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Search Results: 1 - 10 of 126508 matches for " Miguel O. Bernabeu "
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Analyzing and Modeling the Performance of the HemeLB Lattice-Boltzmann Simulation Environment
Derek Groen,James Hetherington,Hywel B. Carver,Rupert W. Nash,Miguel O. Bernabeu,Peter V. Coveney
Physics , 2012, DOI: 10.1016/j.jocs.2013.03.002
Abstract: We investigate the performance of the HemeLB lattice-Boltzmann simulator for cerebrovascular blood flow, aimed at providing timely and clinically relevant assistance to neurosurgeons. HemeLB is optimised for sparse geometries, supports interactive use, and scales well to 32,768 cores for problems with ~81 million lattice sites. We obtain a maximum performance of 29.5 billion site updates per second, with only an 11% slowdown for highly sparse problems (5% fluid fraction). We present steering and visualisation performance measurements and provide a model which allows users to predict the performance, thereby determining how to run simulations with maximum accuracy within time constraints.
Coalesced communication: a design pattern for complex parallel scientific software
Hywel B. Carver,Derek Groen,James Hetherington,Rupert W. Nash,Miguel O. Bernabeu,Peter V. Coveney
Computer Science , 2012,
Abstract: We present a new design pattern for high-performance parallel scientific software, named coalesced communication. This pattern allows for a structured way to improve the communication performance through coalescence of multiple communication needs using two communication management components. We apply the design pattern to several simulations of a lattice-Boltzmann blood flow solver with streaming visualisation which engenders a reduction in the communication overhead of approximately 40%.
Weighted decomposition in high-performance lattice-Boltzmann simulations: are some lattice sites more equal than others?
Derek Groen,David Abou Chacra,Rupert W. Nash,Jiri Jaros,Miguel O. Bernabeu,Peter V. Coveney
Computer Science , 2014,
Abstract: Obtaining a good load balance is a significant challenge in scaling up lattice-Boltzmann simulations of realistic sparse problems to the exascale. Here we analyze the effect of weighted decomposition on the performance of the HemeLB lattice-Boltzmann simulation environment, when applied to sparse domains. Prior to domain decomposition, we assign wall and in/outlet sites with increased weights which reflect their increased computational cost. We combine our weighted decomposition with a second optimization, which is to sort the lattice sites according to a space filling curve. We tested these strategies on a sparse bifurcation and very sparse aneurysm geometry, and find that using weights reduces calculation load imbalance by up to 85%, although the overall communication overhead is higher than some of our runs.
Impact of blood rheology on wall shear stress in a model of the middle cerebral artery
Miguel O. Bernabeu,Rupert W. Nash,Derek Groen,Hywel B. Carver,James Hetherington,Timm Krüger,Peter V. Coveney
Physics , 2012, DOI: 10.1098/rsfs.2012.0094
Abstract: Perturbations to the homeostatic distribution of mechanical forces exerted by blood on the endothelial layer have been correlated with vascular pathologies including intracranial aneurysms and atherosclerosis. Recent computational work suggests that in order to correctly characterise such forces, the shear-thinning properties of blood must be taken into account. To the best of our knowledge, these findings have never been compared against experimentally observed pathological thresholds. In the current work, we apply the three-band diagram (TBD) analysis due to Gizzi et al. to assess the impact of the choice of blood rheology model on a computational model of the right middle cerebral artery. Our results show that, in the model under study, the differences between the wall shear stress predicted by a Newtonian model and the well known Carreau-Yasuda generalized Newtonian model are only significant if the vascular pathology under study is associated with a pathological threshold in the range 0.94 Pa to 1.56 Pa, where the results of the TBD analysis of the rheology models considered differs. Otherwise, we observe no significant differences.
Choice of boundary condition for lattice-Boltzmann simulation of moderate Reynolds number flow in complex domains
Rupert W. Nash,Hywel B. Carver,Miguel O. Bernabeu,James Hetherington,Derek Groen,Timm Krüger,Peter V. Coveney
Physics , 2012, DOI: 10.1103/PhysRevE.89.023303
Abstract: Modeling blood flow in larger vessels using lattice-Boltzmann methods comes with a challenging set of constraints: a complex geometry with walls and inlet/outlets at arbitrary orientations with respect to the lattice, intermediate Reynolds number, and unsteady flow. Simple bounce-back is one of the most commonly used, simplest, and most computationally efficient boundary conditions, but many others have been proposed. We implement three other methods applicable to complex geometries (Guo, Zheng and Shi, Phys Fluids (2002); Bouzdi, Firdaouss and Lallemand, Phys. Fluids (2001); Junk and Yang Phys. Rev. E (2005)) in our open-source application \HemeLB{}. We use these to simulate Poiseuille and Womersley flows in a cylindrical pipe with an arbitrary orientation at physiologically relevant Reynolds (1--300) and Womersley (4--12) numbers and steady flow in a curved pipe at relevant Dean number (100--200) and compare the accuracy to analytical solutions. We find that both the Bouzidi-Firdaouss-Lallemand and Guo-Zheng-Shi methods give second-order convergence in space while simple bounce-back degrades to first order. The BFL method appears to perform better than GZS in unsteady flows and is significantly less computationally expensive. The Junk-Yang method shows poor stability at larger Reynolds number and so cannot be recommended here. The choice of collision operator (lattice Bhatnagar-Gross-Krook vs.\ multiple relaxation time) and velocity set (D3Q15 vs.\ D3Q19 vs.\ D3Q27) does not significantly affect the accuracy in the problems studied.
Computer simulations reveal complex distribution of haemodynamic forces in a mouse retina model of angiogenesis
Miguel O. Bernabeu,Martin Jones,Jens H. Nielsen,Timm Krüger,Rupert W. Nash,Derek Groen,Sebastian Schmieschek,James Hetherington,Holger Gerhardt,Claudio A. Franco,Peter V. Coveney
Computer Science , 2013, DOI: 10.1098/rsif.2014.0543
Abstract: There is currently limited understanding of the role played by haemodynamic forces on the processes governing vascular development. One of many obstacles to be overcome is being able to measure those forces, at the required resolution level, on vessels only a few micrometres thick. In the current paper, we present an in silico method for the computation of the haemodynamic forces experienced by murine retinal vasculature (a widely used vascular development animal model) beyond what is measurable experimentally. Our results show that it is possible to reconstruct high-resolution three-dimensional geometrical models directly from samples of retinal vasculature and that the lattice-Boltzmann algorithm can be used to obtain accurate estimates of the haemodynamics in these domains. We generate flow models from samples obtained at postnatal days (P) 5 and 6. Our simulations show important differences between the flow patterns recovered in both cases, including observations of regression occurring in areas where wall shear stress gradients exist. We propose two possible mechanisms to account for the observed increase in velocity and wall shear stress between P5 and P6: i) the measured reduction in typical vessel diameter between both time points, ii) the reduction in network density triggered by the pruning process. The methodology developed herein is applicable to other biomedical domains where microvasculature can be imaged but experimental flow measurements are unavailable or difficult to obtain.
An automated multiscale ensemble simulation approach for vascular blood flow
Mohamed A. Itani,Ulf D. Schiller,Sebastian Schmieschek,James Hetherington,Miguel O. Bernabeu,Hoskote Chandrashekar,Fergus Robertson,Peter V. Coveney,Derek Groen
Computer Science , 2015, DOI: 10.1016/j.jocs.2015.04.008
Abstract: Cerebrovascular diseases such as brain aneurysms are a primary cause of adult disability. The flow dynamics in brain arteries, both during periods of rest and increased activity, are known to be a major factor in the risk of aneurysm formation and rupture. The precise relation is however still an open field of investigation. We present an automated ensemble simulation method for modelling cerebrovascular blood flow under a range of flow regimes. By automatically constructing and performing an ensemble of multiscale simulations, where we unidirectionally couple a 1D solver with a 3D lattice-Boltzmann code, we are able to model the blood flow in a patient artery over a range of flow regimes. We apply the method to a model of a middle cerebral artery, and find that this approach helps us to fine-tune our modelling techniques, and opens up new ways to investigate cerebrovascular flow properties.
Novel T-Violation observable open to any pair of decay channels at meson factories
Jose Bernabeu,Francisco J. Botella,Miguel Nebot
Physics , 2013, DOI: 10.1016/j.physletb.2013.11.031
Abstract: Quantum Entanglement between the two neutral mesons produced in meson factories has allowed the first indisputable direct observation of Time Reversal Violation in the time evolution of the neutral meson between the two decays. The exceptional meson transitions are directly connected to semileptonic and CP-eigenstate decay channels. The possibility of extending the observable asymmetries to more decay channels confronts the problem of the "orthogonality condition", which can be stated with this tongue-twister: Given a decay channel $f$, Which is the decay channel $f'$ such that the meson state not decaying to $f'$ is orthogonal to the meson state not decaying to $f$? In this paper we propose an alternative $T$-Violation Asymmetry at meson factories which allows its opening to any pair of decay channels. Instead of searching which is the pair of decay channels associated to the $T$-reverse meson transition, we build an asymmetry which tags the initial states of both the Reference and the $T$-reverse meson transitions. This observable filters the appropriate final states by means of two measurable survival probabilities. We discuss the methodology to be followed in the analysis of the new observable and the results expected in specific examples.
Flexible composition and execution of high performance, high fidelity multiscale biomedical simulations
Derek Groen,Joris Borgdorff,Carles Bona-Casas,James Hetherington,Rupert W. Nash,Stefan J. Zasada,Ilya Saverchenko,Mariusz Mamonski,Krzysztof Kurowski,Miguel O. Bernabeu,Alfons G. Hoekstra,Peter V. Coveney
Computer Science , 2012, DOI: 10.1098/rsfs.2012.0087
Abstract: Multiscale simulations are essential in the biomedical domain to accurately model human physiology. We present a modular approach for designing, constructing and executing multiscale simulations on a wide range of resources, from desktops to petascale supercomputers, including combinations of these. Our work features two multiscale applications, in-stent restenosis and cerebrovascular bloodflow, which combine multiple existing single-scale applications to create a multiscale simulation. These applications can be efficiently coupled, deployed and executed on computers up to the largest (peta) scale, incurring a coupling overhead of 1 to 10% of the total execution time.
The p75 neurotrophin receptor is expressed by adult mouse dentate progenitor cells and regulates neuronal and non-neuronal cell genesis
Ramon O Bernabeu, Frank M Longo
BMC Neuroscience , 2010, DOI: 10.1186/1471-2202-11-136
Abstract: In a first series of studies focusing on proliferation, mice received a single BrdU injection and were sacrificed 2, 10 and 48 hours later. Proliferating, BrdU-positive cells were found to express p75NTR. In a second series of studies, BrdU was administered by six daily injections and mice were sacrificed 1 day later. Dentate gyrus sections demonstrated a large proportion of BrdU/p75NTR co-expressing cells expressing either the NeuN neuronal or GFAP glial marker, indicating that p75NTR expression persists at least until early stages of maturation. In p75NTR (-/-) mice, there was a 59% decrease in the number of BrdU-positive cells, with decreases in the number of BrdU cells co-labeled with NeuN, GFAP or neither marker of 35%, 60% and 64%, respectively.These findings demonstrate that p75NTR is expressed by adult dentate progenitor cells and point to p75NTR as an important receptor promoting the proliferation and/or early maturation of not only neural, but also glial and other cell types.Neurons and astrocytes in the dentate gyrus of the hippocampus continue to be replaced throughout adult life in several species including humans [1-6]. Given the therapeutic implications of promoting neurogenesis in the dentate gyrus [7,8], it is becoming increasingly important to identify the mechanisms involved in the early stages of adult stem cell proliferation and differentiation. Receptors amendable to small molecule therapeutic targeting are of particular interest.Several lines of evidence raise the possibility that neurotrophins and their receptors might be capable of regulating dentate progenitor proliferation and/or differentiation. Mature neurotrophins interact with two types of receptors: the Trk tyrosine kinase receptors (TrkA, TrkB, and TrkC) and the p75 neurotrophin receptor (p75NTR) [9]. p75NTR receptors promote neuronal death or survival depending on the cellular context and the actions of a complex array of intracellular adaptors [10-12]. In in vitro studies, p75NTR-l
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