8,186 research outputs found

    Reinforcement Learning-based User-centric Handover Decision-making in 5G Vehicular Networks

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    The advancement of 5G technologies and Vehicular Networks open a new paradigm for Intelligent Transportation Systems (ITS) in safety and infotainment services in urban and highway scenarios. Connected vehicles are vital for enabling massive data sharing and supporting such services. Consequently, a stable connection is compulsory to transmit data across the network successfully. The new 5G technology introduces more bandwidth, stability, and reliability, but it faces a low communication range, suffering from more frequent handovers and connection drops. The shift from the base station-centric view to the user-centric view helps to cope with the smaller communication range and ultra-density of 5G networks. In this thesis, we propose a series of strategies to improve connection stability through efficient handover decision-making. First, a modified probabilistic approach, M-FiVH, aimed at reducing 5G handovers and enhancing network stability. Later, an adaptive learning approach employed Connectivity-oriented SARSA Reinforcement Learning (CO-SRL) for user-centric Virtual Cell (VC) management to enable efficient handover (HO) decisions. Following that, a user-centric Factor-distinct SARSA Reinforcement Learning (FD-SRL) approach combines time series data-oriented LSTM and adaptive SRL for VC and HO management by considering both historical and real-time data. The random direction of vehicular movement, high mobility, network load, uncertain road traffic situation, and signal strength from cellular transmission towers vary from time to time and cannot always be predicted. Our proposed approaches maintain stable connections by reducing the number of HOs by selecting the appropriate size of VCs and HO management. A series of improvements demonstrated through realistic simulations showed that M-FiVH, CO-SRL, and FD-SRL were successful in reducing the number of HOs and the average cumulative HO time. We provide an analysis and comparison of several approaches and demonstrate our proposed approaches perform better in terms of network connectivity

    Smart Handover with Predicted User Behavior using Convolutional Neural Networks for WiGig Systems

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    WiGig networks and 60 GHz frequency communications have a lot of potential for commercial and personal use. They can offer extremely high transmission rates but at the cost of low range and penetration. Due to these issues, WiGig systems are unstable and need to rely on frequent handovers to maintain high-quality connections. However, this solution is problematic as it forces users into bad connections and downtime before they are switched to a better access point. In this work, we use Machine Learning to identify patterns in user behaviors and predict user actions. This prediction is used to do proactive handovers, switching users to access points with better future transmission rates and a more stable environment based on the future state of the user. Results show that not only the proposal is effective at predicting channel data, but the use of such predictions improves system performance and avoids unnecessary handovers.Comment: Submitted to IEEE Networ

    OLIG2 neural progenitor cell development and fate in Down syndrome

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    Down syndrome (DS) is caused by triplication of human chromosome 21 (HSA21) and is the most common genetic form of intellectual disability. It is unknown precisely how triplication of HSA21 results in the intellectual disability, but it is thought that the global transcriptional dysregulation caused by trisomy 21 perturbs multiple aspects of neurodevelopment that cumulatively contribute to its etiology. While the characteristics associated with DS can arise from any of the genes triplicated on HSA21, in this work we focus on oligodendrocyte transcription factor 2 (OLIG2). The progeny of neural progenitor cells (NPCs) expressing OLIG2 are likely to be involved in many of the cellular changes underlying the intellectual disability in DS. To explore the fate of OLIG2+ neural progenitors, we took advantage of two distinct models of DS, the Ts65Dn mouse model and induced pluripotent stem cells (iPSCs) derived from individuals with DS. Our results from these two systems identified multiple perturbations in development in the cellular progeny of OLIG2+ NPCs. In Ts65Dn, we identified alterations in neurons and glia derived from the OLIG2 expressing progenitor domain in the ventral spinal cord. There were significant differences in the number of motor neurons and interneurons present in the trisomic lumbar spinal cord depending on age of the animal pointing both to a neurodevelopment and a neurodegeneration phenotype in the Ts65Dn mice. Of particular note, we identified changes in oligodendrocyte (OL) maturation in the trisomic mice that are dependent on spatial location and developmental origin. In the dorsal corticospinal tract, there were significantly fewer mature OLs in the trisomic mice, and in the lateral funiculus we observed the opposite phenotype with more mature OLs being present in the trisomic animals. We then transitioned our studies into iPSCs where we were able to pattern OLIG2+ NPCs to either a spinal cord-like or a brain-like identity and study the OL lineage that differentiated from each progenitor pool. Similar to the region-specific dysregulation found in the Ts65Dn spinal cord, we identified perturbations in trisomic OLs that were dependent on whether the NPCs had been patterned to a brain-like or spinal cord-like fate. In the spinal cord-like NPCs, there was no difference in the proportion of cells expressing either OLIG2 or NKX2.2, the two transcription factors whose co-expression is essential for OL differentiation. Conversely, in the brain-like NPCs, there was a significant increase in OLIG2+ cells in the trisomic culture and a decrease in NKX2.2 mRNA expression. We identified a sonic hedgehog (SHH) signaling based mechanism underlying these changes in OLIG2 and NKX2.2 expression in the brain-like NPCs and normalized the proportion of trisomic cells expressing the transcription factors to euploid levels by modulating the activity of the SHH pathway. Finally, we continued the differentiation of the brain-like and spinal cord-like NPCs to committed OL precursor cells (OPCs) and allowed them to mature. We identified an increase in OPC production in the spinal cord-like trisomic culture which was not present in the brain-like OPCs. Conversely, we identified a maturation deficit in the brain-like trisomic OLs that was not present in the spinal cord-like OPCs. These results underscore the importance of regional patterning in characterizing changes in cell differentiation and fate in DS. Together, the findings presented in this work contribute to the understanding of the cellular and molecular etiology of the intellectual disability in DS and in particular the contribution of cells differentiated from OLIG2+ progenitors

    Interference mitigation in LiFi networks

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    Due to the increasing demand for wireless data, the radio frequency (RF) spectrum has become a very limited resource. Alternative approaches are under investigation to support the future growth in data traffic and next-generation high-speed wireless communication systems. Techniques such as massive multiple-input multiple-output (MIMO), millimeter wave (mmWave) communications and light-fidelity (LiFi) are being explored. Among these technologies, LiFi is a novel bi-directional, high-speed and fully networked wireless communication technology. However, inter-cell interference (ICI) can significantly restrict the system performance of LiFi attocell networks. This thesis focuses on interference mitigation in LiFi attocell networks. The angle diversity receiver (ADR) is one solution to address the issue of ICI as well as frequency reuse in LiFi attocell networks. With the property of high concentration gain and narrow field of view (FOV), the ADR is very beneficial for interference mitigation. However, the optimum structure of the ADR has not been investigated. This motivates us to propose the optimum structures for the ADRs in order to fully exploit the performance gain. The impact of random device orientation and diffuse link signal propagation are taken into consideration. The performance comparison between the select best combining (SBC) and maximum ratio combining (MRC) is carried out under different noise levels. In addition, the double source (DS) system, where each LiFi access point (AP) consists of two sources transmitting the same information signals but with opposite polarity, is proven to outperform the single source (SS) system under certain conditions. Then, to overcome issues around ICI, random device orientation and link blockage, hybrid LiFi/WiFi networks (HLWNs) are considered. In this thesis, dynamic load balancing (LB) considering handover in HLWNs is studied. The orientation-based random waypoint (ORWP) mobility model is considered to provide a more realistic framework to evaluate the performance of HLWNs. Based on the low-pass filtering effect of the LiFi channel, we firstly propose an orthogonal frequency division multiple access (OFDMA)-based resource allocation (RA) method in LiFi systems. Also, an enhanced evolutionary game theory (EGT)-based LB scheme with handover in HLWNs is proposed. Finally, due to the characteristic of high directivity and narrow beams, a vertical-cavity surface-emitting laser (VCSEL) array transmission system has been proposed to mitigate ICI. In order to support mobile users, two beam activation methods are proposed. The beam activation based on the corner-cube retroreflector (CCR) can achieve low power consumption and almost-zero delay, allowing real-time beam activation for high-speed users. The mechanism based on the omnidirectional transmitter (ODTx) is suitable for low-speed users and very robust to random orientation

    Development of in-vitro in-silico technologies for modelling and analysis of haematological malignancies

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    Worldwide, haematological malignancies are responsible for roughly 6% of all the cancer-related deaths. Leukaemias are one of the most severe types of cancer, as only about 40% of the patients have an overall survival of 10 years or more. Myelodysplastic Syndrome (MDS), a pre-leukaemic condition, is a blood disorder characterized by the presence of dysplastic, irregular, immature cells, or blasts, in the peripheral blood (PB) and in the bone marrow (BM), as well as multi-lineage cytopenias. We have created a detailed, lineage-specific, high-fidelity in-silico erythroid model that incorporates known biological stimuli (cytokines and hormones) and a competing diseased haematopoietic population, correctly capturing crucial biological checkpoints (EPO-dependent CFU-E differentiation) and replicating the in-vivo erythroid differentiation dynamics. In parallel, we have also proposed a long-term, cytokine-free 3D cell culture system for primary MDS cells, which was firstly optimized using easily-accessible healthy controls. This system enabled long-term (24-day) maintenance in culture with high (>75%) cell viability, promoting spontaneous expansion of erythroid phenotypes (CD71+/CD235a+) without the addition of any exogenous cytokines. Lastly, we have proposed a novel in-vitro in-silico framework using GC-MS metabolomics for the metabolic profiling of BM and PB plasma, aiming not only to discretize between haematological conditions but also to sub-classify MDS patients, potentially based on candidate biomarkers. Unsupervised multivariate statistical analysis showed clear intra- and inter-disease separation of samples of 5 distinct haematological malignancies, demonstrating the potential of this approach for disease characterization. The work herein presented paves the way for the development of in-vitro in-silico technologies to better, characterize, diagnose, model and target haematological malignancies such as MDS and AML.Open Acces

    The Adirondack Chronology

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    The Adirondack Chronology is intended to be a useful resource for researchers and others interested in the Adirondacks and Adirondack history.https://digitalworks.union.edu/arlpublications/1000/thumbnail.jp

    Identificación de nuevas rutas de patogénesis y dianas terapéuticas en la enfermedad de Parkinson mediante el uso de modelos biomédicos

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    La enfermedad de Parkinson (EP) es la segunda enfermedad neurodegenerativa más común, caracterizada por la pérdida progresiva de neuronas dopaminérgicas en la substantia nigra pars compacta. Esto conduce a una disminución de los niveles de dopamina en el núcleo estriado, causando los síntomas motores típicos de la enfermedad. Entre las principales causas de la neurodegeneración se encuentran el estrés oxidativo (EO) y la disfunción mitocondrial. Aunque la mayoría de los casos de EP son idiopáticos, se ha demostrado que entre el 5 y el 10% de ellos son formas familiares de la enfermedad causadas por mutaciones en determinados genes. Uno de ellos es el gen DJ-1, cuyas mutaciones están asociadas a casos familiares de la EP de inicio temprano. Además, se ha demostrado que en los cerebros de los pacientes con formas idiopáticas de la EP se acumula una forma sobreoxidada e inactiva de la proteína DJ-1. Curiosamente, DJ-1 desempeña un papel esencial en la defensa contra el EO y participa en la homeostasis mitocondrial, entre otras muchas funciones. En la actualidad, la EP es una enfermedad incurable cuya fisiopatología aún no está clara. Además, es urgente descubrir nuevos biomarcadores y dianas terapéuticas para facilitar su diagnóstico y tratamiento. En este contexto, se han desarrollado modelos de la EP en varios organismos que han permitido descubrir diferentes mecanismos patogénicos subyacentes a esta enfermedad. En este trabajo se ha empleado un modelo de la EP generado en Drosophila y basado en la falta de función de DJ-1β (ortólogo en Drosophila del gen DJ-1 humano). Las moscas mutantes DJ-1β muestran fenotipos relacionados con la enfermedad, como defectos motores, aumento de los niveles de EO e incremento de la carbonilación de proteínas. Dado que la modificación oxidativa de las proteínas puede alterar su función, nos planteamos identificar aquellas específicamente carboniladas en las moscas modelo para aumentar nuestra comprensión de la patogénesis de la EP, así como para descubrir posibles dianas terapéuticas para el desarrollo de nuevas estrategias de tratamiento. Para ello, se realizó un ensayo de proteómica redox en los mutantes DJ-1β en el que se identificaron proteínas con niveles aumentados de carbonilación en estas moscas respecto a las moscas control. El análisis de algunas de las proteínas identificadas en el modelo de la EP en Drosophila mostró un aumento en la actividad de enzimas de la ruta glucolítica, como la fosfofructoquinasa y la enolasa, y una disminución de la función de la proteína SERCA, implicada en el mantenimiento de la homeostasis del calcio. Estos resultados fueron confirmados en un modelo de la EP generado en células humanas de neuroblastoma deficientes en DJ-1. En conjunto, estos sugieren que la pérdida de función de DJ-1 provoca un aumento de la tasa glucolítica y que la alteración de la actividad de la proteína SERCA podría estar implicada en la fisiopatología de la EP. También demostramos que el tratamiento con compuestos que aumentan la glucólisis, como la meclizina o el dimetilfumarato, o que aumentan la actividad de SERCA, como el CDN1163, suprimen los fenotipos presentes en ambos modelos de la EP basados en la falta de función de DJ-1. Además, realizamos un estudio metabolómico en moscas deficientes en DJ-1β con el fin de identificar otras rutas metabólicas que podrían estar implicadas en la patogénesis de la EP. Nuestros resultados mostraron que las moscas modelo de la EP presentan alteraciones en el metabolismo de las proteínas, el ciclo del ácido cítrico, y un cambio en la ruta principal de obtención de energía hacia la glucólisis, además de un aumento en la expresión de algunas enzimas del ciclo de la urea. Así, estas alteraciones metabólicas podrían estar contribuyendo a la patogénesis de la EP y constituir potenciales dianas terapéuticas y/o biomarcadores para esta enfermedad

    Channel estimation and beam training with machine learning applications for millimetre-wave communication systems

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    The fifth generation (5G) wireless system will extend the capabilities of the fourth generation (4G) standards to serve more users and provide timely communication. To this end, the carriers of 5G systems will be able to operate at higher frequency bands, such as the millimetre-wave (mmWave) bands that span from 30 GHz to 300 GHz, to obtain greater bandwidths and higher data rates. As a result, the deployment of 5G networks is required to accommodate more antennas and offer pervasive coverage with controlled power consumption. The complexity of 5G systems introduces new challenges to traditional signal processing techniques. To address these challenges, a major step is to integrate machine learning (ML) algorithms into wireless communication systems. ML can learn patterns from datasets to achieve control and optimisation of complex radio frequency (RF) networks. This PhD thesis focuses on developing efficient channel estimation methods and beam training strategies with the application of ML algorithms for mmWave wireless systems. Firstly, the channel estimation and signal detection problem is investigated for orthogonal frequency-division multiplexing (OFDM) systems that operate at mmWave bands. A deep neural network (DNN)-based joint channel estimation and signal detection approach is proposed to achieve multi-user detection in a one-shot process for non-orthogonal multiple access (NOMA) systems. The DNN acts as the receiver, which can recover the transmitted data by learning the channel implicitly from suitable training. The proposed approach can be adapted to work for both single-input and single-output (SISO) systems and multiple-output and multipleoutput (MIMO) systems. This DNN-based approach is shown to provide good performance for OFDM systems that suffer from severe inter-symbol interference or where small numbers of pilot symbols are used. Secondly, the beam training and tracking problem is studied for mmWave channels with receiver mobility. To reduce the signalling overhead caused by frequent beam training, a lowcomplexity beam training strategy is proposed for mobile mmWave channels, which searches a set of selected beams obtained based on the recent beam search results. By searching only the adjacent beams to the one recently used, the proposed beam training strategy can reduce the beam training delay significantly while maintaining high transmission rates. The proposed strategy works effectively for channel datasets generated using either the stochastic or the raytracing channel model. This strategy is shown to approach the performance for an exhaustive beam search while saving up to 92% on the required beam training overhead. Thirdly, the proposed low-complexity beam training strategy is enhanced with the use of deep reinforcement learning (DRL) for mobile mmWave channels. A DRL-based beam training algorithm is proposed, which can intelligently switch between different beam training methods such that the average beam training overhead is minimised while achieving good spectral efficiency or energy efficiency performance. Given the desired performance requirement in the reward function for the DRL model, the spectral efficiency or energy efficiency can be maximised for the current channel condition by controlling the number of activated RF chains. The DRL-based approach can adjust the amount of beam training overhead required according to the dynamics of the environment. This approach can provide a good overhead-performance trade-off and achieve higher data rates in channels with significant levels of signal blockage
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