Dissertations / Theses on the topic 'Antithrombin'
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Skinner, Richard. "Structural biology of antithrombin." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627475.
Full textBruce, David. "Antithrombin : structural variants and thrombosis." Thesis, Open University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386084.
Full textFitton, Hazel Louise. "Modulation of antithrombin by heparin." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624993.
Full textJin, L. "Antithrombin structures and the heparin pentasaccharide." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.605606.
Full textChristey, Peter B. "Heparin binding and activation of antithrombin." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315820.
Full textCORNO, ANNA ROSA. "CARENZA CONGENITA DI ANTITROMBINA E DIAGNOSI DI LABORTORIO: QUALE TEST FUNZIONALE?" Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/233996.
Full textIntroduction – Antithrombin (AT) deficiency, associated with an increased risk for venous thrombosis, is classified into type I (quantitative defect) and type II (qualitative defect). Qualitative defects may affect the reactive site (RS), the heparin binding site (HBS) of AT, or they may have a pleiotropic effect (PE). Screening tests, which measure the ability of AT, in the presence of heparin, to inhibits either thrombin (anti-IIa activity) or FXa (anti-Xa activity), are able to detect most AT deficiencies; however, few cases of discrepancies have been described (i.e. normal vs. pathological value) with the two different methods. Aim of the study was the evaluation of agreement between an anti-Xa assay and an anti-IIa assay for AT, and the evaluation of their ability in detecting AT defects. Materials and Methods – The study population consisted of the “routine and thrombophilic” group (493 patients for which AT test was required) and the “historical deficiencies” group (23 subjects with known AT deficiency and 18 relatives). Anti-Xa HemosIL Antithrombin kit (from Instrumentation Laboratory) and a home-made anti-IIa method were used to measure AT activities. A control group (n= 100) was used to determine AT reference ranges. SERPINC1 gene analysis was carried out for 21 patients (Universitair Ziekenhuis in Bruxelles). Results – The results provided by the two methods showed a high correlation (Spearman rho>0.70); however, 8 discrepant results were observed (3 in the “routine and thrombophilia” group and 5 in the “historical deficiencies” group). Gene analysis confirmed the presence of a molecular defect in 18/21 subjects, 5 of which had also descrepant AT results. In fact, normal anti-Xa AT values were obtained for Cambridge II defect (RS), whereas anti-IIa test provided normal values for a HBS defect. Both methods provided pathological AT values for 5 type I deficiencies but normal AT values for other 2 HBS defects. In the study population AT anti-Xa and AT anti-IIa sensitivity was 61.1% and 55.6%, respectively; when both tests were used, sensitivity increased to 72.2%. When the ratio between AT anti-IIa and AT anti-Xa was added, sensitivity increased to 88.9%. Conclusions – Currently avaible screening tests are not able to detect all molecular defects. However, when anti-Xa assay is carried out together with anti-IIa method, and the ratio between the results provided by both is considered, the diagnostic power is increased. Anyway, laboratory test results should be considered together with personal and familiar clinical history of the single subject under evaluation.
Chen, Iris Ye Wu. "The interactions between human antithrombin and heparin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0005/NQ42731.pdf.
Full textPerry, David James. "The genetic basis of human antithrombin deficiency." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283014.
Full textBelzar, Klara Jane. "The allosteric activation of antithrombin by heparin." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621213.
Full textBourti, Yasmine. "Evaluation d'un variant d'antithrombine dans différentes indications thérapeutiques." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS404/document.
Full textOur team topic focuses on the structural-function relationship of a natural anticoagulant, antithrombin (AT), in order to develop potential therapeutic agents. AT inhibits several serine proteases of the coagulation cascade and its inhibitory activity is increased when AT binds to a pentasaccharidic motif contained within in the heparin derivatives. At high concentrations (500%), AT also exerts anti-inflammatory and cytoprotective properties through its binding to heparan sulfate proteoglycans, making it a good candidate for supportive therapy in clinical settings associating inflammation and coagulation activation. Indeed, AT has already been evaluated in vivo in various models of ischemia-reperfusion injury (IRI) and AT even reached a large-scale clinical trial in severe sepsis. However, the high concentrations of AT that are needed to exert anti-inflammatory properties are inconsistent with the safety profile of this anticoagulant protein.In this context we have further characterized an AT variant (AT-N135Q-Pro394) with increased affinity to heparin but devoid of anticoagulant activity. Indeed, this variant was described to be able to trap heparin derivatives and our work was to pursue the characterization of this variant as an antidote toward heparin derivatives in clinical situations of overdosing. In addition, this AT variant binds to heparan sulfate proteoglycans with higher affinity, as compared to native AT, and appears as a promising cytoprotective agent whose administration would not be associated with any bleeding risk.To test the latter hypothesis, we developed a murine model of renal IRI in which the renal function was severely impaired, as attested by increased kidney injury markers (urea, creatinine, kim-1) and local kidney inflammation (renal gene expression of il-6 and cxcl-1). Indeed, in 2003, Mizutani et al. reported a protective effect of AT in a similar murine model of renal IRI. Surprisingly, we observed none of the described protective effects, neither on inflammation nor renal function, with plasma AT, recombinant AT and an equimolar mixture of native and latent AT. Nevertheless, the same model enabled us to highlight the nephroprotective and anti-inflammatory properties of another anticoagulant protein, activated protein C (APC), as previously reported. These disappointing results coincided with the withdrawal in 2013 of the study of Mizutani et al., and our work allowed us to clarify the literature and to claim that neither recombinant nor plasma-derived native nor latent forms of AT exhibit a protective effect in renal IRI in mice. Under these conditions, AT-N135Q-Pro394 variant has not been tested in our model.AT-N135Q-Pro394 has also been previously shown to efficiently neutralise the anticoagulant activity of heparin derivatives, including unfractionated heparin (UFH), low molecular weight heparins (LMWH) and fondaparinux in vivo. Nevertheless, this reversal effect was only explored by anti-factor Xa assays whereas AT inhibits a number of coagulation proteases, including factors VIIa, IXa and IIa. Therefore, we explored AT-N135Q-Pro394 variant in a more global coagulation assay, the thrombin-generation assay (TGA), in order to compare its activity with non-specific reversal agents used toward heparin derivative overdose (recombinant-activated factor VII, activated prothrombin-complex concentrate or protamine). Interestingly, in plasma mimicking an overdose, our variant demonstrated greater reversal efficiency as compared to hemostatic agents and protamine sulfate toward fondaparinux and LMWH, respectively, and was as efficient as protamine sulfate toward UFH. Finally, when added to native plasma (in the absence of heparin derivative), AT-N135Q-Pro394 showed no effect on thrombin generation unlike hemostatics and protamine sulfate that all significantly affect the TGA profile
Mushunje, Alec. "Antithrombin conformational transitions and their implications in thrombosis." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620006.
Full textBrinkmeyer, Stephan. "Experimente zur Aktivierung von Heparinkofaktor II durch Heparin und Dermatansulfat unter Verwendung eines reversiblen molekularen Schalters." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963784730.
Full textZilker, Susanne. "Aktivitätsgesteuerte Therapie der schweren chirurgischen Sepsis mit Antithrombin III." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-99495.
Full textOldeen, Molly Elisabeth. "Optimizing Anticoagulation Therapy in ECMO Patients using Antithrombin III." Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/228500.
Full textFazavana, Judicaël. "Développement d’une antithrombine modifiée inactive comme antidote des anticoagulants hépariniques." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114855/document.
Full textUnfractionnated heparin (UFH), low molecular weight heparins (LMWH), and fondaparinux are used therapeutically as anticoagulants. They potentiate antithrombin (AT): a physiological inhibitor of coagulation. Their therapeutic use is associated with a major risk of bleeding. Currently, protamine sulfate is the only antidote available for UFH. It is partially effective for LMWH, and has no effect against fondaparinux, which has no antidote. So, we propose modified inactive AT, but able to bind heparin molecules as antidote of these heparins. These molecules would compete with plasmatic AT for binding to heparins, and neutralize their anticoagulant effect. To produce that AT, we realized a genetic approach and a chemical approach. In the first approach, we expressed the variant AT-N135Q-Pro394 that had an anti-Xa or anti-IIa activity below 0.02% in the presence of heparins, and heparin affinity three times higher, compared to the plasmatic AT. In the chemical approach, we modified the plasmatic AT by 2,3-butanedione (AT-BD), a chemical reagent for arginin’s characterization. The AT-BD had a moderate loss of anticoagulant activity, and a heparin affinity 20 times higher, compared to the plasmatic AT. Despite these differences in biochemical properties, these two modified AT neutralize similarly heparins in vitro and in a mouse model. Moreover, unlike protamine sulfate, our antidotes had not an intrinsic anticoagulant effect in activated partial thromboplastin test. Thus, this PhD-work offers the first and the only specific antidote described to fondaparinux, and it can be used too alternatively for all anticoagulant heparins
Elnerud, Maja. "Method development for studying the interactions between antithrombin and heparin." Thesis, Linköping University, The Department of Physics, Chemistry and Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-11208.
Full textAntithrombin (AT) is one of the most important anticoagulant factors in the blood, and its effects are increased by the interaction with glycosaminoglycans, especially heparin. AT appears in two additional variants, other than the native form, and those variants have antiangiogenic properties and also bind to heparin. AT is found in two distinct isoforms (alfa, beta) where the difference lie in the degree of glycosylation. This project has shown interesting results regarding the dependence of calcium ions on the binding between heparin and antithrombin. The results show that the beta-isoform increases its affinity for heparin in the presence of calcium in contrast to the alfa-isoform, which shows a decrease in the heparin affinity under the same conditions. This project has also given results that after further investigation and development could be used for an improved set-up of the immobilisation of AT variants in a surface plasmon resonance system. The results show that immobilisation of a protein in the reference channel gives a better shielding effect between the negatively charged heparin molecules and the negatively charged dextran matrix. Furthermore a more significant difference was seen between the two heparin moieties used during binding affinity studies, especially for native AT.
Wells, Michael John. "Identification and characterization of rabbit hepatic receptors for thrombin-antithrombin complexes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0003/NQ42771.pdf.
Full textKittel, Florina Luisa [Verfasser], and Hinnak [Akademischer Betreuer] Northoff. "Schwingquarzbasierte Bestimmung von Antithrombin III / Florina Luisa Kittel ; Betreuer: Hinnak Northoff." Tübingen : Universitätsbibliothek Tübingen, 2015. http://d-nb.info/1197057986/34.
Full textEvington, 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.
Full textKittel, Florina [Verfasser], and Hinnak [Akademischer Betreuer] Northoff. "Schwingquarzbasierte Bestimmung von Antithrombin III / Florina Luisa Kittel ; Betreuer: Hinnak Northoff." Tübingen : Universitätsbibliothek Tübingen, 2015. http://d-nb.info/1197057986/34.
Full textVan, der Merwe Liesel Laura. "The effect of haemolysis on antithrombin concentration as determined by a chromogenic method." Diss., University of Pretoria, 2005. http://hdl.handle.net/2263/22875.
Full textDissertation (MMedVet (Med))--University of Pretoria, 2005.
Companion Animal Clinical Studies
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Hagel, Stefan. "Protein C- und Antithrombin III-Aktivität : Stellenwert bei der Diagnose und Verlaufsbeurteilung unterschiedlicher systemischer Entzündungssyndrome bei kritisch kranken Patienten /." Saarbrücken VDM Verlag Dr. Müller, 2006. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=015040669&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
Full textZamorskii, I. I. "Antithrombin DNA aptamers as a renoprotective agents against the rhabdomyolysis-induced acute kidney injury." Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18254.
Full textPfannenschmidt, Gerd. "Der Effekt von Antithrombin III auf die pulmonalvaskuläre Freisetzung von Big Endothelin-1, Endothelin-1 und Prostanoiden unter septischen und nichtseptischen Bedingungen sowie seine Mechanismen." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2000. http://dx.doi.org/10.18452/14540.
Full textThe aim of the present study was to clarify if the pulmonary protective effects of AT III in LPS-induced ARDS can be attributed to a stimulation of the pulmonary vascular release of PGI2. The pulmonary vascular release of big ET-1 and ET-1 under septic conditions and the possible influence of AT III was to be investigated. To this end, we used the model of the isolated perfused rat lung. Exposure of the lung to LPS increased the release of 6-Keto-PGF1(, the stable metabolite of PGI2, 1.6fold and the production of TxB2, the stable metabolite of TxA2, 2.9fold compared with control lungs. The release of ET-1 increased 1.6fold under LPS, whereas the concentration of big ET-1 was unchanged. The application of AT III had no effect on the release of PGI2 and TxA2. The effects following combined application of LPS and AT III were similar to the effects of LPS alone. Compared with controls, AT III, at 2 U/ml, increased the perfusate levels of big ET-1 and ET-1 1.7fold and 1.2fold, respectively; the administration of 5 U/ml AT III raised big ET-1 and ET-1 1.6fold and 1.3fold, respectively. Combined application of LPS and AT III resulted in a 2.6fold rise of big ET-1 levels compared with controls, whereas concentrations of ET-1 did not differ from those in the presence of LPS or AT III alone. Cicaprost, a stable PGI2 analogue, affected neither the basal nor the AT III plus LPS-stimulated release of big ET-1 and ET-1. Nicardipin, an L-type calcium channel blocker, heparin and N-acetyl heparin, a heparin derivative devoid of AT III affinity, each antagonized completely the AT III-stimulated increase in big ET-1 and ET-1 levels. Staurosporin, an inhibitor of protein kinase C, and genistein, an inhibitor of tyrosine kinases, did not influence the AT III effects on endothelins. CONCLUSIONS: In ARDS, the well-known rise in plasma PGI2 in response to AT III obviously originates from non-pulmonary sources. PGI2 does not suppress the pulmonary ET-1 secretion; therefore, this mechanism seems not involved in the AT III-induced lung protection during septic ARDS. The AT III-mediated stimulation of the release of pulmonary endothelins is of potential pathophysiological relevance, because it may blunt the protective effects of AT III in ARDS. In the intact rat lung, this stimulatory effect of AT III is mediated neither by protein kinase C nor by tyrosine kinases. Moreover, the observed effect of AT III on pulmonary endothelins is based on calcium influx through L-type calcium channels and depends on the intracellular calcium activity. The equipotency of heparin and N-acetyl heparin in inhibiting the AT III action demonstrates that direct binding of AT III is not essential for the blocking effect of heparins. This fact points to additional involvement of an IP3-dependent intracellular calcium release.
Borg, Jeanne-Yvonne. "Antithrombines trois rouen : anomalies constitutionnelles avec defaut isole de liaison a l'heparine : etude structurale et fonctionnelle, analyse physiopathologique." Paris 7, 1987. http://www.theses.fr/1987PA077193.
Full textYamashiro, Kenji. "Inhibitory Effects of Antithrombin III against Leukocyte Rolling and Infiltration during Endotoxin-induced Uveitis in Rats." Kyoto University, 2003. http://hdl.handle.net/2433/148459.
Full textRaghuraman, Arjun. "Designing Non-saccharide Heparin/Heparan Sulfate Mimics." Online version available 8/19/2013, 2008. http://hdl.handle.net/10156/2269.
Full textde, la Morena Barrio Mª Eugenia. "Identificación de nuevos elementos implicados en la regulación de antitrombina= Identification of new elements involved in antithrombin regulation." Doctoral thesis, Universidad de Murcia, 2013. http://hdl.handle.net/10803/116861.
Full textLa deficiencia de antitrombina causada por mutaciones en el gen SERPINC1 incrementa el riesgo trombótico. Nuestro objetivo fue identificar nuevos mecanismos implicados en la deficiencia de este anticoagulante. Empleando metodología molecular, celular y bioquímica estudiamos 29 pacientes con deficiencia de antitrombina sin mutaciones en SERPINC1, un estudio familiar, tres estudios caso-control (2,980 pacientes/3,996 controles) y dos pacientes con trastornos congénitos de glicosilación (CDG). Identificamos la primera mutación en el promotor de SERPINC1 que causa deficiencia de antitrombina. Confirmamos la baja variabilidad genética en SERPINC1 y su escasa influencia en la heredabilidad de antitrombina. Un GWAS y experimentos de silenciamiento mostraron que LARGE es el primer gen modulador de antitrombina. Diagnosticamos un CDG por la deficiencia de antitrombina de un paciente con trombosis recurrente y descubrimos nuevo desorden con patrón bioquímico similar al CDG pero solo con trombosis que es causado por una sola mutación en PMM2 y consumo de alcohol.
Zani, Karen de Morais. "Estudo da atividade anti-inflamatória da antitrombina nativa da serpente Bothrops jararaca. Clonagem da antitrombina." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-06062013-154512/.
Full textB. jararaca antithrombin was isolated by affinity chromatography using HiTrap Heparin HP column (GE Healthcare). The interaction analysis of human or B. jararaca antithrombin with heparin using a BIAcoreT200 system (GE Healthcare) demonstrated that the affinity of B. jararaca antithrombin for heparin is higher than human antithrombin. Regarding the anti-inflammatory activity of B. jararaca antithrombin, the results showed the anti-inflammatory effect of pre- and post-treatment with this molecule in acute inflammation. The proteomic analysis of inflammatory exudate of mice identified some proteins possibly related to the mechanism of inhibition of antithrombin, such as C3 complement, serum transferrin, a1-antitrypsin, apolipoprotein AI, fibrinogen, albumin and kininogen. The molecular cloning process allowed the determination of the complete sequence of B. jararaca antithrombin and despite the evolutionary distance between snakes and human, a number of characteristics are preserved in antithrombin molecule.
Morais, Karen Batista de. "Purificação e caracterização da antitrombina do plasma da serpente Bothrops jararaca (Wied, 1824) (Ophidia: Viperidae, Crotalinae)." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-13072009-160524/.
Full textThe aim of the present work was to characterize the seed development of Araucaria angustifolia through proteomics in order to understand the physiological and biochemical changes during this process. For that, initially, three different protein extraction methods were evaluated. The extraction based on protein solubilization in 7 M urea, 2 M thiourea, 1% dithiothreitol, 2% Triton-100, 1 mM phenylmethylsulphonyl fluoride, 5 µM pepstatin, followed by 20% trichloroacetic acid precipitation showed the highest gel resolution and reprodutivity and, thus, was chosen to be used in the analysis of the proteome of A. angustifolia seeds. One aspect that hampers the proteome study of unsequenced species is the low protein representativity in databases. So, protein identification is usually carried out through homology. Strategies based on 2-DE result in high keratin contamination. In the present work a spectra filtering software was developed and evaluated for use in homology driven proteomics. The software reduced the time of search, improved alignment quality and did not result in lost of positive identifications. Finally, using the described strategies, the changes in the proteome of A. angustifolia seeds were studied. Ninety six proteins were identified and classified according to their biological functions and expression profiles during seed development. The identified proteins may be used as protein markers of early and late embryogenesis. Proteins involved in the control of oxidative metabolism were highly expressed during the early stages of seed development; while, carbon metabolism and storage proteins were highly expressed in late stages. Considerations on the improvement and control of somatic embryogenesis through medium manipulation and protein markers screening using data generated are also discussed.
Vecchietti, D. G. "Low Molecular Weight Heparins : in depth structural characterization to understand their different biological properties." Doctoral thesis, Università degli Studi di Milano, 2008. http://hdl.handle.net/2434/59669.
Full textHashim, R. Bt. "The use of fluorescent probes in the study of the interaction of the interaction of heparin with antithrombin III and polycations." Thesis, University of Salford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356175.
Full textBäck, Jennie. "The Plasma Contact System : New Functional Insights from a Hemostatic and Thrombotic Perspective." Doctoral thesis, Uppsala universitet, Klinisk immunologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-160343.
Full textWahlgren, Carl Magnus. "Mechanisms of thrombosis and restenosis after vascular injury /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-260-8/.
Full textPfannenschmidt, Gerd. "Der Effekt von Antithrombin-III auf die pulmonalvaskuläre Freisetzung von Big-Endothelin-1, Endothelin-1 und Prostanoiden unter septischen und nichtseptischen Bedingungen sowie seine Mechanismen." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=960868755.
Full textSanchez, Caroline. "Influences génétique et environnementale de la génération de thrombine." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX20658.
Full textIn this work, we studied genetic and environmental modulators of thrombin generation by endogenous thrombin potential (ETP).We showed that plasma levels of antithrombin (AT) can be considered as risk factors for thrombosis. ETP levels are higher in patients presenting a quantitative defect of AT. In addition, mutation AT Cambridge II is also associated with an increase of ETP. Besides the AT, we confirmed a positive effect of the prothrombin 20210A allele on thrombin generation, especially in presence of venous thrombosis antecedents. These contributions, we have confirmed the role of plasma fibrinogen and factor II, blood group and oral contraceptives on thrombin generation.In addition, our results also showed an effect of high fat diet on thrombin generation in rats. Conversely to the standard fat diet, high fat diet maintened high levels of ETP after weaning. High fat diet-induced effects persisted four weeks after switching to standard fat diet. This effect could be partially explained by higher rates of coagulation factors VII and did not follow classical changes in glucidolipidic metabolism.In conclusion our data suggest that ETP can be considered as an indicator of the prothrombotic state in patients, but require more explanation to predict a risk of venous thrombosis. The measurement of thrombin generation may be a useful tool for assessing the impact of changes in diet or medication to treat obesity on circulating procoagulant potential
Arnljots, Björn. "On prevention of microarterial thrombosis role of protein C and protein S and thrombin inhibition /." Lund : Dept. of Plastic and Reconstructive Surgery, Malmö University Hospital, University of Lund, 1995. http://catalog.hathitrust.org/api/volumes/oclc/39055869.html.
Full textMigoney, Touze Véronique. "Fonctionnalisation de la surface interne de matériaux tubulaires : étude de l'inhibition de la thrombine par l'antithrombine III à la surface de ces matériaux." Paris 13, 1986. http://www.theses.fr/1986PA132006.
Full textNienaber, Cornelie. "Haemostatic variables in African adolescents : the PLAY study / Cornelie Nienaber." Thesis, North-West University, 2006. http://hdl.handle.net/10394/1322.
Full textSié, Pierre. "Biologie et pharmacologie du second cofacteur de l'heparine." Paris 7, 1987. http://www.theses.fr/1987PA077082.
Full textLinden, Matthew D. "The haemostatic defect of cardiopulmonary bypass." University of Western Australia. School of Surgery and Pathology, 2003. http://theses.library.uwa.edu.au/adt-WU2006.0009.
Full textDesroys, du Roure François. "Influence de la concentration en chlorure de sodium sur l'inhibition de la thrombine par l'antithrombine III en présence d'héparine standard et de trois héparines de bas poids moléculaire." Paris 5, 1993. http://www.theses.fr/1993PA05P010.
Full textCamprubí, Rimblas Marta. "Nebulized anti-coagulants as a therapy for acute lung injury and acute respiratory distress syndrome." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/663961.
Full textAcute respiratory distress syndrome (ARDS) is an acute respiratory failure with a global incidence in Europe of 17.9 per 100,000 person-year. Although significant advances have been performed in supportive care of patients with ARDS, mortality remains high (40%) and survivors present persistent sequelae. An effective pharmacological therapy for this syndrome is not available yet. ARDS pathophysiology involves pulmonary activated coagulation and inflammation together with the breakdown of the alveolar-capillary barrier. This leads to proteinaceous edema, neutrophils infiltration into the alveolar compartment and the activation of macrophages towards a pro-inflammatory phenotype. Beneficial effects of anti-coagulants have been proved in pre-clinical models of acute lung injury (ALI) and in ARDS patients, although systemic bleeding offset its positive effects. Anti-coagulants could be effective for their anti-inflammatory activity in addition to their anti-coagulant properties. Moreover, given the cross talk of these pathways and their influence on permeability, anti-coagulants could also restore the alveolar-capillary barrier. Nebulization of anti-coagulants directly into the alveolar compartment might increase local efficacy and decrease the risk of systemic bleeding. The hypothesis of this thesis is that nebulized heparin and/or antithrombin (ATIII) limit the pro-inflammatory and pro-coagulant response in the lungs after ALI, also promoting the restoration of the alveolar-capillary barrier. The co-administration of both anti-coagulants directly into the lungs via nebulization produces a synergistic effect enhancing the properties of heparin and ATIII, reducing lung injury and avoiding the risk of systemic bleeding. As part of this thesis we are showing the results of the action of heparin or ATIII in specific primary human injured cell lung populations and the direct administration of heparin and/or ATIII into the lungs by nebulization in a rat model of ALI. Nebulized heparin and/or ATIII attenuated pulmonary inflammation and coagulation and did not produce systemic bleeding in the model of ALI. Treatment with nebulized heparin modulated alveolar macrophages through reducing TGF-β and NF-κB effectors and the coagulation pathway and decreased the recruitment of neutrophils into the alveolar space. Local administration of ATIII alone increased beneficial effects in coagulation, while combined ATIII and heparin had a higher impact reducing permeability and decreasing the infiltration of macrophages into the alveolar compartment. The translational action into humans of both anti-coagulants was also studied. In injured human cell lung populations isolated from lung biopsies, heparin diminished the expression of pro-inflammatory markers in alveolar macrophages and deactivated the NF-κB pathway in alveolar type II cells; decreasing the expression of its mediators and effectors. Also, ATIII decreased levels of pro-inflammatory mediators and increased levels of tight junctions in injured alveolar type II cells. The current studies prove that nebulized heparin and ATIII might be a potential treatment for ARDS, as they act in different pathways and processes of the pathophysiology of this syndrome. Local administration of anti-coagulants attenuates lung injury decreasing inflammation, coagulation and proving ameliorations on permeability without causing systemic bleeding.
Kuusisto, M. (Milla). "Translational research on challenges in the treatment of diffuse large B-cell lymphoma." Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526210643.
Full textTiivistelmä Tutkimuksessa arvioitiin osaa yleisimmän pahanlaatuisen imukudossyövän eli lymfooman, diffuusin suurisoluisen B-solulymfooman, hoidon haasteista. Osa potilaista saa ensilinjan hoidon jälkeen joko paikallisen tai aivoston alueen taudin uusiutuman. Uusiutuneen taudin hoito on haasteellista, ja hoitoyrityksistä huolimatta osa potilaista kuolee tautiinsa. Solunsalpaajille resistentti tauti on myös yksi haastavista hoitotilanteista, ja osa potilaista kärsiikin hoitojen läpi etenevästä taudista. Antioksidatiivisia entsyymejä, kuten peroksiredoksiineja ja tioredoksiinia, arvioitiin ennusteellisina ja ennakoivina merkkiaineina diffuusissa suurisoluisessa B-solulymfoomassa. Peroksiredoksiini VI:n korkea sytosolinen ilmaantuvuus korreloi tavallista huonompaan diffuusin suurisoluisen B-solulymfooman ennusteeseen. Tioredoksiinin hiljentäminen lymfoomasoluviljelyssä paljasti sen mahdollisen ennakoivan merkityksen hoitoon liittyvässä päätöksenteossa. Solut herkistyivät tiodredoksiinin hiljentämisen vuoksi doksorubisiinille, jota käytetään laajalti diffuusin suurisoluisen B-solulymfooman solunsalpaajahoidoissa. Etoposidi, joka on huomattavasti myrkyllisempi solunsalpaaja, päinvastoin tappoi enemmän tavallisia diffuusia suurisoluisia B-solulymfoomaa edustavia soluja kuin doksorubisiini. Potilaat, joilla oli korkea tioredoksiinin määrä taudin diagnostisessa vaiheessa, hyötyivät etoposidia sisältävästä korkea-annoshoidosta sekä autologisesta kantasolusiirrosta. Näille potilaille ei kehittynyt kantasolusiirron jälkeisiä taudin uusiutumia kuin taas niitä kehittyi potilaille, joilla oli tioredoksiini negatiivinen. Antitrombiini III:a on ehdotettu soveltuvaksi aikaisempien tutkimusten perusteella aivoston lymfooman merkkiaineeksi aivo-selkäydinnesteestä. Tässä tutkimuksessa antitrombiini III:n määrää mitattiin potilailta, joilla oli aivoston lymfooma tai neurologinen sairaus. Korkeat konsentraatiot antitrombiini III:a aivo-selkäydinnesteessä kuitenkin vain heijastivat veri-aivoesteen vuotamisen määrää, ja näin ollen antitrombiini III:a ei tulisi käyttää kliinisessä käytössä
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Full textVidaud, Dominique. "Pathologie des inhibiteurs des sérines protéases (serpines) : Etude moléculaire d'un cas d'alpha1-antitrypsine Pittsburgh et de plusieurs déficits en antithrombine III." Paris 13, 1991. http://www.theses.fr/1991PA132003.
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Full textFazavana, Judicaël. "Développement d'une antithrombine modifiée inactive comme antidote des anticoagulants hépariniques." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00976551.
Full textMauray, Sandrine. "Activités anticoagulante et antithrombotique de polysaccharides sulfatés." Paris 13, 1995. http://www.theses.fr/1995PA132026.
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