Methods: The calf garments of two IPC devices (WizAir, Medical Compression Systems,

Inc, Ltd, Or-Akiva, Israel; VenaFlow, AirCast Inc, Summit, NJ) were tested in five healthy volunteers. The interface pressure was measured with Tactilus Human Body Interface sensor system (Sensor Products Inc, Madison, NJ). Changes in tissue volumes were assessed with MRI. Velocity and flow changes in the great saphenous vein (GSV) and femoral veins (FV) were evaluated by DUS scans.

Results. The spatial distribution of interface pressure differed substantially between the two devices. These differences were in the location and percentage of calf surface area to which different pressure was applied. Both devices produced the tissue compression consistent with each device’s unique pattern

of the interface pressure distribution. Compression MX69 by the IPC devices was associated with a measurable decrease in the volume of subcutaneous tissue under the garment, the total volume of superficial veins, and the volume of the GSV. No measurable changes occurred in subfascial volume of the calf. Compression was associated with significant increase in flow velocities in the GSV and FV. The increase of volume flow was significant in FV, but not in GSV. Comparing hemodynamic data with MRI data showed that the flow velocity increase in FV and GSV caused by IPC highly correlated with decrease in volume of superficial veins and subcutaneous

tissue measured by MRI, but not with changes in subfascial volume. A single strongest predictor of venous DNA Damage inhibitor flow increase was the change in subcutaneous veins volume.

Conclusions. This methodology provides means Silibinin for the investigation of relationships between the pressure in the garment, interface pressure, tissue deformation, and hemodynamic respond to IPC. The clinical efficacy of IPC should not be explicitly attributed to the magnitude of the pressure in the garment. Similar hemodynamic responses to IPC can be produced by different spatial distributions of pressure resulting in different patterns of tissue compression. Further investigation of biomechanical mechanisms of IPC is needed to guide the development of better engineering solutions for mechanical devices aimed at prevention of venous thrombosis.”
“Amyloid-beta (A beta) is one of the main factors to cause Alzheimer’s disease. Although fibrillar A beta (fA beta) activates microglial cells that release toxic compounds to induce partial neuronal death, the mechanism of interaction between A beta and microglia remains unclear. Therefore, we examined the interaction of microglial cells (BV2) and fA beta on a gelatin-precoated plate. The binding was markedly enhanced by RhoA inactivation using Tat-C3, dominant negative RhoA, and si-RhoA. To identify the receptor for fA beta, we tested various antibodies to mask receptors.