Analysis of Particle Trajectories in Aortic Artery Bifurcations With Stenosis

1989 ◽  
Vol 111 (4) ◽  
pp. 311-315 ◽  
Author(s):  
M. Nazemi ◽  
C. Kleinstreuer
Keyword(s):  
Shear Stress ◽  
Element Model ◽  
Spherical Particles ◽  
Shear Stresses ◽  
Atherosclerotic Lesions ◽  
Aortic Artery ◽  
Diseased Segment ◽  
Low Shear Stress ◽  
Accelerated Growth ◽  
Low Shear

The fluid-particle dynamics in a two-dimensonal symmetric branching channel with local occlusions representing a diseased segment of an aortic artery bifurcation has been analyzed. The validated finite element model simulates the trajectories and landing or impact sites of spherical particles for laminar flow in bifurcation channels with generalized wall conditions. Two hypotheses relating critical wall shear stress levels and plaque formation, previously postulated by Kleinstreuer et al. (1988) and Nazemi et al. (1989), have been confirmed. Low shear stress may contribute to the onset of atherosclerotic lesions and areas of critically low and high shear stresses are susceptible to accelerated growth of plaque.

CXCR4 expression in atherosclerotic lesions induced by low shear stress

2008 ◽  
Vol 32 (3) ◽  
pp. S18-S19
Author(s):  
Dang Heng Wei ◽  
Gui Xue Wang ◽  
Yi Ping Xia ◽  
Jian Jun Lei ◽  
Lu Shang Liu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Cxcr4 Expression ◽  
Atherosclerotic Lesions ◽  
Low Shear Stress ◽  
Low Shear

scholarly journals Restoring vascular endothelial autophagic flux reduces atherosclerotic lesions

2021 ◽  
Author(s):  
Shruti Chatterjee ◽  
Marouane Kheloufi ◽  
Stephane M.I Mazlan ◽  
Xavier Loyer ◽  
Timothy A. McKinsey ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Stress Conditions ◽  
Intercellular Adhesion Molecule ◽  
Autophagic Flux ◽  
Histone Deacetylase 6 ◽  
Tubulin Acetylation ◽  
Atherosclerotic Lesions ◽  
Low Shear Stress ◽  
Low Shear

Atherosclerotic lesions preferentially develop in arterial areas exposed to low shear stress, where endothelial cells express a pro-inflammatory, apoptotic, and senescent phenotype. Autophagy is a lysosomal mechanism that recycles damaged organelles and protein aggregates to maintain cellular homeostasis. Stimulation of autophagy in high shear stress conditions is an atheroprotective process. Conversely, endothelial cells exposed to atheroprone low shear stress present a defective autophagic flux, which favors a pro-inflammatory phenotype and the formation of atherosclerotic lesions. Since an efficient autophagic flux is dependent on α-tubulin acetylation, which is reduced under low shear stress, we hypothesized that increasing α-tubulin acetylation could restore adequate levels of autophagy in endothelial cells exposed to low shear stress. We found that blocking Histone Deacetylase 6 (HDAC6) activity, either by pharmacological inhibition (Tubastatin-A) or genetic approaches (shHDAC6), raised levels of acetylated α-tubulin, as well as LC3-II/I ratio, LC3 punctae area and autophagic flux in cultured endothelial cells exposed to low shear stress. This effect was associated with a reduced expression of inflammatory markers (Intercellular adhesion molecule-1 (ICAM-1), Vascular cell Adhesion Protein-1 (VCAM-1) and Monocyte Chemoattractant Protein-1 (MCP-1)) in Tumor Necrosis Factor-alpha (TNF-α)-stimulated cells. We observed increased endothelial autophagic flux in the aortic arch of the HDAC6-/-/ApoE-/- mice. Subsequently, atherosclerotic plaque size was significantly reduced in the atheroprone areas of chimeric HDAC6-/-/ApoE-/- mice, transplanted with HDAC6+/+/ApoE-/- bone marrow, when compared to HDAC6+/+/ApoE-/- littermate controls. Taken together, these results indicate that targeting α-tubulin acetylation, via HDAC6-inhibition, may be an interesting strategy to restore endothelial autophagic flux and to promote an atheroprotective endothelial phenotype despite unfavorable shear stress conditions.

Endothelial Cell Morphometry of Atherosclerotic Lesions and Flow Profiles at Aortic Bifurcations in Cholesterol Fed Rabbits

1992 ◽  
Vol 114 (3) ◽  
pp. 301-308 ◽  
Author(s):  
Mitsuji Okano ◽  
Yoji Yoshida
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Lipid Deposition ◽  
High Shear ◽  
High Shear Stress ◽  
Atherosclerotic Lesions ◽  
Flow Profiles ◽  
Flow Divider ◽  
Low Shear Stress ◽  
Low Shear

Observations on shapes of endothelial cells both in sudanophilic and nonsudanophilic regions at bifurcations of the brachiocephalic (BC) and left subclavian (SA) arteries in hyperlipidemic rabbits were performed under a SEM. The stagnation point of flow and leading edges of flow dividers were nonsudanophilic and covered by round and long fusiform endothelial cells, respectively. The hips of flow dividers of both branchings, proven to be relatively low shear stress regions, by movement of microspheres in steady flow, were sudanophilic and covered by ellipsoidal cells. Similar studies were carried out in normolipidemic rabbits. It might be concluded that lipid deposition in hyperlipidemic rabbits occurs in relatively low shear stress regions, where endothelial cells are functionally activated, rather than in laminar high shear stress regions at the flow divider.

scholarly journals Computing of Low Shear Stress-Driven Endothelial Gene Network Involved in Early Stages of Atherosclerotic Process

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Federico Vozzi ◽  
Jonica Campolo ◽  
Lorena Cozzi ◽  
Gianfranco Politano ◽  
Stefano Di Carlo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Shear Stress ◽  
Transcription Factors ◽  
Gene Network ◽  
Bioinformatics Analysis ◽  
Atherosclerotic Disease ◽  
Cell Phenotype ◽  
Shear Stresses ◽  
Low Shear Stress ◽  
Low Shear

Background. In the pathogenesis of atherosclerosis, a central role is represented by endothelial inflammation with influx of chemokine-mediated leukocytes in the vascular wall. Aim of this study was to analyze the effect of different shear stresses on endothelial gene expression and compute gene network involved in atherosclerotic disease, in particular to homeostasis, inflammatory cell migration, and apoptotic processes.Methods. HUVECs were subjected to shear stress of 1, 5, and 10 dyne/cm2in a Flow Bioreactor for 24 hours to compare gene expression modulation. Total RNA was analyzed by Affymetrix technology and the expression of two specific genes (CXCR4 and ICAM-1) was validated by RT-PCR. To highlight possible regulations between genes and as further validation, a bioinformatics analysis was performed.Results. At low shear stress (1 dyne/cm2) we observed the following: (a) strong upregulation of CXCR4; (b) mild upregulation of Caspase-8; (c) mild downregulation of ICAM-1; (d) marked downexpression of TNFAIP3. Bioinformatics analysis showed the presence of network composed by 59 new interactors (14 transcription factors and 45 microRNAs) appearing strongly related to shear stress.Conclusions. The significant modulation of these genes at low shear stress and their close relationships through transcription factors and microRNAs suggest that all may promote an initial inflamed endothelial cell phenotype, favoring the atherosclerotic disease.

Finite Element Analysis of Tire/Rim Interface Forces Under Braking and Cornering Loads

1992 ◽  
Vol 20 (2) ◽  
pp. 83-105 ◽  
Author(s):  
J. P. Jeusette ◽  
M. Theves
Keyword(s):  
Finite Element ◽  
Shear Stress ◽  
Contact Pressure ◽  
Element Model ◽  
Shear Stresses ◽  
Detailed Knowledge ◽  
Stress Distributions ◽  
Element Analysis ◽  
Plane Shear ◽  
Normal Contact

Abstract During vehicle braking and cornering, the tire's footprint region may see high normal contact pressures and in-plane shear stresses. The corresponding resultant forces and moments are transferred to the wheel. The optimal design of the tire bead area and the wheel requires a detailed knowledge of the contact pressure and shear stress distributions at the tire/rim interface. In this study, the forces and moments obtained from the simulation of a vehicle in stationary braking/cornering conditions are applied to a quasi-static braking/cornering tire finite element model. Detailed contact pressure and shear stress distributions at the tire/rim interface are computed for heavy braking and cornering maneuvers.

Low shear stress-induced endothelial mesenchymal transformation via the down-regulation of TET2

2021 ◽  
Vol 545 ◽  
pp. 20-26
Author(s):  
AFang Li ◽  
LiLan Tan ◽  
ShuLei Zhang ◽  
Jun Tao ◽  
Zuo Wang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Down Regulation ◽  
Low Shear Stress ◽  
Mesenchymal Transformation ◽  
Low Shear

Plaque and Shear Stress Distribution in Human Coronary Bifurcations: a Multi-Slice Computed Tomography Study

2007 ◽  
Author(s):  
Alina G. van der Giessen ◽  
Jolanda J. Wentzel ◽  
Frans N. van de Vosse ◽  
Antonius F. van der Steen ◽  
Pim J. de Feyter ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Shear Stress ◽  
Outer Wall ◽  
Atherosclerotic Plaques ◽  
Advanced Stage ◽  
Flow Divider ◽  
Low Shear Stress ◽  
Curved Vessels ◽  
Early Atherosclerosis ◽  
Low Shear

It is generally accepted that early atherosclerosis develops in low shear-stress (SS) regions such as the outer wall of arterial bifurcations and the inner bend of curved vessels (1). However, in clinical practice, it is common to observe atherosclerotic plaques at the flow-divider, or carina, of coronary bifurcations (2). Plaques at the carina are more frequently found in symptomatic patients, and may represent a more advanced stage of atherosclerosis. The carina is located in a region which is exposed to high SS. We hypothesize that if plaques are located in atheroprotective high SS regions, they have grown circumferentially from the atherogenic low SS regions.

scholarly journals Low Shear Stress Induced HMGB1 Translocation and Release via PECAM-1/PARP-1 Pathway to Induce Inflammation Response

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0120586 ◽  
Author(s):  
Wei-dong Qin ◽  
Shao-hua Mi ◽  
Chen Li ◽  
Gui-xia Wang ◽  
Jian-ning Zhang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Inflammation Response ◽  
Low Shear Stress ◽  
Parp 1 ◽  
Low Shear
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