Impact of Cross-Tie Properties on the Modal Behavior of Cable Networks on Cable-Stayed Bridges.

Dynamic behaviour of cable networks is highly dependent on the installation location, stiffness, and damping of cross-ties. Thus, these are the important design parameters for a cable network. While the effects of the former two on the network response have been investigated to some extent in the past, the impact of cross-tie damping has rarely been addressed.

The expression of tissue factor and tissue factor pathway inhibitor in aortic smooth muscle cells is up-regulated in synthetic compared to contractile phenotype.

Tissue factor (TF) and its specific inhibitor TF pathway inhibitor (TFPI) are produced by vascular smooth muscle cells (SMCs) in vitro and are increased in vivo in atherosclerotic compared to normal vessels. Besides local regulation of the hemostatic balance, this may be related to non-hemostatic TF/protease dependent functions such as SMC proliferation, adhesion and migration. The aim of the study was to compare the expression of both proteins between the contractile (normal adult) and synthetic (neo-intimal) SMC phenotypes.

Anti-thrombotic and haemorrhagic effects of active site-inhibited factor VIIa in rats.

Active site-inhibited factor VIIa (FFR-rFVIIa) competes with factor VIIa (FVIIa) for binding to tissue factor (TF) and exerts an anti-thrombotic effect. We report an evaluation of the anti-thrombotic properties of FFR-rFVIIa in a model of thrombosis involving two thrombogenic surfaces. Uncoated glass capillaries or glass capillaries coated with TF were incorporated into an arterioarterial shunt in the rat and the occlusion time (OT) of the shunt was determined.

Arachidonic-acid-selective cytosolic phospholipase A2 is involved in gastrin-induced AR4-2J-cell proliferation.

Gastrin/CCK(B) G protein-coupled receptors have been shown to mediate proliferation stimulated by their endogenous ligands. The present study demonstrates the proliferative effect of arachidonic acid on AR4-2J cells. Gastrin induces an [3H]arachidonic-acid release in a dose-dependent manner.