Oscillatory Shear Stress Research Articles

Influence of disturbed blood flow on endothelial function in people living with HIV

Abstract Introduction People infected with human immunodeficiency virus (HIV) are more susceptible to endothelial dysfunction due to the virus itself, side effects of the antiretroviral therapy and classical risk factors. Endothelial damage is most prominent at the locations where laminar blood flow is disturbed and oscillatory shear stress with retrograde blood flow is dominating. Purpose The goal of this study was to assess the endothelial function in people with HIV, and to determine whether their endothelium is more susceptible to a short-term increase in retrograde blood flow in comparison to healthy individuals. Methods The study included 62 people with HIV infection and 38 people without HIV infection, in whom endothelial function was assessed using flow-mediated dilatation, which was presented in absolute (FMD) and relative (FMD%) values. The intervention produced oscillatory shear stress and retrograde blood flow during 20 minutes, after which the endothelial function assessment was repeated. Results Baseline FMD (0.30±0.07 vs. 0.36±0.07 mm; p<0.05) and FMD% (6.84±1.57 vs. 7.89±1.19 %, p<0.05) were lower in the HIV group in compare to controls. FMD and FMD% decreased in the HIV group by 0.03 mm and 0.7% (p<0.05), while in the control group they decreased by 0.09 mm and 2.0% (p<0.05). The post-intervention FMD and FMD% were not different between the groups (p>0.05). Conclusion People with HIV infection express worse endothelial function in compare to healthy individuals. Retrograde blood flow and oscillatory shear stress deteriorate endothelial function in both HIV patients and healthy controls, although this decline is more pronounced in healthy individuals.

Piezo1-Mediated Mechanotransduction Contributes to Disturbed Flow-Induced Atherosclerotic Endothelial Inflammation.

Disturbed flow generates oscillatory shear stress (OSS), which in turn leads to endothelial inflammation and atherosclerosis. Piezo1, a biomechanical force sensor, plays a crucial role in the cardiovascular system. However, the specific role of Piezo1 in atherosclerosis remains to be fully elucidated. We detected the expression of Piezo1 in atherosclerotic mice and endothelial cells from regions with disturbed blood flow. The pharmacological inhibitor Piezo1 inhibitor (GsMTx4) was used to evaluate the impact of Piezo1 on plaque progression and endothelial inflammation. We examined Piezo1's direct response to OSS invitro and its effects on endothelial inflammation. Furthermore, mechanistic studies were conducted to explore the potential molecular cascade through which Piezo1 mediates endothelial inflammation in response to OSS. Our findings revealed the upregulation of Piezo1 in apoE-/- (apolipoprotein E) atherosclerotic mice, which is associated with disturbed flow. Treatment with GsMTx4 not only delayed plaque progression but also mitigated endothelial inflammation in both chronic and disturbed flow-induced atherosclerosis. Piezo1 was shown to facilitate calcium ions (Ca2+)influx in response to OSS, thereby activating endothelial inflammation. This inflammatory response was attenuated in the absence of Piezo1. Additionally, we identified that under OSS, Piezo1 activates the Ca2+/CaM/CaMKII (calmodulin/calmodulin-dependent protein kinases Ⅱ) pathways, which subsequently stimulate downstream kinases FAK (focal adhesion kinase) and Src. This leads to the activation of the OSS-sensitive YAP (yes-associated protein), ultimately triggering endothelial inflammation. Our study highlights the key role of Piezo1 in atherosclerotic endothelial inflammation, proposing the Piezo1-Ca2+/CaM/CaMKII-FAK/Src-YAP axis as a previously unknown endothelial mechanotransduction pathway. Piezo1 is expected to become a potential therapeutic target for atherosclerosis and cardiovascular diseases.

EPHB4-RASA1 Inhibition of PIEZO1 Ras Activation Drives Lymphatic Valvulogenesis.

EPHB4 (ephrin receptor B4) and the RASA1 (p120 Ras GTPase-activating protein) are necessary for the development of lymphatic vessel (LV) valves. However, precisely how EPHB4 and RASA1 regulate LV valve development is unknown. In this study, we examine the mechanisms by which EPHB4 and RASA1 regulate the development of LV valves. We used LV-specific inducible EPHB4-deficient mice and EPHB4 knockin mice that express a form of EPHB4 that is unable to bind RASA1 yet retains protein tyrosine kinase activity (EPHB4 2YP) to study the role of EPHB4 and RASA1 in LV valve development in the embryo and LV valve maintenance in adults. We also used human dermal lymphatic endothelial cells in vitro to study the role of EPHB4 and RASA1 as regulators of LV valve specification induced by oscillatory shear stress, considered the trigger for LV valve specification in vivo. LV valve specification, continued valve development postspecification, and LV valve maintenance were blocked upon induced loss of EPHB4 in LV. LV specification and maintenance were also impaired in EPHB4 2YP mice. Defects in LV development were reversed by inhibition of the Ras-MAPK (mitogen-activated protein kinase) signaling pathway. In human dermal lymphatic endothelial cells, loss of expression of EPHB4 or its ephrin b2 ligand, loss of expression of RASA1, and inhibition of physical interaction between EPHB4 and RASA1 resulted in dysregulated oscillatory shear stress-induced Ras-MAPK activation and impaired expression of LV specification markers that could be rescued by Ras-MAPK pathway inhibition. The same results were observed when human dermal lymphatic endothelial cells were stimulated with the Yoda1 agonist of the PIEZO1 oscillatory shear stress sensor. Although Yoda1 increased the number of LV valves when administered to wild-type embryos, it did not increase LV valve number when administered to EPHB4 2YP embryos. EPHB4 is necessary for LV valve specification, continued valve development postspecification, and valve maintenance. LV valve specification requires physical interaction between EPHB4 and RASA1 to limit activation of the Ras-MAPK pathway in lymphatic endothelial cells. Specifically, EPHB4-RASA1 physical interaction is necessary to dampen Ras-MAPK activation induced through the PIEZO1 oscillatory shear stress sensor. These findings reveal the mechanism by which EPHB4 and RASA1 regulate the development of LV valves.

Impact of peripheral venoarterial extracorporeal membrane oxygenation support for heart failure on systemic hemodynamics and aortic blood flow

Peripheral venoarterial extracorporeal membrane oxygenation (VA-ECMO) is an advanced temporary life support system for patients with refractory cardiogenic shock or severe cardiopulmonary failure. However, the reperfusion of oxygenated blood into the arterial system via a peripheral artery will induce substantial hemodynamic changes that might contribute to the development of complications. In this study, we developed two types of computational models to quantify the hemodynamic changes induced by the peripheral VA-ECMO support for systolic heart failure (HF) of various severities. One was a lumped-parameter model used for exploring the optimal workload of extracorporeal membrane oxygenation (ECMO) for a specific severity of HF, whereas the other one was a geometrical multiscale model capable of simulating the detailed flow field in the aorta while accounting for the hemodynamic coupling of VA-ECMO with the cardiovascular system. Numerical results revealed that the retrograde transmission of ECMO-supplied blood flow toward the heart not only considerably inhibited cardiac output but also induced marked flow disturbance and regionally high or oscillatory wall shear stress (WSS) in the aorta that may increase the risk of thrombosis and vascular dysfunction. The major characteristics of flow disturbance and spatial distribution of abnormal WSS were codetermined by the cardiac function and workload of ECMO while less influenced by the morphology of aorta. These findings emphasized the importance of tuning the workload of ECMO based on patient-specific cardiac function to balance the amount of blood oxygenation support by ECMO against the risk of complications associated with hemodynamic abnormalities.

Elucidating the hemodynamic impact of residual stenosis post-carotid artery stenting: A numerical study.

Residual stenosis (RS) and hemodynamics demonstrate a significant correlation with postoperative in-stent restenosis/thrombosis following carotid artery stenting (CAS). This study endeavors to elucidate the potential associations between RS and adverse postoperative hemodynamic factors. This study utilized 46 patient-specific carotid artery models post-stenting, which were categorized into two groups based on the presence of RS: the normal group (N, n=23) and the RS group (RS, n=23). A comparative analysis was conducted to evaluate the discrepancies in geometry and adverse hemodynamic parameters, alongside investigating the potential correlation between hemodynamic and geometric parameters. The results reveal that a higher reflux flow volume is discernible in the RS group during low-velocity phases of the cardiac cycle, concomitant with an augmented extent of areas exposed to oscillatory shear stress and extended particle residence time. Moreover, the adverse hemodynamic parameters exhibit a positive correlation with the degree of stent expansion, stent length in the common carotid artery (CCA), and the distal slope of the RS. The distal slope and tortuosity of RS significantly influence the development of adverse hemodynamic conditions post-stenting, exacerbating the hemodynamic environment near the stenosis. Interestingly, while an extended stent length in the internal carotid artery (ICA) region improves hemodynamics by reducing flow disturbance, a longer stent in the CCA significantly worsens these conditions. Hence, it is prudent to analyze the characteristics of the local lesion regions to optimize the strategy for stent implantation.

Low or oscillatory shear stress and endothelial permeability in atherosclerosis.

Endothelial shear stress is a tangential stress derived from the friction of the flowing blood on the endothelial surface of the arterial wall and is expressed in units of force/unit area (dyne/cm2). Branches and bends of arteries are exposed to complex blood flow patterns that generate low or oscillatory endothelial shear stress, which impairs glycocalyx integrity, cytoskeleton arrangement and endothelial junctions (adherens junctions, tight junctions, gap junctions), thus increasing endothelial permeability. The lipoproteins and inflammatory cells penetrating intima due to the increased endothelial permeability characterizes the pathological changes in early stage of atherosclerosis. Endothelial cells are critical sensors of shear stress, however, the mechanisms by which the complex shear stress regulate endothelial permeability in atherosclerosis remain unclear. In this review, we focus on the molecular mechanisms of the endothelial permeability induced by low or oscillatory shear stress, which will shed a novel sight in early stage of atherosclerosis.

Rictor, an mTORC2 Protein, Regulates Murine Lymphatic Valve Formation Through the AKT-FOXO1 Signaling.

Lymphatic valves are specialized structures in collecting lymphatic vessels and are crucial for preventing retrograde lymph flow. Mutations in valve-forming genes have been clinically implicated in the pathology of congenital lymphedema. Lymphatic valves form when oscillatory shear stress from lymph flow signals through the PI3K/AKT pathway to promote the transcription of valve-forming genes that trigger the growth and maintenance of lymphatic valves. Conventionally, in many cell types, AKT is phosphorylated at Ser473 by the mTORC2 (mammalian target of rapamycin complex 2). However, mTORC2 has not yet been implicated in lymphatic valve formation. In vivo and in vitro techniques were used to investigate the role of Rictor, a critical component of mTORC2, in lymphatic endothelium. Here, we showed that embryonic and postnatal lymphatic deletion of Rictor, a critical component of mTORC2, led to a significant decrease in lymphatic valves and prevented the maturation of collecting lymphatic vessels. RICTOR knockdown in human dermal lymphatic endothelial cells not only reduced the level of activated AKT and the expression of valve-forming genes under no-flow conditions but also abolished the upregulation of AKT activity and valve-forming genes in response to oscillatory shear stress. We further showed that the AKT target, FOXO1 (forkhead box protein O1), a repressor of lymphatic valve formation, had increased nuclear activity in Rictor knockout mesenteric lymphatic endothelial cells in vivo. Deletion of Foxo1 in Rictor knockout mice restored the number of valves to control levels in lymphatic vessels of the ear and mesentery. Our work identifies a novel role for RICTOR in the mechanotransduction signaling pathway, wherein it activates AKT and prevents the nuclear accumulation of the valve repressor, FOXO1, which ultimately enables the formation and maintenance of lymphatic valves.

Numerical simulation of non-Newtonian blood flow in a human arterial bifurcation model

Hemodynamic factors play a role in atherogenesis and the localization of atherosclerotic plaques. The human aorta and coronary arteries are susceptible to arterial disease, and there have been many studies of flows in models of these vessels. Atherosclerosis is a systemic disease occurring in specific sections of the cardiovascular tree such as the carotid and the coronary arteries. This paper aims to simulate the human arterial bifurcation and investigates some hemodynamic parameters as blood propagates from the aortic artery toward the carotid artery. We analyze the velocity, static pressure, shear stress. The simulation results showed disturbed flow patterns, such as flow separation and stagnation, as well as abnormal hemodynamic parameters (HPs) distributions including the low and high wall shear stress (WSS) and oscillation of wall shear stress. Based on our simulating characteristic results, the CFD tools can not only monitor the hemodynamic parameters obviously, but also help to analyze the diagnostic for the treatment of vascular diseases. CFD can be an effective technology for the examination and treatment of patients with failure of blood supply of the head and brain.

Targeting the tyrosine kinase Src in endothelium attenuates inflammation and atherogenesis induced by disturbed flow.

Previous studies have shown that Src can regulate inflammation and tumour progression. However, the mechanisms by which Src regulates the inflammatory response of vascular endothelium and atherogenesis are currently poorly understood. This study aimed to investigate the role of Src in endothelial inflammation and atherogenesis, as well as the underlying mechanisms. Real-time quantitative PCR was used to measure the mRNA levels of inflammatory genes. The phosphorylation and localization of proteins were examined using western blotting and immunofluorescence, respectively. The level of p-Src Y416 in mouse endothelium was directly determined using en face staining. Endothelial-specific knockdown of Src was achieved by tail vein injection of AAV-sgSrc in ApoE-/-; Cas9LSL/LSL; Cdh5-cre mice. Atherosclerosis was induced by partial ligation of the carotid artery. Oscillatory shear stress (OSS) promotes the phosphorylation of Src at Y416 in endothelial cells, and Piezo1 is required for this regulatory process. Overexpression of constitutively active Src promotes endothelial inflammation, as well as phosphorylation of Stat3 (at Y705) and its nuclear translocation. Endothelial inflammation induced by OSS was abolished by the Src inhibitor dasatinib or si-Src. Dasatinib, when administered orally, reduced endothelial inflammation and plaque formation in ApoE-/- mice induced by partial carotid artery ligation. Additionally, plaque formation was decreased in the ligated left carotid artery of mice with endothelial-specific Src knockdown. Disturbed flow promotes endothelial inflammation and atherogenesis through the Piezo1-Src-Stat3 pathway. Therefore, inhibiting Src in endothelial cells could be a promising therapeutic strategy to treat atherogenesis.

Computational model-based hemodynamic comparisons of traditional and modified idealized models of autologous radiocephalic fistula.

Autologous arteriovenous fistula (AVF) is a commonly used vascular access (VA) for hemodialysis, and hemodynamic changes are one of the main factors for its failure. To explore the effect of geometry on the hemodynamics in the AVF, a modified model is built with a gradual and smooth turn at the anastomosis and is compared with the traditional model, which has an abrupt sharp turn at the anastomisis. Transient computational fluid dynamics (CFD) simulations were performed for the comparison and analysis of the hemodynamic fields of the two models at different stages of the pulse cycle. The results showed that the low shear stress region and high oscillatory shear stress region in the modified AVF model coincided with regions of intimal hyperplasia that have been identified by previous studies. A comparison with the blood flow velocities measured in vivo was performed, and the error between the simulation results and the medical data was reduced by 22% in the modified model, which verifies the rationality and utility of the modified model.

The sphingosine-1-phosphate receptor 1 mediates the atheroprotective effect of eicosapentaenoic acid.

Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) have been associated with potential cardiovascular benefits, partly attributed to their bioactive metabolites. However, the underlying mechanisms responsible for these advantages are not fully understood. We previously reported that metabolites of the cytochrome P450 pathway derived from eicosapentaenoic acid (EPA) mediated the atheroprotective effect of ω-3 PUFAs. Here, we show that 17,18-epoxyeicosatetraenoic acid (17,18-EEQ) and its receptor, sphingosine-1-phosphate receptor 1 (S1PR1), in endothelial cells (ECs) can inhibit oscillatory shear stress- or tumor necrosis factor-α-induced endothelial activation in cultured human ECs. Notably, the atheroprotective effect of 17,18-EEQ and purified EPA is circumvented in male mice with endothelial S1PR1 deficiency. Mechanistically, the anti-inflammatory effect of 17,18-EEQ relies on calcium release-mediated endothelial nitric oxide synthase (eNOS) activation, which is abolished upon inhibition of S1PR1 or Gq signaling. Furthermore, 17,18-EEQ allosterically regulates the conformation of S1PR1 through a polar interaction with Lys34Nter. Finally, we show that Vascepa, a prescription drug containing highly purified and stable EPA ethyl ester, exerts its cardiovascular protective effect through the 17,18-EEQ-S1PR1 pathway in male and female mice. Collectively, our findings indicate that the anti-inflammatory effect of 17,18-EEQ involves the activation of the S1PR1-Gq-Ca2+-eNOS axis in ECs, offering a potential therapeutic target against atherosclerosis.

Abstract 3019: Piezo-1 Expression Decreases Under Disturbed Flow Model Of Femoral Atherosclerosis.

Background: Peripheral arterial disease (PAD) is often manifest by focal atherosclerotic plaque formation in the infra-inguinal arteries. However, murine models of atherosclerosis in the infra-inguinal arteries are lacking. It is well known that low and oscillatory wall shear stress, which occurs around blockages in PAD, promotes focal atherosclerotic plaque, but this has not been tested in vivo. Piezo1 is a mechanosensitive ion channel associated with hemodynamic changes in the arterial wall, but its role in flow-mediated atherosclerotic plaque deposition is not known. Objective: To develop a flow-mediated murine model of focal atherosclerotic plaque in the femoral arteries. Methods: 8 male and female S129 mice underwent partial femoral artery ligation (Figure A/B). Wall shear stress was calculated from duplex ultrasound imaging (Figure C/D). Atherogenic conditions were imposed with PCSK9 infection and high fat diet; this was initiated 1 week prior to partial femoral ligation. Histologic comparison of the left (partial femoral ligation) and right (normal stable flow) was performed. Results: Low wall shear stress was induced in this model (Figure C/D). Piezo1 expression was decreased in both male and female arteries under these conditions in this model (Figure E). Atherosclerotic plaque was induced by the partial femoral artery ligation but not on the normal stable flow side (Figure F). Conclusions: We have successfully developed a flow-mediated model of focal atherosclerotic plaque in murine femoral arteries. This is associated with downregulation of Piezo1 gene expression. Ongoing work is examining the causative role of Piezo1 on endothelial response to disturbed flow.

Abstract 1039: Endothelial Deletion Of Nck1 Reduces Atherosclerosis In Apoe-/- Mice Through The Nck1-atf3 Axis

The Nck family of signaling adaptors, including both Nck1 and Nck2, classically regulate cell motility during vascular development and postnatal angiogenesis. While Nck1 and Nck2 play redundant roles in this regard with deletion of both isoforms required to affect tissue remodeling, we demonstrated that global Nck1 deletion was sufficient to reduce atherosclerotic plaque formation and selective Nck1 inhibition reduces proinflammatory endothelial activation in response to oscillatory shear stress. Therefore, we sought to determine the role of endothelial Nck1 in atherosclerosis and ischemic angiogenesis using novel endothelial-specific Nck1 knockout mice. Endothelial-specific Nck1 deletion significantly reduced Western diet-induced atherosclerotic plaque formation at multiple sites compared to mice expressing endothelial-specific Cre alone or to endothelial-specific Nck2 knockout mice. This reduced plaque formation was characterized by diminished macrophage and smooth muscle incorporation despite enhanced weight gain in endothelial Nck1 knockout mice. RNA Sequencing analysis of endothelial cells in culture showed that Nck1 depletion reduces the expression of a variety of proinflammatory pathways but enhances the expression of genes involved in central carbon metabolism and proliferation. While Nck1 deletion is sufficient to blunt atherogenic inflammation, Nck1 inhibition did not affect angiogenesis or limb perfusion in the femoral artery ligation model of hind limb ischemia. To further characterized Nck1’s proinflammatory role, we utilized affinity precipitation-mass spectrometry and identified Activating Transcription Factor 3 ATF3 as a Nck1-selective binding partner. While no studies to date have examined endothelial ATF3 signaling in atherosclerosis, our preliminary data show that Nck1 is required for ATF3 expression in response to disturbed flow in vitro and in vivo , but the mechanism by which disturbed flow stimulates ATF3 expression remains unknown. ATF3 knockdown reduces disturbed flow-induced proinflammatory gene expression, suggesting that the Nck1-ATF3 signaling axis is a novel regulator of flow-induced inflammation.

EXPERIMENTAL STUDY OF NON-EQUILIBRIUM RHEOLOGICAL EFFECTS DURING THE FLOW OF PARAFFINIC OILS OF TIMAN-PECHORA BASIN. THIXOTROPY, SUPER ANOMALOUS VISCOSITY, OSCILLATIONS OF SHEAR STRESS

Laboratory experiments were carried out to study the non-stationary and non-equilibrium flow regimes of some paraffinic and high paraffinic crude oils of the Timan-Pechora Basin in a rotational viscometer. The presence of thixotropic properties (shear thinnig and hy steresis loops on the flow curves) is shown. The threshold character of the dependence of the area of the hysteresis loop on the oil tempera ture is demonstrated. Experiments have shown that under certain conditions on the flow curves of the studied oils, there are areas of a decrease in shear stress with an increase in shear rate, similar to areas of a «super anomalous» viscosity (SAV) in plastic lubricants. The shape and size of these areas, i.e. the intensity of the «superanomality» manifestation strongly depends on the experiment conditions and are poorly reproducible from experiment to experiment. In experiments, the SAV phenomenon at temperatures below the gelation temperature was always observed when the sample of paraffinic oil was at rest for a sufficiently long time before deformation. If, however, it was in the gap between the viscometer cylinders after the end of the next measurement cycle for a short time (no more than a few minutes), then at the next cycle of recording the flow curve, the SAV phenomenon can be practically imperceptible, although the hysteresis remains. Experiments show that if a sample of high paraffinic oil is deformed at a constant low shear rate, i.e. constant angular velocity of rotation of the device cylinder, and a temperature below the temperature of gelation, then on the falling curve of the dependence of shear stress on time («shear thinning»), oscillations in shear stress with a period equal to the period of rotation of the viscometer cylinder can be observed.

Oscillatory shear stress promotes endothelial senescence and atherosclerosis via STING activation

Endothelial dysfunction is an initiating factor in atherosclerosis. Endothelial cells (ECs) are constantly subject to blood flow shear stress, and atherosclerotic plaques tend to occur in aortic bends or bifurcations impaired by low oscillatory shear stress (OSS). However, the mechanism that how OSS affects the initiation and progression of atherosclerosis remains to be explored. Here, we first reported that OSS can promote endothelial dysfunction and atherogenesis in vivo and in vitro by activating STING pathway. Mechanistically, at atherosclerosis-prone areas, OSS caused mitochondria damage in ECs, leading to the leakage of mitochondrial DNA (mtDNA) into the cytoplasm. The cytoplasmic mtDNA was recognized by cGAS to produce cGAMP, activating the STING pathway and leading to endothelial senescence, which resulted in endothelial dysfunction and atherosclerosis. We found that STING was activated in plaques of atherosclerotic patients and in aortic arch ECs of high-fat diet (HFD)-fed ApoeKO mice, as well as in ECs exposed to OSS. STING-specific deficiency in ECs attenuates endothelial senescence and resulted in a significant reduction in aortic arch plaque area in HFD-fed ApoeKO mice. Consistently, specific deficiency or pharmacological inhibition of STING attenuated OSS-induced senescence and endothelial dysfunction. Pharmacological depletion of mtDNA ameliorated OSS-induced senescence and endothelial dysfunction. Taken together, our study linked hemodynamics and endothelial senescence, and revealed a novel mechanism by which OSS leads to endothelial dysfunction. Our study provided new insights into the development of therapeutic strategies for endothelial senescence and atherosclerosis.

Importance of sign conventions on analytical solutions to the wave-induced cyclic response of a poro-elastic seabed

This paper discusses the influence of different sign conventions for strains and stresses, i.e. the solid mechanics sign convention and the soil mechanics sign convention, on the form of governing partial differential equations (the static equilibrium equations and the continuity equation) used to describe the wave-induced cyclic response of a poro-elastic seabed due to propagation of a sinusoidal surface water-wave. Some selected analytical solutions, obtained by different authors and published in specialist literature in the form of complex functions describing the wave-induced pore-fluid pressure, effective normal stress and shear stress oscillations in the seabed, have been analysed and compared with each other mainly with respect to different sign conventions for stains and stresses and also with regard to different orientations of the positive vertical axis of the two-dimensional coordinate system and different directions of surface water-wave propagation. The performed analyses of the analytical solutions has indicated many inaccuracies, or even evident errors and exemplary mistakes of wrong-signed values of basic wave-induced response parameters (the shear stress in particular), thereby disqualifying these solutions and their final equations from practical engineering applications. Most of the mistakes found in the literature must be linked to authors’ lack of understanding and consistency in an uniform application of a certain sign convention for strains and stresses in the soil matrix at both stages of mathematical formulation of the governing problem and correct interpretation of equations of the final analytical solution. The present paper, based mostly on a thorough literature review, ought to draw attention and arouse interest among coastal scientists and engineers in proper identification and use of the existing analytical solutions to the wave-induced cyclic seabed response – solutions which differ very often in the applied sign convention for stresses in the soil matrix.

A Strange Result Regarding Some MHD Motions of Generalized Burgers’ Fluids with a Differential Expression of Shear Stress on the Boundary

In this work, we investigate isothermal MHD motions of a large class of rate type fluids through a porous medium between two infinite horizontal parallel plates when a differential expression of the non-trivial shear stress is prescribed on the boundary. Exact expressions are provided for the dimensionless steady state velocities, shear stresses and Darcy’s resistances. Obtained solutions can be used to find the necessary time to touch the steady state or to bring to light certain characteristics of the fluid motion. Graphical representations showed the fluid moves slower in presence of a magnetic field or porous medium. In addition, contrary to our expectations, the volume flux across a plane orthogonal to the velocity vector per unit width of this plane is zero. Finally, based on a simple remark regarding the governing equations of velocity and shear stress for MHD motions of incompressible generalized Burgers’ fluids between infinite parallel plates, provided were the first exact solutions for MHD motions of these fluids when the two plates apply oscillatory or constant shear stresses to the fluid. This important remark offers the possibility to solve any isothermal MHD motion of these fluids between infinite parallel plates or over an infinite plate when the non-trivial shear stress is prescribed on the boundary. As an application, steady state solutions for MHD motions of same fluids have been developed when a differential expression of the fluid velocity is prescribed on the boundary.

Viscous dissipation effect on amplitude and oscillating frequency of heat transfer and electromagnetic waves of magnetic driven fluid flow along the horizontal circular cylinder

The significant importance of present research is to remove the extreme temperature along the magnetic driven horizontal circular cylinder. The induced electromagnetic field is applied around the surface of cylinder. The main novelty of current research is to control thermal and magnetic boundary layer in the presence of viscous dissipation and induced electromagnetic field. The dimensional mathematical form is developed with defined boundary conditions. The dimensional equations are transformed into dimensionless equations to generate physical factors. The primitive form is used to reduce dimensionless equations into convenient form for smooth algorithm. The finite difference method with Gaussian elimination technique is applied for numerical results in FORTRAN language tool. The velocity, temperature and electromagnetic field are sketched graphically with asymptotic sequence. The oscillatory shear stress, oscillating heat rate and periodical current density is plotted graphically and numerically. It is found that fluid velocity improves significantly as buoyancy force increases around each position. It is noticed that the increasing oscillations in heat transfer are sketched for maximum choice of Prandtl number. It is found that the maximum oscillations in current density are obtained for each Eckert parameter. It is noticed that the significant distribution in temperature profile is obtained in the presence of viscous dissipation and magnetic field.

Effects of preoperative aortic tortuosity and postoperative hypertension on patient-specific hemodynamics of abdominal aortic aneurysm

Abdominal aortic aneurysm (AAA) is a serious dilated vascular disease. The risk factors of aneurysm rupture and postoperative blood pressure are the major clinical concerns. The purpose of this work is to analyze the hemodynamic difference between preoperative and postoperative AAA using patient-specific boundary conditions and explore the rupture risk of AAA with different torsion and to simulate the blood flow of different degrees of hypertension. A three-element Windkessel model is utilized as the outlet boundary condition. 20-sim software and self-developed user-defined functions are used to calibrate the parameters. To analyze the influence of aortic tortuosity on hemodynamics, five AAA geometries with different torsion degrees are modified and obtained. We also grade the hypertension and explore the effect of hypertension after operation. The analysis results are consistent with the patient-specific situation. The results show that stent implantation for aneurysms reduces the pressure at the lesion site and increase the speed and wall shear stress. Vessels with high torsion have lower time-averaged wall shear stress (TAWSS), higher oscillatory shear stress index (OSI) and relative retention time, and more disordered blood flow. After stent implantation, with the increase in blood pressure, TAWSS and OSI continue to increase, and the blood flow speed is also faster. AAA with high torsion is more likely to rupture. In clinical practice, attention should be paid to the degree of torsion of the lesion site. Furthermore, blood pressure should be monitored and controlled in time to prevent postoperative complications.

Hemodynamics in arterial bypass graft anastomoses with varying cuff sizes and proximal flow paths: a fluid–structure interaction study

This article investigates the effect of the cuff size of arterial bypass grafts and the flow conditions on the hemodynamics in the anastomosis (connection) to the artery, using numerical simulations. We consider a fluid-structure interaction problem which is solved based on a partitioned scheme. Additionally, we employ computational fluid dynamics to investigate the effect of a rigid wall assumption. The work focuses on clinically relevant hemodynamic quantities associated with the development of intimal hyperplasia. We also include a model for the prediction of hemolysis into the simulation. The results show that even minor changes of the cuff size can result into significant differences in the corresponding quantities of interest. The importance of the inflow path is shown to be lower than that of the cuff size. The usually employed rigid wall assumption is found to be adequate to address wall shear stress oscillations but falls short on predicting maximum and minimum wall shear stress-related quantities of interest.