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Relevant bibliographies by topics / Coagulation cascade

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Academic literature on the topic 'Coagulation cascade'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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Journal articles on the topic "Coagulation cascade"

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GREEN, David. "Coagulation cascade." Hemodialysis International 10, S2 (2006): S2—S4. http://dx.doi.org/10.1111/j.1542-4758.2006.00119.x.

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Olah, Zsolt, Zsuzsanna Bereczky, Mariann Szarvas, and Zoltan Boda. "Coagulation: cascade!" Lancet 378, no. 9792 (2011): 740. http://dx.doi.org/10.1016/s0140-6736(11)60875-1.

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Amour, A., M. Bird, L. Chaudry, J. Deadman, D. Hayes, and C. Kay. "General considerations for proteolytic cascades." Biochemical Society Transactions 32, no. 1 (2004): 15–16. http://dx.doi.org/10.1042/bst0320015.

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Proteases are involved in the regulation of a wide variety of essential physiological processes, often by participating in a highly orchestrated sequence of events termed a ‘proteolytic cascade’. Four major proteolytic cascades with disease relevance are candidates for therapeutic intervention, namely caspase-mediated apoptosis, blood coagulation, the matrix metalloproteinase cascade and the complement cascade. Understanding the various steps involved in the functioning of a cascade is key to deciding possible points of intervention for the design of potential drug molecules. This brief review

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HOFFMAN, Maureane, Zhi Hong MENG, Harold R. ROBERTS, and Dougald M. MONROE. "Rethinking the Coagulation Cascade." Japanese Journal of Thrombosis and Hemostasis 16, no. 1 (2005): 70–81. http://dx.doi.org/10.2491/jjsth.16.70.

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Schenone, Monica, Barbara C. Furie, and Bruce Furie. "The blood coagulation cascade." Current Opinion in Hematology 11, no. 4 (2004): 272–77. http://dx.doi.org/10.1097/01.moh.0000130308.37353.d4.

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Monroe, Dougald M., and Maureane Hoffman. "The Coagulation Cascade in Cirrhosis." Clinics in Liver Disease 13, no. 1 (2009): 1–9. http://dx.doi.org/10.1016/j.cld.2008.09.014.

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Hoffman, Maureane. "Remodeling the Blood Coagulation Cascade." Journal of Thrombosis and Thrombolysis 16, no. 1/2 (2003): 17–20. http://dx.doi.org/10.1023/b:thro.0000014588.95061.28.

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Wang, Ling, Julie Bastarache, and Lorraine Ware. "The Coagulation Cascade in Sepsis." Current Pharmaceutical Design 14, no. 19 (2008): 1860–69. http://dx.doi.org/10.2174/138161208784980581.

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Nicolle, AL, KL Talks, and JP Hanley. "Congenital and acquired bleeding problems in elderly patients." Reviews in Clinical Gerontology 15, no. 1 (2005): 9–26. http://dx.doi.org/10.1017/s0959259805001735.

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Bleeding in elderly patients is most commonly due to an underlying structural problem or an acquired coagulopathy. Occasionally, previously asymptomatic congenital bleeding disorders may present at an advanced age. When considering the possible causes of a clinical bleeding problem, the coagulation cascade is still a good starting-point. However, it is important to realize that the traditional model of the coagulation cascade has been superceded by the concept of a ‘coagulation network’. This updated model recognizes the importance of tissue factor in the initiation of coagulation. Despite the

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Yang, Zhangsheng, Milomir O. Simovic, Bin Liu, et al. "Indices of complement activation and coagulation changes in trauma patients." Trauma Surgery & Acute Care Open 7, no. 1 (2022): e000927. http://dx.doi.org/10.1136/tsaco-2022-000927.

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ObjectivesEarly complementopathy and coagulopathy are shown often after trauma. However, the prevalence of any interplay between complement cascade (ComC) and coagulation cascade (CoaC) after trauma remains unclear. This study intended to explore whether complement-coagulation crosstalk exists, which may provide a reliable guide to clinical implications in trauma patients.MethodsThis single-center cohort study of trauma patients enrolled 100 patients along with 20 healthy volunteers. Blood samples from patients were collected at admission, 45, 90, 135 minutes, and 18 hours after admission. Dem

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Dissertations / Theses on the topic "Coagulation cascade"

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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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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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Petts, Gemma Susan. "The role of the coagulation cascade in liver injury." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/43367.

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Liver disease affects approximately 600,000 people in England and Wales and is the third biggest cause of premature death. Acute and chronic liver injury occur due to a number of aetiologies and affect the function of the liver in the short and long term through pathological inflammation and fibrosis. Given the variety of aetiologies and growing burden of disease in the population, there is a need to find universal therapies that alter the progression of liver injury and fibrosis beyond the initiating insult. This work focuses on investigating the role of the coagulation cascade, specifically

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Anderson, Julia A. M. "A hypersulphated oligosaccharide inhibits intrinsic tenase and prothrombinase : key components of the blood coagulation cascade." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/21290.

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The action of thrombin is central to the processes of thrombosis and haemostasis. Thrombin is generated following the activation of prothrombin by 'prothrombinase' (II-ase), the phospholipid membrane-bound factor Xa (fXa)-factor Va (fVa) complex, which in turn is dependent upon the generation of fXa by 'intrinsic tenase' (X-ase), the phospholipid membrane-bound factor IXa (fIXa)-factor VIIIa (fVIIIa) complex. Thrombin not only converts fibrinogen to fibrin, but also amplifies its own formation by activating the cofactors in II-ase and X-ase, factor V and factor VIII, respectively. The critical

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Silva, Ludmila Bezerra da. "Identificação de proteases de Leptospira envolvidas na degradação de proteínas da matriz extracelular e do plasma humano." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/10/10134/tde-31012018-112506/.

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Leptospiras são bactérias espiroquetas altamente móveis dotadas de estratégias que possibilitam grande eficiência nos processos de invasão e disseminação no hospedeiro. Nosso grupo demonstrou previamente que leptospiras patogênicas secretam proteases capazes de clivar e inativar moléculas-chave do sistema complemento humano, o que confere a essas bactérias a capacidade de driblar os mecanismos de defesa do sistema imune inato. Dada a rápida disseminação das leptospiras durante o processo de infecção, aventou-se a hipótese de que essas proteases secretadas pudessem alvejar uma gama maior de mo

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Winbanks, Catherine, and winbanks@unimelb edu au. "Novel Aspects of Renal Tubulointerstitial Fibrosis." RMIT University. Medical Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080617.143850.

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Tubulointerstitial fibrosis is the key histological predictor of the progression of declining renal function and the final common pathway of progressive kidney disease, regardless of aetiology. Despite its significance, there are currently no treatments available to abrogate this process and those that suffer with this burden eventually succumb to renal failure. Tubulointerstitial fibrosis is largely mediated by fibroblasts and myofibroblasts present in the interstitium. In response to injury, activated fibroblasts differentiate into myofibroblasts which serves as a histological hallmark of

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Hall, David. "The effects of protease-activated receptor 2 on atherosclerosis." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1459438552.

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Chelle, Pierre. "Vers une définition patient-spécifique du taux cible de facteur anti-hémophilique à partir de la génération de thrombine : Apports des approches expérimentales et des modèles dynamiques de la cascade de la coagulation." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEM014/document.

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L’hémophilie est une maladie génétique se traduisant par la déficience des facteurs VIII et IX de la coagulation et conduisant à une tendance hémorragique. L’intensité des traitements substitutifs en facteur VIII et IX est définie essentiellement sur le taux basal du facteur déficitaire et non pas sur la capacité propre à chaque patient à générer de la thrombine qui est l’enzyme clé dans la formation du caillot de fibrine. Le test de génération de thrombine pourrait être utilisé pour permettre une individualisation du traitement anti-hémophilique. En effet, le taux de facteur VIII ou IX nécess

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Karegli, Julieta. "The potential for localised inhibition of complement and coagulation cascades in high risk renal transplantation." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/the-potential-for-localised-inhibition-of-complement-and-coagulation-cascades-in-high-risk-renal-transplantation(a65dc840-89fc-4244-8df3-2eec53777fbc).html.

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Transplantation is the preferred treatment for patients with end-stage kidney disease. However, antibodies against blood group and histocompatibility antigens on transplanted organs pose a high risk of accelerated humoral rejection. Allograft transplantation into sensitised recipients initiates complement activation and early thrombotic processes. The aim of the research described here was to determine whether cell protective therapy targeting the complement and coagulation cascades is effective at preventing graft rejection in highly sensitised renal allograft recipients. In this thesis, usin

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Oliveira, Daniella Gorete Lourenço de [UNESP]. "Purificação e caracterização de proteínas de venenos de serpentes que interferem na cascata de coagulação sanguínea." Universidade Estadual Paulista (UNESP), 2006. http://hdl.handle.net/11449/87536.

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Made available in DSpace on 2014-06-11T19:22:55Z (GMT). No. of bitstreams: 0 Previous issue date: 2006-12-08Bitstream added on 2014-06-13T20:10:06Z : No. of bitstreams: 1 oliveira_dgl_me_sjrp.pdf: 2024541 bytes, checksum: 9e617f882421a4dd2f2cc715da6fb79f (MD5)<br>Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)<br>Toxins isolated from vemos have been used as molecular tools to understand many physiological processes. The enzymes isolated from the venoms of Crotalus and Bothrops species interfere with the control and balance of the hemostatic system (PEREZ et al., 1996) and thus,

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Books on the topic "Coagulation cascade"

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Parlato, Marianna, and Jean-Marc Cavaillon. Innate immunity and the inflammatory cascade. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0299.

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Inflammation results from a complex interaction between a large number of mediators able to induce each other and to favour the generation of other inflammatory molecules (e.g. free radicals, lipid mediators, and proteases). The perpetuation of inflammation by these cascades of mediators is favoured by their ability to induce coagulation, leukocyte recruitment, and cell and tissue alteration (apoptosis, necrosis, and barrier disruption). Other cascades of mediators occur to generate anti-inflammatory mediators favouring the healing process. A neuroendocrine loop and neuromediators from central

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Matthey, Dr Francis. Anticoagulation and transfusion. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.00012.

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Chapter 12 covers anticoagulation and transfusion as they present in the acutely unwell patient, and includes information about the coagulation cascade and coagulation tests, hypercoagulable disorders, anticoagulation, factors contributing to coagulation failure and DIC, blood and blood components, bleeding disorders, and transfusion and management of bleeding.

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Wiersinga, W. Joost, and Tom van der Poll. The host response to infection in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0303.

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Infection continues to be a leading cause of intensive care unit death. The host response to infection can be seen as a pattern recognition receptor (PRR)-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. A measured and rapid response to microbial invasion is essential to health. The same immunological and coagulation systems that protect against localized infection can act to our disadvantage when these systems are activated systemically during generalized microbial infection. Toll-

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Dawson, Dana, and Keith Fox. Anti-Platelet and Anti-Thrombotic Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0004.

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• Acute coronary syndromes (ACS) encompass a spectrum of presentations which include unstable angina, non-ST-elevation myocardial infarction (NSTEMI or NSTE-ACS), and ST-elevation myocardial infarction (STEMI or STE-ACS)• Anti-platelet and anti-thrombotic agents are administered as ancillary therapy to myocardial reperfusion in patients presenting with an acute coronary syndrome, to maintain the patency of the infarct-related coronary artery• More specific and potent inhibitors of platelet activation and of the coagulation cascade are emerging with the aim being to further improve clinical out

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Wijdicks, Eelco F. M., and Sarah L. Clark. Antifibrinolytics and Thrombolytics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0008.

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There is a balance between activation of the coagulation cascade leading to thrombin and the fibrinolytic system dissolving clots. Antifibrinolytic drugs and fibrinolytic drugs are commonly used in the neurosciences intensive care unit. Antifibrinolytics, mostly tranexamic acid, are used to prevent rebleeding of recently ruptured intracranial aneurysms because fibrinolysis is considered the main mechanism of rebleeding. Drugs resulting in fibrinolysis are commonly used in vascular medicine and in cardiology. In acute ischemic stroke with disability, intravenous alteplase is the main fibrinolyt

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Albert, Tyler J., and Erik R. Swenson. The blood cells and blood count. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0265.

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Blood is a dynamic fluid consisting of cellular and plasma components undergoing constant regeneration and recycling. Like most physiological systems, the concentrations of these components are tightly regulated within narrow limits under normal conditions. In the critically-ill population, however, haematological abnormalities frequently occur and are largely due to non-haematological single- or multiple-organ pathology. Haematopoiesis originates from the pluripotent stem cell, which undergoes replication, proliferation, and differentiation, giving rise to cells of the erythroid, myeloid, and

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Book chapters on the topic "Coagulation cascade"

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Boland, John Edward, and David E. Connor. "Coagulation and the coagulation cascade." In Interventional Cardiology and Cardiac Catheterisation. CRC Press, 2019. http://dx.doi.org/10.1201/9781351060356-4.

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Ramanan, Siddharth Venkat, Jayanth Rajan, and Shobana Rajan. "The Coagulation Cascade." In Transfusion Practice in Clinical Neurosciences. Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-0954-2_25.

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Crawley, James T. B., Jose R. Gonzalez-Porras, and David A. Lane. "The Coagulation Cascade and Its Regulation." In Textbook of Pulmonary Vascular Disease. Springer US, 2010. http://dx.doi.org/10.1007/978-0-387-87429-6_23.

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Thielemans, Lieze, Moghees Hanif, and James Crawley. "The Coagulation Cascade and its Therapeutic Modulation." In Heart of the Matter. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24219-0_16.

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Cafuir, Lorraine, and Ana Antun. "Overview of the Coagulation Cascade and Thrombophilic Disorders." In PERT Consortium Handbook of Pulmonary Embolism. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-030-70904-4_12-1.

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George, Lindsey A., and Michele P. Lambert. "Coagulation Cascade and Fibrinolysis Pathway: Assessment in the Laboratory." In Nonmalignant Hematology. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30352-9_20.

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Davie, Earl W., Kazuo Fujikawa, Kotoku Kurachi, and Walter Kisiel. "The Role of Serine Proteases in the Blood Coagulation Cascade." In Advances in Enzymology - and Related Areas of Molecular Biology. John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/9780470122938.ch6.

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Castaldi, Davide, Daniele Maccagnola, Daniela Mari, and Francesco Archetti. "Stochastic Simulation of the Coagulation Cascade: A Petri Net Based Approach." In Lecture Notes in Computer Science. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36949-0_28.

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Efendiev, Messoud. "The Blood Coagulation Cascade in a Perfusion Experiment: Example from the Pharmaceutical Industry." In International Series of Numerical Mathematics. Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0615-2_6.

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Ogawa, Rei. "Ideal Wound Closure Methods for Minimizing Scarring After Surgery." In Textbook on Scar Management. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_21.

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AbstractWound-healing phenomena are the result of a cascade of complex biochemical events that can be categorized into four general overlapping phases: coagulation, inflammation, proliferation, and remodeling. Significantly, all four phases of wound healing are influenced by both intrinsic and extrinsic mechanical forces. These mechanical forces provoke chronic inflammation of the dermis, namely, the unceasing influx and activation of inflammatory cells, the persistent generation of blood vessels and nerve fibers, and the constant production of collagen by the activated fibroblasts. This chron

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Conference papers on the topic "Coagulation cascade"

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Bellini, Matteo, Daniela Besozzi, Paolo Cazzaniga, Giancarlo Mauri, and Marco S. Nobile. "Simulation and Analysis of the Blood Coagulation Cascade Accelerated on GPU." In 2014 22nd Euromicro International Conference on Parallel, Distributed and Network-Based Processing (PDP). IEEE, 2014. http://dx.doi.org/10.1109/pdp.2014.52.

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Cheadle, Rhonda, Andy Maczuszenko, and Cindra Widrig Opalsky. "Design and Development of a Unit-Use Cartridge for Coagulation Testing in Whole Blood." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0325.

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Abstract The following describes the development of a disposable cartridge for use at the patient bedside to perform traditional coagulation assays on fresh whole blood samples. The cartridge provides a means by which a blood sample can be metered and quantitatively mixed with reagents that activate the coagulation cascade. Clot formation is subsequently detected using a microfabricated sensor housed within the cartridge. The functional features of the cartridge and sensor are described.

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Tucker, Torry A., Ann Jeffers, Alexia Alvarez, Kathleen Koenig, L. Vijaya M. Rao, and Steven Idell. "Coagulation Cascade Proteases Induce Mesenchymal Transition In Human Pleural Mesothelial Cells: Implications For Pleural Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5568.

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Narahara, N., H. Sadakata, T. Uchiyama, et al. "MECHANISM OF ACTIVATION OF BLOOD COAGULATION BY LEUKOCYTE PROCOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643161.

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To investigate the process of activation mechanism of blood coagulation by leukocytes, binding of radiolabelled Factor X and the activation of Factor X on the cell surface of leukocytes were studied by using cultured leukemia cell line, Molt-4 cells. Cells were cultured in RPMI 1640 medium with 10% inactivated fetal, calf serum at a concentration of 1x106cells/ml. After 6 hours' stimulation with 1 ug/ml of endotoxin(LPS: Escherichia coli 026:B6), cells were separated by centrifugation, washed three times with Tris containing NaCl buffer(pH 7.5, TBS), and then suspended in TBS containing 0.5% b

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Mouraret, A., E. Gerard, J. Le Gall, and R. Curien. "Ostéonécrose du prémaxillaire consécutive à une coagulation intravasculaire disséminée : à propos d’un cas." In 66ème Congrès de la SFCO. EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206603011.

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La coagulation intravasculaire disséminée (CIVD) est une pathologie rare correspondant à l’activation systémique de la cascade de coagulation. Les thrombi fibrineux formés, auxquels s’ajoute un éventuel vasospasme, conduisent à l’ischémie et à la nécrose des tissus. La CIVD est fréquemment associée à un traumatisme, une blessure, une complication obstétrique ou à un choc septique. De nombreux cas d’ostéonécrose dus à une CIVD ont été décrits dans la littérature orthopédique (principalement concernant la tête fémorale), mais très peu de cas sont retrouvés concernant la région maxillo-mandibulai

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Pavlov, Valeri, Michael Zorn, and Roland Kraemer. "Probing single-stranded DNA and its biomolecular interactions through direct catalytic activation of factor XII, a protease of the blood coagulation cascade." In XIVth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2008. http://dx.doi.org/10.1135/css200810268.

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Arai, Tsunenori, Tetsumi Sumiyoshi, Kyota Naruse та ін. "Laser-tissue interaction of a continuous-wave 2-μm, 3-μm cascade oscillation fiber laser: sharp incision with controlled coagulation layer thickness". У BiOS 2000 The International Symposium on Biomedical Optics, редактори Donald D. Duncan, Jeffrey O. Hollinger та Steven L. Jacques. SPIE, 2000. http://dx.doi.org/10.1117/12.388052.

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Morrissey, J. H., D. S. Fair, and T. S. Edgington. "STRUCTURE AND PROPERTIES OF THE HUMAN TISSUE FACTOR APOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643738.

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Tissue factor (TF), an integral membrane glycoprotein, is an initiating molecule for the coagulation protease cascade. TF must reside in a phospholipid membrane for optimal activity where it functions as the receptor and essential allosteric activator for factor Vll/VIIa.TF apoprotein was purified from human brain and placenta using factor Vll-affinity chromatography or immunoaffinity chromatography with a mouse anti-TF monoclonal antibody. Both methods resulted in a homogeneous preparation consisting of a highly glycosylated 47 kDa heavy chain and a 12.5 kDa light chain.Removal of asparagine-

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Zhang, Peng, Jawaad Sheriff, João S. Soares, et al. "Multiscale Modeling of Flow Induced Thrombogenicity Using Dissipative Particle Dynamics and Coarse Grained Molecular Dynamics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14187.

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The coagulation cascade of blood may be initiated by flow induced platelet activation, which prompts clot formation in prosthetic cardiovascular devices and arterial disease processes. While platelet activation may be induced by biochemical agonists, shear stresses arising from pathological flow patterns enhance the propensity of platelets to activate and initiate the intrinsic pathway of coagulation, leading to thrombosis. Upon activation platelets undergo complex biochemical and morphological changes: organelles are centralized, membrane glycoproteins undergo conformational changes, and adhe

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Bluestein, Danny, João S. Soares, Peng Zhang, et al. "Multiscale Modeling of Flow Induced Thrombogenicity Using Dissipative Particle Dynamics and Molecular Dynamics." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93094.

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The coagulation cascade of blood may be initiated by flow induced platelet activation, which prompts clot formation in prosthetic cardiovascular devices and arterial disease processes. While platelet activation may be induced by biochemical agonists, shear stresses arising from pathological flow patterns enhance the propensity of platelets to activate and initiate the intrinsic pathway of coagulation, leading to thrombosis. Upon activation platelets undergo complex biochemical and morphological changes: organelles are centralized, membrane glycoproteins undergo conformational changes, and adhe

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