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Fibrinogen platelets

IL-6 participates in both atherogenesis and inflammatory processes. In one interesting mouse model that was double deficient at the apoE and IL-6 loci, animals displayed similar hypercholesterolemia compared to apoE-null mice, but disclosed larger and more calcified lesions at 1 year of age (Klinge 2001). Thus, IL-6 appears to be involved at the fibrous plaque stage of the atherosclerotic process. Moreover, IL-6 is a key factor in the generation of the hepatic acute-phase response and so increases the levels of CRP, fibrinogen, platelet... [Pg.231]

Fibrinogen-platelet binding inhibitors ticlipidine hydrochloride... [Pg.611]

Sample Blood Fibrinogen, Platelets, Thrombin Heparin... [Pg.121]

Fibrinogen/platelet interaction changes due to surface treatment on polyvinyl chloride. [Pg.255]

In 50 children taking valproate there were significant changes in fibrinogen, platelet count, and von Willebrand factor, but no patient developed the laboratory changes that are typical of von Willebrand s syndrome [375 ]. [Pg.172]

A method for the fractionation of plasma, allowing albumin, y-globulin, and fibrinogen to become available for clinical use, was developed during World War II (see also Fractionation, blood-plasma fractionation). A stainless steel blood cell separation bowl, developed in the early 1950s, was the earhest blood cell separator. A disposable polycarbonate version of the separation device, now known as the Haemonetics Latham bowl for its inventor, was first used to collect platelets from a blood donor in 1971. Another cell separation rotor was developed to faciUtate white cell collections. This donut-shaped rotor has evolved to the advanced separation chamber of the COBE Spectra apheresis machine. [Pg.519]

Primary blood components iaclude plasma, red blood cells (erythrocytes), white blood cells (leukocytes), platelets (thrombocytes), and stem cells. Plasma consists of water dissolved proteias, ie, fibrinogen, albumins, and globulins coagulation factors and nutrients. The principal plasma-derived blood products are siagle-donor plasma (SDP), produced by sedimentation from whole blood donations fresh frozen plasma (FFP), collected both by apheresis and from whole blood collections cryoprecipitate, produced by cryoprecipitation of FFP albumin, collected through apheresis and coagulation factors, produced by fractionation from FFP and by apheresis (see Fractionation, blood-plasma fractionation). [Pg.520]

Thrombin, the two-chain derivative of the prothrombin molecule, has a molecular weight of approximately 37,000 daltons. Its proteolytic properties induce the conversion of fibrinogen to fibrin to produce the initial visible manifestation of coagulation, the soluble fibrin clot. In addition, thrombin influences the activity of Factors V, VIII, and XIII and plasmin. Thrombin affects platelet function by inducing viscous metamorphosis and the release reaction with subsequent aggregation. [Pg.173]

Components/ mechanism of action Human plasma, fibrinogen and thrombin, virally inactivated, hemostat, sealant. Autologous fibrinogen -t-platelet-rich plasma, hemostatic gel. Bovine collagen, bovine thrombin, plus autologous human plasma, hemostatic agent. Bovine collagen and bovine thrombin. Expands 20% which aids in hemostatic effect. [Pg.1106]

Most antiplatelet dtugs only partially inhibit platelet activation. In contrast, blockers of GPIIb/llla interfere at the end of the pathway common to platelet aggregation. They prevent fibrinogen and vWf from... [Pg.168]

Platelets are the formed elements of the blood which participate in hemostasis. Platelets are enucleated, discoid fragments which arise from mature megakaryocytes in the bone marrow. Under normal circumstances, platelets do not adhere to endothelial surfaces of blood vessels. However, platelets can adhere to damaged areas of blood vessels and become activated in such a way that they can also bind fibrinogen. [Pg.985]

Hematological Effects. Leukocytosis and decreased platelet counts were reported in a group of subjects shortly after they ingested an unknown amount of endosulfan (Blanco-Coronado et al. 1992). One subject from that study, who eventually died, had prolonged partial thromboplastin time and prothrombin time with thrombocytopenia, and decreased fibrinogen two days after being admitted to the hospital. Elevated white cell count was also observed in an additional case of fatal acute poisoning with... [Pg.81]

A number of laboratory tests are available to measure the phases of hemostasis described above. The tests include platelet count, bleeding time, activated partial thromboplastin time (aPTT or PTT), prothrombin time (PT), thrombin time (TT), concentration of fibrinogen, fibrin clot stabifity, and measurement of fibrin degradation products. The platelet count quantitates the number of platelets, and the bleeding time is an overall test of platelet function. aPTT is a measure of the intrinsic pathway and PT of the extrinsic pathway. PT is used to measure the effectiveness of oral anticoagulants such as warfarin, and aPTT is used to monitor heparin therapy. The reader is referred to a textbook of hematology for a discussion of these tests. [Pg.608]

Glycoprotein llb/llla Platelets allbps ICAM-2 Fibrinogen, fibronectin, von Willebrand factor Platelet adhesion and aggregation... [Pg.622]

Fibrinogen-GPIIB/IIIA. A complex responsible for aggregation of platelets in the bloodstream. [Pg.250]

Check CBC, PT, PTT, platelets, fibrinogen and D-dimer. Repeat every 2 hours until bleeding is controlled... [Pg.74]


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See also in sourсe #XX -- [ Pg.527 ]




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