It is worth rehearsing just how big an effect this is in molar terms: fibrinogen (MW 340 kDa) is present at in plasma at concentrations of approximately 2–4 g l−1 (Weisel's authoritative review  gives 2.5 g l−1), and its levels are increased during inflammation (see above), while the LPS (MW 10–20 kDa) was added at a concentration of 0.2 ng l−1. We will assume 15 kDa for the MW of LPS and 30 fg LPS per cell. Thus, 0.2 ng l−1 = 13 fM and 2.5 g l−1 fibrinogen approximately 7.35 µM which is a molar ratio of LPS; fibrinogen monomer in the WB of less than 10−8 : 1. As we are here only looking at the terminal stages of clotting, we considered that fibrinogen might be an important mediator of the LPS-induced hypercoagulation. Thus, we also added both LPS types to purified fibrinogen (30 s and 10 min exposure time) with added thrombin. Even the 30 s exposure time changed the fibrin fibres to form fibrils or dense matted deposits without any individual fibres visible (figure 5). Figure 5.(a) Purified fibrinogen with added thrombin but no LPS; (b) purified fibrinogen with added O111:B4 LPS (30 s exposure) and 0.2 ng l−1 LPS; (c) as panel (b) but 10 min exposure.