In computed tomography (CT), the beam hardening effect has been known to be one of the major sources of deterministic error that leads to inaccuracy and artifact in the reconstructed images. Because of the polychromatic nature of the x-ray source used in CT and the energy-dependent attenuation of most materials, Beer's law no longer holds. As a result, errors are present in the acquired line integrals or measurements of the attenuation coefficients of the scanned object. In the past, many studies have been conducted to combat image artifacts induced by beam hardening. In this paper, we present an iterative beam hardening correction approach for cone beam CT. An algorithm that utilizes a tilted parallel beam geometry is developed and subsequently employed to estimate the projection error and obtain an error estimation image, which is then subtracted from the initial reconstruction. A theoretical analysis is performed to investigate the accuracy of our methods. Phantom and animal experiments are conducted to demonstrate the effectiveness of our approach.

Rates of restenosis vary with stent geometry, but whether stents affect spatial and temporal distributions of wall shear stress (WSS) in vivo is unknown. We tested the hypothesis that alterations in spatial WSS after stent implantation predict sites of NH in rabbit iliac arteries. Antegrade iliac artery stent implantation was performed under angiography, and blood flow was measured before casting 14 or 21 days after implantation. Iliac artery blood flow domains were obtained from three-dimensional microfocal X-ray computed tomography imaging and reconstruction of the arterial casts. Indexes of WSS were determined using three-dimensional computational fluid dynamics. Vascular histology was unchanged proximal and distal to the stent. Time-dependent NH was localized within the stented region and was greatest in regions exposed to low WSS and acute elevations in spatial WSS gradients. The lowest values of WSS spatially localized to the stented area of a theoretical artery progressively increased after 14 and 21 days as NH occurred within these regions. This NH abolished spatial disparity in distributions of WSS. The results suggest that stents may introduce spatial alterations in WSS that modulate NH in vivo.computational fluid dynamics; restenosis; computational modeling; computed tomography; image reconstruction; wall shear stress RESTENOSIS after stent implantation remains a persistent clinical problem (1,6,8,28,40,45). The mechanisms of restenosis are incompletely understood, but direct endothelial and smooth muscle cell damage, reduced compliance, and alterations in the distributions of wall shear stress (WSS) within the stented region have been implicated as potential triggering events that stimulate neointimal hyperplasia (11,19,44,47). Vascular damage to the vessel during implantation may be minimized by using an appropriate stent-to-artery deployment ratio (11,46). The rigid framework of the stent causes differences in compliance between the stented and native regions of the artery, but this stent rigidity provides structural scaffolding that is associated with reduced restenosis rates compared with angioplasty alone (4,8). Novel stent designs that reduce compliance mismatch at the proximal and distal edges of the stent have also been developed (2). Previous studies have suggested that there may be a correlation between stent-induced alterations in WSS and neointimal hyperplasia during pathological processes including primary atherogenesis and restenosis after angioplasty (17,18,20,21,30). However, few studies have examined detailed time-and space-dependent distributions of WSS or attempted to correlate these alterations in WSS with neointimal hyperplasia after stent implantation in vivo. Moreover, it is well known that restenosis varies with stent geometry (11,32,35,50), but the geometric influence of stent properties on spatial and temporal WSS patterns has not been thoroughly investigated. Thus we tested the hypothesis that local alterations in spatial WSS associated with stent implantation temporally pr...

Objective-Atherosclerosis is a vascular disease that involves lesion formation at sites of disturbed flow under the influence of genetic and environmental factors. Endothelial expression of adhesion molecules that enable infiltration of immune cells is important for lesion development. Platelet/endothelial cell adhesion molecule-1 (PECAM-1; CD31) is an adhesion and signaling receptor expressed by many cells involved in atherosclerotic lesion development. PECAM-1 transduces signals required for proinflammatory adhesion molecule expression at atherosusceptible sites; thus, it is predicted to be proatherosclerotic. PECAM-1 also inhibits inflammatory responses, on which basis it is predicted to be atheroprotective. Methods and Results-We evaluated herein the effect of PECAM-1 deficiency on development of atherosclerosis in LDL receptor-deficient mice. We found that PECAM-1 has both proatherosclerotic and atheroprotective effects, but that the former dominate in the inner curvature of the aortic arch whereas the latter dominate in the aortic sinus, branching arteries, and descending aorta. Endothelial cell expression of PECAM-1 was sufficient for its atheroprotective effects in the aortic sinus but not in the descending aorta, where the atheroprotective effects of PECAM-1 also required its expression on bone marrow-derived cells. Conclusion-We conclude that PECAM-1 influences initiation and progression of atherosclerosis both positively and negatively, and that it does so in a site-specific manner. Key Words:therosclerosis is a chronic inflammatory disease that involves formation, at discrete regions within the vasculature, of lesions characterized by the presence of inflammatory cells, lipid deposits, and extracellular matrix deposition. 1 Atherosclerotic lesions form preferentially at sites of vessel branching or high vessel curvature, which are exposed to low shear stresses or oscillatory or turbulent flow; however, genetic and environmental factors that determine circulating lipid levels, gender and immune status strongly influence lesion development in atherosusceptible regions. 2 Endothelial cells respond to low shear stress in atherosusceptible regions with increased expression of adhesion molecules that enable recruitment and infiltration of immune cells that contribute to lesion development. 3 Nevertheless, the roles of individual adhesion molecules in regulating atherosclerotic lesion development are not completely understood. See accompanying article on page 1887PECAM-1 is expressed on the surfaces of many cells involved in atherosclerotic lesion development, including monocytes, lymphocytes, platelets, and endothelial cells. 4 PECAM-1 expression is equally distributed over the entire surface of the aorta, including advanced lesions, and does not appear to be affected by hemodynamic forces or lipid levels. 5,6 PECAM-1 engages in homophilic 7 and heterophilic 8 interactions at sites of cell-cell contact. On the basis of its role as a critical component of a mechanotransducing complex that is required for ex...