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Inhibitors, viii

Figure 4.5 Examples of kinase inhibitors, which use diverse binding modes. Further information is in the following references ABFGNF-5 (4.10),18 AKT-Inhibitor VIII (4.11),20 p38-biarylbutyranilide (4.12),21 JNK-docking groove binder (4.13),22 p38-allosteric site (4.14),23 JNK-allosteric site (4.15),23 CHK-allosteric site (4.16),25 JAK-substrate competitive (4.17).27... Figure 4.5 Examples of kinase inhibitors, which use diverse binding modes. Further information is in the following references ABFGNF-5 (4.10),18 AKT-Inhibitor VIII (4.11),20 p38-biarylbutyranilide (4.12),21 JNK-docking groove binder (4.13),22 p38-allosteric site (4.14),23 JNK-allosteric site (4.15),23 CHK-allosteric site (4.16),25 JAK-substrate competitive (4.17).27...
Two nucleation processes important to many people (including some surface scientists ) occur in the formation of gallstones in human bile and kidney stones in urine. Cholesterol crystallization in bile causes the formation of gallstones. Cryotransmission microscopy (Chapter VIII) studies of human bile reveal vesicles, micelles, and potential early crystallites indicating that the cholesterol crystallization in bile is not cooperative and the true nucleation time may be much shorter than that found by standard clinical analysis by light microscopy [75]. Kidney stones often form from crystals of calcium oxalates in urine. Inhibitors can prevent nucleation and influence the solid phase and intercrystallite interactions [76, 77]. Citrate, for example, is an important physiological inhibitor to the formation of calcium renal stones. Electrokinetic studies (see Section V-6) have shown the effect of various inhibitors on the surface potential and colloidal stability of micrometer-sized dispersions of calcium oxalate crystals formed in synthetic urine [78, 79]. [Pg.338]

Factor VIII, immunoglobulin, and albumin are all held as protein precipitates, the first as cryoprecipitate and the others as the Cohn fractions FI + II + III (or FII + III) and FIV + V (or FV), respectively (Table 7, Fig. 2). Similarly, Fractions FIVj + FIV can provide an intermediate product for the preparation of antithrombin III and a-1-proteinase inhibitor. This abiUty to reduce plasma to a number of compact, stable, intermediate products, together with the bacteriacidal properties of cold-ethanol, are the principal reasons these methods are stiU used industrially. [Pg.531]

Treatment of Patients with Factor VIII or IX Inhibitors... [Pg.991]

Factor VIII and IX inhibitors are antibodies that develop in 20% and 12% of hemophilia A and hemophilia B patients, respectively, in response to replacement therapy. These antibodies bind to and neutralize the activity of infused factor concentrates. Although the inhibitors do not increase hemorrhage frequency, their existence challenges the treatment of bleeding episodes. Titers of inhibitors are measured and... [Pg.991]

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]

The individual responsiveness to desmopressin is consistent, and a test dose administered at the time of diagnosis or prior to therapy is the best predictor of response. Generally, DDAVP is more effective in vWD than in hemophilia patients, with an average 30% to 50% increase in vWF and factor VIII levels. In patients with an adequate response, desmopressin is first-line therapy because it allows for once-daily administration (elevates plasma levels for 8-10 hours), does not pose a threat in terms of viral transmission, and the cost is substantially less than that of the plasma-derived products. Fibrinolysis inhibitors (50-60 mg/kg of aminocapriotic acid every 4—6 hours or trenex-amic acid 10-15 mg/kg every 8-12 hours) and OCs are used successfully in the management of epistaxis and menorrhagia or as adjuvant treatments. [Pg.993]

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]

The procoagulant factors produced by endothelial cells are the coagulation factors von Willebrand factor (WF), F-V, F-VIII, tissue factor (TF), and plasminogen activator inhibitor (PAI), which blocks the activators u-PA and t-PA and counteracts fibrinolysis (G21, FI6). It has been shown that under the influence of complement activation (C9), in response to endotoxin in vitro (C24), in experimental E. coli sepsis in baboons (D30), and after stimulation with TNF (Al, N6), endothelial cells up-regulate the expression of TF, down-regulate TM and inhibit the production of t-PA and PAF. Thus, the balance may shift in the procoagulant direction with a large excess of PAI-1. [Pg.83]

Proplex T (Factor IX Complex)—used for factor VIII inhibitors, and factor VII or IX deficiency... [Pg.161]

Factor VIII inhibitor dose = 75 factor IX units/kg... [Pg.161]

Factor VIII process, 12 143 Factor IX, 4 86-87 Factor IXa, 4 86-87, 89 Factor IXa inhibitors, 4 103 Factor IX concentrates, properties of, 72 152t... [Pg.345]

Mechanism of action - Argatroban is a synthetic, direct thrombin inhibitor that reversibly binds to the thrombin active site. It inhibits thrombin-catalyzed or induced reactions, including fibrin formation activation of coagulation factors V, VIII, and XIII protein C and platelet aggregation. [Pg.154]

Hemophilia There have been reports of spontaneous bleeding in patients with hemophilia A and B treated with protease inhibitors. In some patients, additional Factor VIII was required. [Pg.1803]

VIII. Table of PDB-Entries Enzyme-Inhibitor Complexes of Imino Sugars and Selected... [Pg.187]

Therapy is determined by the level of factor VIII deficiency. Severely affected patients have concentrations less than 1 %, in moderate disease this is present between 1 and 5 % whereas plasma levels between 5 and 30 % may be associated with bleeding only after trauma such as dental extraction. Additionally, the choice of replacement is modified by the site of bleeding and the presence or absence of inhibitors that interfere with the function of the factor. Cryoprecipitate or lyophilised concentrate is becom-... [Pg.743]


See other pages where Inhibitors, viii is mentioned: [Pg.558]    [Pg.558]    [Pg.55]    [Pg.558]    [Pg.558]    [Pg.55]    [Pg.526]    [Pg.529]    [Pg.153]    [Pg.1009]    [Pg.130]    [Pg.345]    [Pg.76]    [Pg.991]    [Pg.76]    [Pg.45]    [Pg.161]    [Pg.502]    [Pg.193]    [Pg.14]    [Pg.605]    [Pg.606]    [Pg.28]    [Pg.224]    [Pg.62]   
See also in sourсe #XX -- [ Pg.3 , Pg.6 , Pg.45 , Pg.47 , Pg.49 , Pg.63 , Pg.144 , Pg.190 , Pg.192 , Pg.199 , Pg.212 , Pg.261 , Pg.262 , Pg.275 , Pg.276 , Pg.278 , Pg.280 , Pg.284 , Pg.301 , Pg.306 , Pg.318 ]




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