33 research outputs found

    Characterizing throughput and convergence time in dynamic multi-connectivity 5G deployments

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    Fifth-generation (5G) mobile communications are expected to integrate multiple radio access technologies (RATs) within a unified access network by allowing the user equipment (UE) to utilize them concurrently. As a consequence, mobile users face even more heterogeneous connectivity options, which creates challenges for efficient decision-making when selecting a network dynamically. In this work, with the tools of queuing theory, integral geometry, and optimization theory, we develop a novel mobility-centric analytical methodology for multi-RAT deployments. Particularly, we first contribute a framework for optimal data rate allocation in the network-assisted regime. Then, we characterize the convergence time of the distributed optimization algorithms based on reinforcement learning to reduce the signaling overheads. Our findings suggest that network-assisted strategies may improve the UE throughput by up to 60% depending on the considered deployment, where the gains increase with a higher density of millimeter-wave New Radio (NR) base stations. A user-centric solution based on reinforcement learning mechanisms is capable of approaching the performance of the network-assisted scheme. However, the associated convergence time may be prohibitive, on the order of several minutes. To improve the latter, we further propose and evaluate a transfer learning-based algorithm that allows to decrease the convergence time by up to 10 times, thus becoming a simple solution for rate-optimized operation in future 5G NR deployments. © 2022 The Author(s

    Enabling Social- and Location-Aware IoT Applications in Smart Cities

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    In the last decade, governments, municipalities, and industries have invested large amounts of funds on research on smart cities with the main goal of developing services to improve people’s quality of life. Many proposals focus on a Cloud-centric network architecture in which all the data collected from a myriad of sensors devices is transferred to the Cloud for processing. However, this approach presents significant limitations when faced with the formidable traffic generated by the Internet of Things and with the need for low-latency services. The deployment of IoT devices in compact groups, connected to the smart city network infrastructure by relatively powerful “gateways”, opens the possibility to depart from the centralized architectures and move the computation closer to the data sources. To this end, this paper proposes SPF, a new middleware solution that supports IoT application and service development, deployment, and management. SPF runs IoT services on capable devices located at the edge of the network and proposes a programming model that enables to take advantage of decentralized computation resources in a seamless fashion. SPF also leverages an information dissemination solution designed for constrained network environments and adopts Value-of-Information based methods to prioritize transmission of essential information

    Compound heterozygous mutations P336L and I1660V in the human cardiac sodium channel associated with the Brugada syndrome

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    BACKGROUND - Loss-of-function mutations in SCN5A have been associated with the Brugada syndrome. We report the first Brugada syndrome family with compound heterozygous mutations in SCN5A. The proband inherited 1 mutation from each parent and transmitted 1 to each daughter. METHODS AND RESULTS - The effects of the mutations on the function of the sodium channel were evaluated with heterologous expression in TSA201 cells, patch-clamp study, and confocal microscopy. Genetic analysis revealed that the proband carried 2 heterozygous missense mutations (P336L and I1660V) on separate alleles. He displayed a coved-type ST-segment elevation and a prolonged PR interval (280 ms). One daughter inherited P336L and exhibited a prolonged PR (210 ms). The other daughter inherited mutation I1660V and displayed a normal PR interval. Both daughters had a slightly elevated, upsloping ST-segment elevation. The parents had normal ECGs. Patch-clamp analysis showed that the P336L mutation reduced INa by 85% relative to wild type. The I1660V mutation produced little measurable current, which was rescued by room temperature incubation for 48 hours. Sodium channel blockers also rescued the I1660V current, with mexiletine proving to be the most effective. Confocal immunofluorescence showed that I1660V channels conjugated to green fluorescent protein remained trapped in intracellular organelles. CONCLUSIONS - Mutation P336L produced a reduction in cardiac INa, whereas I1660V abolished it. Only the proband carrying both mutations displayed the Brugada syndrome phenotype, whereas neither mutation alone produced the clinical phenotype. I1660V channels could be rescued pharmacologically and by incubation at room temperature. The present data highlight the role of compound heterozygosity in modulating the phenotypic expression and penetrance of Brugada syndrome. © 2006 American Heart Association, Inc

    Comparison of rinsing and sanitizing procedures for reducing bacterial pathogens on fresh cantaloupes and bell peppers

    No full text
    BACKGROUND - Loss-of-function mutations in SCN5A have been associated with the Brugada syndrome. We report the first Brugada syndrome family with compound heterozygous mutations in SCN5A. The proband inherited 1 mutation from each parent and transmitted 1 to each daughter. METHODS AND RESULTS - The effects of the mutations on the function of the sodium channel were evaluated with heterologous expression in TSA201 cells, patch-clamp study, and confocal microscopy. Genetic analysis revealed that the proband carried 2 heterozygous missense mutations (P336L and I1660V) on separate alleles. He displayed a coved-type ST-segment elevation and a prolonged PR interval (280 ms). One daughter inherited P336L and exhibited a prolonged PR (210 ms). The other daughter inherited mutation I1660V and displayed a normal PR interval. Both daughters had a slightly elevated, upsloping ST-segment elevation. The parents had normal ECGs. Patch-clamp analysis showed that the P336L mutation reduced INa by 85% relative to wild type. The I1660V mutation produced little measurable current, which was rescued by room temperature incubation for 48 hours. Sodium channel blockers also rescued the I1660V current, with mexiletine proving to be the most effective. Confocal immunofluorescence showed that I1660V channels conjugated to green fluorescent protein remained trapped in intracellular organelles. CONCLUSIONS - Mutation P336L produced a reduction in cardiac INa, whereas I1660V abolished it. Only the proband carrying both mutations displayed the Brugada syndrome phenotype, whereas neither mutation alone produced the clinical phenotype. I1660V channels could be rescued pharmacologically and by incubation at room temperature. The present data highlight the role of compound heterozygosity in modulating the phenotypic expression and penetrance of Brugada syndrome. " 2006 American Heart Association, Inc.",,,,,,"10.1161/CIRCULATIONAHA.106.627489",,,"http://hdl.handle.net/20.500.12104/40264","http://www.scopus.com/inward/record.url?eid=2-s2.0-33750731284&partnerID=40&md5=ea83d39951b11e466aedab197b444c99",,,,,,"19",,"Circulation",,"202
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