A fiber Bragg grating sensor system for train axle counting

Railway signaling facilitates two main functions, namely, train detection and train control, in order to maintain safe separations among the trains. Track circuits are the most commonly used train detection means with the simple open/close circuit principles; and subsequent adoption of axle counters further allows the detection of trains under adverse track conditions. However, with electrification and power electronics traction drive systems, aggravated by the electromagnetic interference in the vicinity of the signaling system, railway engineers often find unstable or even faulty operations of track circuits and axle counting systems, which inevitably jeopardizes the safe operation of trains. A new means of train detection, which is completely free from electromagnetic interference, is therefore required for the modern railway signaling system. This paper presents a novel optical fiber sensor signaling system. The sensor operation, field setup, axle detection solution set, and test results of an installation in a trial system on a busy suburban railway line are given.

A comprehensive condition monitoring of modern railway

The demand for high quality rail services in the twenty-first century has put an ever increasing demand on all rail operators. In order to meet the expectation of their patrons, the maintenance regime of railway systems has to be tightened up, the track conditions have to be well looked after, the rolling stock must be designed to withstand heavy duty. In short, in an ideal world where resources are unlimited, one needs to implement a very rigorous inspection regime in order to take care of the modem needs of a railway system [1]. If cost were not an issue, the maintenance engineers could inspect the train body by the most up-to-date techniques such as ultra-sound examination, x-ray inspection, magnetic particle inspection, etc. on a regular basis. However it is inconceivable to have such a perfect maintenance regime in any commercial railway. Likewise, it is impossible to have a perfect rolling stock which can weather all the heavy duties experienced in a modem railway. Hence it is essential that some condition monitoring schemes are devised to pick up potential defects which could manifest into safety hazards. This paper introduces an innovative condition monitoring system for track profile and, together with an instrumented car to carry out surveillance of the track, will provide a comprehensive railway condition monitoring system which is free from the usual difficulty of electromagnetic compatibility issues in a typical railway environment

Remediation strategies of shaft and common mode voltages in adjustable speed drive systems

AC motors are largely used in a wide range of modern systems, from household appliances to automated industry applications such as: ventilations systems, fans, pumps, conveyors and machine tool drives. Inverters are widely used in industrial and commercial applications due to the growing need for speed control in ASD systems. Fast switching transients and the common mode voltage, in interaction with parasitic capacitive couplings, may cause many unwanted problems in the ASD applications. These include shaft voltage and leakage currents. One of the inherent characteristics of Pulse Width Modulation (PWM) techniques is the generation of the common mode voltage, which is defined as the voltage between the electrical neutral of the inverter output and the ground. Shaft voltage can cause bearing currents when it exceeds the amount of breakdown voltage level of the thin lubricant film between the inner and outer rings of the bearing. This phenomenon is the main reason for early bearing failures. A rapid development in power switches technology has lead to a drastic decrement of switching rise and fall times. Because there is considerable capacitance between the stator windings and the frame, there can be a significant capacitive current (ground current escaping to earth through stray capacitors inside a motor) if the common mode voltage has high frequency components. This current leads to noises and Electromagnetic Interferences (EMI) issues in motor drive systems. These problems have been dealt with using a variety of methods which have been reported in the literature. However, cost and maintenance issues have prevented these methods from being widely accepted. Extra cost or rating of the inverter switches is usually the price to pay for such approaches. Thus, the determination of cost-effective techniques for shaft and common mode voltage reduction in ASD systems, with the focus on the first step of the design process, is the targeted scope of this thesis. An introduction to this research – including a description of the research problem, the literature review and an account of the research progress linking the research papers – is presented in Chapter 1. Electrical power generation from renewable energy sources, such as wind energy systems, has become a crucial issue because of environmental problems and a predicted future shortage of traditional energy sources. Thus, Chapter 2 focuses on the shaft voltage analysis of stator-fed induction generators (IG) and Doubly Fed Induction Generators DFIGs in wind turbine applications. This shaft voltage analysis includes: topologies, high frequency modelling, calculation and mitigation techniques. A back-to-back AC-DC-AC converter is investigated in terms of shaft voltage generation in a DFIG. Different topologies of LC filter placement are analysed in an effort to eliminate the shaft voltage. Different capacitive couplings exist in the motor/generator structure and any change in design parameters affects the capacitive couplings. Thus, an appropriate design for AC motors should lead to the smallest possible shaft voltage. Calculation of the shaft voltage based on different capacitive couplings, and an investigation of the effects of different design parameters are discussed in Chapter 3. This is achieved through 2-D and 3-D finite element simulation and experimental analysis. End-winding parameters of the motor are also effective factors in the calculation of the shaft voltage and have not been taken into account in previous reported studies. Calculation of the end-winding capacitances is rather complex because of the diversity of end winding shapes and the complexity of their geometry. A comprehensive analysis of these capacitances has been carried out with 3-D finite element simulations and experimental studies to determine their effective design parameters. These are documented in Chapter 4. Results of this analysis show that, by choosing appropriate design parameters, it is possible to decrease the shaft voltage and resultant bearing current in the primary stage of generator/motor design without using any additional active and passive filter-based techniques. The common mode voltage is defined by a switching pattern and, by using the appropriate pattern; the common mode voltage level can be controlled. Therefore, any PWM pattern which eliminates or minimizes the common mode voltage will be an effective shaft voltage reduction technique. Thus, common mode voltage reduction of a three-phase AC motor supplied with a single-phase diode rectifier is the focus of Chapter 5. The proposed strategy is mainly based on proper utilization of the zero vectors. Multilevel inverters are also used in ASD systems which have more voltage levels and switching states, and can provide more possibilities to reduce common mode voltage. A description of common mode voltage of multilevel inverters is investigated in Chapter 6. Chapter 7 investigates the elimination techniques of the shaft voltage in a DFIG based on the methods presented in the literature by the use of simulation results. However, it could be shown that every solution to reduce the shaft voltage in DFIG systems has its own characteristics, and these have to be taken into account in determining the most effective strategy. Calculation of the capacitive coupling and electric fields between the outer and inner races and the balls at different motor speeds in symmetrical and asymmetrical shaft and balls positions is discussed in Chapter 8. The analysis is carried out using finite element simulations to determine the conditions which will increase the probability of high rates of bearing failure due to current discharges through the balls and races.

Near infrared for non-destructive testing of articular cartilage

The concept of non-destructive testing (NDT) of materials and structures is of immense importance in engineering and medicine. Several NDT methods including electromagnetic (EM)-based e.g. X-ray and Infrared; ultrasound; and S-waves have been proposed for medical applications. This paper evaluates the viability of near infrared (NIR) spectroscopy, an EM method for rapid non-destructive evaluation of articular cartilage. Specifically, we tested the hypothesis that there is a correlation between the NIR spectrum and the physical and mechanical characteristics of articular cartilage such as thickness, stress and stiffness. Intact, visually normal cartilage-on-bone plugs from 2-3yr old bovine patellae were exposed to NIR light from a diffuse reflectance fibre-optic probe and tested mechanically to obtain their thickness, stress, and stiffness. Multivariate statistical analysis-based predictive models relating articular cartilage NIR spectra to these characterising parameters were developed. Our results show that there is a varying degree of correlation between the different parameters and the NIR spectra of the samples with R2 varying between 65 and 93%. We therefore conclude that NIR can be used to determine, nondestructively, the physical and functional characteristics of articular cartilage.

A simple orientation robust transmit polarization signalling scheme

A special transmit polarization signalling scheme is presented to alleviate the power reduction as a result of polarization mismatch from random antenna orientations. This is particularly useful for hand held mobile terminals typically equipped with only a single linearly polarized antenna, since the average signal power is desensitized against receiver orientations. Numerical simulations also show adequate robustness against incorrect channel estimations.

Applying incremental EM to Bayesian classifiers in the learning of hyperspectral remote sensing data

In this paper, we apply the incremental EM method to Bayesian Network Classifiers to learn and interpret hyperspectral sensor data in robotic planetary missions. Hyperspectral image spectroscopy is an emerging technique for geological investigations from airborne or orbital sensors. Many spacecraft carry spectroscopic equipment as wavelengths outside the visible light in the electromagnetic spectrum give much greater information about an object. The algorithm used is an extension to the standard Expectation Maximisation (EM). The incremental method allows us to learn and interpret the data as they become available. Two Bayesian network classifiers were tested: the Naive Bayes, and the Tree-Augmented-Naive Bayes structures. Our preliminary experiments show that incremental learning with unlabelled data can improve the accuracy of the classifier.

The low-affinity site of the β1-adrenoceptor and its relevance to cardiovascular pharmacology

β-Adrenoceptor blocking agents (β-blockers) that at low concentrations antagonize cardiostimulant effects of catecholamines, but at high concentrations also cause cardiostimulation, have been appearing since the late 1960s. These cardiostimulant β-blockers, coined non-conventional partial agonists, antagonize the effects of catecholamines through a high-affinity site (β1HAR), but cause cardiostimulation mainly through a low-affinity site (β1LAR) of the myocardial β1-adrenoceptor. The experimental non-conventional partial agonist (−)-CGP12177 increases cardiac L-type Ca2+ current density and Ca2+ transients, shortens action potential duration but augments action potential plateau, increases heart rate and force, as well as causes arrhythmic Ca2+ transients and arrhythmic cardiocyte contractions. Other β-blockers, which do not cause cardiostimulation, consistently have lower affinity for β1LAR than β1HAR. These sites were verified and the cardiac pharmacology of non-conventional partial agonists confirmed on recombinant β1-adrenoceptors and on β1-adrenoceptors overexpressed into the heart. A targeted mutation of Asp138 to Glu138 virtually abolished the pharmacology of β1HAR but left intact the pharmacology of β1LAR. Non-conventional partial agonists may be beneficial for the treatment of peripheral autonomic neuropathy but probably due to their arrhythmic propensities, may be harmful for the treatment of chronic heart failure.

Dimensions of coupling in middleware

It is well accepted that different types of distributed architectures require different degrees of coupling. For example, in client-server and three-tier architectures, application components are generally tightly coupled, both with one another and with the underlying middleware. Meanwhile, in off-line transaction processing, grid computing and mobile applications, the degree of coupling between application components and with the underlying middleware needs to be minimized. Terms such as ‘synchronous’, ‘asynchronous’, ‘blocking’, ‘non-blocking’, ‘directed’, and ‘non-directed’ are often used to refer to the degree of coupling required by an architecture or provided by a middleware. However, these terms are used with various connotations. Although various informal definitions have been provided, there is a lack of an overarching formal framework to unambiguously communicate architectural requirements with respect to (de-)coupling. This article addresses this gap by: (i) formally defining three dimensions of (de-)coupling; (ii) relating these dimensions to existing middleware; and (iii) proposing notational elements to represent various coupling integration patterns. This article also discusses a prototype that demonstrates the feasibility of its implementation.

In vitro and in vivo examination of the cell surface glycoprotein CDCP1

A number of reports have demonstrated the importance of the CUB domaincontaining protein 1 (CDCP1) in facilitating cancer progression in animal models and the potential of this protein as a prognostic marker in several malignancies. CDCP1 facilitates metastasis formation in animal models by negatively regulating anoikis, a type of apoptosis triggered by the loss of attachment signalling from cell-cell contacts or cell-extra cellular matrix (ECM) contacts. Due to the important role CDCP1 plays in cancer progression in model systems, it is considered a potential drug target to prevent the metastatic spread of cancers. CDCP1 is a highly glycosylated 836 amino acid cell surface protein. It has structural features potentially facilitating protein-protein interactions including 14 N-glycosylation sites, three CUB-like domains, 20 cysteine residues likely to be involved in disulfide bond formation and five intracellular tyrosine residues. CDCP1 interacts with a variety of proteins including Src family kinases (SFKs) and protein kinase C ä (PKCä). Efforts to understand the mechanisms regulating these interactions have largely focussed on three CDCP1 tyrosine residues Y734, Y743 and Y762. CDCP1-Y734 is the site where SFKs phosphorylate and bind to CDCP1 and mediate subsequent phosphorylation of CDCP1-Y743 and -Y762 which leads to binding of PKCä at CDCP1-Y762. The resulting trimeric protein complex of SFK•CDCP1•PKCä has been proposed to mediate an anti-apoptotic cell phenotype in vitro, and to promote metastasis in vivo. The effect of mutation of the three tyrosines on interactions of CDCP1 with SFKs and PKCä and the consequences on cell phenotype in vitro and in vivo have not been examined. CDCP1 has a predicted molecular weight of ~90 kDa but is usually detected as a protein which migrates at ~135 kDa by Western blot analysis due to its high degree of glycosylation. A low molecular weight form of CDCP1 (LMWCDCP1) of ~70 kDa has been found in a variety of cancer cell lines. The mechanisms leading to the generation of LMW-CDCP1 in vivo are not well understood but an involvement of proteases in this process has been proposed. Serine proteases including plasmin and trypsin are able to proteolytically process CDCP1. In addition, the recombinant protease domain of the serine protease matriptase is also able to cleave the recombinant extracellular portion of CDCP1. Whether matriptase is able to proteolytically process CDCP1 on the cell surface has not been examined. Importantly, proteolytic processing of CDCP1 by trypsin leads to phosphorylation of its cell surface-retained portion which suggests that this event leads to initiation of an intracellular signalling cascade. This project aimed to further examine the biology of CDCP1 with a main of focus on exploring the roles played by CDCP1 tyrosine residues. To achieve this HeLa cells stably expressing CDCP1 or the CDCP1 tyrosine mutants Y734F, Y743F and Y762F were generated. These cell lines were used to examine: • The roles of the tyrosine residues Y734, Y743 and Y762 in mediating interactions of CDCP1 with binding proteins and to examine the effect of the stable expression on HeLa cell morphology. • The ability of the serine protease matriptase to proteolytically process cell surface CDCP1 and to examine the consequences of this event on HeLa cell phenotype and cell signalling in vitro. • The importance of these residues in processes associated with cancer progression in vitro including adhesion, proliferation and migration. • The role of these residues on metastatic phenotype in vivo and the ability of a function-blocking anti-CDCP1 antibody to inhibit metastasis in the chicken embryo chorioallantoic membrane (CAM) assay. Interestingly, biochemical experiments carried out in this study revealed that mutation of certain CDCP1 tyrosine residues impacts on interactions of this protein with binding proteins. For example, binding of SFKs as well as PKCä to CDCP1 was markedly decreased in HeLa-CDCP1-Y734F cells, and binding of PKCä was also reduced in HeLa-CDCP1-Y762F cells. In contrast, HeLa-CDCP1-Y743F cells did not display altered interactions with CDCP1 binding proteins. Importantly, observed differences in interactions of CDCP1 with binding partners impacted on basal phosphorylation of CDCP1. It was found that HeLa-CDCP1, HeLa-CDCP1-Y743F and -Y762F displayed strong basal levels of CDCP1 phosphorylation. In contrast, HeLa-CDCP1-Y734F cells did not display CDCP1 phosphorylation but exhibited constitutive phosphorylation of focal adhesion kinase (FAK) at tyrosine 861. Significantly, subsequent investigations to examine this observation suggested that CDCP1-Y734 and FAK-Y861 are competitive substrates for SFK-mediated phosphorylation. It appeared that SFK-mediated phosphorylation of CDCP1- Y734 and FAK-Y861 is an equilibrium which shifts depending on the level of CDCP1 expression in HeLa cells. This suggests that the level of CDCP1 expression may act as a regulatory mechanism allowing cells to switch from a FAK-Y861 mediated pathway to a CDCP1-Y734 mediated pathway. This is the first time that a link between SFKs, CDCP1 and FAK has been demonstrated. One of the most interesting observations from this work was that CDCP1 altered HeLa cell morphology causing an elongated and fibroblastic-like appearance. Importantly, this morphological change depended on CDCP1- Y734. In addition, it was observed that this change in cell morphology was accompanied by increased phosphorylation of SFK-Y416. This suggests that interactions of SFKs with CDCP1-Y734 increases SFK activity since SFKY416 is critical in regulating kinase activity of these proteins. The essential role of SFKs in mediating CDCP1-induced HeLa cell morphological changes was demonstrated using the SFK-selective inhibitor SU6656. This inhibitor caused reversion of HeLa-CDCP1 cell morphology to an epithelial appearance characteristic of HeLa-vector cells. Significantly, in vitro studies revealed that certain CDCP1-mediated cell phenotypes are mediated by cellular pathways dependent on CDCP1 tyrosine residues whereas others are independent of these sites. For example, CDCP1 expression caused a marked increase in HeLa cell motility that was independent of CDCP1 tyrosine residues. In contrast, CDCP1- induced decrease in HeLa cell proliferation was most prominent in HeLa- CDCP1-Y762F cells, potentially indicating a role for this site in regulating proliferation in HeLa cells. Another cellular event which was identified to require phosphorylation of a particular CDCP1 tyrosine residue is adhesion to fibronectin. It was observed that the CDCP1-mediated strong decrease in adhesion to fibronectin is mostly restored in HeLa-CDCP1-Y743F cells. This suggests a possible role for CDCP1-Y743 in causing a CDCP1-mediated decrease in adhesion. Data from in vivo experiments indicated that HeLa-CDCP1-Y734F cells are more metastic than HeLa-CDCP1 cells in vivo. This indicates that interaction of CDCP1 with SFKs and PKCä may not be required for CDCP1-mediated metastasis formation of HeLa cells in vivo. The metastatic phenotype of these cells may be caused by signalling involving FAK since HeLa-CDCP1- Y734F cells are the only CDCP1 expressing cells displaying constitutive phosphorylation of FAK-Y861. HeLa-CDCP1-Y762F cells displayed a very low metastatic ability which suggests that this CDCP1 tyrosine residue is important in mediating a pro-metastatic phenotype in HeLa cells. More detailed exploration of cellular events occurring downstream of CDCP1-Y734 and -Y762 may provide important insights into the mechanisms altering the metastatic ability of CDCP1 expressing HeLa cells. Complementing the in vivo studies, anti-CDCP1 antibodies were employed to assess whether these antibodies are able to inhibit metastasis of CDCP1 and CDCP1 tyrosine mutants expressing HeLa cells. It was found that HeLa- CDCP1-Y734F cells were the only cell line which was markedly reduced in the ability to metastasise. In contrast, the ability of HeLa-CDCP1, HeLa- CDCP1-Y743F and -Y762F cells to metastasise in vivo was not inhibited. These data suggest a possible role of interactions of CDCP1 with SFKs, occurring at CDCP1-Y734, in preventing an anti-metastatic effect of anti- CDCP1 antibodies in vivo. The proposal that SFKs may play a role in regulating anti-metastatic effects of anti-CDCP1 antibodies was supported by another experiment where differences between HeLa-CDCP1 cells and CDCP1 expressing HeLa cells (HeLa-CDCP1-S) from collaborators at the Scripps Research Institute were examined. It was found that HeLa-CDCP1-S cells express different SFKs than CDCP1 expressing HeLa cells generated for this study. This is important since HeLa-CDCP1-S cells can be inhibited in their metastatic ability using anti-CDCP1 antibodies in vivo. Importantly, these data suggest that further examinations of the roles of SFKs in facilitating anti-metastatic effects of anti-CDCP1 antibodies may give insights into how CDCP1 can be blocked to prevent metastasis in vivo. This project also explored the ability of the serine protease matriptase to proteolytically process cell surface localised CDCP1 because it is unknown whether matriptase can cleave cell surface CDCP1 as it has been reported for other proteases such as trypsin and plasmin. Furthermore, the consequences of matriptase-mediated proteolysis on cell phenotype in vitro and cell signalling were examined since recent reports suggested that proteolysis of CDCP1 leads to its phosphorylation and may initiate cell signalling and consequently alter cell phenotype. It was found that matriptase is able to proteolytically process cell surface CDCP1 at low nanomolar concentrations which suggests that cleavage of CDCP1 by matriptase may facilitate the generation of LWM-CDCP1 in vivo. To examine whether matriptase-mediated proteolysis induced cell signalling anti-phospho Erk 1/2 Western blot analysis was performed as this pathway has previously been examined to study signalling in response to proteolytic processing of cell surface proteins. It was found that matriptase-mediated proteolysis in CDCP1 expressing HeLa cells initiated intracellular signalling via Erk 1/2. Interestingly, this increase in phosphorylation of Erk 1/2 was also observed in HeLa-vector cells. This suggested that initiation of cell signalling via Erk 1/2 phosphorylation as a result of matriptase-mediated proteolysis occurs by pathways independent of CDCP1. Subsequent investigations measuring the flux of free calcium ions and by using a protease-activated receptor 2 (PAR2) agonist peptide confirmed this hypothesis. These data suggested that matriptase-mediated proteolysis results in cell signalling via a pathway induced by the activation of PAR2 rather than by CDCP1. This indicates that induction of cell signalling in HeLa cells as a consequence of matriptase-mediated proteolysis occurs via signalling pathways which do not involve phosphorylation of Erk 1/2. Consequently, it appears that future attempts should focus on the examination of cellular pathways other than Erk 1/2 to elucidate cell signalling initiated by matriptase-mediated proteolytic processing of CDCP1. The data presented in this thesis has explored in vitro and in vivo aspects of the biology of CDCP1. The observations summarised above will permit the design of future studies to more precisely determine the role of CDCP1 and its binding partners in processes relevant to cancer progression. This may contribute to further defining CDCP1 as a target for cancer treatment.

Functional role of cell surface CUB domain-containing protein 1 in tumour cell dissemination

The function of CUB domain-containing protein 1 (CDCP1), a recently described transmembrane protein expressed on the surface of hematopoietic stem cells and normal and malignant cells of different tissue origin, is not well defined. The contribution of CDCP1 to tumor metastasis was analyzed by using HeLa carcinoma cells overexpressing CDCP1 (HeLa-CDCP1) and a high-disseminating variant of prostate carcinoma PC-3 naturally expressing high levels of CDCP1 (PC3-hi/diss). CDCP1 expression rendered HeLa cells more aggressive in experimental metastasis in immunodeficient mice. Metastatic colonization by HeLa-CDCP1 was effectively inhibited with subtractive immunization-generated, CDCP1-specific monoclonal antibody (mAb) 41-2, suggesting that CDCP1 facilitates relatively late stages of the metastatic cascade. In the chick embryo model, time- and dose-dependent inhibition of HeLa-CDCP1 colonization by mAb 41-2 was analyzed quantitatively to determine when and where CDCP1 functions during metastasis. Quantitative PCR and immunohistochemical analyses indicated that CDCP1 facilitated tumor cell survival soon after vascular arrest. Live cell imaging showed that the function-blocking mechanism of mAb 41-2 involved enhancement of tumor cell apoptosis, confirmed by attenuation of mAb 41-2–mediated effects with the caspase inhibitor z-VAD-fmk. Under proapoptotic conditions in vitro, CDCP1 expression conferred HeLa-CDCP1 cells with resistance to doxorubicin-induced apoptosis, whereas ligation of CDCP1 with mAb 41-2 caused additional enhancement of the apoptotic response. The functional role of naturally expressed CDCP1 was shown by mAb 41-2–mediated inhibition of both experimental and spontaneous metastasis of PC3-hi/diss. These findings confirm that CDCP1 functions as an antiapoptotic molecule and indicate that during metastasis CDCP1 facilitates tumor cell survival likely during or soon after extravasation.

Reduction rules for reset/inhibitor nets

Reset/inhibitor nets are Petri nets extended with reset arcs and inhibitor arcs. These extensions can be used to model cancellation and blocking. A reset arc allows a transition to remove all tokens from a certain place when the transition fires. An inhibitor arc can stop a transition from being enabled if the place contains one or more tokens. While reset/inhibitor nets increase the expressive power of Petri nets, they also result in increased complexity of analysis techniques. One way of speeding up Petri net analysis is to apply reduction rules. Unfortunately, many of the rules defined for classical Petri nets do not hold in the presence of reset and/or inhibitor arcs. Moreover, new rules can be added. This is the first paper systematically presenting a comprehensive set of reduction rules for reset/inhibitor nets. These rules are liveness and boundedness preserving and are able to dramatically reduce models and their state spaces. It can be observed that most of the modeling languages used in practice have features related to cancellation and blocking. Therefore, this work is highly relevant for all kinds of application areas where analysis is currently intractable.

Minimising capacitive couplings and distributing copper losses in planar magnetic elements

Planar magnetic elements are becoming a replacement for their conventional rivals. Among the reasons supporting their application, is their smaller size. Taking less bulk in the electronic package is a critical advantage from the manufacturing point of view. The planar structure consists of the PCB copper tracks to generate the desired windings .The windings on each PCB layer could be connected in various ways to other winding layers to produce a series or parallel connection. These windings could be applied coreless or with a core depending on the application in Switched Mode Power Supplies (SMPS). Planar shapes of the tracks increase the effective conduction area in the windings, brings about more inductance compared to the conventional windings with the similar copper loss case. The problem arising from the planar structure of magnetic inductors is the leakage current between the layers generated by a pulse width modulated voltage across the inductor. This current value relies on the capacitive coupling between the layers, which in its turn depends on the physical parameters of the planar scheme. In order to reduce this electrical power dissipation due to the leakage current and Electromagnetic Interference (EMI), reconsideration in the planar structure might be effective. The aim of this research is to address problem of these capacitive coupling in planar layers and to find out a better structure for the planar inductance which offers less total capacitive coupling and thus less thermal dissipation from the leakage currents. Through Finite Element methods (FEM) several simulations have been carried out for various planar structures. The labs prototypes of these structures are built with the similar specification of the simulation cases. The capacitive couplings of the samples are determined with Spectrum Analyser whereby the test analysis verified the simulation results.

Space : Irrealis objects and their role in a new political economy

In this paper, I show how new spaces are being prefigured for colonisation in the language of contemporary technology policy. Drawing on a corpus of 1.3 million words collected from technology policy centres throughout the world, I show the role of policy language in creating the foundations of an emergent form of political economy. The analysis is informed by principles from critical discourse analysis (CDA) and classical political economy. It foregrounds a functional aspect of language called process metaphor to show how aspects of human activity are prefigured for mass commodification by the manipulation of irrealis spaces. I also show how the fundamental element of any new political economy, the property element, is being largely ignored. The potential creation of a global space as concrete as landed property – electromagnetic spectrum – has significant ramifications for the future of social relations in any global “knowledge economy”.

From Greek temple to bird's nest : mapping, assessing and understanding national integrity systems

In this paper, I would like to outline the approach we have taken to mapping and assessing integrity systems and how this has led us to see integrity systems in a new light. Indeed, it has led us to a new visual metaphor for integrity systems – a bird’s nest rather than a Greek temple. This was the result of a pair of major research projects completed in partnership with Transparency International (TI). One worked on refining and extending the measurement of corruption. This, the second, looked at what was then the emerging institutional means for reducing corruption – ‘national integrity systems’