Fig. 4.

Cross-linking stabilizes plasma ‘thrombi’ and alters the pattern of fibrin degradation products. (A) Plasma from normal individuals was used to form ‘thrombi’, in the absence (○) and the presence (•) of transglutaminase (TG) inhibitor, and these were compared with plasma ‘thrombi’ from the FXIII-deficient patient (Δ). Lysis with tissue-type plasminogen activator (1 μg mL⁻¹) was recorded as release of fluorescence over time, and results are expressed as mean ± standard error of the mean (n = 3). The difference in lysis rate upon addition of TG inhibitor to plasma ‘thrombi’ was significant (P < 0.005), as was the difference between the normal control and the patient (P < 0.005). (B) After the final time point (4 h), samples were taken from the bathing fluid of the model thrombi formed in the absence (1) and presence (2) of TG inhibitor or from the FXIII-deficient patient (3). Samples were separated on 4–12% polyacrylamide gels before staining in Coomassie Brilliant Blue R or transferring to nitrocellulose and staining with an antibody to the γ-chain of fibrinogen.