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B J Ballermann - One of the best experts on this subject based on the ideXlab platform.
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Shear Stress and the endothelium
Kidney International, 1998Co-Authors: B J Ballermann, Alan DardikAbstract:Shear Stress and the endothelium. Vascular endothelial cells (ECs) in vivo are influenced by two distinct hemodynamic forces: cyclical strain due to vessel wall distention by transmural pressure, and Shear Stress, the frictional force generated by blood flow. Shear Stress acts at the apical cell surface to deform cells in the direction of blood flow; wall distention tends to deform cells in all directions. The Shear Stress response differs, at least partly, from the cyclical strain response, suggesting that cytoskeletal strain alone cannot explain it. Acute Shear Stress in vitro elicits rapid cytoskeletal remodeling and activates signaling cascades in ECs, with the consequent acute release of nitric oxide and prostacyclin; activation of transcription factors nuclear factor (NF)κB, c- fos , c- jun and SP-1; and transcriptional activation of genes, including ICAM-1, MCP-1, tissue factor, platelet-derived growth factor-B (PDGF-B), transforming growth factor (TGF)-β1, cyclooxygenase-II, and endothelial nitric oxide synthase (eNOS). This response thus shares similarities with EC responses to inflammatory cytokines. In contrast, ECs adapt to chronic Shear Stress by structural remodeling and flattening to minimize Shear Stress. Such cells become very adherent to their substratum and show evidence of differentiation. Increased adhesion following chronic Shear Stress has been exploited to generate vascular grafts with confluent EC monolayers, retained after implantation in vivo , thus overcoming a major obstacle to endothelialization of vascular prostheses.
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Shear Stress and the endothelium.
Kidney international. Supplement, 1998Co-Authors: B J Ballermann, Alan DardikAbstract:Shear Stress and the endothelium. Vascular endothelial cells (ECs) in vivo are influenced by two distinct hemodynamic forces: cyclical strain due to vessel wall distention by transmural pressure, and Shear Stress, the frictional force generated by blood flow. Shear Stress acts at the apical cell surface to deform cells in the direction of blood flow; wall distention tends to deform cells in all directions. The Shear Stress response differs, at least partly, from the cyclical strain response, suggesting that cytoskeletal strain alone cannot explain it. Acute Shear Stress in vitro elicits rapid cytoskeletal remodeling and activates signaling cascades in ECs, with the consequent acute release of nitric oxide and prostacyclin; activation of transcription factors nuclear factor (NF)kappaB, c-fos, c-jun and SP-1; and transcriptional activation of genes, including ICAM-1, MCP-1, tissue factor, platelet-derived growth factor-B (PDGF-B), transforming growth factor (TGF)-beta1, cyclooxygenase-II, and endothelial nitric oxide synthase (eNOS). This response thus shares similarities with EC responses to inflammatory cytokines. In contrast, ECs adapt to chronic Shear Stress by structural remodeling and flattening to minimize Shear Stress. Such cells become very adherent to their substratum and show evidence of differentiation. Increased adhesion following chronic Shear Stress has been exploited to generate vascular grafts with confluent EC monolayers, retained after implantation in vivo, thus overcoming a major obstacle to endothelialization of vascular prostheses.
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Shear Stress-conditioned, endothelial cell-seeded vascular grafts: Improved cell adherence in response to in vitro Shear Stress
Surgery, 1995Co-Authors: B J BallermannAbstract:Background . Prosthetic vascular grafts with adherent endothelial cell monolayers may prove useful for small-caliber vessel bypass. However, endothelial cells adhere poorly to prosthetic graft material, and they are stripped when exposed to in vivo Shear Stress. This study sought to determine whether in vitro Shear Stress conditioning improves endothelial cell adhesion and decreases thrombogenicity of endothelial cell-seeded grafts. Methods . The lumens of 1.5 mm (inside diameter) spun polyurethane polymer vascular grafts were seeded with bovine aortic endothelial cells and cultured in vitro for 6 days with or without continuous laminar Shear Stress, first at 1 to 2 dynes/cm 2 for 3 days, then at approximately 25 dynes/cm 2 for 3 days. Grafts preconditioned by Shear Stress and the static control grafts were then exposed to arterial Shear Stress at 25 dynes/cm 2 for 25 seconds. The number of dislodged cells was counted, and the grafts were examined by light and scanning electron microscopy. Whole blood clotting time in the grafts was also determined. Results . Exposure of grafts to acute Shear Stress dislodged 1.35×10 6 ±0.44×10 6 cells from static grafts compared with 1.05×10 4 ±0.16×10 4 cells from grafts preconditioned by Shear Stress. By light and electron microscopy an intact endothelial monolayer was observed to cover the lumen of Shear Stress-conditioned grafts, whereas few cells remained on the luminal surface of grafts not previously exposed to Shear Stress. The clotting time in Shear Stress-conditioned grafts was significantly prolonged in relation to grafts not exposed to Shear Stress. Conclusions . These findings show that endothelial cell adhesion and retention on vascular grafts in vitro is markedly enhanced by preconditioning the seeded endothelial cell monolayer with long-term Shear Stress. Consequently, vascular grafts containing Shear Stress-conditioned endothelial monolayers are less thrombogenic in vitro than small-caliber vascular grafts without intact endothelial cell monolayers.
Barbara J. Ballermann - One of the best experts on this subject based on the ideXlab platform.
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Shear Stress-conditioned, endothelial cell-seeded vascular grafts: Improved cell adherence in response to in vitro Shear Stress
Surgery, 1995Co-Authors: Barbara J. BallermannAbstract:Background . Prosthetic vascular grafts with adherent endothelial cell monolayers may prove useful for small-caliber vessel bypass. However, endothelial cells adhere poorly to prosthetic graft material, and they are stripped when exposed to in vivo Shear Stress. This study sought to determine whether in vitro Shear Stress conditioning improves endothelial cell adhesion and decreases thrombogenicity of endothelial cell-seeded grafts. Methods . The lumens of 1.5 mm (inside diameter) spun polyurethane polymer vascular grafts were seeded with bovine aortic endothelial cells and cultured in vitro for 6 days with or without continuous laminar Shear Stress, first at 1 to 2 dynes/cm 2 for 3 days, then at approximately 25 dynes/cm 2 for 3 days. Grafts preconditioned by Shear Stress and the static control grafts were then exposed to arterial Shear Stress at 25 dynes/cm 2 for 25 seconds. The number of dislodged cells was counted, and the grafts were examined by light and scanning electron microscopy. Whole blood clotting time in the grafts was also determined. Results . Exposure of grafts to acute Shear Stress dislodged 1.35×10 6 ±0.44×10 6 cells from static grafts compared with 1.05×10 4 ±0.16×10 4 cells from grafts preconditioned by Shear Stress. By light and electron microscopy an intact endothelial monolayer was observed to cover the lumen of Shear Stress-conditioned grafts, whereas few cells remained on the luminal surface of grafts not previously exposed to Shear Stress. The clotting time in Shear Stress-conditioned grafts was significantly prolonged in relation to grafts not exposed to Shear Stress. Conclusions . These findings show that endothelial cell adhesion and retention on vascular grafts in vitro is markedly enhanced by preconditioning the seeded endothelial cell monolayer with long-term Shear Stress. Consequently, vascular grafts containing Shear Stress-conditioned endothelial monolayers are less thrombogenic in vitro than small-caliber vascular grafts without intact endothelial cell monolayers.
Wolfgang Schroder - One of the best experts on this subject based on the ideXlab platform.
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Measurements of the wall-Shear Stress distribution in turbulent channel flow using the micro-pillar Shear Stress sensor MPS3
Experimental Thermal and Fluid Science, 2019Co-Authors: Michael Klaas, Wolfgang SchroderAbstract:Abstract This study investigates the wall-Shear Stress (WSS) distribution in turbulent channel flow at friction Reynolds numbers of Re τ = 860 and 1300 using the micro-pillar Shear-Stress sensor (MPS3). The probability density functions and the joint probability density functions of the wall-Shear Stress vectors indicate that the intermittency of the flow increases for higher Reynolds numbers. Extreme events occurring at the wall, such as wall-normal velocity spikes and backflow events, are detected and analyzed based on the wall-Shear Stress patterns. The events representing the wall-normal spikes are conditionally sampled from the wall-normal velocity component, which is determined from the local wall-Shear Stress gradients. The results show that the negative velocity spikes tend to co-occur with strong streamwise wall-Shear Stress motions, and that the positive spikes are likely to accompany large spanwise motions. Rare backflow events are detected from the wall-Shear Stress distribution for both Reynolds numbers, serving as an experimental evidence of near-wall flow reversal events in turbulent channel flow. The diameter of the detected backflow region is approximately 20 viscous units. The data confirm the results from previous numerical studies. The wall-normal velocity spikes and the backflow events are likely to be three-dimensional, suggesting an energy and momentum transfer between the viscous sublayer and the outer part of the turbulent channel flow.
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Development of a Shear Stress sensor to analyse the influence of polymers on the turbulent wall Shear Stress
Journal of Physics: Condensed Matter, 2011Co-Authors: Bernardo Nottebrock, Sebastian Grosse, Wolfgang SchroderAbstract:The drag reducing effect of polymers in a channel flow is well known and it is assumed that the polymer filaments interfere with the turbulent structures in the very near-wall flow. To analyse their precise effect, a micro-pillar Shear Stress sensor (MPS3) measurement system is developed which allows the detection of wall Shear Stress at high spatial and temporal resolutions. Different manufacturing techniques for the required micro-pillars are discussed and their influence on the flow is investigated evidencing the non-intrusive character of the pillars. Subsequently, a complete calibration is presented to relate the recorded deflection to wall Shear Stress values and to assure the correct detection over the whole expected frequency spectrum. A feasibility study about the ability to visualize the two-dimensional wall Shear Stress distribution completes the discussion about the validity of MPS3. In the last step, the drag reduction of a polymer filament grafted on a micro-pillar compared to a plain pillar and the application of MPS3 in an ocean-type polymer solution are investigated. The results confirm the expected behaviour found in the literature.
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Mean wall-Shear Stress measurements using the micro-pillar Shear-Stress sensor MPS3
Measurement Science and Technology, 2007Co-Authors: Sebastian Grosse, Wolfgang SchroderAbstract:A new sensor to measure the mean turbulent wall-Shear Stress in turbulent flows is described. The wall-Shear Stress sensor MPS3 has been tested in a well-defined fully developed turbulent pipe flow at Reynolds numbers Reb based on the bulk velocity Ub and the pipe diameter D in the range of Reb = 10 000–20 000. The results demonstrate a convincing agreement of the mean wall-Shear Stress obtained with the new sensor technique with analytical and experimental results from the literature. The sensor device consists of a flexible micro-pillar that extends from the wall into the viscous sublayer. Bending due to the exerting fluid forces, the pillar-tip deflection serves as a measure for the local wall-Shear Stress. The sensor concept, calibration techniques, the achievable accuracy and error estimates, the fields of application and the sensor limits will be discussed. Furthermore, a first estimate of the pillar dynamic response will be derived showing the potential of the sensor to also measure the turbulent fluctuating wall-Shear Stress.
Jolanda J Wentzel - One of the best experts on this subject based on the ideXlab platform.
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Shear Stress and advanced atherosclerosis in human coronary arteries
Journal of Biomechanics, 2012Co-Authors: Frank J. H. Gijsen, Alina Van Der Giessen, Anton F. W. Van Der Steen, Jolanda J WentzelAbstract:Abstract The role of low and oscillating Shear Stress as a key factor for localizing early atherosclerotic plaques is generally accepted. Once more advanced plaques protrude into the lumen, the Shear Stress they are exposed to changes. The influence of Shear Stress on plaque composition in advanced atherosclerosis is not fully understood. In this review, we discuss our recent studies on the relationship between Shear Stress and plaque composition and the location of plaque rupture in human coronary arteries. We have shown that elevated Shear Stress levels can be found over plaques inducing only mild luminal narrowing and are not subjected to treatment. Regional exposure of certain plaque regions to high Shear Stress is therefore a condition that will pertain for a prolonged period of time. We have also shown that in more advanced atherosclerosis the necrotic core experiences higher Shear Stress. Low Shear Stress plaque regions can be found downstream of the plaque and are stiffer. High Shear Stress plaque regions can be found either at the upstream, shoulder or cap region of the plaque and are softer. The plaque regions with the highest strain levels are the regions that are exposed to the highest Shear Stress. The high Shear Stress plaque regions are the only plaque regions that get softer over time. Finally, high Shear Stress is also associated with the location of plaque rupture in non-culprit lesion in human coronary arteries. Combining our findings with data from literature, we can conclude that advanced coronary plaques grow in the distal regions. The distal plaque regions are exposed to low Shear Stress, are stiffer and have a stable plaque phenotype. The regions exposed to high Shear Stress are softer, and are associated with vulnerable plaque features.
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High Shear Stress influences plaque vulnerability
Netherlands Heart Journal, 2008Co-Authors: Harald C. Groen, Marina S. Ferguson, Frank J. H. Gijsen, Can Yuan, Aad Van Der Lugt, A.f.w. Van Der Steen, Thomas S Hatsukami, Jolanda J WentzelAbstract:Shear Stress of the blood at the vessel wall plays an important role in many processes in the cardiovascular system primarily focused on the regulation of vessel lumen and wall dimensions. There is ample evidence that atherosclerotic plaques are generated at low Shear Stress regions in the cardiovascular system, while high Shear Stress regions are protected. In the course of plaque progression, advanced plaques start to encroach into the lumen, and thereby start to experience high Shear Stress at the endothelium. Until now the consequences of high Shear Stress working at the endothelium of an advanced plaque are unknown. As high Shear Stress influences tissue regression, we hypothesised that high Shear Stress can destabilise the plaque by cap weakening leading to ulceration. We investigated this hypothesis in a magnetic resonance imaging (MRI) dataset of a 67-year-old woman with a plaque in the carotid artery at baseline and an ulcer at ten-month follow-up. The lumen, plaque components (lipid/necrotic core, intraplaque haemorrhage) and ulcer were reconstructed three dimensionally and the geometry at baseline was used for Shear Stress calculation using computational fluid dynamics. Correlation of the change in plaque composition with the Shear Stress at baseline showed that the ulcer was generated exclusively at the high Shear Stress location. In this serial MRI study we found plaque ulceration at the high Shear Stress location of a protruding plaque in the carotid artery. Our data suggest that high Shear Stress influences plaque vulnerability and therefore may become a potential parameter for predicting future events. (Neth Heart J 2008;16:280-3.)
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Shear Stress, vascular remodeling and neointimal formation
Journal of Biomechanics, 2003Co-Authors: Jolanda J Wentzel, Christina J Slager, Patrick W.j.c. Serruys, Nikos Stergiopulos, Frank J. H. Gijsen, Rob KramsAbstract:The role of Shear Stress in atherosclerosis has been well documented. However, its role in restenosis was underexposed. In this paper a novel in vivo measuring technique and several of its applications related to restenosis will be described. The technique consists of a combination of 3D reconstruction of blood vessels and computational fluid dynamics (CFD). The 3D imaging techniques use either of 3D intravascular ultrasound (IVUS) as a stand-alone technique or a fusion of biplane angiography and IVUS (ANGUS). CFD is applied in order to relate local Shear Stress distribution to the morphology of the vessel wall. In the applications of these techniques it will be demonstrated that Shear Stress plays a role in the prediction of neointimal formation in in-stent restenosis and in vascular remodeling after balloon angioplasty. Attempts to locally increase Shear Stress by a newly developed flow divider indicate that Shear Stress reduce in-stent neointimal formation by 50%.
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Shear Stress in atherosclerosis, and vascular remodelling.
Seminars in interventional cardiology : SIIC, 1998Co-Authors: Rob Krams, Jan A. Oomen, Ivan Andhyiswara, Jeroen Kloet, De Smet B, Mark J. Post, Jolanda J Wentzel, Johan C.h. Schuurbiers, Cornelius Borst, Christina J SlagerAbstract:Abstract Shear Stress plays a role in lipid accumulation in primary atherosclerosis and vascular remodelling. We will present applications of a new technique, which enables to quantify Shear Stress in 3D vessel reconstructions. The method is based on 3D IVUS reconstructions of blood vessels either obtained by IVUS pull back (external iliac artery) or by a combination of angiography and IVUS (curved coronary artery). Distribution of wall thickness of a curved human right coronary artery was such that low wall thickness occurred where Shear Stress was high, and wall thickness was high where Shear Stress was low. Consequently, an inverse relationship between Shear Stress and wall thickness was detected. Although vascular remodelling after PTA in external iliac arteries of atherosclerotic Yucatan pigs was predicted both by acute gain and decrements in Shear Stress, the decrement in Shear Stress appeared a better predictor. In conclusion, Shear Stress appears to play a role in primary atherosclerosis and vascular remodelling after PTA.
Abdul R. Asif - One of the best experts on this subject based on the ideXlab platform.
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Advances in endothelial Shear Stress proteomics
Expert Review of Proteomics, 2014Co-Authors: Sabika Firasat, Lutz Binder, Markus Hecker, Abdul R. AsifAbstract:The vascular endothelium lining the luminal surface of all blood vessels is constantly exposed to Shear Stress exerted by the flowing blood. Blood flow with high laminar Shear Stress confers protection by activation of antiatherogenic, antithrombotic and anti-inflammatory proteins, whereas low or oscillatory Shear Stress may promote endothelial dysfunction, thereby contributing to cardiovascular disease. Despite the usefulness of proteomic techniques in medical research, however, there are relatively few reports on proteome analysis of cultured vascular endothelial cells employing conditions that mimic in vivo Shear Stress attributes. This review focuses on the proteome studies that have utilized cultured endothelial cells to identify molecular mediators of Shear Stress and the roles they play in the regulation of endothelial function, and their ensuing effect on vascular function in general. It provides an overview on current strategies in Shear Stress-related proteomics and the key proteins mediating it...
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Advances in endothelial Shear Stress proteomics
Expert review of proteomics, 2014Co-Authors: Sabika Firasat, Lutz Binder, Markus Hecker, Abdul R. AsifAbstract:The vascular endothelium lining the luminal surface of all blood vessels is constantly exposed to Shear Stress exerted by the flowing blood. Blood flow with high laminar Shear Stress confers protection by activation of antiatherogenic, antithrombotic and anti-inflammatory proteins, whereas low or oscillatory Shear Stress may promote endothelial dysfunction, thereby contributing to cardiovascular disease. Despite the usefulness of proteomic techniques in medical research, however, there are relatively few reports on proteome analysis of cultured vascular endothelial cells employing conditions that mimic in vivo Shear Stress attributes. This review focuses on the proteome studies that have utilized cultured endothelial cells to identify molecular mediators of Shear Stress and the roles they play in the regulation of endothelial function, and their ensuing effect on vascular function in general. It provides an overview on current strategies in Shear Stress-related proteomics and the key proteins mediating its effects which have been characterized so far.
