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Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Fibrin in the blood clot is comparatively stable; under certain circumstances, however, it is lysed rapidly. The rapid lysis is not associated with increased proteolytic activity of the tissues or leukocytes, but it is the result of the activation of a proenzyme, the plasminogen activator in the blood itself. Plasminogen is converted to a proteolytic enzyme called plasmin or fibrinolysin. Plasminogen is present in the blood, in lymph, in some other body fluids and tissues, and in exudates in certain conditions. Plasminogen is a protein constituted as a single polypeptide chain with a molecular weight of 81,000 to 92,000 Da. Plasmin contains two chains connected by a disulfide bond, with a molecular weight of about 73,000 to 84,000. The conversion of plasminogen to plasmin due to the cleavage of a single bond resulting in the active molecule and the release of a peptide from the NH2-terminus of the molecule, weighing 8000 Da.379,382
The Spleen
Published in E. George Elias, CRC Handbook of Surgical Oncology, 2020
Patients with leukemia or late stages of lymphoma, who are being considered for splenectomy, should have the preoperative preparations listed on Table 3. The epsilon-aminocaproic acid (AMICAR) should always be available in case of a sudden onset of a fibrinolytic process. In reality, it can be administered preoperatively, i.e., starting 2 hr prior to surgery in a small continuous drip fashion as 5 g of AMICAR in 1000 cc of i.v. solution in patients with late stage lymphomas as well as in those with leukemias. This will minimize the blood loss and binds any fibrinolysin that may be released. A total of 10 g of AMICAR per day will not result in an anticoagulant effect. However, if 11 g of AMICAR is going to be exceeded per day, the patient should be thoroughly studied to make sure that he has fibrinolysin mechanism. An excess of 11 g of AMICAR per 24 hr in the absence of fibrinolysin may result in an anticoagulant effect on the patient.
Hyperfibrinolysis in Liver Cirrhosis
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Other investigators suggested that low levels of inhibitors of fibrinolysis were the cause of hyperfibrinolysis in cirrhosis.62,63 O’Connell et al.64 showed a decrease of inhibitors of fibrinolysis in serum of patients with alcoholic cirrhosis. They measured the inhibitors of plasminogen activators as well as of fibrinolysin (plasmin). Several other studies also showed decreased inhibition of fibrinolysis and it was suggested that this might contribute to the excessive response of plasma fibrinolytic activity of cirrhotic patients.47,49,57
Anti-inflammatory activities of a new VEGF blocker, Conbercept
Published in Immunopharmacology and Immunotoxicology, 2021
In addition to the test the effect of Conbercept on collagen-induced arthritis in rats, we also tested whether Conbercept could inhibit acute inflammation. The method of xylene-induced ear edema is a simple and useful method to evaluate anti-inflammatory agents. Xylene induces an acute inflammatory response associated with certain inflammatory mediators such as histamine, kinin, and fibrinolysin [31]. Dexamethasone is used to treat inflammatory-related diseases such as allergies, arthritis, and breathing disorders. It significantly inhibited xylene-inducible ear edema in our study. Conbercept also significantly inhibited the xylene-induced ear edema. This indicated that inhibition of VEGF-dependent angiogenesis may reduce the release of inflammatory mediators such as histamine, kinin, and fibrinolysin. But the highest concentration of Conbercept (50 mg/kg) did not achieve the same effect as Dexamethasone. This indicated that anti-VEGF treatment showed its limitation to inhibit acute inflammation.
Pancarditis: an unusual complication of a group B streptococcal infection
Published in Acta Clinica Belgica, 2018
Elisa Larrieu-Ardilouze, Luc Christiaens, Nicolas Varroud-Vial, Coralie Madico, Jamil Hajj-Chahine, Michaela B. Rehman
From a bacteriological point of view, S. agalactiae does not produce fibrinolysin [22,23]. It creates large, flaky vegetations, resulting in substantial valve impairment. Streptococcus B has a preference for the mitral valve over the aortic valve and for a native valve over a prosthetic valve (85%) [22,23,25,26]. In 22% of cases, multiple valves are involved [25]. Valve impairment is usually severe, often requiring surgical intervention. In our case, the vegetation was on the aorta and small in size, and did not evolve towards significant aortic valve regurgitation.
Stenotrophomonas maltophilia – a low-grade pathogen with numerous virulence factors
Published in Infectious Diseases, 2019
Angelina Trifonova, Tanya Strateva
Fibrinolysin (also called streptokinase), another proteolytic enzyme produced by S. maltophilia, was described in early reports [6]. Its role as a spreading factor has been elucidated in some Gram-positive bacteria, but data are insufficient for S. maltophilia. According to the few studies published, fibrinolysin degradates the fibrin clot around lesions and facilitates dissemination of S. maltophilia [31,32].