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Fibrinogen measurement

Fig. 6. Double refraction of flow in purified fibrinogen measurements at three glycerol concentrations. Theoretical curves for ellipsoidal molecules 620 and 700 A long are shown for comparison with experimental points. From Edsall, Foster and Sckeinberg (32), page 2734. Fig. 6. Double refraction of flow in purified fibrinogen measurements at three glycerol concentrations. Theoretical curves for ellipsoidal molecules 620 and 700 A long are shown for comparison with experimental points. From Edsall, Foster and Sckeinberg (32), page 2734.
The Clauss assay is the most widely employed method for the measurement of functional fibrinogen, measuring fibrinogen-dependent clot formation. With this assay, fibrinogen concenfrafion is inversely proportional fo fhe time recorded for clot formation. The Clauss assay is commonly performed on an automated coagulometer, although... [Pg.207]

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]

Kudryk B Robinson D., Netre C., et al. Measurement in human blood of fibrinogen/fibrin fragments containing the B beta 15-42 sequence. Thromb Res 1982 25,277-91. [Pg.167]

On the other hand, Cassassa and Berry32,129 conclude from their LS measurements on rod-like fibrinogen in solution that Eq. (86) is followed very well, but the intercept is extremely small or effectively zero. A rather trivial change in the model can be shown to produce a theoretical intercept of zero. Accordingly, they consider that the asymptotic scattering data reveal nothing about M but do give information from the slope on the ratio Ln/Mn. [Pg.198]

Q54 Baseline prothrombin time should be measured in patients receiving abciximab. Abciximab is an antiplatelet agent that acts by increasing the binding of fibrinogen to receptors on platelets. [Pg.145]

An in vitro or ex vivo measure of drug effect, for example, mean inhibitory concentration (MIC) of an antimicrobial against bacterial culture inhibition of ADP-induced platelet aggregation with a fibrinogen receptor antagonist. [Pg.213]

Determination of acute-phase proteins (CRP, orosomucoid, haptoglobin, transferrin, prealbumin), immunoglobulins (IgA, IgG, IgM), compressive markers (albumin, fibrinogen), markers of tissue destruction (Apo A-I, A-II, Apo B), components of complement (C3, C4), proteinase inhibitors (antithrombin HI, a -antitrypsin). The measurement was performed simultaneously in CSF and in serum (plasma) by a laser nephelometric method. The functional state of the blood-CSF barrier was evaluated numerically with the help of the quotient Q = Albcsp/s and also by the intrathecal synthesis of immunoglobulins according to Reiber s formula and for each class—IgG, IgM, IgA. [Pg.38]

Freyssinet, J. M., Torbet.J., Hudry-Clergeon, G., and Maret, G. (1983). Fibrinogen and fibrin structure and fibrin formation measured by using magnetic orientation. Proc. Natl. Acad. Sci. USA 80, 1616-1620. [Pg.289]

It appears that the overall and local inflammatory status at the time of PTCA plays a significant role in the development of restenosis. The current evidence arises from studies combining data from the clinical syndrome and peripheral markers of inflammation. For patients with unstable clinical syndromes and with increased levels of monocytes and CRR there is strong evidence for increased risk of restenosis, The measurement of other inflammatory indices, such as SAA, IL-6, IL-l/3, IL-IRa plasma levels, Lp(a), and fibrinogen, seems to provide additional information. [Pg.317]

Many mediators of inflammation have been identified— cytokines IL-6, tumor necrosis factor alpha cell adhesion molecules intracellular adhesion molecule-1 (ICAM-I), P-selectin and acute phase reactants CR.R fibrinogen, serum amyloid A, and soluble CD40 (Fig. I) (3). Myeloperoxidase is an enzyme secreted from monocytes, neutrophils, and macrophages. A single measurement taken from patient with chest pain in the emergency department predicted the early risk of myocardial infarction and the risk of major cardiac of ends in the next 30 days to six months (15). [Pg.467]

Rgure 7 Course of fibrinogen clotting (measured Unhid i metrically) an addition of 5 NIH-U tfirombin (T) and benzoyl-thrombin [Pg.62]

The results of Figure 11 are in striking contrast. Here, when the liver perfusion is carried out with completely defibrinated blood, there is a remarkable net synthesis of fibrinogen which becomes prominent only after the second to third hour and is impressive by the fifth and sixth hours. The chemically measured circulating level of fibrinogen has increased some 60 mg. % above that present in the zero time specimens. Net synthesis of fibrinogen of this magnitude has been repeatedly obtained in more than 25 perfusion studies which will be detailed elsewhere. [Pg.55]


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