HART: A Hybrid Architecture for Ray Tracing Animated Scenes.

We present a hybrid architecture, inspired by asynchronous BVH construction [1], for ray tracing animated scenes. Our hybrid architecture utilizes heterogeneous hardware resources: dedicated ray-tracing hardware for BVH updates and ray traversal and a CPU for BVH reconstruction. We also present a traversal scheme using a primitive's axis-aligned bounding box (PrimAABB). This scheme reduces ray-primitive intersection tests by reusing existing BVH traversal units and the primAABB data for tree updates; it enables the use of shallow trees to reduce tree build times, tree sizes, and bus bandwidth requirements. Furthermore, we present a cache scheme that exploits consecutive memory access by reusing data in an L1 cache block. We perform cycle-accurate simulations to verify our architecture, and the simulation results indicate that the proposed architecture can achieve real-time Whitted ray tracing animated scenes at 1,920 × 1,200 resolution. This result comes from our high-performance hardware architecture and minimized resource requirements for tree updates.

Tauroursodeoxycholic acid, a bile acid, promotes blood vessel repair by recruiting vasculogenic progenitor cells.

Although serum bile acid concentrations are approximately 10 µM in healthy subjects, the crosstalk between the biliary system and vascular repair has never been investigated. In this study, tauroursodeoxycholic acid (TUDCA) induced dissociation of CD34(+) hematopoietic stem cells (HSCs) from stromal cells by reducing adhesion molecule expression. TUDCA increased CD34(+) /Sca1(+) progenitors in mice peripheral blood (PB), and CD34(+) , CD31(+) , and c-kit(+) progenitors in human PB. In addition, TUDCA increased differentiation of CD34(+) HSCs into EPC lineage cells via Akt activation. EPC invasion was increased by TUDCA, which was mediated by fibroblast activating protein via Akt activation. Interestingly, TUDCA induced integration of EPCs into human aortic endothelial cells (HAECs) by increasing adhesion molecule expression. In the mouse hind limb ischemia model, TUDCA promoted blood perfusion by enhancing angiogenesis through recruitment of Flk-1(+) /CD34(+) and Sca-1(+) /c-kit(+) progenitors into damaged tissue. In GFP(+) bone marrow-transplanted hind limb ischemia, TUDCA induced recruitment of GFP(+) /c-kit(+) progenitors to the ischemic area, resulting in an increased blood perfusion ratio. Histological analysis suggested that GFP(+) progenitors mobilized from bone marrow, integrated into blood vessels, and differentiated into VEGFR(+) cells. In addition, TUDCA decreased cellular senescence by reducing levels of p53, p21, and reactive oxygen species and increased nitric oxide. Transplantation of TUDCA-primed senescent EPCs in hind limb ischemia significantly improved blood vessel regeneration, as compared with senescent EPCs. Our results suggested that TUDCA promoted neovascularization by enhancing the mobilization of stem/progenitor cells from bone marrow, their differentiation into EPCs, and their integration with preexisting endothelial cells.