scholarly journals On the large difference between Benjamin’s and Hanratty’s formulations of perturbed flow over uneven terrain

2019 ◽  
Vol 871 ◽  
pp. 534-561
Author(s):  
Paolo Luchini ◽  
François Charru
Keyword(s):  
Boundary Layer ◽  
Shear Stress ◽  
Stress Response ◽  
Eddy Viscosity ◽  
Laminar Shear Stress ◽  
Uneven Terrain ◽  
Eddy Viscosity Model ◽  
Shear Stress Response ◽  
Sommerfeld Equation ◽  
Laminar Shear

Flow over an uneven terrain is a complex phenomenon that requires a chain of approximations in order to be studied. In addition to modelling the intricacies of turbulence if present, the problem is classically first linearized about a flat bottom and a locally parallel flow, and then asymptotically approximated into an interactive representation that couples a boundary layer and an irrotational region through an intermediate inviscid but rotational layer. The first of these steps produces a stationary Orr–Sommerfeld equation; since this is a one-dimensional problem comparatively easy for any computer, it would seem appropriate today to forgo the second sweep of approximation and solve the Orr–Sommerfeld problem numerically. However, the results are inconsistent! It appears that the asymptotic approximation tacitly restores some of the original problem’s non-parallelism. In order to provide consistent results, Benjamin’s version of the Orr–Sommerfeld equation needs to be modified into Hanratty’s. The large difference between Benjamin’s and Hanratty’s formulations, which arises in some wavenumber ranges but not in others, is here explained through an asymptotic analysis based on the concept of admittance and on the symmetry transformations of the boundary layer. A compact and accurate analytical formula is provided for the wavenumber range of maximum laminar shear-stress response. We highlight that the maximum turbulent shear-stress response occurs in the quasi-laminar regime at a Reynolds-independent wavenumber, contrary to the maximum laminar shear-stress response whose wavenumber scales with a power of the boundary-layer thickness. A numerical computation involving an eddy-viscosity model provides a warning against the inaccuracy of such a model. We emphasize that the range $k\unicode[STIX]{x1D708}/u_{\unicode[STIX]{x1D70F}}<10^{-3}$ of the spectrum remains essentially unexplored, and that the question is still open whether a fully developed turbulent regime, similar to the one predicted by an eddy-viscosity model, ever exists for open flow even in the limit of infinite wavelength.

The procyanidin-induced pseudo laminar shear stress response: a new concept for the reversal of endothelial dysfunction

2004 ◽  
Vol 107 (5) ◽  
pp. 513-517 ◽  
Author(s):  
Roger CORDER ◽  
Richard C. WARBURTON ◽  
Noorafza Q. KHAN ◽  
Ruth E. BROWN ◽  
Elizabeth G. WOOD ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Stress Response ◽  
Endothelial Dysfunction ◽  
Grape Seed ◽  
Similar Response ◽  
Laminar Shear Stress ◽  
Shear Stress Response ◽  
Laminar Shear

Reduced endothelium-dependent vasodilator responses with increased synthesis of ET-1 (endothelin-1) are characteristics of endothelial dysfunction in heart failure and are predictive of mortality. Identification of treatments that correct these abnormalities may have particular benefit for patients who become refractory to current regimens. Hawthorn preparations have a long history in the treatment of heart failure. Therefore we tested their inhibitory effects on ET-1 synthesis by cultured endothelial cells. These actions were compared with that of GSE (grape seed extract), as the vasoactive components of both these herbal remedies are mainly oligomeric flavan-3-ols called procyanidins. This showed extracts of hawthorn and grape seed were equipotent as inhibitors of ET-1 synthesis. GSE also produced a potent endothelium-dependent vasodilator response on preparations of isolated aorta. Suppression of ET-1 synthesis at the same time as induction of endothelium-dependent vasodilation is a similar response to that triggered by laminar shear stress. Based on these results and previous findings, we hypothesize that through their pharmacological properties procyanidins stimulate a pseudo laminar shear stress response in endothelial cells, which helps restore endothelial function and underlies the benefit from treatment with hawthorn extract in heart failure.

Epigenetic histones modification and cardiovascular lineage programming in mouse embryonic stem cells exposed to laminar shear stress

2006 ◽  
Vol 45 (3) ◽  
pp. e56
Author(s):  
Barbara Illi ◽  
Alessandro Scopece ◽  
Simona Nanni ◽  
Antonella Farsetti ◽  
Liliana Morgante ◽  
...  
Keyword(s):  
Stem Cells ◽  
Shear Stress ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cells ◽  
Laminar Shear Stress ◽  
Laminar Shear

scholarly journals Laminar shear stress upregulates endothelial Ca2+-activated K+ channels KCa2.3 and KCa3.1 via a Ca2+/calmodulin-dependent protein kinase kinase/Akt/p300 cascade

2013 ◽  
Vol 305 (4) ◽  
pp. H484-H493 ◽  
Author(s):  
Jun Takai ◽  
Alexandra Santu ◽  
Haifeng Zheng ◽  
Sang Don Koh ◽  
Masanori Ohta ◽  
...  
Keyword(s):  
Shear Stress ◽  
Transcriptional Activation ◽  
Static Condition ◽  
Fold Increase ◽  
Laminar Shear Stress ◽  
Human Coronary Artery ◽  
Intracellular Ca ◽  
Kinase Cascade ◽  
Dependent Protein ◽  
Laminar Shear

In endothelial cells (ECs), Ca2+-activated K+ channels KCa2.3 and KCa3.1 play a crucial role in the regulation of arterial tone via producing NO and endothelium-derived hyperpolarizing factors. Since a rise in intracellular Ca2+ levels and activation of p300 histone acetyltransferase are early EC responses to laminar shear stress (LS) for the transcriptional activation of genes, we examined the role of Ca2+/calmodulin-dependent kinase kinase (CaMKK), the most upstream element of a Ca2+/calmodulin-kinase cascade, and p300 in LS-dependent regulation of KCa2.3 and KCa3.1 in ECs. Exposure to LS (15 dyn/cm2) for 24 h markedly increased KCa2.3 and KCa3.1 mRNA expression in cultured human coronary artery ECs (3.2 ± 0.4 and 45 ± 10 fold increase, respectively; P < 0.05 vs. static condition; n = 8–30), whereas oscillatory shear (OS; ± 5 dyn/cm2 × 1 Hz) moderately increased KCa3.1 but did not affect KCa2.3. Expression of KCa2.1 and KCa2.2 was suppressed under both LS and OS conditions, whereas KCa1.1 was slightly elevated in LS and unchanged in OS. Inhibition of CaMKK attenuated LS-induced increases in the expression and channel activity of KCa2.3 and KCa3.1, and in phosphorylation of Akt (Ser473) and p300 (Ser1834). Inhibition of Akt abolished the upregulation of these channels by diminishing p300 phosphorylation. Consistently, disruption of the interaction of p300 with transcription factors eliminated the induction of these channels. Thus a CaMKK/Akt/p300 cascade plays an important role in LS-dependent induction of KCa2.3 and KCa3.1 expression, thereby regulating EC function and adaptation to hemodynamic changes.

An Assessment of Three-Dimensional Turbulent Boundary Layer Prediction Methods

1973 ◽  
Vol 95 (3) ◽  
pp. 415-421 ◽  
Author(s):  
A. J. Wheeler ◽  
J. P. Johnston
Keyword(s):  
Boundary Layer ◽  
Eddy Viscosity ◽  
Three Dimensional ◽  
High Sensitivity ◽  
Boundary Layer Flows ◽  
Mean Velocity ◽  
Eddy Viscosity Model ◽  
Separating Flow ◽  
Dimensional Boundary ◽  
Stress Models

Predictions have been made for a variety of experimental three-dimensional boundary layer flows with a single finite difference method which was used with three different turbulent stress models: (i) an eddy viscosity model, (ii) the “Nash” model, and (iii) the “Bradshaw” model. For many purposes, even the simplest stress model (eddy viscosity) was adequate to predict the mean velocity field. On the other hand, the profile of shear stress direction was not correctly predicted in one case by any model tested. The high sensitivity of the predicted results to free stream pressure gradient in separating flow cases is demonstrated.

scholarly journals Laminar Shear Stress Inhibits Endothelial Cell Metabolism via KLF2-Mediated Repression of PFKFB3

2015 ◽  
Vol 35 (1) ◽  
pp. 137-145 ◽  
Author(s):  
Anuradha Doddaballapur ◽  
Katharina M. Michalik ◽  
Yosif Manavski ◽  
Tina Lucas ◽  
Riekelt H. Houtkooper ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Metabolism ◽  
Laminar Shear Stress ◽  
Laminar Shear ◽  
Endothelial Cell Metabolism

Endothelial albumin permeability is shear dependent, time dependent, and reversible

1991 ◽  
Vol 260 (6) ◽  
pp. H1992-H1996 ◽  
Author(s):  
H. Jo ◽  
R. O. Dull ◽  
T. M. Hollis ◽  
J. M. Tarbell
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluorescein Isothiocyanate ◽  
Vascular Wall ◽  
Laminar Shear Stress ◽  
Aortic Endothelial Cells ◽  
Transendothelial Permeability ◽  
Steady Laminar Shear Stress ◽  
Laminar Shear

Altered permeability of vascular endothelium to macromolecules may play a role in vascular disease as well as vascular homeostasis. Because the shear stress of flowing blood on the vascular wall is known to influence many endothelial cell properties, an in vitro system to measure transendothelial permeability (Pe) to fluorescein isothiocyanate conjugated bovine serum albumin under defined physiological levels of steady laminar shear stress was developed. Bovine aortic endothelial cells grown on polycarbonate filters pretreated with gelatin and fibronectin constituted the model system. Onset of 1 dyn/cm2 shear stress resulted in a Pe rise from 5.1 +/- 1.3 x 10(-6) cm/s to 21.9 +/- 4.6 X 10(-6) cm/s at 60 min (n = 6); while 10 dyn/cm2 shear stress increased Pe from 4.8 +/- 1.5 X 10(-6) cm/s to 50.2 +/- 6.8 X 10(-6) cm/s at 30 min and 49.6 +/- 8.9 X 10(-6) cm/s at 60 (n = 9). Pe returned to preshear values within 120 and 60 min after removal of 1 and 10 dyn/cm2 shear stress, respectively. The data show that endothelial cell Pe in vitro is acutely sensitive to shear stress.

scholarly journals SENCR stabilizes vascular endothelial cell adherens junctions through interaction with CKAP4

2018 ◽  
Vol 116 (2) ◽  
pp. 546-555 ◽  
Author(s):  
Qing Lyu ◽  
Suowen Xu ◽  
Yuyan Lyu ◽  
Mihyun Choi ◽  
Christine K. Christie ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Noncoding Rna ◽  
Rna Binding ◽  
Adherens Junctions ◽  
Vascular Endothelial Cell ◽  
Membrane Integrity ◽  
Laminar Shear Stress ◽  
Loss Of Function ◽  
Laminar Shear

SENCR is a human-specific, vascular cell-enriched long-noncoding RNA (lncRNA) that regulates vascular smooth muscle cell and endothelial cell (EC) phenotypes. The underlying mechanisms of action of SENCR in these and other cell types is unknown. Here, levels of SENCR RNA are shown to be elevated in several differentiated human EC lineages subjected to laminar shear stress. Increases in SENCR RNA are also observed in the laminar shear stress region of the adult aorta of humanized SENCR-expressing mice, but not in disturbed shear stress regions. SENCR loss-of-function studies disclose perturbations in EC membrane integrity resulting in increased EC permeability. Biotinylated RNA pull-down and mass spectrometry establish an abundant SENCR-binding protein, cytoskeletal-associated protein 4 (CKAP4); this ribonucleoprotein complex was further confirmed in an RNA immunoprecipitation experiment using an antibody to CKAP4. Structure–function studies demonstrate a noncanonical RNA-binding domain in CKAP4 that binds SENCR. Upon SENCR knockdown, increasing levels of CKAP4 protein are detected in the EC surface fraction. Furthermore, an interaction between CKAP4 and CDH5 is enhanced in SENCR-depleted EC. This heightened association appears to destabilize the CDH5/CTNND1 complex and augment CDH5 internalization, resulting in impaired adherens junctions. These findings support SENCR as a flow-responsive lncRNA that promotes EC adherens junction integrity through physical association with CKAP4, thereby stabilizing cell membrane-bound CDH5.

scholarly journals Endothelial Barrier Function is co-regulated at Vessel Bifurcations by Fluid Forces and Sphingosine-1-Phosphate

2020 ◽  
Author(s):  
Ehsan Akbari ◽  
Griffin B. Spychalski ◽  
Miles M. Menyhert ◽  
Kaushik K. Rangharajan ◽  
Shaurya Prakash ◽  
...  
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Barrier Function ◽  
Endothelial Barrier ◽  
Laminar Shear Stress ◽  
Endothelial Barrier Function ◽  
Fluid Forces ◽  
Sphingosine 1 Phosphate ◽  
Laminar Shear ◽  
Vessel Bifurcations

AbstractSphingosine-1-phosphate (S1P) is a blood-borne bioactive lipid mediator of endothelial barrier function. Prior studies have implicated mechanical stimulation due to intravascular laminar shear stress in co-regulating S1P signaling in endothelial cells (ECs). Yet, vascular networks in vivo consist of vessel bifurcations, and this geometry produces hemodynamic forces that are distinct from laminar shear stress. However, the role of these forces at vessel bifurcations in regulating S1P-dependent endothelial barrier function is not known. In this study, we implemented a microfluidic platform that recapitulates the flow dynamics of vessel bifurcations with in situ quantification of the permeability of microvessel analogues. Co-application of S1P with impinging bifurcated fluid flow, which was characterized by approximately zero shear stress and 38 dyn cm-2 stagnation pressure at the vessel bifurcation point, promotes vessel stabilization. Similarly, co-treatment of carrier-free S1P with 3 dyn cm-2 laminar shear stress is also protective of endothelial barrier function. Moreover, it is shown that vessel stabilization due to laminar shear stress, but not bifurcated fluid flow, is dependent on S1P receptor 1 or 2 signaling. Collectively, these findings demonstrate the endothelium-protective function of fluid forces at vessel bifurcations and their involvement in coordinating S1P-dependent regulation of vessel permeability.

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