Exercise regulated cartilage-SB PTOA development in DMM-operated knees in a dose-dependent manner. Our findings shed light on the important role of BMP expression in superficial zone chondrocytes in attenuation of PTOA development following physiological exercise loading. Further studies to support a mechanism by which BMPs would be beneficial in preventing PTOA progression are warranted.

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The pig EVLP system was not affected when ET-K was used instead of PX as the flush/preservation solution. The initial 200 mL of effluent should be discarded when using the ET-K to ensure that the potassium level does not increase.

Methods:We are developing a range of lubricating vectors based on phosphatidylcholine (PC) lipids, where friction reduction is provided by the hydration lubrication mechanism arising at their highly-hydrated phosphocholine headgroups. We have used such vectors a) in model nanotribological studies using a surface force balance, b) to modify tendon/sheath friction in a chicken model using a macroscopic tribometer, and c) injected into destabilized mice joints to examine their effect on subsequent gene regulation. Results: In model studies we find that small and large unilamellar vesicles (SUVs) of suitable PCs can complex with surface attached hyaluronan (HA) molecules and other surface-attached macromolecules to provide extremely good friction at physiologically high pressures (coefficients of friction down to 10 À3 e10 À4 ); such lubrication vectors can also reduce tendon/sheath friction by over 70% in a very sustained manner. Preliminary results in a murine model where PC-SUV-based lubrication vectors were injected into destabilized joints revealed changes in regulation of genes that are associated both with compression and shear stress. Conclusions: Novel lipid-based vectors can act as extremely efficient boundary lubricants in physiological conditions, both on model surfaces and at naturally occurring interfaces such as in tendon/sheath gliding. Preliminary results indicate that they modulate mechano-sensitive gene regulation in murine joints providing mechanistic support for their putative chondroprotective role in vivo.