Research paperDetection of the terminal complement complex in patient plasma following acute myocardial infarction
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Complement C3 activation in the ICU: Disease and therapy as Bonnie and Clyde
2022, Seminars in ImmunologyComplement activation in acute myocardial infarction: An early marker of inflammation and tissue injury?
2018, Immunology LettersCitation Excerpt :Later, Reyes et al. (1984) [22] showed that products of C3 degradation were presented in the plasma of AMI patients and correlated with the severe evolution and bad prognostic of AMI. Plasma concentration of native C3 and C4 [23], as well as C3d and C4d, sC5b9 [12,23], C3a and C5a [24] were also shown to be increased in AMI patients. Although several reports suggest that complement activation is crucial in the pathophysiology of cardiovascular events [25], few studies have investigated the association between serum levels of complement and AMI in a longitudinal follow-up from patient admission to discharge from the hospital.
A polysaccharide (PNPA) from Pleurotus nebrodensis offers cardiac protection against ischemia-reperfusion injury in rats
2015, Carbohydrate PolymersCitation Excerpt :Over the last decade, reintroduction of blood flow to a former ischemic area was the successful logical approach for the treatment of patients with acute obstruction of coronary arteries, during which myocardial ischemia–reperfusion (I/R) injury occurs (Maxwell & Lip, 1997; Verma et al., 2002). The main mechanisms which trigger and modulate myocardial I/R injury have been well characterized, including the generation of reactive oxygen species (ROS), complement activation and inflammatory response (Kilgore & Luchessi, 1993; Langlois & Gawryl, 1998; Romson et al., 1983). Increasing evidence has proposed that the generation of ROS immediately upon reperfusion will in turn accelerate the development and progression of myocardial I/R injury (McCord, 1985).
Complement activation triggered by chondroitin sulfate released by thrombin receptor-activated platelets
2008, Journal of Thrombosis and Haemostasis
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