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Vertical offline stand building and manipulating system

A vertical off-line stand building system includes a mast having a basal portion and an upper portion. An upper pipe elevator is mounted in the upper portion of the mast and is selectively translatable by a selecting actuable first hoist between upper raised and lowered positions. A lower pipe elevator is mounted in the basal portion of the mast and is selectively translatable by a selecting actuable second hoist between basal raised and lowered positions. A horizontal pipe support table is positioned adjacent the base of the mast. A horizontal pipe translator is mounted in the table for translating a pipe single longitudinally along the table so as to engage a first end of the pipe single with the lower pipe elevator when in its basal lowered position. The lower pipe elevator draws the first pipe into the mast through a front opening in the mast. The upper pipe elevator takes the first pipe and elevates it to the top of the mast. The lower pipe elevator raises the next pipe into the mast which is then threaded to the first pipe and the pipe stand then elevated by the upper pipe elevator so that the lower pipe elevator may add successive pipes to the pipe stand. The rear of the mast is entirely open so that the assembled pipe stand may be removed.
Owner:WEATHERFORD CANADA

C-1 Inhibitor prevents non-specific plasminogen activation by a prourokinase mutant without impeding fibrin-specific fibrinolysis

InactiveUS20090010916A1High dose toleranceInhibition of activationPeptide/protein ingredientsBlood disorderTolerabilityC1-inhibitor
A mutant prourokinase plasminogen activator (M5) was developed to make prouPA less subject to spontaneous conversion to tcuPA in blood at therapeutic concentrations. Two-chain M5 was shown to form complexes with C1-inhibitor, which was the principal inhibitor of tcM5 in plasma. The effect of supplemental additions of C1-inhibitor on fibrinolysis and fibrinogenolysis by M5 was determined. Supplemental C1-inhibitor restored the stability of high-dose M5 and prevented fibrinogenolysis but not fibrinolysis, the rate of which was not compromised by the inhibitor. Due to higher dose tolerance of M5 in the presence of supplemental C1-inhibitor, the rate of fibrin-specific lysis reached that achievable by nonspecific fibrinolysis, which is the maximum possible for a plasminogen activator. Plasma C1-inhibitor stabilized M5 in plasma by inhibiting tcM5 which would otherwise greatly amplify non-specific plasminogen activation causing more tcM5 generation from M5. This unusual dissociation of inhibitory effects, whereby fibrinogenolysis and not fibrinolysis is inhibited, has significant implications for improving the safety and efficacy of fibrinolysis. Methods of reducing bleeding and non-specific plasminogen activation during fibrinolysis by administering M5 along with exogenous C1-inhibitor are disclosed.
Owner:THROMBOLYTIC SCI

C1-Inhibitor Prevents Non-Specific Plasminogen Activation by a Prourokinase Mutant without Impeding Fibrin-Specific Fibrinolysis

ActiveUS20110081334A1Attenuation of rateHigh dose tolerancePeptide/protein ingredientsBlood disorderC1-inhibitorHigh doses
A mutant prourokinase plasminogen activator (M5) was developed to make prouPA less subject to spontaneous activation during fibrinolysis. C1-inhibitor complexes with tcM5. The effect of C1-inhibitor on fibrinolysis and fibrinogenolysis by M5 was determined. Supplemental C1-inhibitor restores the stability of M5 but not that of prouPA. Clot lysis by M5 with supplemental C1-inhibitor showed no attenuation of the rate of fibrinolysis, whereas fibrinogenolysis was prevented by C1-inhibitor. Due to higher dose tolerance of M5 with C1-inhibitor, the rate of fibrin-specific lysis reached that achievable by nonspecific fibrinolysis without inhibitor. Plasma C1-inhibitor stabilized M5 in plasma by inhibiting tcM5 and thereby non-specific plasminogen activation. At the same time, fibrin-specific plasminogen activation remained unimpaired. This unusual dissociation of effects has significant implications for improving the safety and efficacy of fibrinolysis. Methods of reducing bleeding and non-specific plasminogen activation during fibrinolysis by administering M5 along with exogenous C1-inhibitor are disclosed.
Owner:THROMBOLYTIC SCI
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