounted for in studies of EOP. Chemokines are supposed to be part of the immune adaptation in pregnancy. We found a decreased expression of CCL18 (Th2/Tregassociated), in trophoblasts from preeclamptic compared to normal pregnant women, indicating a local regulatory defect in preeclampsia, in line with our finding of a possible migratory defect of circulating Treg cells. Due to increased expression of CCL20 (Th17) and CCL22 (Th2) in first trimester placenta and increased circulating levels of CXCL10 (Th1) and CCL20 (Th17) in third trimester preeclamptic women, we suggest that CCL20 and CCL22 may be important for implantation and early placentation while in third trimester of a preeclamptic pregnancy CXCL10 and CCL20 mainly mirror maternal increased endothelial inflammation and aberrant angiogenesis. In summary, we found that preeclampsia is associated with increased inflammation, aberrant angiogenesis and activated coagulation, caused by placental factors in maternal peripheral circulation, more pronounced in the early-onset form of preeclampsia. It also appears that there is a defective modulation of the immune system in preeclamptic pregnancies. The results provide a better understanding of the pathogenesis of preeclampsia and have given suggestions to predictive markers for preeclampsia in the future.

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47

Stepnik, Bertrand. "Émission submillimétrique du milieu interstellaire : coagulation des grains." Paris 6, 2001. http://www.theses.fr/2001PA066529.

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48

Davis, Christina Clarkson. "Understanding and Predicting Water Quality Impacts on Coagulation." Diss., Virginia Tech, 2014. http://hdl.handle.net/10919/70883.

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Effective coagulation is critical to the production of safe, potable drinking water, but variations in the chemical composition of source water can present challenges in achieving targeted contaminant removal and predicting coagulation outcomes. A critical literature review describes factors affecting the hydrolysis reactions of metal salt coagulants and the resulting precipitates. Properties of two key contaminants, turbidity and natural organic matter (NOM), are explored in the context of removal during coagulation, and the influence of co-occurring ions is described. While it is apparent that NOM character determines the minimum achievable organic carbon residual, the effects of water quality—including pH, NOM character and concentration, and concentrations of synergistic and competitive ions—on overall coagulation efficacy and NOM removal may be underestimated. An experimental research plan was devised to investigate the influence of water quality in coagulation and provide data to support the development of a predictive coagulation model. NOM is capable of interfering with ferric iron hydrolysis and influencing the size, morphology, and identity of precipitates. Conversely, calcium is known to increase the size and aggregation of Fe3+ precipitates and increase surface potential, leading to more effective coagulation and widening the pH range of treatment. Experiments and modeling were conducted to investigate the significance of the Fe/NOM ratio and the presence of calcium in coagulation. At the high Fe/NOM ratio, sufficient or excess ferric hydroxide was available for NOM removal, and coagulation proceeded according to expectations based upon the literature. At the low Fe/NOM ratio, however, NOM inhibited Fe3+ hydrolysis, reduced zeta potential, and suppressed the formation of filterable Fe flocs, leading to interference with effective NOM removal. In these dose-limited systems, equilibrating NOM with 1 mM Ca2+ prior to dosing with ferric chloride coagulant increased the extent of Fe3+ hydrolysis, increased zeta potential, decreased the fraction of colloidal Fe, and improved NOM removal. In dose-limited systems without calcium, complexation of Fe species by NOM appears to be the mechanism by which coagulation is disrupted. In systems with calcium, data and modeling indicate that calcium complexation by NOM neutralizes some of the negative organic charge and minimizes Fe complexation, making Fe hydrolysis species available for growth and effective coagulation. Experiments were conducted to investigate the influence of aqueous silica and pH on the removal of natural organic matter (NOM) by coagulation with ferric chloride. Samples with preformed ferric hydroxide were also compared to samples coagulated in situ to assess the role of coprecipitation. The moderate (10 mg/L) and high (50 mg/L) SiO2 concentrations both demonstrated interference with NOM removal at pH 6.5-7.5. In turn, NOM at 2 mg/L as DOC interfered with silica sorption at the moderate silica level and in samples with preformed ferric hydroxide at the high silica level. The combination of NOM and high silica led to decreases in DOC sorption and unexpected increases in silica sorption in the coprecipitated samples. The fraction of colloidal Fe passing a 0.45-μm filter also increased in the coprecipitated samples with both NOM and high silica. It is hypothesized that the combination of NOM and high silica synergistically interfered with Fe precipitation and particle growth processes, with NOM having the greater effect at lower pH and shorter reaction times, and silica exerting greater influence at higher pH and longer reaction time. Direct competition for surface sites and electrostatic repulsion were also influential. An overall goal for this research was the development of a quantitative coagulation model. Previous attempts to model coagulation have been limited by the inherent complexities of simultaneously predicting ligand sorption, metal complexation, floc surface charge, and particle removal. A diffuse layer (DLM) surface complexation model was formulated to simultaneously predict sorption of NOM and other key species, including silica, calcium, and carbonate alkalinity. Predictions of surface potential were used to estimate zeta potential and resulting regimes of effective aggregation and turbidity removal. The model provided good predictive ability for data from bench-scale experiments with synthetic water and jar tests of nine U.S. source waters. Under most conditions, the model provides excellent capability for predicting NOM sorption, calcium sorption, and particle destabilization and adequate capability for predicting silica sorption. Model simulations of hypothetical scenarios and experimental results help to explain practical observations from the literature. The DLM can be optimized to site-specific conditions and expanded to include sorption of additional species, such as arsenic.
Ph. D.

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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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50

Austin, Anthony W. "Effects of Stress-Hemoconcentration on the Coagulation Cascade." Ohio University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1316632604.

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Dissertations / Theses on the topic 'Coagulation'

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