Women had slower 400 m gait speed and this is consistent with previous reports. However, sex was not a predictor of gait speed in LIFE-P. A reason for this may be related to concomitant sex-differences in PP. Women had higher PP than men in LIFE-P and this is also well established in the literature. It is speculated that due to shorter stature and hormonally mediated changes in vascular function, older women have increased arterial stiffness and augmented pressure from wave reflections contributing to higher PP. Interestingly, after adjusting for sex-differences in PP, there were no longer sex-differences in gait speed. Therefore, PP may offer physiologic insight into sex-differences in gait speed in older adults. Limitations to this study should be noted. Presence or absence of PAD was not assessed in LIFE-P. Thus, it is possible that the association between PP and gait speed in LIFE-P was driven in part by the confounding influence of PAD, as previously reported in the Health ABC Study. Self-reports of leg pain during the 400 m walk test were not high in LIFE-P and participants reporting leg pain had similar PP as those participants not reporting leg pain. A specific inclusion criterion for the LIFE-P, and novel aspect of the present cohort, was presence of functional limitation. Thus, present findings may not be extrapolated to older adults with higher functional capacity. The main focus for this study was the exploration of PP as a physiologic correlate of gait. In unadjusted models, PP accounted for 2% of the variance in 400 m gait speed. Although modest, PP was able to improve prediction of slow gate speed using ROC analysis. Future research that appraises clinical outcomes with measures of gait speed and PP are needed to examine the clinical implications of present findings using proper calculation of net reclassification improvement. In conclusion, PP is a predictor of gait speed in communitydwelling older adults. Although noted associations are modest, these findings support that vascular senescence and altered ventricular-vascular coupling may contribute, in part, to the Vorinostat supply deterioration of physical function with advancing age. Future research is needed to examine whether therapeutic interventions that specifically target PP have clinical utility as a means of improving physical function with advancing age. Cardiac valvulogenesis refers to the formation of valves in the heart, an evolutionary conserved mechanism in vertebrates that occurs at mid-gestation and results in the unidirectional flow of blood throughout the heart. Both the semilunar, and atrioventricular valves are thought to arise from endocardial cells that undergo multiple processes governed by an array of growth factors, transcription factors, and extracellular proteins. Endocardial cells destined to become valves undergo an epithelial to mesenchymal transformation upon their stimulation by the TGFb and BMP2/4 growth factors secreted from the underlying myocardium. This process of transformation is dependent on two signaling pathways from within the endocardial cells, specifically the Wnt and NOTCH pathways. The mesenchymal cells will invade the cardiac jelly composed mainly of hyaluronic acid. These cells will undergo proliferation and subsequent differentiation into mature valves, a process that is subject to tight regulation by growth factors amongst which the vascular endothelial growth factor. The final valve structure is made up of at least 2 leaflets composed mainly of endocardially-derived cells. The involvement of neural crest cells in semilunar but not atrioventricular valves formation is supported by conditional knock-outs although neither myocardial nor neural crests cells are detected in the mature valves. The final process of remodeling is governed mainly by apoptosis.