Journal articles: '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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Chambers, R. C., and G. J. Laurent. "Coagulation cascade proteases and tissue fibrosis." Biochemical Society Transactions 30, no. 2 (April 1, 2002): 194–200. http://dx.doi.org/10.1042/bst0300194.

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Fibrotic disorders of the liver, kidney and lung are associated with excessive deposition of extracellular matrix proteins and ongoing coagulation-cascade activity. In addition to their critical roles in blood coagulation, thrombin and the immediate upstream coagulation proteases, Factors Xa and VIIa, influence numerous cellular responses that may play critical roles in subsequent inflammatory and tissue repair processes in vascular and extra-vascular compartments. The cellular effects of these proteases are mediated via proteolytic activation of a novel family of cell-surface receptors, the protease-activated receptors (PAR-1, −2, −3 and −4). Although thrombin is capable of activating PAR-1, −3 and −4, there is accumulating in vitro evidence that the profibrotic effects of thrombin are predominantly mediated via PAR-1. Factor Xa is capable of activating PAR-1 and PAR-2, but its mitogenic effects for fibroblasts are similarly mediated via PAR-1. These proteases do not exert their profibrotic effects directly, but act via the induction of potent fibrogenic mediators, such as platelet-derived growth factor and connective tissue growth factor. In vivo studies using proteolytic inhibitors, PAR-1 antagonists and PAR-1-deficient mice have provided evidence that coagulation proteases play a key role in tissue inflammation and in a number of vascular pathologies associated with hyperproliferation of smooth muscle cells. More recently, coagulation proteases have also been shown to play a role in the pathogenesis of fibrosis but the relative contribution of their cellular versus their procoagulant effects awaits urgent evaluation in vivo. These studies will be informative in determining the potential application of PAR-1 antagonists as antifibrotic agents.

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Chambers, R. C., D. C. J. Howell, O. P. Blanc-Brude, and G. J. Laurent. "Coagulation cascade proteases and tissue fibrosis." Biochemical Society Transactions 30, no. 1 (February 1, 2002): A16. http://dx.doi.org/10.1042/bst030a016a.

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Görlach, Agnes. "Redox Regulation of the Coagulation Cascade." Antioxidants & Redox Signaling 7, no. 9-10 (September 2005): 1398–404. http://dx.doi.org/10.1089/ars.2005.7.1398.

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Nicholson, Andrew C., and David P. Hajjar. "Viral activation of the coagulation cascade." American Heart Journal 138, no. 5 (November 1999): S461—S464. http://dx.doi.org/10.1016/s0002-8703(99)70275-9.

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Anglés-Cano, Eduardo, and Marie-Claude Guillin. "ANTIPHOSPHOLIPID ANTIBODIES AND THE COAGULATION CASCADE." Rheumatic Disease Clinics of North America 27, no. 3 (August 2001): 573–86. http://dx.doi.org/10.1016/s0889-857x(05)70221-0.

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Johari, Vandita, and Chandravathi Loke. "Brief Overview of the Coagulation Cascade." Disease-a-Month 58, no. 8 (August 2012): 421–23. http://dx.doi.org/10.1016/j.disamonth.2012.04.004.

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Roberts, Harold R., and Jay N. Lozier. "New Perspectives on the Coagulation Cascade." Hospital Practice 27, no. 1 (January 15, 1992): 97–112. http://dx.doi.org/10.1080/21548331.1992.11705345.

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Aronovich, Anna, Yaniv Nur, Elias Shezen, Chava Rosen, Yael Zlotnikov Klionsky, Irit Milman, Liran Yarimi, et al. "A novel role for factor VIII and thrombin/PAR1 in regulating hematopoiesis and its interplay with the bone structure." Blood 122, no. 15 (October 10, 2013): 2562–71. http://dx.doi.org/10.1182/blood-2012-08-447458.

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Key PointsThe coagulation cascade via the factor VIII/thrombin/PAR1 axis regulates HSC maintenance. The coagulation cascade via factor VIII/thrombin/PAR1 axis regulates a reciprocal interplay between HSCs and the dynamic bone structure.

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Pant, Asmita, Anna K. Kopec, and James P. Luyendyk. "Role of the blood coagulation cascade in hepatic fibrosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 2 (August 1, 2018): G171—G176. http://dx.doi.org/10.1152/ajpgi.00402.2017.

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Liver is the primary source of numerous proteins that are critical for normal function of the blood coagulation cascade. Because of this, diseases of the liver, particularly when affiliated with severe complications like cirrhosis, are associated with abnormalities of blood clotting. Although conventional interpretation has inferred cirrhosis as a disorder of uniform bleeding risk, it is now increasingly appreciated as a disease wherein the coagulation cascade is precariously rebalanced. Moreover, prothrombotic risk factors are also associated with a more rapid progression of fibrosis in humans, suggesting that coagulation proteases participate in disease pathogenesis. Indeed, strong evidence drawn from experimental animal studies indicates that components of the coagulation cascade, particularly coagulation factor Xa and thrombin, drive profibrogenic events, leading to hepatic fibrosis. Here, we concisely review the evidence supporting a pathologic role for coagulation in the development of liver fibrosis and the potential mechanisms involved. Further, we highlight how studies in experimental animals may shed light on emerging clinical evidence, suggesting that beneficial effects of anticoagulation could extend beyond preventing thrombotic complications to include reducing pathologies like fibrosis.

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Schastlivtsev, I. V., K. V. Lobastov, S. N. Tsaplin, and D. S. Mkrtychev. "Modern view on hemostasis system: cell theory." Medical Council, no. 16 (October 9, 2019): 72–77. http://dx.doi.org/10.21518/2079-701x-2019-16-72-77.

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For many years, there has been no model capable of explaining the complex processes of interaction between various bloodclotting factors leading to a stop of bleeding. One of the most successful models able to partially reflect the mechanisms of hemostasis for a long time was the cascade theory. The cascade model perfectly explains the processes occurring during coagulation in vitro, but was completely inadequate in attempts to evaluate the processes occurring in vivo. A significant drawback of the cascade model is the impossibility to trace the interaction of cells carrying the tissue factor, platelets and plasma coagulation factors on their surface, since these conditions cannot be imitated. The cell theory, which has replaced the cascade theory, pays attention not only to the interaction of plasma coagulation factors, but also takes into account the role of platelets as important participants of coagulation processes. It is based on a four-stage reaction cascade that includes the following stages: initiation, amplification, propagation, and termination.The cell theory of hemostasis is able to reflect the complex process of interaction of all the links of hemostasis and answer questions related to the problems in patients with disorders of the coagulation system. The cell theory of hemostasis allows to reflect more precisely the processes of hemostasis in vivo and to interpret correctly the results of tests and pathophysiological mechanisms of disorders of the coagulation system. Global tests (thrombin generation assay, thromboelastography, thrombodynamics) used for hemostasis system evaluation are more complimentary with cell theory of hemostasis.

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ROHRER, MICHAEL J., and ANITA M. NATALE. "Effect of hypothermia on the coagulation cascade." Critical Care Medicine 20, no. 10 (October 1992): 1402–5. http://dx.doi.org/10.1097/00003246-199210000-00007.

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ROHRER, M. J., and A. M. NATALE. "Effect of Hypothermia on the Coagulation Cascade." Survey of Anesthesiology 37, no. 4 (August 1993): 184. http://dx.doi.org/10.1097/00132586-199308000-00003.

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Woodruff, Rebecca S., and Bruce A. Sullenger. "Modulation of the Coagulation Cascade Using Aptamers." Arteriosclerosis, Thrombosis, and Vascular Biology 35, no. 10 (October 2015): 2083–91. http://dx.doi.org/10.1161/atvbaha.115.300131.

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Davie, Earl W., Kazuo Fujikawa, and Walter Kisiel. "The coagulation cascade: initiation, maintenance, and regulation." Biochemistry 30, no. 43 (October 1991): 10363–70. http://dx.doi.org/10.1021/bi00107a001.

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McCulloch, Scott. "Effect of hypothermia on the coagulation cascade." Annals of Emergency Medicine 22, no. 3 (March 1993): 620. http://dx.doi.org/10.1016/s0196-0644(05)81963-8.

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Foley, Jonathan H., and Edward M. Conway. "Gas6 gains entry into the coagulation cascade." Blood 121, no. 4 (January 24, 2013): 570–71. http://dx.doi.org/10.1182/blood-2012-11-468678.

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Ernoehazy, W. S. "Effect of hypothermia on the coagulation cascade." Journal of Emergency Medicine 11, no. 3 (May 1993): 365–66. http://dx.doi.org/10.1016/0736-4679(93)90069-j.

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Hong, Seung-No, Yu-Lian Zhang, Chae-Seo Rhee, and Dong-Young Kim. "Probable Roles of Coagulation Cascade and Fibrinolysis System in the Development of Allergic Rhinitis." American Journal of Rhinology & Allergy 33, no. 2 (December 6, 2018): 137–44. http://dx.doi.org/10.1177/1945892418816015.

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Background Dysregulation of the coagulation cascade and fibrinolysis system may play an etiologic role in many diseases. Allergic diseases such as bronchial asthma, atopic dermatitis, and conjunctivitis are also associated with fibrin accumulation caused by a change in hemostasis. However, only a few studies have dealt with the relationship between allergic rhinitis (AR) and the coagulation system. Objective We investigated the difference of coagulation and fibrinolysis cascade components between an AR mouse model and a control mice. Methods BALB/c mice were sensitized and challenged with ovalbumin. Multiple parameters of coagulation cascade and fibrinolysis system such as factors II, V, VII, X, and XIII; tissue-type plasminogen activator; urokinase-type plasminogen activator (u-PA); plasminogen activator inhibitor-1 (PAI-1); and fibrin were compared between the AR model group and the control group. Results The symptom scores and eosinophil counts were higher in the AR group than in the control group ( P < .01). The mRNA expression level of u-PA ( P = .040) was significantly lower, and the expression levels of factor II ( P = .038) and factor X ( P = .036) were significantly higher, in the AR group. Immunohistochemical staining revealed that most of the fibrinolysis system and coagulation cascade components were localized to the epithelium, endothelium, and submucosal glands of the nasal mucosa. u-PA was downregulated in the AR group, whereas fibrin deposition was more prominent in the AR group than in the control group. Conclusion In AR, particular components of the coagulation cascade were increased and fibrinolysis system was decreased compared to normal control. This difference may be associated with the fibrin deposition in the mucosa of AR mouse model.

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Strohbach, Anne, and Raila Busch. "Predicting the In Vivo Performance of Cardiovascular Biomaterials: Current Approaches In Vitro Evaluation of Blood-Biomaterial Interactions." International Journal of Molecular Sciences 22, no. 21 (October 21, 2021): 11390. http://dx.doi.org/10.3390/ijms222111390.

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The therapeutic efficacy of a cardiovascular device after implantation is highly dependent on the host-initiated complement and coagulation cascade. Both can eventually trigger thrombosis and inflammation. Therefore, understanding these initial responses of the body is of great importance for newly developed biomaterials. Subtle modulation of the associated biological processes could optimize clinical outcomes. However, our failure to produce truly blood compatible materials may reflect our inability to properly understand the mechanisms of thrombosis and inflammation associated with biomaterials. In vitro models mimicking these processes provide valuable insights into the mechanisms of biomaterial-induced complement activation and coagulation. Here, we review (i) the influence of biomaterials on complement and coagulation cascades, (ii) the significance of complement-coagulation interactions for the clinical success of cardiovascular implants, (iii) the modulation of complement activation by surface modifications, and (iv) in vitro testing strategies.

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Davie, Earl W. "Introduction to the blood coagulation cascade and cloning of blood coagulation factors." Journal of Protein Chemistry 5, no. 4 (August 1986): 247–53. http://dx.doi.org/10.1007/bf01025423.

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Vojacek, Jan F. "Should We Replace the Terms Intrinsic and Extrinsic Coagulation Pathways With Tissue Factor Pathway?" Clinical and Applied Thrombosis/Hemostasis 23, no. 8 (October 18, 2016): 922–27. http://dx.doi.org/10.1177/1076029616673733.

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Present review highlights some new aspects of the role of individual components of blood coagulation process and proposes a modified concept of hemocoagulation cascade. The role of FXII in the initiation of the so-called intrinsic coagulation system is currently questioned. Its role has been recently demonstrated mainly in the thrombus propagation and final stabilization together with factors XI and XIII. The edited concept underlines the common part of the tissue factor (TF) in the initiation of both the intrinsic and extrinsic pathways of the coagulation system and therefore may make it not improperly be called the TF coagulation pathway. The search for new antithrombotic agents shows that the level of the coagulation system blockade depends on which step in the coagulation cascade is targeted and results in different degrees of the antithrombotic efficiency and the risk of bleeding complications.

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Antoniak, Silvio, and Nigel Mackman. "Multiple roles of the coagulation protease cascade during virus infection." Blood 123, no. 17 (April 24, 2014): 2605–13. http://dx.doi.org/10.1182/blood-2013-09-526277.

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Abstract The coagulation cascade is activated during viral infections. This response may be part of the host defense system to limit spread of the pathogen. However, excessive activation of the coagulation cascade can be deleterious. In fact, inhibition of the tissue factor/factor VIIa complex reduced mortality in a monkey model of Ebola hemorrhagic fever. Other studies showed that incorporation of tissue factor into the envelope of herpes simplex virus increases infection of endothelial cells and mice. Furthermore, binding of factor X to adenovirus serotype 5 enhances infection of hepatocytes but also increases the activation of the innate immune response to the virus. Coagulation proteases activate protease-activated receptors (PARs). Interestingly, we and others found that PAR1 and PAR2 modulate the immune response to viral infection. For instance, PAR1 positively regulates TLR3-dependent expression of the antiviral protein interferon β, whereas PAR2 negatively regulates expression during coxsackievirus group B infection. These studies indicate that the coagulation cascade plays multiple roles during viral infections.

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Diosdado, Alicia, Fernando Simón, Rodrigo Morchón, and Javier González-Miguel. "Dirofilaria immitis possesses molecules with anticoagulant properties in its excretory/secretory antigens." Parasitology 147, no. 5 (January 29, 2020): 559–65. http://dx.doi.org/10.1017/s0031182020000104.

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AbstractDirofilaria immitis is a parasitic nematode that survives in the circulatory system of suitable hosts for many years, causing the most severe thromboembolisms when simultaneous death of adult worms occurs. The two main mechanisms responsible for thrombus formation in mammals are the activation and aggregation of platelets and the generation of fibrin through the coagulation cascade. The aim of this work was to study the anticoagulant potential of excretory/secretory antigens from D. immitis adult worms (DiES) on the coagulation cascade of the host. Anticoagulant and inhibition assays respectively showed that DiES partially alter the coagulation cascade of the host and reduce the activity of the coagulation factor Xa, a key enzyme in the coagulation process. In addition, a D. immitis protein was identified by its similarity to the homologous serpin 6 from Brugia malayi as a possible candidate to form an inhibitory complex with FXa by sodium dodecyl sulfate polyacrylamide gel electrophoresis and mass spectrometry. These results indicate that D. immitis could use the anticoagulant properties of its excretory/secretory antigens to control the formation of blood clots in its immediate intravascular habitat as a survival mechanism.

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Bernard, Aline M., and Gordon R. Bernard. "The Immune Response: Targets for the Treatment of Severe Sepsis." International Journal of Inflammation 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/697592.

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The clinical process of severe sepsis is characterized by extreme inflammation interlinked with potent stimulation of the coagulation cascade often followed by a state of relative immune paralysis. In this paper, we will review many of the potential therapies directed at various steps along the inflammatory cascade from modulation of inflammatory mediators eliciting the immune response, alteration of the host's immune response in both a stimulatory and depressive manner, and taming the overexuberant coagulation response triggered by the fierce coagulation-inflammation cycle. Finally, we will discuss further opportunities for research to improve our ability to design effective therapies.

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Faqihi, Fahimeh, Marcus A. Stoodley, and Lucinda S. McRobb. "The Evolution of Safe and Effective Coaguligands for Vascular Targeting and Precision Thrombosis of Solid Tumors and Vascular Malformations." Biomedicines 9, no. 7 (July 4, 2021): 776. http://dx.doi.org/10.3390/biomedicines9070776.

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In cardiovascular and cerebrovascular biology, control of thrombosis and the coagulation cascade in ischemic stroke, myocardial infarction, and other coagulopathies is the focus of significant research around the world. Ischemic stroke remains one of the largest causes of death and disability in developed countries. Preventing thrombosis and protecting vessel patency is the primary goal. However, utilization of the body’s natural coagulation cascades as an approach for targeted destruction of abnormal, disease-associated vessels and tissues has been increasing over the last 30 years. This vascular targeting approach, often termed “vascular infarction”, describes the deliberate, targeted delivery of a thrombogenic effector to diseased blood vessels with the aim to induce localized activation of the coagulation cascade and stable thrombus formation, leading to vessel occlusion and ablation. As systemic delivery of pro-thrombotic agents may cause consternation amongst traditional stroke researchers, proponents of the approach must suitably establish both efficacy and safety to take this field forward. In this review, we describe the evolution of this field and, with a focus on thrombogenic effectors, summarize the current literature with respect to emerging trends in “coaguligand” development, in targeted tumor vessel destruction, and in expansion of the approach to the treatment of brain vascular malformations.

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HASHIGUCHI, Teruto. "Extrinsic coagulation cascade and diversity of prothrombin time." Japanese Journal of Thrombosis and Hemostasis 27, no. 6 (2016): 631–35. http://dx.doi.org/10.2491/jjsth.27.631.

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Saiah, Eddine, and Chris Soares. "Small Molecule Coagulation Cascade Inhibitors in the Clinic." Current Topics in Medicinal Chemistry 5, no. 16 (December 1, 2005): 1677–95. http://dx.doi.org/10.2174/156802605775009702.

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Davie, Earl W. "Biochemical and Molecular Aspects of the Coagulation Cascade." Thrombosis and Haemostasis 74, no. 01 (1995): 001–6. http://dx.doi.org/10.1055/s-0038-1642645.

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Altieri, D. C., and T. S. Edgington. "Sequential receptor cascade for coagulation proteins on monocytes." Journal of Biological Chemistry 264, no. 5 (February 1989): 2969–72. http://dx.doi.org/10.1016/s0021-9258(19)81707-6.

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Pukrittayakamee, S., N. J. White, R. Clemens, S. Chittamas, H. E. Karges, V. Desakorn, S. Looareesuwan, and D. Bunnag. "Activation of the coagulation cascade in falciparum malaria." Transactions of the Royal Society of Tropical Medicine and Hygiene 83, no. 6 (November 1989): 762–66. http://dx.doi.org/10.1016/0035-9203(89)90321-0.

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Chambers, Rachel C., and Chris J. Scotton. "Coagulation Cascade Proteinases in Lung Injury and Fibrosis." Proceedings of the American Thoracic Society 9, no. 3 (July 15, 2012): 96–101. http://dx.doi.org/10.1513/pats.201201-006aw.

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Overbey, Douglas M., Edward L. Jones, and Thomas N. Robinson. "How Hemostatic Agents Interact With the Coagulation Cascade." AORN Journal 100, no. 2 (August 2014): 148–59. http://dx.doi.org/10.1016/j.aorn.2013.12.012.

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Embi Bs, Abraham A. "ENERGY DETECTION IN THE FORM OF LIGHT RADIATION AT END OF HUMAN BLOOD COAGULATION CASCADE- THE OPTICAL ABSORPTION OF WATER VS. FIBRIN BURST ENERGY RELEASE." International Journal of Research -GRANTHAALAYAH 7, no. 9 (September 30, 2019): 200–212. http://dx.doi.org/10.29121/granthaalayah.v7.i9.2019.602.

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The human blood coagulation cascade had been extensively researched from a biochemistry and molecular perspective. The purpose of this manuscript is to introduce a biophysical phenomenon detected via optical microscopy at the end of the human blood coagulation cascade. This could be described as a sudden energy event in the form of light radiation observed once blood tissue movement stops being attracted to metal iron filings or carbon based graphite particles used as sentinels. Upon close examination of video recordings, the sudden movements of iron particles images coincided with light at the end of the coagulation cascade. A literature search confirmed that both metal filings and graphite particles to possess excellent electrical conductivity. A biophysical light radiation event discharge is hypothesized as result of a burst in the conversion of fibrinogen to fibrin signaling the end of a coagulation cycle; perhaps combined with a piezoelectric effect induced by a sudden clumping of RBCs, or from the optical absorption or water. Method: Metal iron filings or graphite particles were randomly sprinkled on fresh TIBS preparations. The sample was then readily focused and selected particles chosen for video analysis. Equipment used was a video microscope Celestron Model # 44348, glass slides and author’s blood drops. The data was digitally transferred and stored in an Apple computer photo application for further review. Results: When metal iron filings or graphite particles were sprinkled on freshly prepared TIBS slides, video analysis show light radiation emitted at the end of the blood coagulation cascade. Discussion: Since the light radiation emission occurred at the end of the blood coagulation cycle, it is theorized that blood tissue compression could induce piezoelectricity coinciding with energy released by a fibrin burst, or by the optical absorption of water.

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Marinkovic, Sanja Petrusevska, Irena Kondova Topuzovska, Zvonko Milenkovic, and Biserka Kaeva. "The Role of Serum Coagulation Factors in the Differential Diagnosis of Patients with Pneumonia and Parapneumonic Effusion." PRILOZI 37, no. 2-3 (November 1, 2016): 81–88. http://dx.doi.org/10.1515/prilozi-2016-0020.

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Abstract The aim of this study was to identify the participations of the serum coagulations and fibrinolysis factors that contribute to the differential diagnosis of the patients with community-acquired pneumonia (CAP) without effusion, uncomplicated parapneumonic effusion (UCPPE) and complicated parapneumonic effusion (CPPE). The coagulations system is fundamental for the maintenance of homeostasis, and contributes to the inflammatory process responsible for CAP and the parapneumonic effusion. The factors of coagulations and fibrinolysis participate in the cellular proliferation and migration as in the synthesis of the inflammatory mediators. We evaluated the laboratory profile of coagulations and fibrinolysis in the serum of 148 patients with CAP without effusion, 50 with UCPPE and 44 with CPPE. We determined the test of the coagulation cascade which measures the time elapsed from the activation of the coagulation cascade at different points to the fibrin generation. As a consequence, there is an activation of the fibrinolytic system with the increased D-dimer levels measured in the plasma in the three groups. The patients were with mean age ± SD (53,82 ± 17,5) min – max 18–93 years. A significantly higher number of thrombocytes was in the group with CPPE with median 412 × 109/L (rank 323–513 × 109/L). The extended activation of the prothrombin time (aPTT) was significantly higher in the same group of patients with median of 32 sec. (rank 30–35 sec). The mean D-dimer plasma level was 3266,5 ± 1292,3 ng/ml in patients with CPPE, in CAP without effusion 1646,6 ± 1204 ng/ml and in UCPPE 1422,9 ± 970 ng/ml. The coagulations system and the fibrinolysis play important role in the development and pathophysiology of CAP and the parapneumonic effusions.

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Cugno, Massimo, Marco Cicardi, Bianca Bottasso, Raffaella Coppola, Raffaella Paonessa, Pier Mannuccio Mannucci, and Angelo Agostoni. "Activation of the Coagulation Cascade in C1-Inhibitor Deficiencies." Blood 89, no. 9 (May 1, 1997): 3213–18. http://dx.doi.org/10.1182/blood.v89.9.3213.

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AbstractActivation of the contact and complement systems in C1-inhibitor deficiencies is thought to contribute to the pathogenesis of angioedema attacks by releasing kinins. Trigger stimuli of attacks may also activate coagulation. This is particularly important because experimental data suggest that thrombin, the main enzyme of the coagulation cascade, increases vascular permeability and can thus influence edema formation. We have studied 19 patients with hereditary angioedema (HAE) during remission, 5 HAE patients during acute attacks, and 6 patients with acquired angioedema (AAE) during remission and during seven attacks. Thirty normal subjects, matched for sex and age, served as controls. Generation of thrombin was measured by enzyme-linked immunosorbent assay (ELISA) as plasma levels of the prothrombin fragment 1 + 2 (F1 + 2); the initiators of the tissue factor and contact coagulation pathways were investigated by measuring plasma levels of activated factor VII (FVIIa) coagulometrically and activated factor XII (FXIIa) by ELISA. Cleavage of high molecular weight kininogen (HK) was evaluated by immunoblotting analysis. F1 + 2 was slightly increased during remission and further significantly increased during attacks in both HAE (P = .0115) and AAE. FVIIa and FXIIa, normal during remission, increased strikingly during attacks in both HAE (P = .0022 and P = .0044) and AAE. During remission, cleaved HK was normal in HAE and high in AAE; during attacks it increased in HAE (P = .0008) and remained elevated in AAE. Our data indicate that in C1-inhibitor deficient patients there is increased generation of thrombin during attacks, with signs of activation of both the contact and tissue factor coagulation pathways. In conclusion, C1-inhibitor deficiency, whether hereditary or acquired, has demonstrable activation of the coagulation and kinin-forming cascades during attacks and that thrombin should be considered a possible contributing factor in the pathogenesis of edema in HAE and AAE.

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Sampson, M. T., and A. K. Kakkar. "Coagulation proteases and human cancer." Biochemical Society Transactions 30, no. 2 (April 1, 2002): 201–7. http://dx.doi.org/10.1042/bst0300201.

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Tumours are capable of activating blood coagulation through the expression of procoagulant molecules such as tissue factor, cancer procoagulant and hepsin. Initiation of the clotting cascade results in the generation of the activated serine proteases factor VIIa, factor Xa and thrombin. These proteases act via protease-activated receptors and tissue factor to alter gene expression, thereby modulating tumour cell growth, invasion, metastasis and angiogenesis.

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Maruyama, Ikuro. "Recombinant Thrombomodulin and Activated Protein C in the Treatment of Disseminated Intravascular Coagulation." Thrombosis and Haemostasis 82, no. 08 (1999): 718–21. http://dx.doi.org/10.1055/s-0037-1615902.

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IntroductionThe blood coagulation cascade is regulated by the luminal surface of the endothelial cell lining.1 Endothelial cells synthesize tissue factor pathway inhibitor (TFPI), which, in part, binds to the cell surface glycosaminoglycans and inhibits factors Xa, VIIa, and tissue factor.2 Endothelial cells also produce and exhibit thrombomodulin (TM) on their luminal surface.3 TM is a kind of thrombin receptor that forms a 1:1 complex with thrombin. In this complex, thrombin activates protein C (PC) more than 1,000-fold more than thrombin alone. TM then loses its procoagulant activities, which include fibrinogen clotting, activation of factors V and VIII, and platelet activation. Thus, TM converts thrombin from a procoagulant protease to an anticoagulant. Pathologic states, such as an endothelial injury or perturbation or continuous rapid coagulation cascade activation, overcomes the endothelial regulating activity, resulting in the development of intravascular coagulation and the induction of disseminated intravascular coagulation (DIC). Theoretically, then, supplementing soluble TM or activated PC (APC) to reconstitute the endothelial coagulation regulation system in the circulation and regulate pathologically-activated blood coagulation could be beneficial. In this chapter, application of soluble TM and APC in the treatment of DIC is reviewed.

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Sullivan, Bradley P., Anna K. Kopec, Nikita Joshi, Holly Cline, Juliette A. Brown, Stephanie C. Bishop, Karen M. Kassel, Cheryl Rockwell, Nigel Mackman, and James P. Luyendyk. "Hepatocyte tissue factor activates the coagulation cascade in mice." Blood 121, no. 10 (March 7, 2013): 1868–74. http://dx.doi.org/10.1182/blood-2012-09-455436.

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Lipinski, S., L. Bremer, T. Lammers, F. Thieme, S. Schreiber, and P. Rosenstiel. "Coagulation and inflammation." Hämostaseologie 31, no. 02 (2011): 94–104. http://dx.doi.org/10.5482/ha-1134.

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SummaryOverwhelming evidence has linked inflammatory disorders to a hypercoagulable state. In fact, thromboembolic complications are among the leading causes of disability and death in many acute and chronic inflammatory diseases. Despite this clinical knowledge, coagulation and immunity were long regarded as separate entities. Recent studies have unveiled molecular underpinnings of the intimate interconnection between both systems. The studies have clearly shown that distinct pro-inflammatory stimuli also activate the clotting cascade and that coagulation in turn modulates inflammatory signaling pathways.In this review, we use evidence from sepsis and inflammatory bowel diseases as a paradigm for acute and chronic inflammatory states in general and rise hypotheses how a systematic molecular understanding of the “inflammation-coagulation” crosstalk may result in novel diagnostic and therapeutic strategies that target the inflammation-induced hypercoagulable state.

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Amour, A., J. Hutchinson, A. M. Ruiz Avendaño, S. Ratcliffe, E. Alvarez, J. Martin, J. R. Toomey, S. Senger, M. Wolfendale, and C. Mooney. "The quest for Factor VIIa exosite inhibitors." Biochemical Society Transactions 35, no. 3 (May 22, 2007): 555–58. http://dx.doi.org/10.1042/bst0350555.

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Coagulation proteases are involved in a highly orchestrated proteolytic cascade which is essential for haemostasis and blood clotting. In particular, the initiator of the coagulation cascade, Factor VIIa, binds to its cofactor, tissue factor, and its substrate, Factor X, via exosite interactions to form a ternary catalytic complex named extrinsic Xase. These exosite interactions have also been shown to allosterically induce the active conformation of the catalytic site of Factor VIIa. We have developed a direct continuous fluorescence polarization-based extrinsic Xase assay, which has been used to screen in excess of 1 million structurally diverse low-molecular-mass compounds as a potential starting point for the development of anticoagulants. The primary screen hits were categorized with deconvolution assays into either active-site or exosite inhibitors. The latter category of hits displayed both competitive and uncompetitive modalities of inhibition with respect to Factor X activation. An uncompetitive mechanism of action is of particular interest as it offers a hypothetical inhibitory advantage in the context of inhibiting a proteolytic cascade such as the blood coagulation pathway.

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Journal articles on the topic 'Coagulation cascade'

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