Papers

AVS2001 Session BI-SuA: Biomaterials Plenary Session

Sunday, October 28, 2001 3:00 PM in Room 102

Sunday Afternoon

Start	Invited?	Item
3:00 PM		BI-SuA-1 Living Nightmares: Facing the Growing Threat of Biological Weapons S. Block (Stanford University) Please submit an abstract.
3:40 PM		BI-SuA-3 Protein Biochips: Powerful New Tools to Unravel the Complexity of Proteomics P. Wagner (Zyomyx Inc.) Novel high-throughput biological applications in the drug discovery process, disease diagnosis, and the development and application of patient-specific medicines require highly parallel, miniaturized device technology applied to proteins and their biochemical pathways. While technological innovation has adapted the analysis of genetic material to a miniaturized format, the more delicate nature of protein structures has precluded the development of analogous devices for proteins. Protein biochips have started to emerge recently based on new developments and integration efforts in advanced materials, protein engineering, and detection physics. Recent developments and selected examples will be presented with an emphasis on the technical challenges in surface and assay methodologies.
4:20 PM		BI-SuA-5 The Biocompatibility Challenge: Arterial Interfaces in 2001 R.S. Schwartz (Mayo Foundation) The lack of a suitable prosthetic arterial conduit remains a major problem in clinical medicine today. The breadth of such a need is immense in scope, encompassing peripheral vessels, cerebral arteries, and coronary arteries and grafts. Problems such as restenosis of both coronary stents and following stenting will be shortly solved. The principal mechanism of instent restenosis is by neointimal hyperplasia forming in injured arteries after oversized coronary stents. The cellular events of neointima occur in 3 stages: Thrombus formation occurs after injury (generally less than 24 hours), with fibrin-rich thrombus accumulates around the platelet site. The second stage is cellular recruitment, where the thrombus develops cells having the appearance of endothelial cells. Cell infiltration consists of monocytes and lymphocytes. The third stage is proliferative, occurring late with actin-positive cells colonizing the thrombus from the lumen, forming a "cap" across the top. The cells progressively proliferate toward the injured media, resorbing thrombus until it is gone and replaced by neointimal cells. In coronary models, denudation of endothelium alone does not cause neointimal formation. It is only when the internal elastic lamina is disrupted and media injured that neointima occurs. We hypothesize that the media plays an important role in limiting neointimal hyperplasia and believe in the importance of normal medial cells to limit neointimal hyperplasia. If a "living stent" could be made with medial cells present, neointimal limitation might be possible. Such as stent would represent a short segment of "total artificial artery", placed over artery injury sites to function immediately as a new vessel. We are developing such a stent with porcine carotid smooth muscle cells. The cells are grown in culture into a stent with a three-dimensional matrix. The cells may be transfected with a marker gene (GFP) and re-implanted into the coronary arteries 3 weeks later. Early studies show cell survival within the stent, with strong GFP expression. Such a "living stent" may have application for limiting neointima. Moreover, if the techniques are successful, this would represent a step toward the artificial artery.