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Vascular Tissue Engineering belongs to a rapidly expanding discipline. Tissue engineered vascular grafts (TEVG) have a broad range of clinical application extending from use as small diameter vascular grafts in adult peripheral vasculature to serving as large vessel conduits in pediatric cardiovascular surgery. Several approaches have been utilized by different groups to design these grafts. Preliminary outcomes are exceedingly promising. These grafts have demonstrated the ability to transform into living blood vessels with growth potential and while the underlying mechanisms remain to be elucidated, it has been shown that inflammatory pathways may play an important role. Small animal experiments, development of cell seeding techniques and the application of nanotechnology have all contributed vastly to our understanding of the mechanisms involved in TEVG remodeling. The application of nanomedicine in TEVG design continues to expand at a rapid rate and has provided some clues as to how vascular graft design can be pursued in the future. In this review we discuss the current state of the field of tissue engineered vascular grafts and how the principles of nanomedicine are being applied to aid in the design of second-generation grafts.

Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the beta 2-subunit of the nicotinic acetylcholine receptor (beta 2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta 2-/- mice a 43% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta 2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta 2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta 2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.