Characterization of Interfacial Corrosion Behavior of Hybrid Laminate EN AW-6082 ∪ CFRP.

The corrosion behavior of a hybrid laminate consisting of laser-structured aluminum EN AW-6082 ∪ carbon fiber-reinforced polymer was investigated. Specimens were corroded in aqueous NaCl electrolyte (0.1 mol/L) over a period of up to 31 days and characterized continuously by means of scanning electron and light microscopy, supplemented by energy dispersive X-ray spectroscopy. Comparative linear sweep voltammetry was employed on the first and seventh day of the corrosion experiment. The influence of different laser morphologies and production process parameters on corrosion behavior was compared. The corrosion reaction mainly arises from the aluminum component and shows distinct differences in long-term corrosion morphology between pure EN AW-6082 and the hybrid laminate. Compared to short-term investigations, a strong influence of galvanic corrosion on the interface is assumed. No distinct influences of different laser structuring and process parameters on the corrosion behavior were detected. Weight measurements suggest a continuous loss of mass attributed to the detachment of corrosion products.

Irregular dynamics of cellular blood flow in a model microvessel.

The flow of red blood cells within cylindrical vessels is complex and irregular, so long as the vessel diameter is somewhat larger than the nominal cell size. Long-time-series simulations, in which cells flow 10^{5} vessel diameters, are used to characterize the chaotic kinematics, particularly to inform reduced-order models. The simulation model used includes full coupling between the elastic red blood cell membranes and surrounding viscous fluid, providing a faithful representation of the cell-scale dynamics. Results show that the flow has neither classifiable recurrent features nor a dominant frequency. Instead, its kinematics are sensitive to the initial flow configuration in a way consistent with chaos and Lagrangian turbulence. Phase-space reconstructions show that a low-dimensional attractor does not exist, so the observed long-time dynamics are effectively stochastic. Based on this, a simple Markov chain model for the dynamics is introduced and shown to reproduce the statistics of the cell positions.

Anisotropic shear stress patterns predict the orientation of convergent tissue movements in the embryonic heart.

Myocardial contractility and blood flow provide essential mechanical cues for the morphogenesis of the heart. In general, endothelial cells change their migratory behavior in response to shear stress patterns, according to flow directionality. Here, we assessed the impact of shear stress patterns and flow directionality on the behavior of endocardial cells, the specialized endothelial cells of the heart. At the early stages of zebrafish heart valve formation, we show that endocardial cells are converging to the valve-forming area and that this behavior depends upon mechanical forces. Quantitative live imaging and mathematical modeling allow us to correlate this tissue convergence with the underlying flow forces. We predict that tissue convergence is associated with the direction of the mean wall shear stress and of the gradient of harmonic phase-averaged shear stresses, which surprisingly do not match the overall direction of the flow. This contrasts with the usual role of flow directionality in vascular development and suggests that the full spatial and temporal complexity of the wall shear stress should be taken into account when studying endothelial cell responses to flow in vivo.

Ultrasound-Induced Bubble Clusters in Tissue-Mimicking Agar Phantoms.

Therapeutic ultrasound can drive bubble activity that damages soft tissues. To study the potential mechanisms of such injury, transparent agar tissue-mimicking phantoms were subjected to multiple pressure wave bursts of the kind being considered specifically for burst wave lithotripsy. A high-speed camera recorded bubble activity during each pulse. Various agar concentrations were used to alter the phantom's mechanical properties, especially its stiffness, which was varied by a factor of 3.5. However, the maximum observed bubble radius was insensitive to stiffness. During 1000 wave bursts of a candidate burst wave lithotripsy treatment, bubbles appeared continuously in a region that expanded slowly, primarily toward the transducer. Denser bubble clouds are formed at higher pulse repetition frequency. The specific observations are used to inform the incorporation of damage mechanisms into cavitation models for soft materials.

Cavitation-induced damage of soft materials by focused ultrasound bursts: A fracture-based bubble dynamics model.

A generalized Rayleigh-Plesset-type bubble dynamics model with a damage mechanism is developed for cavitation and damage of soft materials by focused ultrasound bursts. This study is linked to recent experimental observations in tissue-mimicking polyacrylamide and agar gel phantoms subjected to bursts of a kind being considered specifically for lithotripsy. These show bubble activation at multiple sites during the initial pulses. More cavities appear continuously through the course of the observations, similar to what is deduced in pig kidney tissues in shock-wave lithotripsy. Two different material models are used to represent the distinct properties of the two gel materials. The polyacrylamide gel is represented with a neo-Hookean elastic model and damaged based upon a maximum-strain criterion; the agar gel is represented with a strain-hardening Fung model and damaged according to the strain-energy-based Griffith's fracture criterion. Estimates based upon independently determined elasticity and viscosity of the two gel materials suggest that bubble confinement should be sufficient to prevent damage in the gels, and presumably injury in some tissues. Damage accumulation is therefore proposed to occur via a material fatigue, which is shown to be consistent with observed delays in widespread cavitation activity.

Blood flow mechanics in cardiovascular development.

Hemodynamic forces are fundamental to development. Indeed, much of cardiovascular morphogenesis reflects a two-way interaction between mechanical forces and the gene network activated in endothelial cells via mechanotransduction feedback loops. As these interactions are becoming better understood in different model organisms, it is possible to identify common mechanogenetic rules, which are strikingly conserved and shared in many tissues and species. Here, we discuss recent findings showing how hemodynamic forces potentially modulate cardiovascular development as well as the underlying fluid and tissue mechanics, with special attention given to the flow characteristics that are unique to the small scales of embryos.

Algal cell disruption using microbubbles to localize ultrasonic energy.

Microbubbles were added to an algal solution with the goal of improving cell disruption efficiency and the net energy balance for algal biofuel production. Experimental results showed that disruption increases with increasing peak rarefaction ultrasound pressure over the range studied: 1.90 to 3.07 MPa. Additionally, ultrasound cell disruption increased by up to 58% by adding microbubbles, with peak disruption occurring in the range of 10(8)microbubbles/ml. The localization of energy in space and time provided by the bubbles improve efficiency: energy requirements for such a process were estimated to be one-fourth of the available heat of combustion of algal biomass and one-fifth of currently used cell disruption methods. This increase in energy efficiency could make microbubble enhanced ultrasound viable for bioenergy applications and is expected to integrate well with current cell harvesting methods based upon dissolved air flotation.

The wall-stress footprint of blood cells flowing in microvessels.

It is well known that mechanotransduction of hemodynamic forces mediates cellular processes, particularly those that lead to vascular development and maintenance. Both the strength and space-time character of these forces have been shown to affect remodeling and morphogenesis. However, the role of blood cells in the process remains unclear. We investigate the possibility that in the smallest vessels blood's cellular character of itself will lead to forces fundamentally different than the time-averaged forces usually considered, with fluctuations that may significantly exceed their mean values. This is quantitated through the use of a detailed simulation model of microvessel flow in two principal configurations: a diameter D=6.5 µm tube-a model for small capillaries through which red blood cells flow in single-file-and a D=12 µm tube-a model for a nascent vein or artery through which the cells flow in a confined yet chaotic fashion. Results in both cases show strong sensitivity to the mean flow speed U. Peak stresses exceed their means by greater than a factor of 10 when U/D≲10 s(-1), which corresponds to the inverse relaxation time of a healthy red blood cell. This effect is more significant for smaller D cases. At faster flow rates, including those more commonly observed under normal, nominally static physiological conditions, the peak fluctuations are more comparable with the mean shear stress. Implications for mechanotransduction of hemodynamic forces are discussed.

Simulation of platelet, thrombus and erythrocyte hydrodynamic interactions in a 3D arteriole with in vivo comparison.

Cylindrical blood vessels, ellipsoid platelets and biconcave-shaped deformable erythrocytes (RBCs) are important participants in hemostasis and thrombosis. However, due to the challenge of combining these components in simulation tools, few simulation studies have included all of them in realistic three-dimensional models. In the present study, we apply a recently developed simulation model to incorporate these components and analyze the flow in a thrombotic tubular arteriole, particularly the detailed hydrodynamic interactions between the thrombus shape, RBCs and platelets. It was found that at certain azimuth positions, the velocity drops in the proximity of both the upstream and downstream edge of the thrombus, which is accompanied by a rapid velocity increase in the narrowed region. The RBCs alter the flow profiles significantly from the typical low Reynolds (Re) number flow, and also enhance the deposition of free flowing platelets onto the thrombus. By evaluating the platelet-thrombus interaction and platelet-RBC interaction together, several mechanisms of platelet deposition augmentation are identified. With in vivo data comparison, our model illustrates the potential of future thrombosis studies that incorporate detailed receptor-ligand adhesion modules.

Pulse propagation by a capacitive mechanism drives embryonic blood flow.

Pulsatile flow is a universal feature of the blood circulatory system in vertebrates and can lead to diseases when abnormal. In the embryo, blood flow forces stimulate vessel remodeling and stem cell proliferation. At these early stages, when vessels lack muscle cells, the heart is valveless and the Reynolds number (Re) is low, few details are available regarding the mechanisms controlling pulses propagation in the developing vascular network. Making use of the recent advances in optical-tweezing flow probing approaches, fast imaging and elastic-network viscous flow modeling, we investigated the blood-flow mechanics in the zebrafish main artery and show how it modifies the heart pumping input to the network. The movement of blood cells in the embryonic artery suggests that elasticity of the network is an essential factor mediating the flow. Based on these observations, we propose a model for embryonic blood flow where arteries act like a capacitor in a way that reduces heart effort. These results demonstrate that biomechanics is key in controlling early flow propagation and argue that intravascular elasticity has a role in determining embryonic vascular function.

A Diffuse Interface Model with Immiscibility Preservation.

A new, simple, and computationally efficient interface capturing scheme based on a diffuse interface approach is presented for simulation of compressible multiphase flows. Multi-fluid interfaces are represented using field variables (interface functions) with associated transport equations that are augmented, with respect to an established formulation, to enforce a selected interface thickness. The resulting interface region can be set just thick enough to be resolved by the underlying mesh and numerical method, yet thin enough to provide an efficient model for dynamics of well-resolved scales. A key advance in the present method is that the interface regularization is asymptotically compatible with the thermodynamic mixture laws of the mixture model upon which it is constructed. It incorporates first-order pressure and velocity non-equilibrium effects while preserving interface conditions for equilibrium flows, even within the thin diffused mixture region. We first quantify the improved convergence of this formulation in some widely used one-dimensional configurations, then show that it enables fundamentally better simulations of bubble dynamics. Demonstrations include both a spherical bubble collapse, which is shown to maintain excellent symmetry despite the Cartesian mesh, and a jetting bubble collapse adjacent a wall. Comparisons show that without the new formulation the jet is suppressed by numerical diffusion leading to qualitatively incorrect results.

Forces on a wall-bound leukocyte in a small vessel due to red cells in the blood stream.

As part of the inflammation response, white blood cells (leukocytes) are well known to bind nearly statically to the vessel walls, where they must resist the force exerted by the flowing blood. This force is particularly difficult to estimate due to the particulate character of blood, especially in small vessels where the red blood cells must substantially deform to pass an adhered leukocyte. An efficient simulation tool with realistically flexible red blood cells is used to estimate these forces. At these length scales, it is found that the red cells significantly augment the streamwise forces that must be resisted by the binding. However, interactions with the red cells are also found to cause an average wall-directed force, which can be anticipated to enhance binding. These forces increase significantly as hematocrit values approach 25% and decrease significantly as the leukocyte is made flatter on the wall. For a tube hematocrit of 25% and a spherical protrusion with a diameter three-quarters that of the vessel, the average forces are increased by ~40% and the local forces are more than double those estimated with an effective-viscosity-homogenized blood. Both the enhanced streamwise and wall-ward forces and their unsteady character are potentially important in regard to binding mechanisms.

Fluid flows and forces in development: functions, features and biophysical principles.

Throughout morphogenesis, cells experience intracellular tensile and contractile forces on microscopic scales. Cells also experience extracellular forces, such as static forces mediated by the extracellular matrix and forces resulting from microscopic fluid flow. Although the biological ramifications of static forces have received much attention, little is known about the roles of fluid flows and forces during embryogenesis. Here, we focus on the microfluidic forces generated by cilia-driven fluid flow and heart-driven hemodynamics, as well as on the signaling pathways involved in flow sensing. We discuss recent studies that describe the functions and the biomechanical features of these fluid flows. These insights suggest that biological flow determines many aspects of cell behavior and identity through a specific set of physical stimuli and signaling pathways.

Effect of solid properties on slip at a fluid-solid interface.

The dependence of velocity slip at a liquid-solid interface upon the character of the solid is studied using atomistic simulation methods for Lennard-Jones model systems. The effect of the thermostatting mechanisms, often used in such simulations, is also investigated. The solid atom vibrational frequency is shown not to have a significant effect on the slip length for the range of parameters investigated; however, it is found that application of a thermostat to the fluid changes the slip length at low shear rates and results in an unphysical divergent slip behavior at high shear rates. On the other hand, removing the generated heat through the walls, which is more analogous to a laboratory condition, results in a nonlinearly decreasing slip length with shear rate that asymptotes to the no-slip limit at high shear rates. This effect is due to viscous heating, which increases the fluid temperature and pressure. A nonlinear relationship between the slip length and the shear rate collapses the shear-rate-slip-length dependence onto a single curve for a range of cases when heat is more realistically removed through the walls.

Mechanistic basis of otolith formation during teleost inner ear development.

Otoliths, which are connected to stereociliary bundles in the inner ear, serve as inertial sensors for balance. In teleostei, otolith development is critically dependent on flow forces generated by beating cilia; however, the mechanism by which flow controls otolith formation remains unclear. Here, we have developed a noninvasive flow probe using optical tweezers and a viscous flow model in order to demonstrate how the observed hydrodynamics influence otolith assembly. We show that rotational flow stirs and suppresses precursor agglomeration in the core of the cilia-driven vortex. The velocity field correlates with the shape of the otolith and we provide evidence that hydrodynamics is actively involved in controlling otolith morphogenesis. An implication of this hydrodynamic effect is that otolith self-assembly is mediated by the balance between Brownian motion and cilia-driven flow. More generally, this flow feature highlights an alternative biological strategy for controlling particle localization in solution.

Suppression of shocked-bubble expansion due to tissue confinement with application to shock-wave lithotripsy.

Estimates are made of the effect of tissue confinement on the response of small bubbles subjected to lithotriptor shock pressures. To do this the Rayleigh-Plesset equation, which governs the dynamics of spherical bubbles, is generalized to treat a bubble in a liquid region (blood), which is in turn encased within an elastic membrane (like a vessel's basement membrane), beyond which a Voigt viscoelastic material models the exterior tissue. Material properties are estimated from a range of measurements available for kidneys and similar soft tissues. Special attention is given to the constitutive modeling of the basement membranes because of their expected importance due to their proximity to the bubble and their toughness. It is found that the highest expected values for the elasticity of the membrane and surrounding tissue are insufficient to suppress bubble growth. The reduced confinement of a cylindrical vessel should not alter this conclusion. Tissue viscosities taken from ultrasound measurements suppress bubble growth somewhat, though not to a degree expected to resist injury. However, the higher reported viscosities measured by other means, which are arguably more relevant to the deformations caused by growing bubbles, do indeed significantly suppress bubble expansion.

A cumulative shear mechanism for tissue damage initiation in shock-wave lithotripsy.

Evidence suggests that inertial cavitation plays an important role in the renal injury incurred during shock-wave lithotripsy. However, it is unclear how tissue damage is initiated, and significant injury typically occurs only after a sufficient dose of shock waves. Although it has been suggested that shock-induced shearing might initiate injury, estimates indicate that individual shocks do not produce sufficient shear to do so. In this paper, we hypothesize that the cumulative shear of the many shocks is damaging. This mechanism depends on whether there is sufficient time between shocks for tissue to relax to its unstrained state. We investigate the mechanism with a physics-based simulation model, wherein the basement membranes that define the tubules and vessels in the inner medulla are represented as elastic shells surrounded by viscous fluid. Material properties are estimated from in-vitro tests of renal basement membranes and documented mechanical properties of cells and extracellular gels. Estimates for the net shear deformation from a typical lithotripter shock (approximately 0.1%) are found from a separate dynamic shock simulation. The results suggest that the larger interstitial volume (approximately 40%) near the papilla tip gives the tissue there a relaxation time comparable to clinical shock delivery rates (approximately 1 Hz), thus allowing shear to accumulate. Away from the papilla tip, where the interstitial volume is smaller (approximately 20%), the model tissue relaxes completely before the next shock would be delivered. Implications of the model are that slower delivery rates and broader focal zones should both decrease injury, consistent with some recent observations.

The effect of LVAD aortic outflow-graft placement on hemodynamics and flow: Implantation technique and computer flow modeling.

Axial-flow ventricular assist devices (VADs) can be implanted either through a left thoracotomy with outflow-graft anastomosis to the descending thoracic aorta or through a midline sternotomy with anastomosis to the ascending aorta. Each method has advantages and disadvantages. Because these VADs produce nonpulsatile flow, their hemodynamic characteristics differ from those of pulsatile devices. These differences may have important clinical consequences, particularly in relation to the outflow-graft configuration. We describe a computer-generated flow model that we created to illustrate the flow dynamics and possible clinical consequences of each method. The simulations indicate that the location of the anastomosis has important qualitative effects on flow in the ascending aorta and aortic arch. At high VAD outputs (> or =75%), native cardiac output cannot supply the carotid and subclavian arteries. With a descending aortic anastomosis, net backward flow occurs in the descending aorta to supply these branches. Consequently, the aortic arch has a region with almost no net flow, where fluid particles stagnate over many cardiac cycles, possibly causing thrombogenesis. With an ascending aortic anastomosis, the arch has no stagnant region, although flow turbulence still occurs. When the aortic valve remains closed, so that the total output occurs through the VAD, the aortic root has a region of nearly stagnant flow. With an ascending aortic anastomosis, a small degree of recirculatory flow may prevent complete stagnation at the aortic root. With the descending aortic anastomosis, however, no recirculation occurs. These results help delineate the complex flow dynamics and the advantages and drawbacks of each technique.