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Abstract In this paper, we investigate the problem of age of information (AoI)-aware radio resource management for expected long-term performance optimization in a Manhattan grid vehicle-to-vehicle network. With the observation of global network state at each scheduling slot, the roadside unit (RSU) allocates the frequency bands and schedules packet transmissions for all vehicle user equipment-pairs (VUE-pairs). We model the stochastic decision-making procedure as a discrete-time single-agent Markov decision process (MDP). The technical challenges in solving the optimal control policy originate from high spatial mobility and temporally varying traffic information arrivals of the VUE-pairs. To make the problem solving tractable, we first decompose the original MDP into a series of per-VUE-pair MDPs. Then we propose a proactive algorithm based on long short-term memory and deep reinforcement learning techniques to address the partial observability and the curse of high dimensionality in local network state space faced by each VUE-pair. With the proposed algorithm, the RSU makes the optimal frequency band allocation and packet scheduling decision at each scheduling slot in a decentralized way in accordance with the partial observations of the global network state at the VUE-pairs. Numerical experiments validate the theoretical analysis and demonstrate the significant performance improvements from the proposed algorithm.
Abstract Network slicing is a proposing technology to support diverse services from mobile users (MUs) over a common physical network infrastructure. In this paper, we consider radio access network (RAN)-only slicing, where the physical RAN is tailored to accommodate both computation and communication functionalities. Multiple service providers (SPs, i.e., multiple tenants) compete with each other to bid for a limited number of channels across the scheduling slots, aiming to provide their subscribed MUs the opportunities to access the RAN slices. An eavesdropper overhears data transmissions from the MUs. We model the interactions among the non-cooperative SPs as a stochastic game, in which the objective of a SP is to optimize its own expected long-term payoff performance. To approximate the Nash equilibrium solutions, we first construct an abstract stochastic game using the channel auction outcomes. Then we linearly decompose the per-SP Markov decision process to simplify the decision- makings and derive a deep reinforcement learning based scheme to approach the optimal abstract control policies. TensorFlow-based experiments verify that the proposed scheme outperforms the three baselines and yields the best performance in average utility per MU per scheduling slot.
Abstract This paper investigates an unmanned aerial vehicle (UAV)-assisted mobile-edge computing (MEC) system, in which the UAV provides complementary computation resource to the terrestrial MEC system. The UAV processes the received computation tasks from the mobile users (MUs) by creating the corresponding virtual machines. Due to finite shared I/O resource of the UAV in the MEC system, each MU competes to schedule local as well as remote task computations across the decision epochs, aiming to maximize the expected long-term computation performance. The non-cooperative interactions among the MUs are modeled as a stochastic game, in which the decision makings of a MU depend on the global state statistics and the task scheduling policies of all MUs are coupled. To approximate the Nash equilibrium solutions, we propose a proactive scheme based on the long short-term memory and deep reinforcement learning (DRL) techniques. A digital twin of the MEC system is established to train the proactive DRL scheme offline. Using the proposed scheme, each MU makes task scheduling decisions only with its own information. Numerical experiments show a significant performance gain from the scheme in terms of average utility per MU across the decision epochs.
Abstract This paper investigates an air-ground integrated multi-access edge computing system, which is deployed by an infrastructure provider (InP). Under a business agreement with the InP, a third-party service provider provides computing services to the subscribed mobile users (MUs). MUs compete for the shared spectrum and computing resources over time to achieve their distinctive goals. From the perspective of an MU, we deliberately define the age of update to capture the staleness of information from refreshing computation outcomes. Given the system dynamics, we model the interactions among MUs as a stochastic game. In the Nash equilibrium without cooperation, each MU behaves in accordance with the local system states and conjectures. We can hence transform the stochastic game into a single-agent Markov decision process. As another major contribution, we develop an online deep reinforcement learning (RL) scheme that adopts two separate double deep Q-networks to approximate the Q-factor and the post-decision Q-factor, respectively. The deep RL scheme allows each MU to optimize the behaviours with unknown dynamic statistics. Numerical experiments show that our proposed scheme outperforms the baselines in terms of the average utility under various system conditions.
Abstract Mobile data traffic has been growing exponentially over the past few years. A report from Cisco shows that the mobile data traffic in 2014 grew 69 percent and was nearly 30 times the size of the entire global Internet in 2000 [item 1) in the Appendix]. One of the primary contributors to the explosive mobile traffic growth is the rapid proliferation of mobile social applications running on multimedia mobile devices (particularly smartphones). These sharp increases in mobile traffic (particularly from mobile social applications) are projected to continue in the foreseeable future. As mobile networks by and large are designed and deployed to meet people’s social needs, people’s behaviors and interactions in the social domain will shape their ways to access mobile services. Therefore, there is an urgent need to integrate social effects into the design of mobile networks.
Abstract Vanadium(V)-substituted cerium niobate [Ce(Nb1–xVx)O4, CNVx] ceramics were prepared to explore their structure–microwave (MW) property relations and application in C-band dielectric resonator antennas (DRAs). X-ray diffraction and Raman spectroscopy revealed that CNVx (0.0 ≤ x ≤ 0.4) ceramics exhibited a ferroelastic phase transition at a critical content of V (xc = 0.3) from a monoclinic fergusonite structure to a tetragonal scheelite structure (TF–S), which decreased in temperature as a function of x according to thermal expansion analysis. Optimum microwave dielectric performance was obtained for CNV0.3 with permittivity (εr) of ∼16.81, microwave quality factor (Qf) of ∼41 300 GHz (at ∼8.7 GHz), and temperature coefficient of the resonant frequency (TCF) of ∼ –3.5 ppm/°C. εr is dominated by Ce–O phonon absorption in the microwave band; Qf is mainly determined by the porosity, grain size, and proximity of TF–S; and TCF is controlled by the structural distortions associated with TF–S. Terahertz (THz) (0.20–2.00 THz, εr ∼ 12.52 ± 0.70, and tan δ ∼ 0.39 ± 0.17) and infrared measurements are consistent, demonstrating that CNVx (0.0 ≤ x ≤ 0.4) ceramics are effective in the sub-millimeter as well as MW regime. A cylindrical DRA prototype antenna fabricated from CNV0.3 resonated at 7.02 GHz (|S11| = −28.8 dB), matching simulations, with >90% radiation efficiency and 3.34–5.93 dB gain.
Abstract Background: DNA methylation at the GFI1-locus has been repeatedly associated with exposure to smoking from the foetal period onwards. We explored whether DNA methylation may be a mechanism that links exposure to maternal prenatal smoking with offspring’s adult cardio-metabolic health. Methods: We meta-analysed the association between DNA methylation at GFI1-locus with maternal prenatal smoking, adult own smoking, and cardio-metabolic phenotypes in 22 population-based studies from Europe, Australia, and USA (n = 18,212). DNA methylation at the GFI1-locus was measured in whole-blood. Multivariable regression models were fitted to examine its association with exposure to prenatal and own adult smoking. DNA methylation levels were analysed in relation to body mass index (BMI), waist circumference (WC), fasting glucose (FG), high-density lipoprotein cholesterol (HDL—C), triglycerides (TG), diastolic, and systolic blood pressure (BP). Findings: Lower DNA methylation at three out of eight GFI1-CpGs was associated with exposure to maternal prenatal smoking, whereas, all eight CpGs were associated with adult own smoking. Lower DNA methylation at cg14179389, the strongest maternal prenatal smoking locus, was associated with increased WC and BP when adjusted for sex, age, and adult smoking with Bonferroni-corrected P < 0·012. In contrast, lower DNA methylation at cg09935388, the strongest adult own smoking locus, was associated with decreased BMI, WC, and BP (adjusted 1 × 10−7 < P < 0.01). Similarly, lower DNA methylation at cg12876356, cg18316974, cg09662411, and cg18146737 was associated with decreased BMI and WC (5 × 10−8 < P < 0.001). Lower DNA methylation at all the CpGs was consistently associated with higher TG levels. Interpretation: Epigenetic changes at the GFI1 were linked to smoking exposure in-utero/in-adulthood and robustly associated with cardio-metabolic risk factors. Fund: European Union’s Horizon 2020 research and innovation programme under grant agreement no. 633595 DynaHEALTH.
Abstract We performed a multi-ethnic Epigenome Wide Association study on 22,774 individuals to describe the DNA methylation signature of chronic low-grade inflammation as measured by C-Reactive protein (CRP). We find 1,511 independent differentially methylated loci associated with CRP. These CpG sites show correlation structures across chromosomes, and are primarily situated in euchromatin, depleted in CpG islands. These genomic loci are predominantly situated in transcription factor binding sites and genomic enhancer regions. Mendelian randomization analysis suggests altered CpG methylation is a consequence of increased blood CRP levels. Mediation analysis reveals obesity and smoking as important underlying driving factors for changed CpG methylation. Finally, we find that an activated CpG signature significantly increases the risk for cardiometabolic diseases and COPD.
Background: DNA methylation at the GFI1-locus has been repeatedly associated with exposure to smoking from the foetal period onwards. We explored whether DNA methylation may be a mechanism that links exposure to maternal prenatal smoking with offspring's adult cardio-metabolic health. Methods: We meta-analysed the association between DNA methylation at GFI1-locus with maternal prenatal smoking, adult own smoking, and cardio-metabolic phenotypes in 22 population-based studies from Europe, Australia, and USA (n = 18,212). DNA methylation at the GFI1-locus was measured in whole-blood. Multivariable regression models were fitted to examine its association with exposure to prenatal and own adult smoking. DNA methylation levels were analysed in relation to body mass index (BMI), waist circumference (WC), fasting glucose (FG), high-density lipoprotein cholesterol (HDL—C), triglycerides (TG), diastolic, and systolic blood pressure (BP). Findings: Lower DNA methylation at three out of eight GFI1-CpGs was associated with exposure to maternal prenatal smoking, whereas, all eight CpGs were associated with adult own smoking. Lower DNA methylation at cg14179389, the strongest maternal prenatal smoking locus, was associated with increased WC and BP when adjusted for sex, age, and adult smoking with Bonferroni-corrected P b 0·012. In contrast, lower DNA methylation at cg09935388, the strongest adult own smoking locus, was associated with decreased BMI, WC, and BP (adjusted 1 × 10−7 b P b 0.01). Similarly, lower DNA methylation at cg12876356, cg18316974, cg09662411, and cg18146737 was associated with decreased BMI and WC (5 × 10−8 b P b 0.001). Lower DNA methylation at all the CpGs was consistently associated with higher TG levels. Interpretation: Epigenetic changes at the GFI1 were linked to smoking exposure in-utero/in-adulthood and robustly associated with cardio-metabolic risk factors.