Effect of the base station antenna beam tilting on energy consumption in cellular networks

The objective of this paper is to combine the antenna downtilt selection with the cell size selection in order to reduce the overall radio frequency (RF) transmission power in the homogeneous High-Speed Packet Downlink (HSDPA) cellular radio access network (RAN). The analysis is based on the concept of small cells deployment. The energy consumption ratio (ECR) and the energy reduction gain (ERG) of the cellular RAN are calculated for different antenna tilts when the cell size is being reduced for a given user density and service area. The results have shown that a suitable antenna tilt and the RF power setting can achieve an overall energy reduction of up to 82.56%. Equally, our results demonstrate that a small cell deployment can considerably reduce the overall energy consumption of a cellular network.

Application of IEEE 802.16 mesh networks as the backhaul of multihop cellular networks

Cellular networks have been widely used to support many new audio-and video-based multimedia applications. The demand for higher data rate and diverse services has driven the research on multihop cellular networks (MCNs). With its ad hoc network features, an MCN can offer many additional advantages, such as increased network throughput, scalability and coverage. However, providing ad hoc capability to MCNs is challenging as it may require proper wireless interfaces. In this article, the architecture of IEEE 802.16 network interface to provide ad hoc capability for MCNs is investigated, with its focus on the IEEE 802.16 mesh networking and scheduling. Several distributed routing algorithms based on network entry mechanism are studied and compared with a centralized routing algorithm. It is observed from the simulation results that 802.16 mesh networks have limitations on providing sufficient bandwidth for the traffic from the cellular base stations when a cellular network size is relatively large. © 2007 IEEE.

Progmosis:evaluating risky individual behavior during epidemics using mobile network data

The possibility to analyze, quantify and forecast epidemic outbreaks is fundamental when devising effective disease containment strategies. Policy makers are faced with the intricate task of drafting realistically implementable policies that strike a balance between risk management and cost. Two major techniques policy makers have at their disposal are: epidemic modeling and contact tracing. Models are used to forecast the evolution of the epidemic both globally and regionally, while contact tracing is used to reconstruct the chain of people who have been potentially infected, so that they can be tested, isolated and treated immediately. However, both techniques might provide limited information, especially during an already advanced crisis when the need for action is urgent. In this paper we propose an alternative approach that goes beyond epidemic modeling and contact tracing, and leverages behavioral data generated by mobile carrier networks to evaluate contagion risk on a per-user basis. The individual risk represents the loss incurred by not isolating or treating a specific person, both in terms of how likely it is for this person to spread the disease as well as how many secondary infections it will cause. To this aim, we develop a model, named Progmosis, which quantifies this risk based on movement and regional aggregated statistics about infection rates. We develop and release an open-source tool that calculates this risk based on cellular network events. We simulate a realistic epidemic scenarios, based on an Ebola virus outbreak; we find that gradually restricting the mobility of a subset of individuals reduces the number of infected people after 30 days by 24%.

Bidirectional transport between the trans-Golgi network and the endosomal system

The exchange of proteins and lipids between the trans-Golgi network (TGN) and the endosomal system requires multiple cellular machines, whose activities are coordinated in space and time to generate pleomorphic, tubulo-vesicular carriers that deliver their content to their target compartments. These machines and their associated protein networks are recruited and/or activated on specific membrane domains where they select proteins and lipids into carriers, contribute to deform/elongate and partition membrane domains using the mechanical forces generated by actin polymerization or movement along microtubules. The coordinated action of these protein networks contributes to regulate the dynamic state of multiple receptors recycling between the cell surface, endosomes and the TGN, to maintain cell homeostasis as exemplified by the biogenesis of lysosomes and related organelles, and to establish/maintain cell polarity. The dynamic assembly and disassembly of these protein networks mediating the exchange of membrane domains between the TGN and endosomes regulates cell-cell signalling and thus the development of multi-cellular organisms. Somatic mutations in single network components lead to changes in transport dynamics that may contribute to pathological modifications underlying several human diseases such as mental retardation.

Advanced handover procedure for cellular communication systems

Third Generation cellular communication systems are expected to support mixed cell architecture in which picocells, microcells and macrocells are used to achieve full coverage and increase the spectral capacity. Supporting higher numbers of mobile terminals and the use of smaller cells will result in an increase in the number of handovers, and consequently an increase in the time delays required to perform these handovers. Higher time delays will generate call interruptions and forced terminations, particularly for time sensitive applications like real-time multimedia and data services. Currently in the Global System for Mobile communications (GSM), the handover procedure is initiated and performed by the fixed part of the Public Land Mobile Network (PLMN). The mobile terminal is only capable of detecting candidate base stations suitable for the handover; it is the role of the network to interrogate a candidate base station for a free channel. Handover signalling is exchanged via the fixed network and the time delay required to perform the handover is greatly affected by the levels of teletraffic handled by the network. In this thesis, a new handover strategy is developed to reduce the total time delay for handovers in a microcellular system. The handover signalling is diverted from the fixed network to the air interface to prevent extra delays due to teletraffic congestion, and to allow the mobile terminal to exchange signalling directly with the candidate base station. The new strategy utilises Packet Reservation Multiple Access (PRMA) technique as a mechanism to transfer the control of the handover procedure from the fixed network to the mobile terminal. Simulation results are presented to show a dramatic reduction in the handover delay as compared to those obtained using fixed channel allocation and dynamic channel allocation schemes.

Analysis and simulation of computer controlled cellular mobile radio systems

Cellular mobile radio systems will be of increasing importance in the future. This thesis describes research work concerned with the teletraffic capacity and the canputer control requirements of such systems. The work involves theoretical analysis and experimental investigations using digital computer simulation. New formulas are derived for the congestion in single-cell systems in which there are both land-to-mobile and mobile-to-mobile calls and in which mobile-to-mobile calls go via the base station. Two approaches are used, the first yields modified forms of the familiar Erlang and Engset formulas, while the second gives more complicated but more accurate formulas. The results of computer simulations to establish the accuracy of the formulas are described. New teletraffic formulas are also derived for the congestion in multi -cell systems. Fixed, dynamic and hybrid channel assignments are considered. The formulas agree with previously published simulation results. Simulation programs are described for the evaluation of the speech traffic of mobiles and for the investigation of a possible computer network for the control of the speech traffic. The programs were developed according to the structured progranming approach leading to programs of modular construction. Two simulation methods are used for the speech traffic: the roulette method and the time-true method. The first is economical but has some restriction, while the second is expensive but gives comprehensive answers. The proposed control network operates at three hierarchical levels performing various control functions which include: the setting-up and clearing-down of calls, the hand-over of calls between cells and the address-changing of mobiles travelling between cities. The results demonstrate the feasibility of the control netwvork and indicate that small mini -computers inter-connected via voice grade data channels would be capable of providing satisfactory control

Capacity improvements for a direct-sequence code division multiple access network

The rapidly increasing demand for cellular telephony is placing greater demand on the limited bandwidth resources available. This research is concerned with techniques which enhance the capacity of a Direct-Sequence Code-Division-Multiple-Access (DS-CDMA) mobile telephone network. The capacity of both Private Mobile Radio (PMR) and cellular networks are derived and the many techniques which are currently available are reviewed. Areas which may be further investigated are identified. One technique which is developed is the sectorisation of a cell into toroidal rings. This is shown to provide an increased system capacity when the cell is split into these concentric rings and this is compared with cell clustering and other sectorisation schemes. Another technique for increasing the capacity is achieved by adding to the amount of inherent randomness within the transmitted signal so that the system is better able to extract the wanted signal. A system model has been produced for a cellular DS-CDMA network and the results are presented for two possible strategies. One of these strategies is the variation of the chip duration over a signal bit period. Several different variation functions are tried and a sinusoidal function is shown to provide the greatest increase in the maximum number of system users for any given signal-to-noise ratio. The other strategy considered is the use of additive amplitude modulation together with data/chip phase-shift-keying. The amplitude variations are determined by a sparse code so that the average system power is held near its nominal level. This strategy is shown to provide no further capacity since the system is sensitive to amplitude variations. When both strategies are employed, however, the sensitivity to amplitude variations is shown to reduce, thus indicating that the first strategy both increases the capacity and the ability to handle fluctuations in the received signal power.

Hypoxia-inducible factor (HIF) network:insights from mathematical models

Oxygen is a crucial molecule for cellular function. When oxygen demand exceeds supply, the oxygen sensing pathway centred on the hypoxia inducible factor (HIF) is switched on and promotes adaptation to hypoxia by up-regulating genes involved in angiogenesis, erythropoiesis and glycolysis. The regulation of HIF is tightly modulated through intricate regulatory mechanisms. Notably, its protein stability is controlled by the oxygen sensing prolyl hydroxylase domain (PHD) enzymes and its transcriptional activity is controlled by the asparaginyl hydroxylase FIH (factor inhibiting HIF-1).To probe the complexity of hypoxia-induced HIF signalling, efforts in mathematical modelling of the pathway have been underway for around a decade. In this paper, we review the existing mathematical models developed to describe and explain specific behaviours of the HIF pathway and how they have contributed new insights into our understanding of the network. Topics for modelling included the switch-like response to decreased oxygen gradient, the role of micro environmental factors, the regulation by FIH and the temporal dynamics of the HIF response. We will also discuss the technical aspects, extent and limitations of these models. Recently, HIF pathway has been implicated in other disease contexts such as hypoxic inflammation and cancer through crosstalking with pathways like NF?B and mTOR. We will examine how future mathematical modelling and simulation of interlinked networks can aid in understanding HIF behaviour in complex pathophysiological situations. Ultimately this would allow the identification of new pharmacological targets in different disease settings.

Gene network and proteomic analyses of cardiac responses to pathological and physiological stress

Background—The molecular mechanisms underlying similarities and differences between physiological and pathological left ventricular hypertrophy (LVH) are of intense interest. Most previous work involved targeted analysis of individual signaling pathways or screening of transcriptomic profiles. We developed a network biology approach using genomic and proteomic data to study the molecular patterns that distinguish pathological and physiological LVH. Methods and Results—A network-based analysis using graph theory methods was undertaken on 127 genome-wide expression arrays of in vivo murine LVH. This revealed phenotype-specific pathological and physiological gene coexpression networks. Despite >1650 common genes in the 2 networks, network structure is significantly different. This is largely because of rewiring of genes that are differentially coexpressed in the 2 networks; this novel concept of differential wiring was further validated experimentally. Functional analysis of the rewired network revealed several distinct cellular pathways and gene sets. Deeper exploration was undertaken by targeted proteomic analysis of mitochondrial, myofilament, and extracellular subproteomes in pathological LVH. A notable finding was that mRNA–protein correlation was greater at the cellular pathway level than for individual loci. Conclusions—This first combined gene network and proteomic analysis of LVH reveals novel insights into the integrated pathomechanisms that distinguish pathological versus physiological phenotypes. In particular, we identify differential gene wiring as a major distinguishing feature of these phenotypes. This approach provides a platform for the investigation of potentially novel pathways in LVH and offers a freely accessible protocol (http://sites.google.com/site/cardionetworks) for similar analyses in other cardiovascular diseases.