Numerical simulation of flow-induced cavity noise in self-sustained oscillations

The generation and near-field radiation of aerodynamic sound from a low-speed unsteady flow over a two-dimensional automobile door cavity is simulated by using a source-extraction-based coupling method. In the coupling procedure, the unsteady cavity flow field is first computed solving the Reynolds averaged Navier–Stokes (RANS) equations. The radiated sound is then calculated by using a set of acoustic perturbation equations with acoustic source terms which are extracted from the time-dependent solutions of the unsteady flow. The aerodynamic and its resulting acoustic field are computed for the Reynolds number of 53,266 based on the base length of the cavity. The free stream flow velocity is taken to be 50.9m/s. As first stage of the numerical investigation of flow-induced cavity noise, laminar flow is assumed. The CFD solver is based on a cell-centered finite volume method. A dispersion-relation-preserving (DRP), optimized, fourth-order finite difference scheme with fully staggered-grid implementation is used in the acoustic solver

Numerical simulation of incompressible flow problems using an unstructured staggered mesh method

A number of two dimensional staggered unstructured discretisation schemes for the solution of fluid flow and heat transfer problems have been developed. All schemes store and solve velocity vector components at cell faces with scalar variables solved at cell centres. The velocity is resolved into face-normal and face-parallel components and the various schemes investigated differ in the treatment of the parallel component. Steady-state and time-dependent fluid flow and thermal energy equations are solved with the well known pressure correction scheme, SIMPLE, employed to couple continuity and momentum. The numerical methods developed are tested on well known benchmark cases: the Lid-Driven Cavity, Natural Convection in a Cavity and Melting of Gallium in a rectangular domain. The results obtained are shown to be comparable to benchmark, but with accuracy dependent on scheme selection.

Numerical solutions of certain nonlinear models in European options on a distributed computing environment

Financial modelling in the area of option pricing involves the understanding of the correlations between asset and movements of buy/sell in order to reduce risk in investment. Such activities depend on financial analysis tools being available to the trader with which he can make rapid and systematic evaluation of buy/sell contracts. In turn, analysis tools rely on fast numerical algorithms for the solution of financial mathematical models. There are many different financial activities apart from shares buy/sell activities. The main aim of this chapter is to discuss a distributed algorithm for the numerical solution of a European option. Both linear and non-linear cases are considered. The algorithm is based on the concept of the Laplace transform and its numerical inverse. The scalability of the algorithm is examined. Numerical tests are used to demonstrate the effectiveness of the algorithm for financial analysis. Time dependent functions for volatility and interest rates are also discussed. Applications of the algorithm to non-linear Black-Scholes equation where the volatility and the interest rate are functions of the option value are included. Some qualitative results of the convergence behaviour of the algorithm is examined. This chapter also examines the various computational issues of the Laplace transformation method in terms of distributed computing. The idea of using a two-level temporal mesh in order to achieve distributed computation along the temporal axis is introduced. Finally, the chapter ends with some conclusions.

A unified 3D model of the VAR process

A 3D time-dependent model of the VAR process has been developed using CFD techniques. The model solves the coupled field equations for fluid flow, heat transfer (including phase change) and electromagnetic field, for both the electrode and the ingot. The motion of the electic arc 'preferred spot' can be specified based on observations. Correlations are sought between the local gap height, resulting from instantaneous liquid pool surface shape and electrode tip shape, and the arc motion. The detailed behaviour of the melting film on the electrode tip is studies using a spectral free surface technique, which allows investigation of the drops' detachment and drip shorts.

Models for magnetohydrodynamics of aluminium electrolysis cells

The electric current and the associated magnetic field in aluminium electrolysis cells create effects limiting the cell productivity and possibly cause instabilities: surface waving, ‘anode effects’, erosion of pot lining, feed material sedimentation, etc. The instructive analysis is presented via a step by step inclusion of different physical coupling factors affecting the magnetic field, electric current, velocity and wave development in the electrolysis cells. The full time dependent model couples the nonlinear turbulent fluid dynamics and the extended electromagnetic field in the cell, and the whole bus bar circuit with the ferromagnetic effects. Animated examples for the high amperage cells are presented. The theory and numerical model of the electrolysis cell is extended to the cases of variable cell bottom of aluminium layer and the variable thickness of the electrolyte due to the anode non-uniform burn-out process and the presence of the anode channels. The problem of the channel importance is well known Moreau-Evans model) for the stationary interface and the velocity field, and was validated against measurements in commercial cells, particularly with the recently published ‘benchmark’ test for the MHD models of aluminium cells [1]. The presence of electrolyte channels requires also to reconsider the previous magnetohydrodynamic instability theories and the dynamic wave development models. The results indicate the importance of a ‘sloshing’ parametrically excited MHD wave development in the aluminium production cells.

Effect of varying electromagnetic field on the VAR process

The three-dimensional, time-dependent electromagnetic field arising from the precession of the arc centre in a vacuum arc remelting furnace is shown (in a numerical simulation) to affect the fluid flow and heat transfer conditions near the solidification front in the upper part of the ingot.

Magnetic damping of levitated liquid droplets in AC and DC field

The intense AC magnetic field required to produce levitation in terrestrial conditions, along with the buoyancy and thermo-capillary forces, results in turbulent convective flow within the droplet. The use of a homogenous DC magnetic field allows the convective flow to be damped. However the turbulence properties are affected at the same time, leading to a possibility that the effective turbulent damping is considerably reduced. The MHD modified K-Omega turbulence model allows the investigation of the effect of magnetic field on the turbulence. The model incorporates free surface deformation, the temperature dependent surface tension, turbulent momentum transport, electromagnetic and gravity forces. The model is adapted to incorporate a periodic laser heating at the top of the droplet, which have been used to measure the thermal conductivity of the material by calculating the phase lag between the frequency of the laser heating and the temperature response at the bottom. The numerical simulations show that with the gradual increase of the DC field the fluid flow within the droplet is initially increasing in intensity. Only after a certain threshold magnitude of the field the flow intensity starts to decrease. In order to achieve the flow conditions close to the ‘laminar’ a D.C. magnetic field >4 Tesla is required to measure the thermal conductivity accurately. The reduction in the AC field driven flow in the main body of the drop leads to a noticeable thermo-capillary convection at the edge of the droplet. The uniform vertical DC magnetic field does not stop a translational oscillation of the droplet along the field, which is caused by the variation in total levitation force due to the time-dependent surface deformation.

Modeling the structural breakdown of solder paste using the structural kinetic model

Solder paste is the most important strategic bonding material used in the assembly of surface mount devices in electronic industries. It is known to exhibit a thixotropic behavior, which is recognized by the decrease in apparent viscosity of paste material with time when subjected to a constant shear rate. The proper characterization of this time-dependent rheological behavior of solder pastes is crucial for establishing the relationships between the pastes structure and flow behavior; and for correlating the physical parameters with paste printing performance. In this article, we present a novel method which has been developed for characterizing the time-dependent and non-Newtonian rheological behavior of solder pastes and flux mediums as a function of shear rates. We also present results of the study of the rheology of the solder pastes and flux mediums using the structural kinetic modeling approach, which postulates that the network structure of solder pastes breaks down irreversibly under shear, leading to time and shear-dependent changes in the flow properties. Our results show that for the solder pastes used in the study, the rate and extent of thixotropy was generally found to increase with increasing shear rate. The technique demonstrated in this study has wide utility for R&D personnel involved in new paste formulation, for implementing quality control procedures used in solder-paste manufacture and packaging; and for qualifying new flip-chip assembly lines.

Effects of formalin preservation on stable carbon and nitrogen isotope signatures in Calanoid copepods: implications for the use of Continuous Plankton Recorder Survey samples in stable isotope analyses

Preserved and archived organic material offers huge potential for the conduct of retrospective and long-term historical ecosystem reconstructions using stable isotope analyses, but because of isotopic exchange with preservatives the obtained values require validation. The Continuous Plankton Recorder (CPR) Survey is the most extensive long-term monitoring program for plankton communities worldwide and has utilised ships of opportunity to collect samples since 1931. To keep the samples intact for subsequent analysis, they are collected and preserved in formalin; however, previous studies have found that this may alter stable carbon and nitrogen isotope ratios in zooplankton. A maximum ~0.9‰ increase of δ15N and a time dependent maximum ~1.0‰ decrease of δ13C were observed when the copepod, Calanus helgolandicus, was experimentally exposed to two formalin preservatives for 12 months. Applying specific correction factors to δ15N and δ13C values for similarly preserved Calanoid species collected by the CPR Survey within 12 months of analysis may be appropriate to enable their use in stable isotope studies. The isotope values of samples stored frozen did not differ significantly from those of controls. Although the impact of formalin preservation was relatively small in this and other studies of marine zooplankton, changes in isotope signatures are not consistent across taxa, especially for δ15N, indicating that species-specific studies may be required. Copyright © 2011 John Wiley & Sons, Ltd.

Towards An Acoustic Model-Based Poroelastic Imaging Method: I. Theoretical Foundation

The ultrasonic measurement and imaging of tissue elasticity is currently under wide investigation and development as a clinical tool for the assessment of a broad range of diseases, but little account in this field has yet been taken of the fact that soft tissue is porous and contains mobile fluid. The ability to squeeze fluid out of tissue may have implications for conventional elasticity imaging, and may present opportunities for new investigative tools. When a homogeneous, isotropic, fluid-saturated poroelastic material with a linearly elastic solid phase and incompressible solid and fluid constituents is subjected to stress, the behaviour of the induced internal strain field is influenced by three material constants: the Young's modulus (E(s)) and Poisson's ratio (nu(s)) of the solid matrix and the permeability (k) of the solid matrix to the pore fluid. New analytical expressions were derived and used to model the time-dependent behaviour of the strain field inside simulated homogeneous cylindrical samples of such a poroelastic material undergoing sustained unconfined compression. A model-based reconstruction technique was developed to produce images of parameters related to the poroelastic material constants (E(s), nu(s), k) from a comparison of the measured and predicted time-dependent spatially varying radial strain. Tests of the method using simulated noisy strain data showed that it is capable of producing three unique parametric images: an image of the Poisson's ratio of the solid matrix, an image of the axial strain (which was not time-dependent subsequent to the application of the compression) and an image representing the product of the aggregate modulus E(s)(1-nu(s))/(1+nu(s))(1-2nu(s)) of the solid matrix and the permeability of the solid matrix to the pore fluid. The analytical expressions were further used to numerically validate a finite element model and to clarify previous work on poroelastography.

Hepatocyte growth factor (HGF) protects c-met-expressing Burkitt''s lymphoma cell lines from apoptotic death induced by DNA damaging agents

The relative sensitivity of neoplastic cells to DNA damaging agents is a key factor in cancer therapy. In this paper, we show that pretreatment of Burkitt's lymphoma cell lines expressing the c-met protooncogene with hepatocyte growth factor (HGF) protects them from death induced by DNA damaging agents commonly used in tumour therapy. This protection was observed in assays based on morphological assessment of apoptotic cells and DNA fragmentation assays. The protection was dose- and time-dependent — maximal protection requiring pre-incubation with 100 ng/ml HGF for 48 h. Western blotting analysis and flow cytometric studies revealed that HGF inhibited doxorubicin- and etoposide-induced decreases in the levels of the anti-apoptotic proteins Bcl-XL, and to a lesser extent Bcl-2, without inducing changes in the pro-apoptotic Bax protein. Overall, these studies suggest that the accumulation of HGF within the microenvironment of neoplastic cells may contribute to the development of a chemoresistant phenotype.

APOLIPROTEIN(A)-INDUCED APOPTOSIS IN VASCULAR ENDOTHELIAL CELLS

Elevated plasma concentrations of lipoprotein(a) (Lp(a)) are a risk factor for a variety of atherosclerotic disorders including coronary heart disease. In the current study, the investigators report that incubation of cultured human umbilical vein endothelial cells (HUVECs) with high concentrations of apolipoprotein(a)(apo(a)/Lp(a)) induces apoptosis and endothelial dysfunction in a dose dependent manner. Apo(a), the component of Lp(a) mediates these effects by inducing externalization of Annexin V, DNA condensation and fragmentation which are the hallmarks of death by apoptosis. The pathway of apo(a)-induced apoptosis is associated with overexpression of Bax, caspase-9, p53 phosphorylation, decreased in Bcl-2 expression and activation of caspase-3. Taken together, the data suggest that elevated concentration of apo(a) induces apoptosis in endothelial cells probably by activating the intrinsic pathway. The data also showed that apo(a) induces increased expression of the growth arrest protein (Gas1), which has been known to induce apoptosis and growth arrest in vitro. In addition the data showed that elevated apo(a)/Lp(a) attenuates endothelial nitric oxide (eNOS) activity and endothelin-1 (ET-1) in a dose and time-dependent manner, particularly with small apo(a) isoforms. In summary, the authors proposed a new signaling pathway by which apo(a)/Lp(a) induce apoptosis and this finding could help explain how apo(a)/Lp(a) mediate atherosclerosis related diseases.

Double-electron above threshold ionization of helium

We present calculations of intense-field multiphoton ionization processes in helium at XUV wavelengths. The calculations are obtained from a full-dimensional integration of the two-electron time-dependent Schrödinger equation. A momentum-space analysis of the ionizing two-electron wavepacket reveals the existence of double-electron above threshold ionization (DATI). In momentum-space two distinct forms of DATI are resolved, namely non-sequential and sequential. In non-sequential DATI correlated electrons resonantly absorb and share energy in integer units of Ïlaser.

Role of p190RhoGAP in beta2 Integrin Regulation of RhoA in Human Neutrophils

We found that engagement of beta 2 integrins on human neutrophils induced activation of RhoA, as indicated by the increased ratio of GTP:GTP 1 GDP recovered on RhoA and translocation of RhoA to a membrane fraction. The clustering of beta 2 integrins also induced a time-dependent increase in GDP bound to RhoA, which correlated with beta 2 integrin-induced activation of p190RhoGAP. The activation of p190RhoGAP was completely blocked by [4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine] (PP1), a selective inhibitor of Src family tyrosine kinases. However, clustering of beta 2 integrins did not increase the basal tyrosine phosphorylation of p190RhoGAP, nor did it affect the amount of p120RasGAP bound to p190RhoGAP. Instead, the beta 2 integrin-induced activation of p190RhoGAP was accompanied by increased tyrosine phosphorylation of a p190RhoGAP-associated protein, p120RasGAP, and accumulation of both p120RasGAP and p190RhoGAP in a membrane fraction. PP1 blocked the beta 2 integrin-induced phosphorylation of p120RasGAP, as well as the translocation of p190RhoGAP and p120RasGAP, but it did not affect the accumulation of RhoA in the membrane fraction. In agreement with the mentioned findings, PP1 also increased the GTP:GTP 1 GDP ratio recovered on RhoA immunoprecipitated from beta2 integrin-stimulated cells. Thus, in neutrophils, beta 2 integrin-induced activation of p190RhoGAP requires a signal from a Src family tyrosine kinase, but it does not occur via the signaling pathway responsible for activation of RhoA.

Glucocorticoid induced muscle atrophy is associated with upregulation of myostatin gene expression

The mechanisms by which excessive glucocorticoids cause muscular atrophy remain unclear. We previously demonstrated that dexamethasone increases the expression of myostatin, a negative regulator of skeletal muscle mass, in vitro. In the present study, we tested the hypothesis that dexamethasone-induced muscle loss is associated with increased myostatin expression in vivo. Daily administration (60, 600, 1,200 micro g/kg body wt) of dexamethasone for 5 days resulted in rapid, dose-dependent loss of body weight (-4.0, -13.4, -17.2%, respectively, P <0.05 for each comparison), and muscle atrophy (6.3, 15.0, 16.6% below controls, respectively). These changes were associated with dose-dependent, marked induction of intramuscular myostatin mRNA (66.3, 450, 527.6% increase above controls, P <0.05 for each comparison) and protein expression (0.0, 260.5, 318.4% increase above controls, P <0.05). We found that the effect of dexamethasone on body weight and muscle loss and upregulation of intramuscular myostatin expression was time dependent. When dexamethasone treatment (600 micro g. kg-1. day-1) was extended from 5 to 10 days, the rate of body weight loss was markedly reduced to approximately 2% within this extended period. The concentrations of intramuscular myosin heavy chain type II in dexamethasone-treated rats were significantly lower (-43% after 5-day treatment, -14% after 10-day treatment) than their respective corresponding controls. The intramuscular myostatin concentration in rats treated with dexamethasone for 10 days returned to basal level. Concurrent treatment with RU-486 blocked dexamethasone-induced myostatin expression and significantly attenuated body loss and muscle atrophy. We propose that dexamethasone-induced muscle loss is mediated, at least in part, by the upregulation of myostatin expression through a glucocorticoid receptor-mediated pathway.