Agent-based model of passenger flows in airport terminals

Passenger flow studies in airport terminals have shown consistent statistical relationships between airport spatial layout and pedestrian movement, facilitating prediction of movement from terminal designs. However, these studies are done at an aggregate level and do not incorporate how individual passengers make decisions at a microscopic level. Therefore, they do not explain the formation of complex movement flows. In addition, existing models mostly focus on standard airport processing procedures such as immigration and security, but seldom consider discretionary activities of passengers, and thus are not able to truly describe the full range of passenger flows within airport terminals. As the route-choice decision-making of passengers involves many uncertain factors within the airport terminals, the mechanisms to fulfill the capacity of managing the route-choice have proven difficult to acquire and quantify. Could the study of cognitive factors of passengers (i.e. human mental preferences of deciding which on-airport facility to use) be useful to tackle these issues? Assuming the movement in virtual simulated environments can be analogous to movement in real environments, passenger behaviour dynamics can be similar to those generated in virtual experiments. Three levels of dynamics have been devised for motion control: the localised field, tactical level, and strategic level. A localised field refers to basic motion capabilities, such as walking speed, direction and avoidance of obstacles. The other two fields represent cognitive route-choice decision-making. This research views passenger flow problems via a "bottom-up approach", regarding individual passengers as independent intelligent agents who can behave autonomously and are able to interact with others and the ambient environment. In this regard, passenger flow formation becomes an emergent phenomenon of large numbers of passengers interacting with others. In the thesis, first, the passenger flow in airport terminals was investigated. Discretionary activities of passengers were integrated with standard processing procedures in the research. The localised field for passenger motion dynamics was constructed by a devised force-based model. Next, advanced traits of passengers (such as their desire to shop, their comfort with technology and their willingness to ask for assistance) were formulated to facilitate tactical route-choice decision-making. The traits consist of quantified measures of mental preferences of passengers when they travel through airport terminals. Each category of the traits indicates a decision which passengers may take. They were inferred through a Bayesian network model by analysing the probabilities based on currently available data. Route-choice decision-making was finalised by calculating corresponding utility results based on those probabilities observed. Three sorts of simulation outcomes were generated: namely, queuing length before checkpoints, average dwell time of passengers at service facilities, and instantaneous space utilisation. Queuing length reflects the number of passengers who are in a queue. Long queues no doubt cause significant delay in processing procedures. The dwell time of each passenger agent at the service facilities were recorded. The overall dwell time of passenger agents at typical facility areas were analysed so as to demonstrate portions of utilisation in the temporal aspect. For the spatial aspect, the number of passenger agents who were dwelling within specific terminal areas can be used to estimate service rates. All outcomes demonstrated specific results by typical simulated passenger flows. They directly reflect terminal capacity. The simulation results strongly suggest that integrating discretionary activities of passengers makes the passenger flows more intuitive, observing probabilities of mental preferences by inferring advanced traits make up an approach capable of carrying out tactical route-choice decision-making. On the whole, the research studied passenger flows in airport terminals by an agent-based model, which investigated individual characteristics of passengers and their impact on psychological route-choice decisions of passengers. Finally, intuitive passenger flows in airport terminals were able to be realised in simulation.

Cyclin A/CDK2 regulates multiple G2 phase pathways

The cell cycle is a carefully choreographed series of phases that when executed successfully will allow the complete replication of the genome and the equal division of the genome and other cellular content into two independent daughter cells. The inability of the cell to execute cell division successfully can result in either checkpoint activation to allow repair and/or apoptosis and/or mutations/errors that may or may not lead to tumourgenesis. Cyclin A/CDK2 is the primary cyclin/CDK regulating G2 phase progression of the cell cycle. Cyclin A/CDK2 activity peaks in G2 phase and its inhibition causes a G2 phase delay that we have termed 'the cyclin A/CDK2 dependent G2 delay'. Understanding the key pathways that are involved in the cyclin A/CDK2 dependent G2 delay has been the primary focus of this study. Characterising the cyclin A/CDK2 dependent G2 delay revealed accumulated levels of the inactive form of the mitotic regulator, cyclin B/CDK1. Surprisingly, there was also increased microtubule nucleation at the centrosomes, and the centrosomes stained for markers of cyclin B/CDK1 activity. Both microtubule nucleation at the centrosomes and phosphoprotein markers were lost with short-term treatment of CDK1/2 inhibition. Cyclin A/CDK2 localised at the centrosomes in late G2 phase after separation of the centrosomes but before the start of prophase. Thus G2 phase cyclin A/CDK2 controls the timing of entry into mitosis by controlling the subsequent activation of cyclin B/CDK1, but also has an unexpected role in coordinating the activation of cyclin B/CDK1 at the centrosome and in the nucleus. In addition to regulating the timing of cyclin B/CDK1 activation and entry into mitosis in the unperturbed cell cycle, cyclin A/CDK2 also was shown to have a role in G2 phase checkpoint recovery. Known G2 phase regulators were investigated to determine whether they had a role in imposing the cyclin A/ CDK2 dependent G2 delay. Examination of the critical G2 checkpoint arrest protein, Chk1, which also has a role during unperturbed G2/M phases revealed the presence of activated Chk1 in G2 phase, in a range of cell lines. Activated Chk1 levels were shown to accumulate in cyclin A/CDK2 depleted/inhibited cells. Further investigations revealed that Chk1, but not Chk2, depletion could reverse the cyclin A/CDK2 dependent G2 delay. It was confirmed that the accumulative activation of Chk1 was not a consequence of DNA damage induced by cyclin A depletion. The potential of cyclin A/CDK2 to regulate Chk1 revealed that the inhibitory phosphorylations, Ser286 and Ser301, were not directly catalysed by cyclin A/CDK2 in G2 phase to regulate mitotic entry. It appeared that the ability of cyclin A/CDK2 to regulate cyclin B/CDK1 activation impacted cyclin B/CDK1s phosphorylation of Chk1 on Ser286 and Ser301, thereby contributing to the delay in G2/M phase progression. Chk1 inhibition/depletion partially abrogated the cyclin A/CDK2 dependent G2 delay, and was less effective in abrogating G2 phase checkpoint suggesting that other cyclin A/CDK2 dependent mechanisms contributed to these roles of cyclin A/CDK2. In an attempt to identify these other contributing factors another G2/M phase regulator known to be regulated by cyclin A/CDK2, Cdh1 and its substrates Plk1 and Claspin were examined. Cdh1 levels were reduced in cyclin A/CDK2 depleted/inhibited cells although this had little effect on Plk1, a known Cdh1 substrate. However, the level of another substrate, Claspin, was increased. Cdh1 depletion mimicked the effect of cyclin A depletion but to a weaker extent and was sufficient at increasing Claspin levels similar to the increase caused by cyclin A depletion. Co-depletion of cyclin A and Claspin blocked the accumulation of activated Chk1 normally seen with cyclin A depletion alone. However Claspin depletion alone did not reduce the cyclin A/CDK2 dependent G2 delay but this is likely to be a result of inhibition of S phase roles of Claspin. Together, these data suggest that cyclin A/CDK2 regulates a number of different mechanisms that contribute to G2/M phase progression. Here it has been demonstrated that in normal G2/M progression and possibly to a lesser extent in G2 phase checkpoint recovery, cyclin A/CDK2 regulates the level of Cdh1 which in turn affects at least one of its substrates, Claspin, and consequently results in the increased level of activated Chk1 observed. However, the involvement of Cdh1 and Claspin alone does not explain the G2 phase delay observed with cyclin A/CDK2 depletion/inhibition. It is likely that other mechanisms, possibly including cyclin A/CDK2 regulation of Wee1 and FoxM1, as reported by others, combine with the mechanism described here to regulate normal G2/M phase progression and G2 phase checkpoint recovery. These findings support the critical role for cyclin A/CDK2 in regulating progression into mitosis and suggest that upstream regulators of cyclin A/CDK2 activation will also be critical controllers of this cell cycle transition. The pathways that work to co-ordinate cell cycle progression are very intricate and deciphering these pathways, required for normal cell cycle progression, is key to understanding tumour development. By understanding cell cycle regulatory pathways it will allow the identification of the pathway/s and their mechanism/s that become affected in tumourgenesis. This will lead to the development of better targeted therapies, inferring better efficacy with fewer side effects than commonly seen with the use of traditional therapies, such as chemotherapy. Furthermore, this has the potential to positively impact the development of personalised medicines and the customisation of healthcare.

Robust control algorithm for grid-interfaced three-phase inverters with high-bandwidth LCL filter

The paper introduces the design of robust current and voltage control algorithms for a grid-connected three-phase inverter which is interfaced to the grid through a high-bandwidth three-phase LCL filter. The algorithms are based on the state feedback control which have been designed in a systematic approach and improved by using oversampling to deal with the issues arising due to the high-bandwidth filter. An adaptive loop delay compensation method has also been adopted to minimize the adverse effects of loop delay in digital controller and to increase the robustness of the control algorithm in the presence of parameter variations. Simulation results are presented to validate the effectiveness of the proposed algorithm.

Utilizing Wide-Area Signals for off-center SVCs to damp interarea oscillations

Wide-Area Measurement Systems (WAMS) provide the opportunity of utilizing remote signals from different locations for the enhancement of power system stability. This paper focuses on the implementation of remote measurements as supplementary signals for off-center Static Var Compensators (SVCs) to damp inter-area oscillations. Combination of participation factor and residue method is used for the selection of most effective stabilizing signal. Speed difference of two generators from separate areas is identified as the best stabilizing signal and used as a supplementary signal for lead-lag controller of SVCs. Time delays of remote measurements and control signals is considered. Wide-Area Damping Controller (WADC) is deployed in Matlab Simulink framework and is tested under different operating conditions. Simulation results reveal that the proposed WADC improve the dynamic characteristic of the system significantly.

Characterisation of microvasulature changes after closed soft tissue trauma by contrast enhanced micro-CT imaging

INTRODUCTION It is known that the vascular morphology and functionality are changed following closed soft tissue trauma (CSTT) [1], and bone fractures [2]. The disruption of blood vessels may lead to hypoxia and necrosis. Currently, most clinical methods for the diagnosis and monitoring of CSTT with or without bone fractures are primarily based on qualitative measures or practical experience, making the diagnosis subjective and inaccurate. There is evidence that CSTT and early vascular changes following the injury delay the soft tissue tissue and bone healing [3]. However, a precise qualitative and quantitative morphological assessment of vasculature changes after trauma is currently missing. In this research, we aim to establish a diagnostic framework to assess the 3D vascular morphological changes after standardized CSTT in a rat model qualitatively and quantitatively using contrast-enhanced micro-CT imaging. METHODS An impact device was used for the application of a controlled reproducible CSTT to the left thigh (Biceps Femoris) of anaesthetized male Wistar rats. After euthanizing the animals at 6 hours, 24 hours, 3 days, 7 days, or 14 days after trauma, CSTT was qualitatively evaluated by macroscopic visual observation of the skin and muscles. For visualization of the vasculature, the blood vessels of sacrificed rats were flushed with heparinised saline and then perfused with a radio-opaque contrast agent (Microfil, MV 122, Flowtech, USA) using an infusion pump. After allowing the contrast agent to polymerize overnight, both hind-limbs were dissected, and then the whole injured and contra-lateral control limbs were imaged using a micro-CT scanner (µCT 40, Scanco Medical, Switzerland) to evaluate the vascular morphological changes. Correlated biopsy samples were also taken from the CSTT region of both injured and control legs. The morphological parameters such as the vessel volume ratio (VV/TV), vessel diameter (V.D), spacing (V.Sp), number (V.N), connectivity (V.Conn) and the degree of anisotropy (DA) were then quantified by evaluating the scans of biopsy samples using the micro-CT imaging system. RESULTS AND DISCUSSION A qualitative evaluation of the CSTT has shown that the developed impact protocols were capable of producing a defined and reproducible injury within the region of interest (ROI), resulting in a large hematoma and moderate swelling in both lateral and medial sides of the injured legs. Also, the visualization of the vascular network using 3D images confirmed the ability to perfuse the large vessels and a majority of the microvasculature consistently (Figure 1). Quantification of the vascular morphology obtained from correlated biopsy samples has demonstrated that V.D and V.N and V.Sp were significantly higher in the injured legs 24 hours after impact in comparison with the control legs (p<0.05). The evaluation of the other time points is currently progressing. CONCLUSIONS The findings of this research will contribute to a better understanding of the changes to the vascular network architecture following traumatic injuries and during healing process. When interpreted in context of functional changes, such as tissue oxygenation, this will allow for objective diagnosis and monitoring of CSTT and serve as validation for future non-invasive clinical assessment modalities.

Investigations of the physical origins of etching LiNbO3 during Ti in-diffusion

We investigate the physical origins of etching observed during Ti diffusion. The relationship between observed etch depth and water vapor content in the annealing environment is quantified. The dynamics of the etching process are also identified. It is discovered that water vapor content is essential for etching and that there is a characteristic delay before etching is observed. From these observations we can conclude that the process is electrochemical in nature with ionic defects diffusing into the Ti strip from the lithium niobate and these defects catalyzing the dissociation of water into reactive ions.

The structured and practical approach in development of decision support system for consultant selection in public sector infrastructure project

Nowadays, most of the infrastructure development projects undertaken are complex in nature. Practically, public clients who do not have a good understanding of the design and management may suffer severe losses, especially for infrastructure projects. There is a need for luring the right consultant to secure client's investment in infrastructure developments. Throughout the project life cycle, consultants play vital role from the inception to completion stage of a project. A few studies in Malaysia show that infrastructure projects involving irrigation and drainage have experience problems such as poor workmanship, delay and cost overrun due to the consultant's inability or the client incompetence of recruiting consultants in time. This highlights the need of aided decision making and an efficient system to select the best consultant by using Decision Support System (DSS). On the other hand, recent trends reveal that most DSS in construction only concentrate on decision model development. These models are impractical and unused as they are complicated or difficult for laymen such as project managers to utilize. Thus, this research attempts to develop an efficient DSS for consultant selection namely consultDeSS. Driven by the motivation and research aims, this study deployed Design Science Research Methodology (DSRM) dominant with a combination of case studies at the Malaysian Department of Irrigation and Drainage (DID). Two real projects involving irrigation and drainage infrastructure were used to design, implement and evaluate the artefact. The 3-tier consultDeSS was revised after the evaluation and the design was significantly improved based on user feedback. By developing desirable tools that fit client's needs will enhance the productivity and minimize conflict within groups and organisations. The tool is more usable and efficient compared to previous studies in construction. Thus, this research has demonstrated a purposeful artefact with a practical and valid structured development approach that is applicable in a variety of problems in construction discipline.

Daxx regulates mitotic progression and prostate cancer predisposition

Mitotic progression of mammalian cells is tightly regulated by the E3 ubiquitin ligase anaphase promoting complex (APC)/C. Deregulation of APC/C is frequently observed in cancer cells and is suggested to contribute to chromosome instability and cancer predisposition. In this study, we identified Daxx as a novel APC/C inhibitor frequently overexpressed in prostate cancer. Daxx interacts with the APC/C coactivators Cdc20 and Cdh1 in vivo, with the binding of Cdc20 dependent on the consensus destruction boxes near the N-terminal of the Daxx protein. Ectopic expression of Daxx, but not the D-box deleted mutant (DaxxΔD-box), inhibited the degradation of APC/Cdc20 and APC/Cdh1 substrates, leading to a transient delay in mitotic progression. Daxx is frequently upregulated in prostate cancer tissues; the expression level positively correlated with the Gleason score and disease metastasis (P = 0.027 and 0.032, respectively). Furthermore, ectopic expression of Daxx in a non-malignant prostate epithelial cell line induced polyploidy under mitotic stress. Our data suggest that Daxx may function as a novel APC/C inhibitor, which promotes chromosome instability during prostate cancer development.

Advances in the systemic therapy of malignant pleural mesothelioma

Malignant pleural mesothelioma is an aggressive thoracic malignancy associated with exposure to asbestos, and its incidence is anticipated to increase during the first half of this century. Chemotherapy is the mainstay of treatment, yet sufficiently robust evidence to substantiate the current standard of care has emerged only in the past 5 years. This Review summarizes the evidence supporting the clinical activity of chemotherapy, discusses the use of end points for its assessment and examines the influence of clinical and biochemical prognostic factors on the natural history of malignant pleural mesothelioma. Early-phase clinical trials of second-line and novel agents are emerging from an increased understanding of mesothelioma cell biology. Coupled with high-quality translational research, such developments have real potential to improve the outlook of patients at a time of increasing incidence.

The effects of the indoor environment of residential care homes on dementia suffers in Hong Kong : a critical incident technique approach

Dementia is an irreversible and incurable syndrome that leads to progressive impairment of cognitive functions and behavioural and psychological symptoms such as agitation, depression and psychosis. Appropriate environmental conditions can help delay its onset and progression, and indoor environmental (IE) factors have a major impact. However, there is no firm understanding of the full range of relevant IE factors and their impact levels. This paper describes a preliminary study to investigate the effects of IE on Hong Kong residential care homes (RCH) dementia residents. This involved six purposively selected focus groups, each comprising the main stakeholders of the dementia residents’ caregivers, RCH staff and/or registered nurses, and architects. Using the Critical Incident Technique, the main context and experiences of behavioural problems of dementia residents caused by IE were explored and the key causal RCH IE quality factors identified, together with the associated responses and stress levels involved. The findings indicate that the acoustic environment, lighting and thermal environment are the most important influencing factors. Many of the remedies provided by the focus groups are quite simple to carry out and are summarised in the form of recommendations to current RCHs providers and users. The knowledge acquired in this initial study will help enrich the knowledge of IE design for dementiaspecific residential facilities. It also provides some preliminary insights for healthcare policymakers and practitioners in the building design/facilities management and dementia-care sectors into the IE factors contributing to a more comfortable, healthy and sustainable RCH living environment in Hong Kong.

The effect of extent of local resection on patterns of disease progression in malignant pleural mesothelioma

Background We sought to determine whether or not there are differences in disease progression after radical or nonradical (debulking) surgical procedures for malignant pleural mesothelioma. Methods Over a 49-month period, 132 patients with malignant pleural mesothelioma underwent surgery. Fifty-three underwent extrapleural pneumonectomy and 79 underwent nonradical procedures. Time to evidence of clinical disease progression was recorded, as was the site(s) of that disease. Results One-hundred nineteen patients were evaluable, of which 59% (22 radical; 48 nonradical) had disease progression. Overall 30-day mortality was 8.5% (7.5% radical; 9% nonradical). The median time to overall disease progression was considerably longer after extrapleural pneumonectomy than debulking surgery (319 days vs 197 days, p = 0.019), as was the time to local disease progression (631 days vs 218 days, p = 0.0018). There was no preponderance of earlier stage disease in the radical surgery group. There was a trend toward prolonged survival in those undergoing radical surgery, but no significant difference between the groups (497 days vs 324 days, p = 0.079). In those who had extrapleural pneumonectomy, time-to-disease progression significantly decreased with N2 disease compared with N0/1 involvement (197 days vs 358 days, p = 0.02). Conclusions Extrapleural pneumonectomy may be preferable to debulking surgery in malignant pleural mesothelioma to delay disease progression and give greater control of local disease. Involvement of N2 nodes is associated with accelerated disease progression and is therefore a contraindication to extrapleural pneumonectomy. © 2004 by The Society of Thoracic Surgeons.

Practical Modbus flooding attack and detection

The Modicon Communication Bus (Modbus) protocol is one of the most commonly used protocols in industrial control systems. Modbus was not designed to provide security. This paper confirms that the Modbus protocol is vulnerable to flooding attacks. These attacks involve injection of commands that result in disrupting the normal operation of the control system. This paper describes a set of experiments that shows that an anomaly-based change detection algorithm and signature-based Snort threshold module are capable of detecting Modbus flooding attacks. In comparing these intrusion detection techniques, we find that the signature-based detection requires a carefully selected threshold value, and that the anomaly-based change detection algorithm may have a short delay before detecting the attacks depending on the parameters used. In addition, we also generate a network traffic dataset of flooding attacks on the Modbus control system protocol.

Modeling bus rapid transit station bus queuing for operational analysis

This paper presents mathematical models for BRT station operation, calibrated using microscopic simulation modelling. Models are presented for station capacity and bus queue length. No reliable model presently exists to estimate bus queue length. The proposed bus queue model is analogous to an unsignalized intersection queuing model.

A pre-clinical functional assessment of an acellular scaffold intended for the treatment of hard-to-heal wounds

Dermal wound healing is a biochemical and cellular process critical to life. While the majority of the population will only ever experience successful wound healing outcomes, some 1-3 % of those aged over 65 years will experience wound healing delay or perpetuation. These hard-to-heal wounds are comprised of degraded and dysfunctional extracellular matrix, yet the integrity of this structure is critical in the processes of normal wound healing. As such, extracellular matrix replacements have been devised that can replace dysfunctional extracellular matrix in hard-to-heal wounds with the aim of restoring normal wound healing processes. Here we evaluated a novel synthetic matrix protein for its ability to act as an acellular scaffold that can replace dysfunctional extracellular matrix. In this regard the synthetic protein demonstrated an ability to rapidly adsorb to the dermal surface, permit cell attachment and facilitate the cellular functions essential to wound healing. When applied to deep partial thickness wounds in a porcine animal model the matrix protein also demonstrated the ability to reduce wound duration. These data provide evidence that the synthetic matrix protein has the ability to function as an acellular scaffold for wound healing purposes.

Differential Regulation of Clusterin Isoforms by the Androgen Receptor

Clusterin (CLU) was initially reported as an androgen-repressed gene which is now shown to be an androgen-regulated ATP-independent cytoprotective molecular chaperone. CLU binds to a wide variety of client proteins to potently inhibit stress-induced protein aggregation and chaperone or stabilise conformations of proteins at times of cell stress. CLU is an enigmatic protein, being ascribed both pro- and anti-apoptotic roles. Recent evidence has shown that both secreted (sCLU) and nuclear (nCLU) isoforms can be produced, and that protein function is dependent on the sub-cellular localisation. We and others have shown that sCLU is cytoprotective, while nCLU is pro-apoptotic. It now seems likely that the apparently dichotomous functions of CLU result from the expression of different but related CLU isoforms and splice variants, and that cell survival depends in part on the relative expression of pro- versus anti-apoptotic CLU proteins. In cancer cells, increased sCLU expression is associated with increased resistance to apoptotic triggers and treatment resistance. CLU is a stress-induced protein upregulated after apoptotic triggers like androgen ablation and chemotherapy. Treatment strategies targeting stress-associated increases in sCLU expression enhance treatment-induced apoptosis and delay the emergence of androgen independence. Differential regulation of CLU isoforms and splice variants by androgens may be a pathway whereby cancer cells develop treatment resistance and evade apoptosis.