Homogenization of the Equations Governing the Flow Between a Slider and a Rough Spinning Disk

We have analyzed the behavior of the flow between a slider bearing and a hard-drive magnetic disk under two types of surface roughness. For both cases the length scale of the roughness along the surface is small as compared to the scale of the slider, so that a homogenization of the governing equations was performed. For the case of longitudinal roughness, we derived a one-dimensional lubrication-type equation for the leading behavior of the pressure in the direction parallel to the velocity of the disk. The coefficients of the equation are determined by solving linear elliptic equations on a domain bounded by the gap height in the vertical direction and the period of the roughness in the span-wise direction. For the case of transverse roughness the unsteady lubrication equations were reduced, following a multiple scale homogenization analysis, to a steady equation for the leading behavior of the pressure in the gap. The reduced equation involves certain averages of the gap height, but retains the same form of the usual steady, compressible lubrication equations. Numerical calculations were performed for both cases, and the solution for the case of transverse roughness was shown be in excellent agreement with a corresponding numerical calculation of the original unsteady equations

Elevated hematocrit enhances platelet accumulation following vascular injury

Red blood cells (RBCs) demonstrate procoagulant properties in vitro, and elevated hematocrit is associated with reduced bleeding and increased thrombosis risk in humans. These observations suggest RBCs contribute to thrombus formation. However, effects of RBCs on thrombosis are difficult to assess because humans and mice with elevated hematocrit typically have coexisting pathologies. Using an experimental model of elevated hematocrit in healthy mice, we measured effects of hematocrit in 2 in vivo clot formation models. We also assessed thrombin generation, platelet-thrombus interactions, and platelet accumulation in thrombi ex vivo, in vitro, and in silico. Compared with controls, mice with elevated hematocrit (RBCHIGH) formed thrombi at a faster rate and had a shortened vessel occlusion time. Thrombi in control and RBCHIGH mice did not differ in size or fibrin content, and there was no difference in levels of circulating thrombin-antithrombin complexes. In vitro, increasing the hematocrit increased thrombin generation in the absence of platelets; however, this effect was reduced in the presence of platelets. In silico, direct numerical simulations of whole blood predicted elevated hematocrit increases the frequency and duration of interactions between platelets and a thrombus.Whenhumanwhole blood was perfused over collagen at arterial shear rates, elevating the hematocrit increased the rate of platelet deposition and thrombus growth. These data suggest RBCs promote arterial thrombosis by enhancing platelet accumulation at the site of vessel injury. Maintaining a normal hematocrit may reduce arterial thrombosis risk in humans

Systems biology of platelet-vessel wall interactions

Platelets are small, anucleated cells that participate in primary hemostasis by forming a hemostatic plug at the site of a blood vessel's breach, preventing blood loss. However, hemostatic events can lead to excessive thrombosis, resulting in life-threatening strokes, emboli, or infarction. Development of multi-scale models coupling processes at several scales and running predictive model simulations on powerful computer clusters can help interdisciplinary groups of researchers to suggest and test new patient-specific treatment strategies