Relevant bibliographies by topics / Coagulation cascade

Academic literature on the topic 'Coagulation cascade'

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Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Coagulation cascade"

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GREEN, David. "Coagulation cascade." Hemodialysis International 10, S2 (October 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 (August 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 (February 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 illustrates some of the common features of proteolytic cascades using the blood coagulation pathway as an example.
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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 (July 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 (February 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 (August 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 (July 1, 2008): 1860–69. http://dx.doi.org/10.2174/138161208784980581.

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Yang, Zhangsheng, Milomir O. Simovic, Bin Liu, Matthew B. Burgess, Andrew P. Cap, Jurandir J. DalleLucca, and Yansong Li. "Indices of complement activation and coagulation changes in trauma patients." Trauma Surgery & Acute Care Open 7, no. 1 (September 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. Demographic characteristics were recorded, blood levels of ComC and CoaC factors, and inflammatory cytokines were measured by ELISA, clot-based assays, or luminex multiplex assay, and partial thromboplastin (PT) and partial thromboplastin time (PTT) were assessed using a Behring blood coagulation system.ResultsCompared with the healthy controls, plasma levels of complement factors (C5b-9 and Bb) and 11 tested inflammatory cytokines increased in moderately and severely injured patients as early as 45 minutes after admission and sustained higher levels up to 18 hours after admission. C5b-9 correlated positively to patients’ hospital stay. In parallel, the consumption of coagulation factors I, II, X, and XIII was shown throughout the first 18 hours after admission in moderately and severely injured patients, whereas PT, PTT, D-dimer, factor VII, and factor VIII values significantly increased from the admission to 135 minutes in moderately and severely injured patients. Along with an inverse correlation between plasma Bb, factors I and II, a positive correlation between C5b-9, Bb, D-dimer, PT, and PTT was evident.ConclusionsThis study demonstrates trauma-induced early activation of plasma cascades including ComC, CoaC, and fibrinolytic cascade, and their correlation between plasma cascades in severe trauma patients. Our study suggests that the simultaneous modulation of plasma cascades might benefit clinical outcomes for trauma patients.Level of evidenceProspective study, level III.
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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 (February 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 complexity of this model, the basic coagulation tests can still be interpreted in relation to the ‘intrinsic’, ‘extrinsic’ and ‘final common pathway’ components of the old-fashioned cascade (Figure 1).
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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 Tissue Factor Pathway Inhibitor (TFPI), in liver injury and it’s use as a potential therapeutic target for altering the progression of acute and chronic liver injury. Using two transgenic strains of mice, expressing TFPI in a cell specific manner I have shown that TFPI decreases the extent and progression of liver injury in models of acute liver injury but does not modify the development of liver fibrosis in a model of chronic liver injury. In the models of acute liver injury there was decreased liver injury associated with decreased fibrin deposition, decreased hepatic stellate cell activation, decreased total liver macrophage content and decreased PAR2 expression. The pattern of changes suggests that TFPI acts early in the injury process, limiting total hepatocyte injury and resulting in a decrease in hepatic stellate cell activation and macrophage recruitment, rather than the other way round. Further work should focus on defining the inflammatory cytokine profile of the liver of these transgenic mice in acute liver injury with the aim of describing the biological mechanism for the action of TFPI in acute liver injury and taking forward the trial of TFPI administration to control mice in a manner that could be carried forward to human studies.
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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 role played by II-ase and X-ase towards thrombin generation makes these membrane-bound enzyme complexes attractive targets for inhibition and offers an effective approach to blocking coagulation. Heparin acts as an anticoagulant by activating antithrombin (AT), which then inactivates thrombin, fXa and other activated clotting factors. However, the heparin-AT complex has limited activity against membrane-bound fIXa and fXa. Recently, in buffer systems, heparin has been shown to have an AT-independent effect on coagulation by directly inhibiting X-ase, an effect that is minimal in plasma where the AT-dependent heparin effect predominates. To capitalise on this AT-independent effect, heparin was chemically modified by periodate oxidation and borohydrate reduction to lower its affinity for AT (from Kd value of 25nM to 43μM); we used LMWH rather than heparin to take advantage of the superior pharmacokinetic profile of LMWH. Using this low affinity LMWH (LA-LMWH), N-desulphated LMWH was prepared using a solvolytic desulphation method. Whereas LA-LMWH inhibited X-ase to a similar extent as LMWH with high AT-affinity (IC50 of 16μg/ml and 13μg/ml respectively), N-desulphated LMWH had minimal inhibitory activity (IC50 of 166μg/ml).
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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 moléculas do hospedeiro. No presente estudo, a atividade proteolítica de proteínas secretadas por leptospiras sobre um painel de moléculas da matriz extracelular e do plasma foi avaliada. O sobrenadante de cultura da estirpe virulenta L. interrogans sorovar Kennewicki Fromm degradou fibrinogênio humano, fibronectina plasmática, colágeno Tipo I, e as proteoglicanas decorina, biglicam e lumicam. A atividade proteolítica foi inibida por 1,10-fenantrolina, sugerindo o envolvimento de metaloproteases. Laminina, matrigel, plasminogênio e trombina não foram clivados por proteases presentes nos sobrenadantes. Ainda, os dados indicam que a produção de proteases deve ser um determinante de virulência importante, uma vez que os sobrenadantes de estirpes saprófitas ou patogênicas atenuadas em cultura não apresentaram atividade proteolítica sobre componentes da matriz ou do plasma. A análise dos genomas de leptospiras disponíveis nos levou à identificação de quatro termolisinas, metaloproteases presentes apenas nas espécies patogênicas. Uma delas, codificada pele LIC13322, foi produzida na forma recombinante e apresentou atividade proteolítica sobre fibrinogênio, biglicam e decorina. Em paralelo, foram também realizadas análises comparativas dos exoproteomas das estirpes Fromm e Patoc I. Algumas metaloproteases que podem estar envolvidas na degradação de moléculas do hospedeiro foram identificadas. A capacidade de clivar moléculas do tecido conjuntivo e proteínas da cascata de coagulação pode certamente contribuir para a invasão e a destruição tecidual observadas durante a infecção por Leptospira.
Leptospires are highly motile spirochetes equipped with strategies for efficient invasion and dissemination within the host. Our group previously demonstrated that pathogenic leptospires secrete proteases capable of cleaving and inactivating key molecules of the human complement system, allowing these bacteria to circumvent host´s innate immune defense mechanisms. Given the successful dissemination of leptospires during infection, we wondered if such proteases would target a broader range of host molecules. In the present study, the proteolytic activity of secreted leptospiral proteases against a panel of extracellular matrix and plasma proteins was assessed. The culture supernatant of the virulent L. interrogans serovar Kennewicki strain Fromm degraded human fibrinogen, plasma fibronectin, collagen Type 1, and the proteoglycans decorin, biglycan, and lumican. Proteolytic activity was inhibited by 1,10-phenanthroline, suggesting the participation of metalloproteases. Laminin, matrigel, plasminogen and thrombin were not cleaved by proteases present in the supernatants. Moreover, production of proteases might be an important virulence determinant since culture-attenuated or saprophytic Leptospira did not display proteolytic acticity against ECM or plasma components. A search against Leptospira genomes allowed identification of four thermolysins, which are metalloproteases found exclusively in pathogenic species. One of them, encoded by LIC13322, was produced in the recombinant form and displayed proteolytic activity against fibrinogen, biglycan and decorin. Comparative exoproteomic analyses using Fromm and Patoc I strains were also performed and allowed identification of a few metalloproteases that could be involved in the degradation of host components. The ability to cleave connective tissue molecules and coagulation cascade proteins may certainly contribute to invasion and tissue destruction observed upon infection with Leptospira.
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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 fibrosis. Myofibroblasts are characterised as the key contributors to interstitial volume and their presence ultimately leads to loss of renal function. The pathological entities leading to fibrosis inextricably depend on complex signalling pathways. Whilst many of the well-known growth factors that exert effects on renal fibroblasts (such as FGF, EGF and PDGF) involve the activation of receptor tyrosine kinases, the intracellular signalling events dictating the response of fibroblasts remain undefined. The kinase mTOR, responsible for integrating stress and amino acids and controlling cell growth, is increasingly recognised for its ability to integrate growth factor signals mediated through the upstream serine/threonine kinase PI3K. A number of recent studies have highlighted the role of PI3K and mTOR in the regulation of key events relevant to fibrosis, serving as a basis for Chapter 3: The role of PI3K and mTOR in the regulation of fibroblast proliferation and collagen synthesis, and the first part of Chapter 5: The role of PI3K and mTOR in the regulation of myofibroblast differentiation. These studies have identified a key role for PI3K and mTOR in the regulation of fibroblast proliferation, differentiation and collagen synthesis. The work described within has also attempted to examine the derivation of myofibroblasts via EMT. EMT is a process that is integral to embryogenesis and may act as an important source of myofibroblasts during fibrosis. This process is examined in Chapter 4: Development and validation of an ex vivo model of EMT. This model aims to better represent the in vivo environment and has also been used to identify novel regulators involved in EMT being utilised in the second part of Chapter 5: The role of PI3K and mTOR in EMT. Although cytokines and growth factors are thought to be chiefly responsible for tubulointerstitial fibrosis, we now know that serine proteases of the coagulation cascade may also play roles in renal disease. However, unlike their role in glomerular diseases, the role of coagulation in tubulointerstitial fibrosis is less well-known. The work described in Chapter 6: Constituents of the coagulation cascade are spatially and functionally related to experimental tubulointerstitial fibrosis has examined temporal and spatial in vivo relationships of coagulation factors and markers of fibrosis that aid our understanding of mechanisms of fibrosis. The aim of this thesis was to examine those facets of renal fibroblast function that are most devastating to renal function and culminate in an expansion of the renal interstitium during fibrosis. This work hopes to provide useful information to aid the understanding of the multifaceted mechanisms involved in renal tubulointerstitial fibrosis.
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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 nécessaire à la normalisation de la génération de thrombine est potentiellement variable d’un patient à l’autre pour une même sévérité d’hémophilie. On peut donc se demander quelle approche expérimentale permettrait de mettre en exergue le lien entre taux de facteur anti-hémophilique et la génération de thrombine. Est-il possible de modéliser mathématiquement la coagulation pour obtenir une relation, soit explicite, soit implicite, entre taux de facteurs et génération de thrombine ? Les modèles existants permettent-ils d'obtenir une telle relation ? Une vaste campagne expérimentale a donc été menée pour mettre en place une base de données qui a permis d’identifier les facteurs déterminants de la génération de thrombine et la relation entre génération de thrombine et taux de facteur anti-hémophilique, de définir leurs valeurs de références, ainsi que d’évaluer et de paramétrer de manière sujet-spécifique des modèles mathématiques de la coagulation
Haemophilia is a genetic disease corresponding to the deficiency of coagulation factor VIII or IX and leading to a bleeding tendency. The current substitutive treatment is defined essentially by the basal level of deficient factor and not the individual capacity to generate thrombin, a key enzyme of the clot formation. The thrombin generation assay could help in the individualisation of the anti-haemophilia treatment. Indeed, the factor VIII or IX level needed to normalise the thrombin generation vary potentially from one patient to another for a same degree of severity. We can wonder which experimental approach could emphasise the relation between level of anti-haemophilic factor and thrombin generation. Is it possible to mathematically model coagulation to obtain a relation, either explicit, or implicit, between factor level and thrombin generation? Could existing models provide this relation? An extensive experimental campaign was carried out to build a database that has been used to identify the determinant coagulation factors of thrombin generation and the individual relation between thrombin generation and anti-haemophilic factor level, to define their reference values, and also to evaluate and parametrise subject-specifically mathematical models of the coagulation cascade
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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, using novel membrane targeting (cytotopic) technology, a therapeutic complement regulator Mirococept (APT070) and coagulation inhibitors (PTL006, Thrombalexin/PTL004) were delivered to the endothelial surface within organs. In these studies, a rat model of hyperimmune rejection of renal allografts from fully MHC disparate donors and recipients was established. In vivo studies revealed the potential of the therapeutic reagents by assessment of graft survival, renal function and pathology. Mirococept only provided modest protection of the endothelium and in renal function, without any prolongation of survival compared to recipients of control-treated grafts. In contrast, treatment of kidneys with either anticoagulant agent (PTL006 or Thrombalexin/PTL004) alone resulted in significant prolongation of graft survival correlating with delayed loss of renal function compared to controls. To explore whether these findings were suitable for translation to clinical application, the investigations were extended to include standard immunosuppressive agents. However, Cyclosporine A treatment was associated with toxic effects in the rats, whereas therapy including Rapamycin failed to prevent lymphocyte migration into the grafts. This study provides evidence that ex vivo graft perfusion of locally acting biological response modifiers can have therapeutic effects in the transplant setting. The approach targets donor organs rather than the recipient. Additional and effective inhibition of cellular immune responses may demonstrate the full potential of this approach to attain graft acceptance against the most severe of immune barriers. These findings make this study clinically relevant.
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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)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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, the determination of their structures is potentially very important. These enzymes are serine proteinases that are similar to tyrpsin in their specificity but are generally referred to as thrombin-like enzymes due to their ability to cleave fibrinogen. The principal aim of this project was to isolate and characterize snake venom poteins that inetefere with the control and regulation of the hemostatic system in quantities and purity required for structural studies. Gel filtration, ion-exchange and HPLC chromatographic techniques were used to isolate convulxin, crotoxin, giroxin and crotamine, the principle components from the venoms of Crotalus durissus collineatus and Crotalus durissus terrificus and the serine and metalo proteinases from the venom of Bothrops jararaca. The purity of the samples was evaluated by SDS-PAGE and the specific activity of the samples was determined. Crystallization experiments were then carried out.
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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 and peripheral nervous system are also involved in the process, allowing a return to homeostasis.
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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-like receptors (TLR), the inflammasomes and other PRRs initiate the host response after recognition of pathogen-associated-molecular-patterns (PAMPs) or endogenous danger-associated-molecular-patterns (DAMPs). The systemic host response to infection will result in activation of coagulation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade and their multidirectional interactions in sepsis should lead towards the development of new therapeutic approaches in the critically ill who are faced with infection.
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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 outcomes in patients presenting with an acute coronary syndrome, without increasing the risks of major bleeding.
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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 fibrinolytic drug, and there is proof of its benefit. Both fibrinolytic and antifibrinolytic drugs are frequently initiated in the emergency department where patients are seen first. The current use, mechanisms, and targets of these medications are reviewed in this chapter.
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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 lymphoid series, as well as megakaryocytes, the precursors to platelets. The haemostatic system is responsible for maintaining blood fluidity and, at the same time, prevents blood loss by initiating rapid, localized, and appropriate blood clotting at sites of vascular damage. This system is complex, comprising both cellular and plasma elements, i.e. platelets, coagulation and fibrinolytic cascades, the natural intrinsic and extrinsic pathways of anticoagulation, and the vascular endothelium. A rapid, reliable, and inexpensive method of examining haematological disorders is the peripheral blood smear, which allows practitioners to assess the functional status of the bone marrow during cytopenic states. Red blood cells, which are primarily concerned with oxygen and carbon dioxide transport, have a normal lifespan of only 120 days and require constant erythropoiesis. White blood cells represent a summation of several circulating cell types, each deriving from the hematopoietic stem cell, together forming the critical components of both the innate and adaptive immune systems. Platelets are integral to haemostasis, and also aid our inflammatory and immune responses, help maintain vascular integrity, and contribute to wound healing.
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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, 33–44. Second edition. | Boca Raton, FL : CRC Press, Taylor & Francis Group, [2019] | Preceded by Cardiology and cardiac catheterisation : the essential guide / edited by John Boland and David W.M. Muller. 2001.: 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, 257–64. Singapore: 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, 357–70. Boston, MA: 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, 193–206. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24219-0_16.

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George, Lindsey A., and Michele P. Lambert. "Coagulation Cascade and Fibrinolysis Pathway: Assessment in the Laboratory." In Nonmalignant Hematology, 221–33. Cham: 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, 277–318. Hoboken, NJ, USA: 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, 248–62. Berlin, Heidelberg: 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, 195–207. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0615-2_6.

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Camera, Marina. "The Coagulative Cascade." In Direct Oral Anticoagulants, 1–8. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-74462-5_1.

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Ogawa, Rei. "Ideal Wound Closure Methods for Minimizing Scarring After Surgery." In Textbook on Scar Management, 185–91. Cham: 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 chronic inflammation blocks the conversion of the granulation tissue into dermis-like tissue by the remodeling process and results in an immature hypertrophic scar that is red, elevated, hard, and painful. These observations suggest that, to prevent pathological scarring after surgery, it is necessary to ensure that the sutures cause the wound edges to adhere to each other without any tension, even when strong extrinsic forces are placed on the wound. This will allow the granulation tissue to convert smoothly into dermis-like tissue, thereby yielding minimal scarring. Another way to prevent pathological scar formation in high-tension areas is to use zigzag suturing techniques such as the Z-plasty.
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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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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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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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Narahara, N., H. Sadakata, T. Uchiyama, K. Andoh, H. Tanaka, N. Kobayashi, and T. Maekawa. "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% bovine serum albumin(TBS-BSA) to the concentration of 5x106 cells/ml. Factors X, VII and IX were purified from fresh-frozen human plasma by the method of Bajaj in a modified version. Factor VIII was purified from cryoprecipitate as starting material. Factor X labelled with 1-125 by the method of McFarlane showed a single band on autoradiography. Specific radioactivity was 0.3 mCi/mg. For the study on binding of Factor X, TBS-BSA solution containing 4 mM of CaClp, various amounts of radiolabelled Factor X with/without purified Factors VII, VIII and IX were added to the LPS-stimulated washed cell suspension and mixed well. N-butyl-phtalate was layered over the reaction mixture after incubation at room temperature for various minutes. Total amount of bound Factor X was calculated from the radioactivity of the cell pellet separated by centrifugation of the reaction mixture. The Xa activity generated in the supernatants was assayed using S2222.Results: Factor X bound specifically to the LPS-stimulated Molt-4 cells. Amount of bound Factor X and the dissociation constant was 1.0 ng/5x10bcells (5.2x103sites/cell) and 5x106M, respectively. More amounts of Factor X bound when Factors VIII and IX were present in the reaction mixture than their absence. Five times more Factor Xa was generated when Factors VII, VIII and IX were present in the reaction mixture as compared with presence of Factor VII, alone. These results suggest that blood coagulation cascade proceeds on the LPS-stimulated leukocyte surface.
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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. Les Ulis, France: 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-mandibulaire. Une patiente de 83 ans se présente en consultation pour l’apparition récente de mobilités au niveau du bloc incisivo-canin maxillaire. L’interrogatoire révèle le diagnostic deux mois auparavant d’une leucémie myéloïde aigue, découverte de manière fortuite suite à un choc septique à E. Coli. Les bilans biologiques réalisés au moment du sepsis étaient en faveur d’une coagulation intravasculaire disséminée (CIVD). Quelques jours après, la patiente se plaignait de douleurs et de mobilités anormales localisées sur les dents antérieures maxillaires. Les examens cliniques et radiographiques (orthopantomogramme et cone beam) objectivent une nécrose osseuse du prémaxillaire limitée par les canines, avec un séquestre indépendant du reste du maxillaire. L’étude d’imputabilité conclut à la responsabilité de la CIVD en l’absence d’autres facteurs déclenchants et en raison d’une chronologie concordante. Le diagnostic de nécrose consécutive à une CIVD est alors posé. La prise en charge consiste en une séquestrotomie sous anesthésie générale et fermeture muqueuse. Un suivi régulier est mis en place avec une évolution favorable. Le prémaxillaire possède une vascularisation très riche assurée par les branches terminales de l’artère carotide externe, et par l’artère maxillaire. Les nécroses avasculaires sont par conséquent rares dans cette région. Cette vascularisation abondante explique le peu de cas décrits dans la littérature. On retrouve deux cas de nécrose consécutive à une CIVD au niveau de la mandibule et deux cas pour le prémaxillaire.
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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. Prague: 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, Miya Ishihara, Shunichi Sato, Makoto Kikuchi, Tadashi Kasamatsu, Hitoshi Sekita, and Minoru Obara. "Laser-tissue interaction of a continuous-wave 2-μm, 3-μm cascade oscillation fiber laser: sharp incision with controlled coagulation layer thickness." In BiOS 2000 The International Symposium on Biomedical Optics, edited by Donald D. Duncan, Jeffrey O. Hollinger, and 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-linked carbohydrate chains with glycopeptidase F reduced the apparentmolecular weight of the heavy chain to 37 kDa but hadno effect on the mobility of the light chain in SDS gel electrophoresis. Electrophoretic analysis of theintact protein with and without reduction indicates that the light chain is disulfide-linked to the heavychain in about half of the TF molecules and is notessential for function.The majority of polyclonal andtwenty- nine monoclonal antibodies against purified TF strongly inhibit coagulation and in all cases aredirected against epitopes on the heavy chain alone. Functional regions of the TF heavy chain have been investigated using a library of twenty-nine monoclonalantibodies and a series of overlapping, synthetic oligopeptides based on sequence information obtained from cloning the cDNA for TF. Supported by NIH grantsHL-16411 and CA-41085.
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Zhang, Peng, Jawaad Sheriff, João S. Soares, Chao Gao, Seetha Pothapragada, Na Zhang, Yuefan Deng, and Danny Bluestein. "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 adhesive pseudopods are extended. Activated platelets polymerize fibrinogen into a fibrin network that enmeshes red blood cells. Activated platelets also cross-talk and aggregate to form thrombi. Current numerical simulations to model this complex process mostly treat blood as a continuum and solve the Navier-Stokes equations governing blood flow, coupled with diffusion-convection-reaction equations. It requires various complex constitutive relations or simplifying assumptions, and is limited to μm level scales. However, molecular mechanisms governing platelet shape change upon activation and their effect on rheological properties can be in the nm level scales. To address this challenge, a multiscale approach which departs from continuum approaches, may offer an effective means to bridge the gap between macroscopic flow and cellular scales. Coarse Grained Molecular dynamics (CGMD) and discrete/dissipative particle dynamics (DPD) methods have been employed in recent years to simulate complex processes at the molecular scales, and various viscous fluids at low-to-high Reynolds numbers at mesoscopic scales. Such particle methods possess important properties at the mesoscopic scale: complex fluids with heterogeneous particles can be modeled, allowing the simulation of processes which are otherwise very difficult to solve by continuum approaches. It is becoming a powerful tool for simulating complex blood flow, red blood cells interactions, and platelet-mediated thrombosis involving platelet activation, aggregation, and adhesion.
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Bluestein, Danny, João S. Soares, Peng Zhang, Chao Gao, Seetha Pothapragada, Na Zhang, Marvin J. Slepian, and Yuefan Deng. "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 adhesive pseudopods are extended. Activated platelets polymerize fibrinogen into a fibrin network that enmeshes red blood cells. Activated platelets also cross-talk and aggregate to form thrombi. Current numerical simulations to model this complex process mostly treat blood as a continuum and solve the Navier-Stokes equations governing blood flow, coupled with diffusion-convection-reaction equations. It requires various complex constitutive relations or simplifying assumptions, and is limited to μm level scales. However, molecular mechanisms governing platelet shape change upon activation and their effect on rheological properties can be in the nm level scales. To address this challenge, a multiscale approach which departs from continuum approaches, may offer an effective means to bridge the gap between macroscopic flow and cellular scales. Molecular dynamics (MD) and dissipative particle dynamics (DPD) methods have been employed in recent years to simulate complex processes at the molecular scales, and various viscous fluids at low-to-high Reynolds numbers at mesoscopic scales. Such particle methods possess important properties at the mesoscopic scale: complex fluids with heterogeneous particles can be modeled, allowing the simulation of processes which are otherwise very difficult to solve by continuum approaches. It is becoming a powerful tool for simulating complex blood flow, red blood cells interactions, and platelet-mediated thrombosis involving platelet activation, aggregation, and adhesion.
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