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Journal articles on the topic 'Disturbed flow'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Laribi, Boualem, and Abdellah Abdellah Hadj. "Analysis of Turbulent Flow Development Downstream Disturbers with Perforated Plate Flow Conditioner." Applied Mechanics and Materials 197 (September 2012): 73–77. http://dx.doi.org/10.4028/www.scientific.net/amm.197.73.

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This article discusses the development and the establishment of turbulent flow downstream of disturbers like a valve 50% open, valve 70% open, Tee and 90° double bend in perpendicular planes. Associated with these disturbers, a perforated plate flow conditioner is installed to examine his performances to produce the fully developed pipe flow as suggested by standards ISO5167 and AGA3. The study focused mainly on the numerical analysis of the velocity contours at several axial stations downstream the disturbers. For the simulation, code CFD Fluent was used. The study of the disturbed flow is examined with three Reynolds numbers. The results show a very good prediction of the CFD code Fluent for the flow development downstream the disturbers and conditioner which makes the code very efficient for conception of a new flow conditioner not described by the standards. It was also found that the valve 50% open could be considered a reference disturber for analyzing the development of turbulent flows. As interesting results, is the effectiveness of the perforated plate to produce the flow developed pipe flow at about z/D=10 downstream the disturber. This result is very important for flow measurement accuracy as suggested by the standards. An experimental study is needed to validate these results.

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2

Gersten, K. "Flow metering with disturbed inflow." Acta Mechanica 201, no. 1-4 (2008): 13–22. http://dx.doi.org/10.1007/s00707-008-0068-9.

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3

Chu, Miao, Clemens von Birgelen, Yingguang Li, et al. "Quantification of disturbed coronary flow by disturbed vorticity index and relation with fractional flow reserve." Atherosclerosis 273 (June 2018): 136–44. http://dx.doi.org/10.1016/j.atherosclerosis.2018.02.023.

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4

Efird, K. D. "Disturbed Flow and Flow-Accelerated Corrosion in Oil and Gas Production." Journal of Energy Resources Technology 120, no. 1 (1998): 72–77. http://dx.doi.org/10.1115/1.2795013.

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The effect of fluid flow on corrosion of steel in oil and gas environments involves a complex interaction of physical and chemical parameters. The basic requirement for any corrosion to occur is the existence of liquid water contacting the pipe wall, which is primarily controlled by the flow regime. The effect of flow on corrosion, or flow-accelerated corrosion, is defined by the mass transfer and wall shear stress parameters existing in the water phase that contacts the pipe wall. While existing fluid flow equations for mass transfer and wall shear stress relate to equilibrium conditions, disturbed flow introduces nonequilibrium, steady-state conditions not addressed by these equations, and corrosion testing in equilibrium conditions cannot be effectively related to corrosion in disturbed flow. The problem in relating flow effects to corrosion is that steel corrosion failures in oil and gas environments are normally associated with disturbed flow conditions as a result of weld beads, pre-existing pits, bends, flanges, valves, tubing connections, etc. Steady-state mass transfer and wall shear stress relationships to steel corrosion and corrosion testing are required for their application to corrosion of steel under disturbed flow conditions. A procedure is described to relate the results of a corrosion test directly to corrosion in an operation system where disturbed flow conditions are expected, or must be considered.

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5

THEOFANOUS, T. G., G. J. LI, T. N. DINH, and C. H. CHANG. "Aerobreakup in disturbed subsonic and supersonic flow fields." Journal of Fluid Mechanics 593 (November 23, 2007): 131–70. http://dx.doi.org/10.1017/s0022112007008853.

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This work concerns the breakup of millimetre-scale liquid droplets in gaseous flow fields that are disturbed from free-stream conditions by the presence of solid obstacles or other drops. A broad range of flow conditions is considered – from subsonic to supersonic, from highly rarefied to ambient pressures, and from fixed cylindrical obstacles to free liquid droplets (as obstacles). The liquid is water or tributyl phosphate, a water-like low-viscosity fluid of very low vapour pressure. We present data on deformation and breakup regimes, and, aided by numerical simulations, we discuss governing mechanisms and the time scaling of these events. Thereby a methodology is demonstrated for conveniently forecasting first-order behaviours in disturbed flow fields more generally. The highly resolved images lend themselves to testing/benchmarking numerical simulations of interfacial flows. These results, along with the experimental capability developed, constitute one of the key building blocks for our overall long-term aim towards predicting ultimate particle-size distributions from such intense aerodynamic interactions involving very large quantities of Newtonian and viscoelastic liquids.

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6

Chiu, J. J., D. L. Wang, S. Chien, R. Skalak, and S. Usami. "Effects of Disturbed Flow On Endothelial Cells." Journal of Biomechanical Engineering 120, no. 1 (1998): 2–8. http://dx.doi.org/10.1115/1.2834303.

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Atherosclerotic lesions tend to localize at curvatures and branches of the arterial system, where the local flow is often disturbed and irregular (e.g., flow separation, recirculation, complex flow patterns, and nonuniform shear stress distributions). The effects of such flow conditions on cultured human umbilical vein endothelial cells (HUVECs) were studied in vitro by using a vertical-step flow channel (VSF). Detailed shear stress distributions and flow structures have been computed by using the finite volume method in a general curvilinear coordinate system. HUVECs in the reattachment areas with low shear stresses were generally rounded in shape. In contrast, the cells under higher shear stresses were significantly elongated and aligned with the flow direction, even for those in the area with reversed flow. When HUVECs were subjected to shearing in VSF, their actin stress fibers reorganized in association with the morphological changes. The rate of DNA synthesis in the vicinity of the flow reattachment area was higher than that in the laminar flow area. These in vitro experiments have provided data for the understanding of the in vivo responses of endothelial cells under complex flow environments found in regions of prevalence of atherosclerotic lesions.

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7

Xu, Qingbo. "Disturbed Flow-Enhanced Endothelial Turnover in Atherosclerosis." Trends in Cardiovascular Medicine 19, no. 6 (2009): 191–95. http://dx.doi.org/10.1016/j.tcm.2009.12.002.

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8

Kheshgi, Haroon S., and L. E. Scriven. "Disturbed film flow on a vertical plate." Physics of Fluids 30, no. 4 (1987): 990. http://dx.doi.org/10.1063/1.866286.

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9

Chien, Shu. "Effects of Disturbed Flow on Endothelial Cells." Annals of Biomedical Engineering 36, no. 4 (2008): 554–62. http://dx.doi.org/10.1007/s10439-007-9426-3.

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10

Qi, Wei Dong, Jin Chun Song, and Guang An Ren. "Analysis on Gas Flow Field in Bell-Type Annealing Furnace by Using FLUENT." Applied Mechanics and Materials 345 (August 2013): 581–85. http://dx.doi.org/10.4028/www.scientific.net/amm.345.581.

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Because temperature decreases sharply, expansion caused by heat and contraction caused by cold are evident, the air in furnace is disturbed greatly and the zone of negative pressure may appear during bell-type furnace annealing. The zone can cause external air permeating the furnace and make steel coil annealed. Therefore it is necessary to analyse the flow field of protective gas in furnace during cooling, whether the air zone of negative pressure can form, the location of the zone and the methods of eliminating the zone. In addition, splitter plate disturbs the flow of gas and its effect on disturbed air is also analyzed. This paper analyses flow field in bell-type annealing furnace by using FLUENT, whether the zone of negative pressure exists and its location.

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11

Chu, Miao, Clemens von Birgelen, Yingguang Li, et al. "TCT-453 Quantification of Disturbed Coronary Blood Flow: Disturbed Vorticity Index and its Relation With Fractional Flow Reserve." Journal of the American College of Cardiology 70, no. 18 (2017): B187. http://dx.doi.org/10.1016/j.jacc.2017.09.562.

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12

Chiu, Jeng-Jiann, and Shu Chien. "Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives." Physiological Reviews 91, no. 1 (2011): 327–87. http://dx.doi.org/10.1152/physrev.00047.2009.

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Vascular endothelial cells (ECs) are exposed to hemodynamic forces, which modulate EC functions and vascular biology/pathobiology in health and disease. The flow patterns and hemodynamic forces are not uniform in the vascular system. In straight parts of the arterial tree, blood flow is generally laminar and wall shear stress is high and directed; in branches and curvatures, blood flow is disturbed with nonuniform and irregular distribution of low wall shear stress. Sustained laminar flow with high shear stress upregulates expressions of EC genes and proteins that are protective against atherosclerosis, whereas disturbed flow with associated reciprocating, low shear stress generally upregulates the EC genes and proteins that promote atherogenesis. These findings have led to the concept that the disturbed flow pattern in branch points and curvatures causes the preferential localization of atherosclerotic lesions. Disturbed flow also results in postsurgical neointimal hyperplasia and contributes to pathophysiology of clinical conditions such as in-stent restenosis, vein bypass graft failure, and transplant vasculopathy, as well as aortic valve calcification. In the venous system, disturbed flow resulting from reflux, outflow obstruction, and/or stasis leads to venous inflammation and thrombosis, and hence the development of chronic venous diseases. Understanding of the effects of disturbed flow on ECs can provide mechanistic insights into the role of complex flow patterns in pathogenesis of vascular diseases and can help to elucidate the phenotypic and functional differences between quiescent (nonatherogenic/nonthrombogenic) and activated (atherogenic/thrombogenic) ECs. This review summarizes the current knowledge on the role of disturbed flow in EC physiology and pathophysiology, as well as its clinical implications. Such information can contribute to our understanding of the etiology of lesion development in vascular niches with disturbed flow and help to generate new approaches for therapeutic interventions.

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13

Gardin, Julius M., and Slawomir M. Lobodzinski. "Do Doppler Color Flow Algorithms for Mapping Disturbed Flow Make Sense?" Journal of the American Society of Echocardiography 3, no. 4 (1990): 310–15. http://dx.doi.org/10.1016/s0894-7317(14)80314-3.

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14

Kim, C. W., A. Pokutta-Paskaleva, S. Kumar, L. H. Timmins, A. D. Morris, and D. W. Kang. "Disturbed Flow Promotes Arterial Stiffening Through Thrombospondin-1." Journal of Vascular Surgery 67, no. 1 (2018): 357. http://dx.doi.org/10.1016/j.jvs.2017.11.031.

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15

Kim, Chan Woo, Anastassia Pokutta-Paskaleva, Sandeep Kumar, et al. "Disturbed Flow Promotes Arterial Stiffening Through Thrombospondin-1." Circulation 136, no. 13 (2017): 1217–32. http://dx.doi.org/10.1161/circulationaha.116.026361.

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16

Jünger, M., T. Klyscz, M. Hahn, and G. Rassner. "Disturbed Blood Flow Regulation in Venous Leg Ulcers." International Journal of Microcirculation 16, no. 5 (1996): 259–65. http://dx.doi.org/10.1159/000179182.

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17

Mahmoud, Marwa, Celine Souilhol, Jovana Serbanovic-Canic, and Paul Evans. "GATA4-Twist1 Signalling in Disturbed Flow-Induced Atherosclerosis." Cardiovascular Drugs and Therapy 33, no. 2 (2019): 231–37. http://dx.doi.org/10.1007/s10557-019-06863-3.

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18

Chen, Cheng-Nan, Shun-Fu Chang, Ya-Chen Ko, and Jeng-Jiann Chiu. "EFFECTS OF DISTURBED FLOW ON LEUKOCYTE TRANSENDOTHELIAL MIGRATION." Cardiovascular Pathology 13, no. 3 (2004): 109. http://dx.doi.org/10.1016/j.carpath.2004.03.327.

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19

Morris, Andrew, Luke P. Brewster, and Luke Timmins. "Developing Models of Disturbed Flow in Infrageniculate Arteries." Journal of the American College of Surgeons 225, no. 4 (2017): S216. http://dx.doi.org/10.1016/j.jamcollsurg.2017.07.498.

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20

Martin, Daniel, Yi Li, Junyao Yang, et al. "Unspliced X-box-binding Protein 1 (XBP1) Protects Endothelial Cells from Oxidative Stress through Interaction with Histone Deacetylase 3." Journal of Biological Chemistry 289, no. 44 (2014): 30625–34. http://dx.doi.org/10.1074/jbc.m114.571984.

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It is well known that atherosclerosis occurs geographically at branch points where disturbed flow predisposes to the development of plaque via triggering of oxidative stress and inflammatory reactions. In this study, we found that disturbed flow activated anti-oxidative reactions via up-regulating heme oxygenase 1 (HO-1) in an X-box-binding protein 1 (XBP1) and histone deacetylase 3 (HDAC3)-dependent manner. Disturbed flow concomitantly up-regulated the unspliced XBP1 (XBP1u) and HDAC3 in a VEGF receptor and PI3K/Akt-dependent manner. The presence of XBP1 was essential for the up-regulation of HDAC3 protein. Overexpression of XBP1u and/or HDAC3 activated Akt1 phosphorylation, Nrf2 protein stabilization and nuclear translocation, and HO-1 expression. Knockdown of XBP1u decreased the basal level and disturbed flow-induced Akt1 phosphorylation, Nrf2 stabilization, and HO-1 expression. Knockdown of HDAC3 ablated XBP1u-mediated effects. The mammalian target of rapamycin complex 2 (mTORC2) inhibitor, AZD2014, ablated XBP1u or HDAC3 or disturbed flow-mediated Akt1 phosphorylation, Nrf2 nuclear translocation, and HO-1 expression. Neither actinomycin D nor cycloheximide affected disturbed flow-induced up-regulation of Nrf2 protein. Knockdown of Nrf2 abolished XBP1u or HDAC3 or disturbed flow-induced HO-1 up-regulation. Co-immunoprecipitation assays demonstrated that XBP1u physically bound to HDAC3 and Akt1. The region of amino acids 201 to 323 of the HDAC3 protein was responsible for the binding to XBP1u. Double immunofluorescence staining revealed that the interactions between Akt1 and mTORC2, Akt1 and HDAC3, Akt1 and XBP1u, HDAC3, and XBP1u occurred in the cytosol. Thus, we demonstrate that XBP1u and HDAC3 exert a protective effect on disturbed flow-induced oxidative stress via up-regulation of mTORC2-dependent Akt1 phosphorylation and Nrf2-mediated HO-1 expression.

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21

Ting, Lucas H., Jessica R. Jahn, Joon I. Jung, et al. "Flow mechanotransduction regulates traction forces, intercellular forces, and adherens junctions." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 11 (2012): H2220—H2229. http://dx.doi.org/10.1152/ajpheart.00975.2011.

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Endothelial cells respond to fluid shear stress through mechanotransduction responses that affect their cytoskeleton and cell-cell contacts. Here, endothelial cells were grown as monolayers on arrays of microposts and exposed to laminar or disturbed flow to examine the relationship among traction forces, intercellular forces, and cell-cell junctions. Cells under laminar flow had traction forces that were higher than those under static conditions, whereas cells under disturbed flow had lower traction forces. The response in adhesion junction assembly matched closely with changes in traction forces since adherens junctions were larger in size for laminar flow and smaller for disturbed flow. Treating the cells with calyculin-A to increase myosin phosphorylation and traction forces caused an increase in adherens junction size, whereas Y-27362 cause a decrease in their size. Since tugging forces across cell-cell junctions can promote junctional assembly, we developed a novel approach to measure intercellular forces and found that these forces were higher for laminar flow than for static or disturbed flow. The size of adherens junctions and tight junctions matched closely with intercellular forces for these flow conditions. These results indicate that laminar flow can increase cytoskeletal tension while disturbed flow decreases cytoskeletal tension. Consequently, we found that changes in cytoskeletal tension in response to shear flow conditions can affect intercellular tension, which in turn regulates the assembly of cell-cell junctions.

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22

Nam, Douglas, Chih-Wen Ni, Amir Rezvan, et al. "Partial carotid ligation is a model of acutely induced disturbed flow, leading to rapid endothelial dysfunction and atherosclerosis." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 4 (2009): H1535—H1543. http://dx.doi.org/10.1152/ajpheart.00510.2009.

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Atherosclerosis is closely associated with disturbed flow characterized by low and oscillatory shear stress, but studies directly linking disturbed flow to atherogenesis is lacking. The major reason for this has been a lack of an animal model in which disturbed flow can be acutely induced and cause atherosclerosis. Here, we characterize partial carotid ligation as a model of disturbed flow with characteristics of low and oscillatory wall shear stress. We also describe a method of isolating intimal RNA in sufficient quantity from mouse carotid arteries. Using this model and method, we found that partial ligation causes upregulation of proatherogenic genes, downregulation of antiatherogenic genes, endothelial dysfunction, and rapid atherosclerosis in 2 wk in a p47phox-dependent manner and advanced lesions by 4 wk. We found that partial ligation results in endothelial dysfunction, rapid atherosclerosis, and advanced lesion development in a physiologically relevant model of disturbed flow. It also allows for easy and rapid intimal RNA isolation. This novel model and method could be used for genome-wide studies to determine molecular mechanisms underlying flow-dependent regulation of vascular biology and diseases.

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23

Johannesen, Asa, Alison M. Dunn, and Lesley J. Morrell. "Disturbed flow in an aquatic environment may create a sensory refuge for aggregated prey." PeerJ 5 (March 28, 2017): e3121. http://dx.doi.org/10.7717/peerj.3121.

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Predators use olfactory cues moved within water and air to locate prey. Because prey aggregations may produce more cue and be easier to detect, predation could limit aggregation size. However, disturbance in the flow may diminish the reliability of odour as a prey cue, impeding predator foraging success and efficiency. We explore how different cue concentrations (as a proxy for prey group size) affect risk to prey by fish predators in disturbed (more turbulent or mixed) and non-disturbed (less mixed) flowing water. We find that increasing odour cue concentration increases predation risk and disturbing the flow reduces predation risk. At high cue concentration fish were able to locate the cue source in both disturbed and non-disturbed flow, but at medium concentrations, predators only located the cue source more often than expected by chance in non-disturbed flow. This suggests that objects disturbing flow provide a sensory refuge allowing prey to form larger groups, but that group sizes may be limited by level of disturbance to the flow.

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24

Abe, Ryuzo, Norio Yamashita, Adrienne Rochier, et al. "Pulsatile to-fro flow induces greater and sustained expression of tissue factor RNA in HUVEC than unidirectional laminar flow." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 4 (2011): H1345—H1351. http://dx.doi.org/10.1152/ajpheart.01197.2010.

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Tissue factor (TF) is expressed in atherosclerotic lesions. Since mechanical forces influence endothelial cell (EC) function and are thought to account for the unique distribution of atherosclerosis in areas exposed to disturbed flow, we hypothesized that disturbed to-fro flow (TFF) and unidirectional pulsatile forward flow (PFF) would have different effects on TF expression in EC. TF RNA expression in HUVEC exposed to mechanical stress in the presence or absence of chemical stimulation with thrombin was determined. TFF induced a significantly higher TF expression than PFF that was sustained for 8 h. Combination of mechanical and chemical stimuli induced significantly higher TF expression than only mechanical stresses, and this effect was synergistic in both TFF and PFF. The MAPK p38 inhibitor SB-203580 significantly inhibited TF expression induced by mechanical and chemical stimulations, but the MEK inhibitor PD-98059 did not inhibit TF induced by TFF. Immunoblotting revealed that ERK1/2 phosphorylation induced by TFF was sustained for 120 min, whereas that induced by PFF was not. We conclude that disturbed flow induced greater and sustained amplification of TF expression, and this synergistic effect may be regulated by p38 MAPK and ERK1/2. These results provide added insight into the mechanism of atherosclerosis in areas of disturbed flow.

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25

Paeng, Dong‐Guk, Min Joo Choi, Suk Wang Yoon, and K. Kirk Shung. "Echogenicity from disturbed blood flow by an eccentric stenosis under pulsatile flow." Journal of the Acoustical Society of America 116, no. 4 (2004): 2560. http://dx.doi.org/10.1121/1.4785224.

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26

Martins, Ramon Silva, Guilherme Siqueira de Aquino, Márcio Ferreira Martins, and Rogério Ramos. "Sensitivity analysis for numerical simulations of disturbed flows aiming ultrasonic flow measurement." Measurement 185 (November 2021): 110015. http://dx.doi.org/10.1016/j.measurement.2021.110015.

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27

Liepsch, D., A. Poll, J. Strigberger, H. N. Sabbah, and P. D. Stein. "Flow Visualization Studies in a Mold of the Normal Human Aorta and Renal Arteries." Journal of Biomechanical Engineering 111, no. 3 (1989): 222–27. http://dx.doi.org/10.1115/1.3168369.

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To study the flow behavior in regions where hemodynamic effects have been suggested to participate in atherogenesis, we evaluated flow in a mold of the aorta and renal arteries of a previously healthy 27-year-old woman who died of trauma. A birefringent solution (vanadium-pentoxide) was used. When diluted, this material behaves like a Newtonian fluid. This method gives a complete picture of the entire flow field. Zones of flow separation and disturbed flow can be seen and the location and size of disturbed areas observed. Unseparated flow regions downstream from disturbed zones can be properly visualized and the method can be used for pulsatile flow as well as steady flow. During steady flow (only at branch to-trunk flow ratios > 0.20), zones of flow separation were observed in the aorta distal to the renal arteries. During pulsatile flow, disturbances were found at nearly all branch-to-trunk flow ratios.

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28

Ma, Ruolong, and William J. Devenport. "Unsteady Periodic Behavior of a Disturbed Tip-Leakage Flow." AIAA Journal 44, no. 5 (2006): 1073–86. http://dx.doi.org/10.2514/1.12082.

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29

Nariai, T., R. Suzuki, T. Nagaoka, et al. "Focally disturbed cerebral blcod flow in post concussive amnesia." Journal of Stroke and Cerebrovascular Diseases 6, no. 6 (1997): 437. http://dx.doi.org/10.1016/s1052-3057(97)80053-5.

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30

Qu, Dan, Li Wang, Mingyu Huo, et al. "Focal TLR4 activation mediates disturbed flow-induced endothelial inflammation." Cardiovascular Research 116, no. 1 (2019): 226–36. http://dx.doi.org/10.1093/cvr/cvz046.

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Abstract Aims Disturbed blood flow at arterial branches and curvatures modulates endothelial function and predisposes the region to endothelial inflammation and subsequent development of atherosclerotic lesions. Activation of the endothelial Toll-like receptors (TLRs), in particular TLR4, contributes to vascular inflammation. Therefore, we investigate whether TLR4 can sense disturbed flow (DF) to mediate the subsequent endothelial inflammation. Methods and results En face staining of endothelium revealed that TLR4 expression, activation, and its downstream inflammatory markers were elevated in mouse aortic arch compared with thoracic aorta, which were absent in Tlr4mut mice. Similar results were observed in the partial carotid ligation model where TLR4 signalling was activated in response to ligation-induced flow disturbance in mouse carotid arteries, and such effect was attenuated in Tlr4mut mice. DF in vitro increased TLR4 expression and activation in human endothelial cells (ECs) and promoted monocyte-EC adhesion, which were inhibited in TLR4-knockdown ECs. Among endogenous TLR4 ligands examined as candidate mediators of DF-induced TLR4 activation, fibronectin containing the extra domain A (FN-EDA) expressed by ECs was increased by DF and was revealed to directly interact with and activate TLR4. Conclusion Our findings demonstrate the indispensable role of TLR4 in DF-induced endothelial inflammation and pinpoint FN-EDA as the endogenous TLR4 activator in this scenario. This novel mechanism of vascular inflammation under DF condition may serve as a critical initiating step in atherogenesis.

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31

Chien, Shu. "Erratum to: Effects of Disturbed Flow on Endothelial Cells." Annals of Biomedical Engineering 38, no. 3 (2010): 1258. http://dx.doi.org/10.1007/s10439-010-9931-7.

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32

Lotz, U., and J. Postlethwaite. "Erosion-corrosion in disturbed two phase liquid/particle flow." Corrosion Science 30, no. 1 (1990): 95–106. http://dx.doi.org/10.1016/0010-938x(90)90239-2.

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33

Postlethwaite, J., S. Nesˇicˇ, G. Adamopoulos, and D. J. Bergstrom. "Predictive models for erosion-corrosion under disturbed flow conditions." Corrosion Science 35, no. 1-4 (1993): 627–33. http://dx.doi.org/10.1016/0010-938x(93)90197-o.

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34

Ferrara, K. W., M. Ostromogilsky, S. Rosenberg, and J. Sokil-Melgar. "Parameter mapping for the detection of disturbed blood flow." Ultrasound in Medicine & Biology 21, no. 4 (1995): 517–25. http://dx.doi.org/10.1016/0301-5629(94)00152-4.

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35

Nešiĉ, S., and J. Postlethwaite. "Hydrodynamics of disturbed flow and erosion-corrosion. Part I - Single-phase flow study." Canadian Journal of Chemical Engineering 69, no. 3 (1991): 698–703. http://dx.doi.org/10.1002/cjce.5450690311.

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36

Nešič, S., and J. Postlethwaite. "Hydrodynamics of disturbed flow and erosion-corrosion. Part II - Two-phase flow study." Canadian Journal of Chemical Engineering 69, no. 3 (1991): 704–10. http://dx.doi.org/10.1002/cjce.5450690312.

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37

Kinlay, Scott, Jasmine Grewal, Deborah Manuelin, et al. "Coronary Flow Velocity and Disturbed Flow Predict Adverse Clinical Outcome After Coronary Angioplasty." Arteriosclerosis, Thrombosis, and Vascular Biology 22, no. 8 (2002): 1334–40. http://dx.doi.org/10.1161/01.atv.0000024569.80106.b4.

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38

Heitmann, F., M. Juling, and J. Steinbock. "Performance of the LDA Volumetric Flow Rate Standard Under Severely Disturbed Flow Conditions." Flow Measurement and Instrumentation 74 (August 2020): 101756. http://dx.doi.org/10.1016/j.flowmeasinst.2020.101756.

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39

Reddy, R. V., and G. S. Lakhina. "Shear flow instabilities in the Earth's magnetotail." Annales Geophysicae 14, no. 8 (1996): 786–93. http://dx.doi.org/10.1007/s00585-996-0786-z.

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Abstract. Shear flow instability is studied in the Earth's magnetotail by treating plasma as compressible. A dispersion relation is derived from the linearized MHD equations using the oscillating boundary conditions at the inner central plasma sheet/outer central plasma sheet (OCPS) interface and OCPS/plasma-sheet boundary layer (PSBL) interface, whereas the surface-mode boundary condition is used at the PSBL/lobe interface. The growth rates and the real frequencies are obtained numerically for near-Earth (∣X∣~10–15 RE) and far-Earth (∣X∣~100 RE) magnetotail parameters. The periods and wavelengths of excited modes depend sensitively on the value of plasma-sheet half thickness, L, which is taken as L=5 RE for quiet time and L=1 RE for disturbed time. The plasma-sheet region is found to be stable for constant plasma flows unless MA3>1.25, where MA3 is the Alfvén Mach number in PSBL. For near-Earth magnetotail, the excited oscillations have periods of 2–20 min (quiet time) and 0.5–4 min (disturbed time) with typical transverse wavelengths of 2–30 RE and 0.5–6.5 RE, respectively; whereas for distant magnetotail, the analysis predicts the oscillation periods of ~8–80 min for quiet periods and 2–16 min for disturbed periods.

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40

Heo, Kyung-Sun, Hakjoo Lee, Patrizia Nigro та ін. "PKCζ mediates disturbed flow-induced endothelial apoptosis via p53 SUMOylation". Journal of Cell Biology 193, № 5 (2011): 867–84. http://dx.doi.org/10.1083/jcb.201010051.

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Atherosclerosis is readily observed in regions of blood vessels where disturbed blood flow (d-flow) is known to occur. A positive correlation between protein kinase C ζ (PKCζ) activation and d-flow has been reported, but the exact role of d-flow–mediated PKCζ activation in atherosclerosis remains unclear. We tested the hypothesis that PKCζ activation by d-flow induces endothelial cell (EC) apoptosis by regulating p53. We found that d-flow–mediated peroxynitrite (ONOO−) increased PKCζ activation, which subsequently induced p53 SUMOylation, p53–Bcl-2 binding, and EC apoptosis. Both d-flow and ONOO− increased the association of PKCζ with protein inhibitor of activated STATy (PIASy) via the Siz/PIAS-RING domain (amino acids 301–410) of PIASy, and overexpression of this domain of PIASy disrupted the PKCζ–PIASy interaction and PKCζ-mediated p53 SUMOylation. En face confocal microscopy revealed increases in nonnuclear p53 expression, nitrotyrosine staining, and apoptosis in aortic EC located in d-flow areas in wild-type mice, but these effects were significantly decreased in p53−/− mice. We propose a novel mechanism for p53 SUMOylation mediated by the PKCζ–PIASy interaction during d-flow–mediated EC apoptosis, which has potential relevance to early events of atherosclerosis.

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Yin, Dongxiao, Hao Wen, Guangqi Wu, et al. "PEGylated gene carriers in serum under shear flow." Soft Matter 16, no. 9 (2020): 2301–10. http://dx.doi.org/10.1039/c9sm02397f.

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Hansen, AJ. "Disturbed Ion Gradients in Brain Anoxia." Physiology 2, no. 2 (1987): 54–57. http://dx.doi.org/10.1152/physiologyonline.1987.2.2.54.

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Anoxia profundly affects brain function. If the blood flow is interrupted for a few minutes, the interstitial fluid shows a dramatic increase of potassium and lowering of sodium, chloride, and calcium concentrations, which lead to arrest of nerve conduction and synaptic transmission. These changes, however, cannot explain that consciousness is lost within seconds. This may be caused by activation of potassium conductance in nerve cell membranes.

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Liu, Xiao, Yubo Fan, X. Yun Xu, and Xiaoyan Deng. "Nitric oxide transport in an axisymmetric stenosis." Journal of The Royal Society Interface 9, no. 75 (2012): 2468–78. http://dx.doi.org/10.1098/rsif.2012.0224.

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To test the hypothesis that disturbed flow can impede the transport of nitric oxide (NO) in the artery and hence induce atherogenesis, we used a lumen–wall model of an idealized arterial stenosis with NO produced at the blood vessel–wall interface to study the transport of NO in the stenosis. Blood flows in the lumen and through the arterial wall were simulated by Navier–Stokes equations and Darcy's Law, respectively. Meanwhile, the transport of NO in the lumen and the transport of NO within the arterial wall were modelled by advection–diffusion reaction equations. Coupling of fluid dynamics at the endothelium was achieved by the Kedem–Katchalsky equations. The results showed that both the hydraulic conductivity of the endothelium and the non-Newtonian viscous behaviour of blood had little effect on the distribution of NO. However, the blood flow rate, stenosis severity, red blood cells (RBCs), RBC-free layer and NO production rate at the blood vessel–wall interface could significantly affect the transport of NO. The theoretical study revealed that the transport of NO was significantly hindered in the disturbed flow region distal to the stenosis. The reduced NO concentration in the disturbed flow region might play an important role in the localized genesis and development of atherosclerosis.

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Takabe, Wakako, Noah Alberts-Grill, and Hanjoong Jo. "Disturbed flow: p53 SUMOylation in the turnover of endothelial cells." Journal of Cell Biology 193, no. 5 (2011): 805–7. http://dx.doi.org/10.1083/jcb.201104140.

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Disturbed blood flow induces apoptosis of vascular endothelial cells, which causes atherosclerosis. In this issue, Heo et al. (2011. J. Cell Biol. doi:10.1083/jcb.201010051) sheds light on p53’s role in this phenomenon. Disturbed flow induces peroxynitrite production, which activates protein kinase C ζ and it’s binding to the E3 SUMO (small ubiquitin-like modifier) ligase PIASy (protein inhibitor of activated STATy). This leads to p53 SUMOylation and its export to the cytosol, where it binds to the antiapoptotic protein Bcl-2 to induce apoptosis.

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Yao, Xin, and Lingjing Li. "Spatial-Temporal Assessment of Debris Flow Risk in the Ms8.0 Wenchuan Earthquake-Disturbed Area." Journal of Disaster Research 11, no. 4 (2016): 720–31. http://dx.doi.org/10.20965/jdr.2016.p0720.

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For 5 years (2009–2013) after the 2008 Ms8.0 Wenchuan earthquake, rainfall led to the transformation of unconsolidated co-seismic deposits into extensive and severe debris flows, causing significant loss of life and property. For debris flows in the earthquake-disturbed area, a few common concerns exist. What is their spatial-temporal distribution? What are the controlling factors? How much is the rainfall threshold for debris flows? What areas are more susceptible? Where suffered the most severe losses of life and property? Using debris flow characteristics, this study analyzes the relationships between seismic geological factors, geomorphologic factors, extreme rainfall, and debris flows in the 5 years following the earthquake, and draws the following conclusions. (1) There are regional differences in the rainfall threshold for generation of debris flows, and the annual maximum 72-hour accumulated rainfall for triggering a debris flow decreases from pre-seismic periods (135–325 mm) to post-seismic periods (75–160 mm) by 44.4–50.8% in study area. (2) Areas with high debris flow susceptibility and hazard are primarily controlled by seismic geological conditions. (3) The long-term risk of debris flows will fall to moderate, and the affected area will shrink to that around the seismogenic fault. The results of this study will help with meteorological early warning systems, deployment of disaster prevention and control projects, and reconstruction site selection in the post-seismic Longmen Mountain area.

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Albarrán-Juárez, Julián, Andras Iring, ShengPeng Wang, et al. "Piezo1 and Gq/G11 promote endothelial inflammation depending on flow pattern and integrin activation." Journal of Experimental Medicine 215, no. 10 (2018): 2655–72. http://dx.doi.org/10.1084/jem.20180483.

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The vascular endothelium is constantly exposed to mechanical forces, including fluid shear stress exerted by the flowing blood. Endothelial cells can sense different flow patterns and convert the mechanical signal of laminar flow into atheroprotective signals, including eNOS activation, whereas disturbed flow in atheroprone areas induces inflammatory signaling, including NF-κB activation. How endothelial cells distinguish different flow patterns is poorly understood. Here we show that both laminar and disturbed flow activate the same initial pathway involving the mechanosensitive cation channel Piezo1, the purinergic P2Y2 receptor, and Gq/G11-mediated signaling. However, only disturbed flow leads to Piezo1- and Gq/G11-mediated integrin activation resulting in focal adhesion kinase-dependent NF-κB activation. Mice with induced endothelium-specific deficiency of Piezo1 or Gαq/Gα11 show reduced integrin activation, inflammatory signaling, and progression of atherosclerosis in atheroprone areas. Our data identify critical steps in endothelial mechanotransduction, which distinguish flow pattern-dependent activation of atheroprotective and atherogenic endothelial signaling and suggest novel therapeutic strategies to treat inflammatory vascular disorders such as atherosclerosis.

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HA, CHANG HOON, SUNGHYEN KIM, JIHWA CHUNG, et al. "Inhibitory effect of soluble RAGE in disturbed flow-induced atherogenesis." International Journal of Molecular Medicine 32, no. 2 (2013): 373–80. http://dx.doi.org/10.3892/ijmm.2013.1393.

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Nesic, S., and J. Postlethwaite. "Relationship Between the Structure of Disturbed Flow and Erosion—Corrosion." CORROSION 46, no. 11 (1990): 874–80. http://dx.doi.org/10.5006/1.3580852.

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Müller, M., H. P. Putzke, E. Siegmund, and W. Dummler. "Significance of disturbed lymph flow for the pathogenesis of pancreatitis." Experimental pathology 33, no. 2 (1988): 95–101. http://dx.doi.org/10.1016/s0232-1513(88)80132-4.

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Faller, Alan J. "Instability and transition of disturbed flow over a rotating disk." Journal of Fluid Mechanics 230 (September 1991): 245–69. http://dx.doi.org/10.1017/s0022112091000782.

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Disturbed flow over a rotating disk can lead to transition of the von Kármán boundary layer at a much lower Reynolds number, Re, (i.e. smaller radius) than that due to the well-known Type 1 stationary mode of instability. This early transition is due to the excitation of the Type 2 instability, similar to that found in the Ekman layer. Detailed numerical values of the growth rates, phase speeds, group velocities, neutral curves, and other characteristics of these two instabilities have been calculated over a wide range of parameters. Neutral curves for the Ekman and Bödewadt boundary layers also are presented. The minimum critical Reynolds numbers for the von Kármán, Ekman and Bödewadt layers are Rec(2) = 69.4, 54.3, and 15.1 with wavelengths L = 22.5, 20.1, and 16.6 and at angles ε = −19.0°, −23.1°, and −33.2°, respectively. These minimum critical values frequently do not well describe laboratory observations, however, because at larger Re other modes grow more rapidly and dominate the flow.The computed results are in excellent agreement with laboratory observations wherever comparison is possible. The growth of representative Type 1 instabilities with radius is shown to lead to N-factors greater than 9 at Re = 520 as appears to be necessary for transition to turbulence by the interaction of Type 1 with the basic flow. The growth of Type 2 instabilities with radius can lead to three additional mechanisms of transition. The necessary levels of excitation of Type 2 for these different mechanisms are estimated.A sequence of photographs from a ciné film illustrate one of the transition mechanisms discussed: the interaction of Type 2 instabilities and a secondary instability that is nearly perpendicular to the Type 2 vortices.

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