Over the past two decades, researchers have applied a wide variety of approaches to investigate the biologic mechanisms that drive a pathologic hyperplasic or vascular remodeling in an effort to identify novel therapeutic strategies to improve clinical outcomes. Vascular adaptation following local injury occurs through a combination of wall thickening (hyperplasia) and expansion or contraction of the lumen. Since many technical avenues for improved patency have been exhausted, the recent belief has been that the future of enhancing the durability of these constructions lies in a better knowledge of the biology of the vein graft healing response. Contemporary data demonstrate restenosis rates following percutaneous coronary interventions to range between 25–35% at 6 months and high grade restenosis (>75%) or occlusion of coronary vein bypass grafts approaching 50% at a year. Despite the escalating need for these often life-saving procedures, their medium and long-term durability remains compromised. Fueled by an epidemic of obesity and diabetes in the United States, substantial increases in the need for these interventions are projected over the next decade. Surgical revascularization using autologous vein also remains a frequent used treatment option, with 427,000 coronary bypass procedures performed in 2004. In 2009, cardiovascular disease was the underlying cause of death accounting for 34.1% of all 2,371,000 deaths, accounting for 1 of every 2.8 deaths in the United States.
Our implementation (i) is modular, (ii) starts from basic mechano-biology principle at the cell level and (iii) facilitates the agile development of the model. Cornerstone to our model is a feedback mechanism between environmental conditions and dynamic tissue plasticity described at the cellular level with an agent based model. We propose a multiscale computational framework of vascular adaptation to develop a bridge between theory and experimental observation and to provide a method for the systematic testing of relevant clinical hypotheses.
Gmsh transfinite line with ruled surface drivers#
Despite incremental progress, specific cause/effect linkages among the primary drivers of the pathology, (hemodynamic factors, inflammatory biochemical mediators, cellular effectors) and vascular occlusive phenotype remain lacking. Over the past two decades, researchers have applied a wide variety of approaches to investigate the primary failure mechanisms, neointimal hyperplasia and aberrant remodeling of the wall, in an effort to identify novel therapeutic strategies. Gmsh.log (27.54 KiB) Downloaded 307 times Screenshot from 13-00-55.png (420.88 KiB) Not downloaded yet t2.geo (27.The failure rate for vascular interventions (vein bypass grafting, arterial angioplasty/stenting) remains unacceptably high. $ gmsh t2.geo -3 -optimize -order 2 > gmsh.log I attached t2.geo, gmsh log-file and ElmerGUI screenshot.Įlmer version is 3.0 Mesa 17.2.8 (Vendor: X.Org, Renderer: AMD TURKS (DRM 2.43.0 / 4.4.0-127-generic, LLVM 5.0.0) ) Is it a convertation problem of mesh, that has been done with transfinite algorithm? And ElmerSolver results wrong.īut when I'm not using transfintie algorithm, everything is allrigth with mesh reading in Elmer. Garfield++ requires mesh elements to be only second-order (quadratic) tetrahedral, thats why I do not use "Recombine" option.īut when I import mesh to ElmerGrid or ElmerGUI, mesh reading seems to be bad, i.e. Since drift tube has a big volume (r_wire = 0.015 mm, r_tube = 5 mm,l_tube is so minimal as possible), I have to use transfinite algorithm (transfinite lines, surfaces and volumes). I'm simulating a drift tube (with special cathode shape) with gmsh, then Elmer and garfield++, according with guide (.
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