Instability of Compacted Residual Soil

Static liquefaction of loose sands has been observed to initiate at stress ratios far less than the steady-state stress ratio. Different collapse surface concepts largely based on undrained triaxial test results have been proposed in the literature to explain the above instability phenomenon of loose sands. Studies of the instability behavior of fill material derived from residual soils remain limited. The present study investigated the instability behavior of a compacted residual soil using the conventional undrained triaxial tests and specially equipped constant shear triaxial tests. The test results were characterized in the p’: q: v space using the current state parameter with respect to the steady-state line for the residual soil. A modified collapse surface that has gradients varying with p’ and v was proposed for the loose residual soil to represent the instability states of undrained loading. Under constant shear stress conditions, the soil can mobilize stress ratios higher than those defined by the modified collapse surface. An instability surface was therefore presented for the instability states reached in static loading. Further, an alternative method of deducing the instability surface from the undrained stress paths was introduced.

Targeting shear gradient activated von Willebrand factor by the novel single-chain antibody A1 reduces occlusive thrombus formation in vitro.

Intraluminal thrombus formation precipitates conditions such as acute myocardial infarction and disturbs local blood flow resulting in areas of rapidly changing blood flow velocities and steep gradients of blood shear rate. Shear rate gradients are known to be pro-thrombotic with an important role for the shear-sensitive plasma protein von Willebrand factor (VWF). Here, we developed a single-chain antibody (scFv) that targets a shear gradient specific conformation of VWF to specifically inhibit platelet adhesion at sites of SRGs but not in areas of constant shear. Microfluidic flow channels with stenotic segments were used to create shear rate gradients during blood perfusion. VWF-GPIbα interactions were increased at sites of shear rate gradients compared to constant shear rate of matched magnitude. The scFv-A1 specifically reduced VWF-GPIbα binding and thrombus formation at sites of SRGs but did not block platelet deposition and aggregation under constant shear rate in upstream sections of the channels. Significantly, the scFv A1 attenuated platelet aggregation only in the later stages of thrombus formation. In the absence of shear, direct binding of scFv-A1 to VWF could not be detected and scFV-A1 did not inhibit ristocetin induced platelet agglutination. We have exploited the pro-aggregatory effects of SRGs on VWF dependent platelet aggregation and developed the shear-gradient sensitive scFv-A1 antibody that inhibits platelet aggregation exclusively at sites of shear rate gradients. The lack of VWF inhibition in non-stenosed vessel segments places scFV-A1 in an entirely new class of anti-platelet therapy for selective blockade of pathological thrombus formation while maintaining normal haemostasis.

Connection between Classical Solutions of Stokes first Problem and those of Simple Couette Flow. Applications

The classical solutions of the first problem of Stokes for viscous fluids, as it was to be expected, are obtained as limiting cases of those of the simple Couette flow. Something similar is valid for the motions of the fluids induced by a constant shear stress on the boundary. As a direct consequence, new exact solutions are immediately obtained for other two classes of motions of the same fluids.