Plasma antecedent

XI Plasma thromboplastin antecedent Intrinsic Activated form (XIa) serves to activate IX... 

Tissue factor/thromboplastin xi Plasma thromboplastin antecedent (PTA) 3.4.27.27... 

Hageman factor (XII), antihemophilic globulin (VIII), Christmas factor (IX), plasma thromboplastin antecedent (XI), calcium (IV), and platelet phospholipids... 

Hageman Factor (Factor XII) and Plasma Thromboplastin Antecedent (Factor XI), /. Lab. Clin. Med. (1972) 80, 704. 

L12. Lindquist, P. A., Fujikawa, K., and Davie, E. W., Activation of bovine Factor IX (Christmas Factor) by Factor XI. (activated plasma thromboplastin antecedent) and a protease from Russell s viper venon. J. Biol. Chem. 253, 1902-1909 (1978). 

Eujikawa, K., Legaz, M.E., Kato, H., Davie, E.W. 1974. The mechanism of activation of bovine factor IX (Ghristmas factor) by bovine factor XIa (activated plasma thromboplastin antecedent). Biochemistry 13, 4508-4516. 

Plasma thromboplastin antecedent Hageman factor Fibrin stabilizing factor... 

I. Chatoor, B.H. Herman, and X Hartzler, Effects of the Opiate Antagonist, Naltrexone, on Binging Antecedents and Plasma 13-Endorphin Concentrations. /. Am. Acad. Child Adolescent Psychiatry, 33,748-752,1994. 

Leaving historic antecedents aside, the following sections discuss the determination of REE by instrumental techniques including nuclear neutron activation, atomic absorption spectrometry, plasma spectrometries and x ray fluorescence spectrometry. In combination, these techniques account for over 90% of all analyses for REE. 

XI Plasma thromboplastin antecedent M, 124000 (bovine), 160000 (human). Glycoprotein composed of 2 similar or identical polypeptides joined by disulfide bond(s). Activates IX.IXa is inhibited by antithrombin III, trypsin inhibitors, a,-trypsin inhibitor and Cl inhibitor. 

Intrinsic thromboplastin is formed in three steps. The first step involves the plasma thromboplastin component the antihemophilic globulin, the thromboplastin antecedent (PTA), the Hageman factor, and the Stuart-Prower factor. All these factors interact rapidly they have not been purified, and therefore nothing is known of their molecular structure. With so little information, it would be rather naive to anticipate that the exact mode of interaction of these different factors would be known. 

Deficiencies in other factors, such as the plasma thromboplastin antecedent, the accelerator globulin, and the serum prothrombin conversion factor have all been described. The deficiencies lead to various forms of hemophilia. The severity of degree of bleeding episodes is much less marked than in classical hemophilia. These deficiencies are usually congenital, transmitted by sex-linked dominant or recessive or by autosomal dominant genes. The manifestations of these deficiencies are usually referred to as hemophilioid states c, d, a, and b, respectively. The major characteristics of these various types of congenital hemophilioid states are summarized in Table 7-4. 

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