Academic literature on the topic 'APS, Complement System, Coagulation Cascade'

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Journal articles on the topic "APS, Complement System, Coagulation Cascade"

1

Panebianco, Lauren M., and Teresa Gentile. "The Role of Monitoring Complement Levels in Catastrophic Antiphospholipid Syndrome: A Case Series of 4 Patients." Blood 134, Supplement_1 (2019): 4872. http://dx.doi.org/10.1182/blood-2019-128297.

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Introduction: Catastrophic antiphospholipid syndrome (CAPS) is characterized by multiple intravascular thrombotic events occurring over a short time period in the presence of persistently detectable antiphospholipid antibodies (APLA). Despite its clinical significance with mortality rate of 40-50%, the underlying pathophysiology remains somewhat enigmatic. More recent focus on the complement system as it interacts with the coagulation cascade has led to off-label use of eculizumab, a humanized monoclonal antibody against C5, in the treatment of CAPS. Consequently, monitoring of disease status
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2

Liang, Yan, Shang-Bo Xie, Chang-Hao Wu, et al. "Coagulation cascade and complement system in systemic lupus erythematosus." Oncotarget 9, no. 19 (2017): 14862–81. http://dx.doi.org/10.18632/oncotarget.23206.

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3

Fletcher-Sandersjöö, Alexander, Marc Maegele, and Bo-Michael Bellander. "Does Complement-Mediated Hemostatic Disturbance Occur in Traumatic Brain Injury? A Literature Review and Observational Study Protocol." International Journal of Molecular Sciences 21, no. 5 (2020): 1596. http://dx.doi.org/10.3390/ijms21051596.

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Despite improvements in medical triage and tertiary care, traumatic brain injury (TBI) remains associated with significant morbidity and mortality. Almost two-thirds of patients with severe TBI develop some form of hemostatic disturbance, which contributes to poor outcome. In addition, the complement system, which is abundant in the healthy brain, undergoes significant intra- and extracranial amplification following TBI. Previously considered to be structurally similar but separate systems, evidence of an interaction between the complement and coagulation systems in non-TBI cohorts has accumul
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4

Berkowitz, Shani, Joab Chapman, Amir Dori, Shany Guly Gofrit, Nicola Maggio, and Efrat Shavit-Stein. "Complement and Coagulation System Crosstalk in Synaptic and Neural Conduction in the Central and Peripheral Nervous Systems." Biomedicines 9, no. 12 (2021): 1950. http://dx.doi.org/10.3390/biomedicines9121950.

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Complement and coagulation are both key systems that defend the body from harm. They share multiple features and are similarly activated. They each play individual roles in the systemic circulation in physiology and pathophysiology, with significant crosstalk between them. Components from both systems are mapped to important structures in the central nervous system (CNS) and peripheral nervous system (PNS). Complement and coagulation participate in critical functions in neuronal development and synaptic plasticity. During pathophysiological states, complement and coagulation factors are upregu
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5

Gavriilaki, Eleni, Akrivi Chrysanthopoulou, Ioanna Sakellari, et al. "Linking Complement Activation, Coagulation, and Neutrophils in Transplant-Associated Thrombotic Microangiopathy." Thrombosis and Haemostasis 119, no. 09 (2019): 1433–40. http://dx.doi.org/10.1055/s-0039-1692721.

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AbstractTransplant-associated thrombotic microangiopathy (TA-TMA) is a severe and life-threatening complication of hematopoietic cell transplantation (HCT) that often coincides with graft-versus-host-disease (GVHD). Although endothelial damage seems to be the common denominator for both disorders, the role of complement system, neutrophils, and coagulation has not been clarified. In an effort to distinguish the pathogenesis of TA-TMA from GVHD, we evaluated markers of complement activation, neutrophil extracellular trap (NET) release, endothelial damage, and activation of coagulation cascade i
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6

Arnout, J. "Mechanism of action of Lupus anticoagulants." Hämostaseologie 21, no. 02 (2001): 44–49. http://dx.doi.org/10.1055/s-0037-1619504.

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SummaryThe antiphospholipid syndrome (APS) is defined as the association of antiphospholipid antibodies (aPL) with thrombosis, fetal loss or thrombocytopenia. Some aPL can be detected via coagulation assays where they present as an aspecific inhibitor termed the lupus anticoagulant (LA). Others can be measured via direct binding to cardiolipin and are termed anticardiolipin antibodies. aPL found in APS patients bind to a variety of PL-binding proteins such as beta-2-glycoprotein I (β2GPI) and prothrombin bound to PL surfaces. LA retard coagulation reactions in vitro by forming stable bivalent
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7

Huber, Silke, Mariam Massri, Marco Grasse, et al. "Systemic Inflammation and Complement Activation Parameters Predict Clinical Outcome of Severe SARS-CoV-2 Infections." Viruses 13, no. 12 (2021): 2376. http://dx.doi.org/10.3390/v13122376.

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Overactivation of the complement system has been characterized in severe COVID-19 cases. Complement components are known to trigger NETosis via the coagulation cascade and have also been reported in human tracheobronchial epithelial cells. In this longitudinal study, we investigated systemic and local complement activation and NETosis in COVID-19 patients that underwent mechanical ventilation. Results confirmed significantly higher baseline levels of serum C5a (24.5 ± 39.0 ng/mL) and TCC (11.03 ± 8.52 µg/mL) in patients compared to healthy controls (p < 0.01 and p < 0.0001, respectively)
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8

Mutch, Nicola J. "Polyphosphate as a haemostatic modulator." Biochemical Society Transactions 44, no. 1 (2016): 18–24. http://dx.doi.org/10.1042/bst20150207.

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Platelets are small anuclear cells that play a central role in haemostasis. Platelets become activated in response to various stimuli triggering release of their granular contents into the surrounding milieu. One of these types of granules, termed dense granules, have been found to contain polyphosphate (polyP) in addition to other inorganic biomolecules, such as serotonin, ADP, ATP, PPi. Individuals deficient in dense granules exhibit bleeding tendencies, emphasizing their importance in haemostasis. Platelet polyP is of a relatively defined size, approximately 60–100 phosphate monomers in len
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9

Tiwari, Ritudhwaj, Anurag R. Mishra, Flora Mikaeloff, et al. "In silico and in vitro studies reveal complement system drives coagulation cascade in SARS-CoV-2 pathogenesis." Computational and Structural Biotechnology Journal 18 (2020): 3734–44. http://dx.doi.org/10.1016/j.csbj.2020.11.005.

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10

Bazargani, Farhan, Russell P. Rother, and Magnus Braide. "The Roles of Complement Factor C5a and CINC-1 in Glucose Transport, Ultrafiltration, and Neutrophil Recruitment during Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 26, no. 6 (2006): 688–96. http://dx.doi.org/10.1177/089686080602600614.

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Background In a recent experimental study, we showed that low molecular weight heparin improved ultrafiltration and blocked complement activation and coagulation in a single peritoneal dialysis (PD) dwell. Objective The aim of the present study was to evaluate the possible contribution of the complement factor C5a and the potential interactions between C5a, the coagulation system, and cytokines of the interleukin (IL)-8 family (cytokine-induced neutrophil chemoattractant; CINC-1). Methods Nonuremic rats were exposed through an indwelling catheter to a single dose of 20 mL glucose- (2.5%) based
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