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Factor II

Products prepared in this manner typically contain significant quantities of coagulation Factors II, VII, and X and other proteins as well as Factor... [Pg.532]

Coagulation Factors II, III, VII, IX, X, XI, and Xlla fragments, thrombin, and plasmin are classified as serine proteases because each possesses a serine residue with neighboring histidine and asparagine residues at its enzymatically active site (Table 3). Factors II, VII, IX, and X, Protein C, Protein S, and Protein Z are dependent on the presence of vitamin K [84-80-0] for their formation as biologically functionally active procoagulant glycoproteins. [Pg.173]

Factor II. Prothrombin is a vitamin K-dependent compound synthesized by the Hver. When prothrombin is activated it is cleaved at two sites, resulting in a two-chain molecule linked by a disulfide bond that has a molecular weight of 37,000 daltons. Thrombin is the serine protease that initiates the conversion of soluble fibrinogen into fibrin. [Pg.174]

Prothrombin (Factor II, from equine blood plasma) [9001-26-7] 72,000. Purified by two... [Pg.562]

From the obtained trajectories the following structural and electronic properties were extracted (i) structure factors, (ii) stability of Sn complexes, in particular, the Zintl anions, and (iii) the electrical conductivities - which yield answers to the questions mentioned in the first paragraph. [Pg.277]

In 1973, the first naturally occurring isobacteriochlorin, iron-containing siroheme, was isolated1 from a sulfite reductase of Escherichia coli. Later it was also discovered in sulfite and nitrite reductases of numerous bacteria and plants.2 Iron-free sirohydrochlorins (also called factor II) were discovered in vitamin B12 producing bacteria.3-4 Together with factor III. a sirohydrochlorin methylated in the 20-position, the reduced forms of factor II and factor III were identified as biosynthetic intermediates in the biosynthesis of vitamin B12.5... [Pg.644]

Zymogen is a precursor protein that is converted to an active protease when one or more of its peptide bonds are cleaved. Zymogens involved in coagulation include factors II (prothrombin), VII, IX, X, and XI. [Pg.1484]

In the final common pathway, factor Xa, produced by either the intrinsic or the extrinsic pathway, activates prothrombin (factor II) to thrombin (factor Ila), which then converts fibrinogen to fibrin (Figure 51-1). [Pg.601]

Coumarin Anticoagulants Inhibit the Vitamin K-Dependent Carboxylation of Factors II, VII, IX, X... [Pg.604]

For activity, factors II, VII, IX, and X and proteins C and S require vitamin K-dependent y-carboxylation of certain glutamate residues, a process that is inhibited by the anticoagulant warfarin. [Pg.608]

If we now apply rotadonal nnmetxy (Factor II given in 2.2.1) to the 14 Bravais lattices, we obtain the 32 Point-Groups which have the factor of symmetry imposed upon the 14 Bravais lattices. The symmetry elements that have been used are ... [Pg.49]

HCII heparin co-factor II TFPI tissue factor pathway inhibitor... [Pg.159]

Factor IX Replacement Hemophilia B therapy may include recombinant (produced via transfection of mammalian cells with the human factor IX gene) or plasma-derived (concentrate from pooled plasma) factor IX (see Table 64-2). Guidelines for choosing the factor-concentrate formulation for hemophilia B are similar to the guidelines for hemophilia A. However, older-generation factor IX concentrates containing other vitamin K-dependent proteins (e.g., factors II, VII, and IX), called prothrombin complex concentrates (PCCs), have been associated with thrombogenic side effects. Consequently, these products are not first-line treatment for hemophilia B.11... [Pg.990]

PCCs contain the vitamin K-dependent factors II, VII, IX, and X. These agents represent another attempt to bypass the factor at which the antibody is directed (see Fig. 64-2). However, PCCs carry the risk of serious thrombotic complications. Porcine factor VIII is most useful when the inhibitor titer is less than 50 BU (see Fig. 64-2 for dose and frequency). Owing to its similarity to human factor VIII, porcine factor VIII participates in the coagulation cascade. However, most inhibitors have very weak neutralizing activity against it. Porcine factor VIII is a third-line agent (only after factor Vila and a PCC have failed) owing to a 15% incidence of cross-reactivity.15... [Pg.991]

Recessively inherited coagulation disorders (RICDs) refer to relatively rare deficiencies in factor II, V, VII, and X-XIII resulting in either decreased clotting factor production or production of a dysfunctional molecule with reduced activity.19 The clinical severity of bleeding varies and generally is poorly correlated with the factor blood levels. Table 64-6 illustrates these clotting factor deficiencies and some of their characteristics. [Pg.994]

Vitamin K is a fat-soluble vitamin cofactor for the activation of factors II, VII, IX, and X in the liver. Almost all neonates are vitamin K-deficient at as a result of (1) insignificant transplacental vitamin K crossover, (2) lack of colonization of the colon by vitamin K-producing bacteria, and (3) inadequate dietary vitamin K intake (especially in breast-fed infants because human milk contains less vitamin K than infant formula or cow s milk). Vitamin K-deficiency bleeding (VKDB) refers to bleeding attributable to vitamin K deficiency within first 6 months of life. It occurs in three general time frames early (0-24 hours), classic (1-7 days), and late (2-12 weeks). Early onset occurs rarely and usually is associated with maternal ingestion of anticonvulsants, rifampin, isoniazid, and warfarin. Classic vitamin K-dependent bleeding usually results from the lack of prophylactic vitamin K administration in... [Pg.997]

The levels of vitamin K-dependent coagulation factors are physiologically low in neonates. Absence of vitamin K impairs y-carboxylation, and the inactive precursors of factors II, VII, IX, and X accumulate in the plasma, unable to bind calcium and cell membranes. Consequently, the precursor levels may decline further, impairing coagulation and potentially leading to VKDB. [Pg.998]

Activated partial thromboplastin time aPTT is performed by adding calcium phospholipids and kaolin to citrated blood and measures the time required for a fibrin clot to form. In this manner, aPTT measures the activity of intrinsic and common pathways. Prolongation of aPTT may be due to a deficiency or inhibitor for factors II, V, VIII, IX, X, XI, and XII. It also may be due to heparin, direct thrombin inhibitors, vitamin K deficiency, liver disease, or lupus anticoagulant. [Pg.1001]

Prothrombin time PT is performed by adding thromboplastin (tissue) factor and calcium to citrate-anticoagulated plasma, recalcifying the plasma, and measuring the clotting time. The major utility of PT is to measure the activity of the vitamin K-dependent factors II, VII, and X. The PT is used in evaluation of liver disease, to monitor warfarin anticoagulant effect, and to assess vitamin K deficiency. [Pg.1001]

Prothrombin A clotting factor that is converted to thrombin also known as factor II. [Pg.1575]

Factors II, VII, and X are stable in plasma maintained under refrigeration for up to 6 hours. Plasma refrigerated for 6 hours and subsequently frozen at — 20°C and at -70°C showed no deterioration in the levels of these factors for up to 14 days. Factor V was stable for 6 hours when plasma was stored at 4°C. However, 20% of the activity of factor V was lost in plasma stored frozen at -20°C for over 7 days (104). Even in samples stored frozen at - 70°C, 10% of the activity of factor V was lost after 7 days (104). [Pg.159]


See other pages where Factor II is mentioned: [Pg.390]    [Pg.528]    [Pg.532]    [Pg.532]    [Pg.532]    [Pg.532]    [Pg.532]    [Pg.170]    [Pg.170]    [Pg.172]    [Pg.178]    [Pg.644]    [Pg.598]    [Pg.108]    [Pg.109]    [Pg.1299]    [Pg.420]    [Pg.600]    [Pg.149]    [Pg.151]    [Pg.720]    [Pg.119]    [Pg.148]    [Pg.148]    [Pg.30]   
See also in sourсe #XX -- [ Pg.600 , Pg.601 ]




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