scholarly journals A Kinetic Analysis of the Tissue Plasminogen Activator and DSPAα1 Cofactor Activities of Untreated and TAFIa-treated Soluble Fibrin Degradation Products of Varying Size

2000 ◽  
Vol 276 (5) ◽  
pp. 3138-3148 ◽  
Author(s):  
John B. Walker ◽  
Michael E. Nesheim
1995 ◽  
Vol 7 (3) ◽  
pp. 380-385 ◽  
Author(s):  
Michelle Henry Barton ◽  
Debra Deem Morris ◽  
Natalie Crowe ◽  
Chrysann Collatos ◽  
Keith W. Prasse

Hemostatic indices were determined in 45 healthy light breed foals, from birth to 1 month of age, and in 20 healthy adult (>2 years of age) light breed horses. Blood samples were obtained from each foal at 4 ages: 1) < 24 hours, 2) 4-7 days, 3) 10-14 days, and 4) 25-30 days. The following hemostatic indices were determined: platelet count; prothrombin and activated partial thromboplastin times; activity concentrations of protein C, antithrombin III, plasminogen, alpha-2 antiplasmin, tissue plasminogen activator, and plasminogen activator inhibitor- 1; plasma protein C antigen and fibrinogen concentrations; and serum fibrin degradation products concentration. Prothrombin and activated partial thromboplastin times were significantly longer at birth than in older foals. The plasma concentrations of the following were significantly lower at birth than in older foals: antithrombin III, plasminogen and tissue plasminogen activator activities, protein C antigen, and fibrinogen. Concentrations of the following were significantly higher at birth than in older foals: protein C and plasminogen activator inhibitor-1 activities and fibrin degradation products. These results indicate that hemostatic indices of neonatal foals differ significantly from those of older foals and adults. With the exceptions of antithrombin III and tissue plasminogen activator activities, all hemostatic indices measured in foals at 1 month of age were equivalent to adult values.


1987 ◽  
Author(s):  
Jessie T Douglas ◽  
G D O Lowe ◽  
R Balendra ◽  
C D Forbes ◽  
L J Creighton ◽  
...  

Acute stroke is normally the result of thromboembolism. Such thromboemboli form and extend by the interaction of platelets and fibrin and elicit a fibrinolytic response. Hence laboratory indices of platelet activation, thrombin formation and plasmin formation may be related to thrombus size and progression, and hence to clinical outcome, ie disability and death. We studied 100 patients with acute paretic stroke and followed them for 1 year. Plasma levels of betathromboglobulin (BTG), fibrinogen, fibrinopeptide A (FPA), fibrin(ogen) fragment BB15-42, serum fragment E, high molecular weight cross-linked fibrin degradation products (X-L FDP) D-dimer, total and tissue plasminogen activator activity, tissue plasminogen activator inhibition and serum fibrin(ogen) degradation products (FDP) were related to death and functional recovery in the 1 year follow up period. The levels of BTG, fibrinogen, FPA, BB15-42, tissue plasminogen activator inhibition and serum fragment E were significantly higher on the first day following stroke, in patients who subsequently died within 1 year when compared to patients who survived. Lowered levels of fibrin plate lysis area as well as raised tPA activity, X-L FDP and D-dimer levels did not achieve significance in patients who subsequently died. In the patients who survived only increased BB15-42 and X-L FDP levels were predictive of functional dependence when compared to patients who became independent. Increased fibrinogen, FPA and fibrin plate lysis area, fragment E and tPA activity and reduced D-dimer did not achieve significance in patients with greater disability when compared to patients with minimal disability. We conclude that several measures of activation of haemostasis are predictive of death in the year following stroke, but only BB15-42 and X-L FDP predict disability in survivors.


1989 ◽  
Vol 61 (03) ◽  
pp. 409-414 ◽  
Author(s):  
M Rånby ◽  
G Nguyen ◽  
P Y Scarabin ◽  
M Samama

SummaryAn enzyme linked immunosorbent assay (ELISA) based on goat polyclonal antibodies against human tissue plasminogen activator (tPA) was evaluated. The relative immunoreactivity of tPA in free form and tPA in complex with inhibitors was estimated by ELISA and found to be 100, 74, 94, 92 and 8l% for free tPA and tPA in complex with PAI-1, PAI-2, α2-antiplasmin and C1-inhibitor, respectively. Addition of tPA to PAI-1 rich plasma resulted in rapid and total loss of tPA activity without detectable loss of ELISA response, indicating an immunoreactivity of tPA in tPA/PAI-1 complex of about l00%. Three different treatments of citrated plasma samples (acidification/reneutralization, addition of 5 mM EDTA or of 0.5 M lysine) prior to determination by ELISA all resulted in increased tPA levels. The fact that the increase was equally large in all three cases along with good analytical recovery of tPA added to plasffi, supported the notion that all tPA antigen present in plasma samples is measured by the ELISA. Analysis by ELISA of fractions obtained by gel filtration of plasma from a patient undergoing tPA treatment identified tPA/inhibitor complexes and free tPA but no low molecular weight degradation products of tPA. Determinations of tPA antigen were made at seven French clinical laboratories on coded and randomized plasma samples with known tPA antigen content. For undiluted samples there was no significant difference between the tPA levels found and those known to be present. The between-assay coefficient of variation was 7 to 10%. In conclusion, the ELISA appeared suited for determination of total tPA antigen in human plasma samples.


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