Load balancing in hybrid LiFi and RF networks

The increasing number of mobile devices challenges the current radio frequency (RF) networks. The conventional RF spectrum for wireless communications is saturating, motivating to develop other unexplored frequency bands. Light Fidelity (LiFi) which uses more than 300 THz of the visible light spectrum for high-speed wireless communications, is considered a promising complementary technology to its RF counterpart. LiFi enables daily lighting infrastructures, i.e. light emitting diode (LED) lamps to realise data transmission, and maintains the lighting functionality at the same time. Since LiFi mainly relies on line-of-sight (LoS) transmission, users in indoor environments may experience blockages which significantly affects users’ quality of service (QoS). Therefore, hybrid LiFi and RF networks (HLRNs) where LiFi supports high data rate transmission and RF offers reliable connectivity, can provide a potential solution to future indoor wireless communications. In HLRNs, efficient load balancing (LB) schemes are critical in improving the traffic performance and network utilisation. In this thesis, the optimisation-based scheme (OBS) and the evolutionary game theory (EGT) based scheme (EGTBS) are proposed for load balancing in HLRNs. Specifically, in OBS, two algorithms, the joint optimisation algorithm (JOA) and the separate optimisation algorithm (SOA) are proposed. Analysis and simulation results show that JOA can achieve the optimal performance in terms of user data rate while requiring high computational complexity. SOA reduces the computational complexity but achieves low user data rates. EGTBS is able to achieve a better performance/complexity trade-off than OBS and other conventional load balancing schemes. In addition, the effects of handover, blockages, orientation of LiFi receivers, and user data rate requirement on the throughput of HLRNs are investigated. Moreover, the packet latency in HLRNs is also studied in this thesis. The notion of LiFi service ratio is introduced, defined as the proportion of users served by LiFi in HLRNs. The optimal LiFi service ratio to minimise system delay is mathematically derived and a low-complexity packet flow assignment scheme based on this optimum ratio is proposed. Simulation results show that the theoretical optimum of the LiFi service ratio is very close to the practical solution. Also, the proposed packet flow assignment scheme can reduce at most 90% of packet delay compared to the conventional load balancing schemes at reduced computational complexity

Robust and Low-Complexity Timing Synchronization for DCO-OFDM LiFi Systems

Personal use of this material is permitted. Permission from IEEE must be obtained for all other uses, in any current or future media, including reprinting/republishing this material for advertising or promotional purposes, creating new collective works, for resale or redistribution to servers or lists, or reuse of any copyrighted component of this work in other works.Light fidelity (LiFi), using light emitting devices such as light emitting diodes (LEDs) which are operating in the visible light spectrum between 400 and 800 THz, provides a new layer of wireless connectivity within existing heterogeneous radio frequency wireless networks. Link data rates of 10 Gbps from a single transmitter have been demonstrated under ideal laboratory conditions. Synchronization is one of these issues usually assumed to be ideal. However, in a practical deployment, this is no longer a valid assumption. Therefore, we propose for the first time a low-complexity maximum likelihood-based timing synchronization process that includes frame detection and sampling clock synchronization for direct current-biased optical orthogonal frequency division multiplexing LiFi systems. The proposed timing synchronization structure can reduce the high-complexity two-dimensional search to two low-complexity one-dimensional searches for frame detection and sampling clock synchronization. By employing a single training block, frame detection can be realized, and then sampling clock offset (SCO) and channels can be estimated jointly. We propose three frame detection approaches, which are robust against the combined effects of both SCO and the low-pass characteristic of LEDs. Furthermore, we derive the Cramér-Rao lower bounds (CRBs) of SCO and channel estimations, respectively. In order to minimize the CRBs and improve synchronization performance, a single training block is designed based on the optimization of training sequences, the selection of training length, and the selection of direct current (DC) bias. Therefore, the designed training block allows us to analyze the trade-offs between estimation accuracy, spectral efficiency, energy efficiency, and complexity. The proposed timing synchronization mechanism demonstrates low complexity and robustness benefits and provides performance significantly better than achieved with existing methods.Peer reviewe

Dual-agonist occupancy of orexin receptor 1 and cholecystokinin A receptor heterodimers decreases G-protein-dependent signaling and migration in the human colon cancer cell line HT-29

The orexin (OX1R) and cholecystokinin A (CCK1R) receptors play opposing roles in the migration of the human colon cancer cell line HT-29, and may be involved in the pathogenesis and pathophysiology of cancer cell invasion and metastasis. OX1R and CCK1R belong to family A of the G-protein-coupled receptors (GPCRs), but the detailed mechanisms underlying their functions in solid tumor development remain unclear. In this study, we investigated whether these two receptors heterodimerize, and the results revealed novel signal transduction mechanisms. Bioluminescence and Förster resonance energy transfer, as well as proximity ligation assays, demonstrated that OX1R and CCK1R heterodimerize in HEK293 and HT-29 cells, and that peptides corresponding to transmembrane domain 5 of OX1R impaired heterodimer formation. Stimulation of OX1R and CCK1R heterodimers with both orexin-A and CCK decreased the activation of Gαq, Gαi2, Gα12, and Gα13 and the migration of HT-29 cells in comparison with stimulation with orexin-A or CCK alone, but did not alter GPCR interactions with β-arrestins. These results suggest that OX1R and CCK1R heterodimerization plays an anti-migratory role in human colon cancer cells. [Abstract copyright: Copyright © 2017. Published by Elsevier B.V.

Chromophore supply modulates cone function and survival in retinitis pigmentosa mouse models.

Retinitis pigmentosa (RP) is an ocular disease characterized by the loss of night vision, followed by the loss of daylight vision. Daylight vision is initiated in the retina by cone photoreceptors, which are gradually lost in RP, often as bystanders in a disease process that initiates in their neighboring rod photoreceptors. Using physiological assays, we investigated the timing of cone electroretinogram (ERG) decline in RP mouse models. A correlation between the time of loss of the cone ERG and the loss of rods was found. To investigate a potential role of the visual chromophore supply in this loss, mouse mutants with alterations in the regeneration of the retinal chromophore, 11-cis retinal, were exam- ined. Reducing chromophore supply via mutations in Rlbp1 or Rpe65 resulted in greater cone function and survival in a RP mouse model. Conversely, overexpression of Rpe65 and Lrat, genes that can drive the regeneration of the chromophore, led to greater cone degeneration. These data suggest that abnormally high chromophore supply to cones upon the loss of rods is toxic to cones, and that a potential therapy in at least some forms of RP is to slow the turnover and/or reduce the level of visual chromophore in the retina

Gain scheduled torque compensation of PMSG-based wind turbine for frequency regulation in an isolated grid

Frequency stability in an isolated grid can be easily impacted by sudden load or wind speed changes. Many frequency regulation techniques are utilized to solve this problem. However, there are only few studies designing torque compensation controllers based on power performances in different Speed Parts. It is a major challenge for a wind turbine generator (WTG) to achieve the satisfactory compensation performance in different Speed Parts. To tackle this challenge, this paper proposes a gain scheduled torque compensation strategy for permanent magnet synchronous generator (PMSG) based wind turbines. Our main idea is to improve the anti-disturbance ability for frequency regulation by compensating torque based on WTG speed Parts. To achieve higher power reserve in each Speed Part, an enhanced deloading method of WTG is proposed. We develop a new small-signal dynamic model through analyzing the steady-state performances of deloaded WTG in the whole range of wind speed. Subsequently, H∞ theory is leveraged in designing the gain scheduled torque compensation controller to effectively suppress frequency fluctuation. Moreover, since torque compensation brings about untimely power adjustment in over-rated wind speed condition, the conventional speed reference of pitch control system is improved. Our simulation and experimental results demonstrate that the proposed strategy can significantly improve frequency stability and smoothen power fluctuation resulting from wind speed variations. The minimum of frequency deviation with the proposed strategy is improved by up to 0.16 Hz at over-rated wind speed. Our technique can also improve anti-disturbance ability in frequency domain and achieve power balance

Ku80 cooperates with CBP to promote COX-2 expression and tumor growth.

Cyclooxygenase-2 (COX-2) plays an important role in lung cancer development and progression. Using streptavidin-agarose pulldown and proteomics assay, we identified and validated Ku80, a dimer of Ku participating in the repair of broken DNA double strands, as a new binding protein of the COX-2 gene promoter. Overexpression of Ku80 up-regulated COX-2 promoter activation and COX-2 expression in lung cancer cells. Silencing of Ku80 by siRNA down-regulated COX-2 expression and inhibited tumor cell growth in vitro and in a xenograft mouse model. Ku80 knockdown suppressed phosphorylation of ERK, resulting in an inactivation of the MAPK pathway. Moreover, CBP, a transcription co-activator, interacted with and acetylated Ku80 to co-regulate the activation of COX-2 promoter. Overexpression of CBP increased Ku80 acetylation, thereby promoting COX-2 expression and cell growth. Suppression of CBP by a CBP-specific inhibitor or siRNA inhibited COX-2 expression as well as tumor cell growth. Tissue microarray immunohistochemical analysis of lung adenocarcinomas revealed a strong positive correlation between levels of Ku80 and COX-2 and clinicopathologic variables. Overexpression of Ku80 was associated with poor prognosis in patients with lung cancers. We conclude that Ku80 promotes COX-2 expression and tumor growth and is a potential therapeutic target in lung cancer

Individual phosphorylation sites at the C-terminus of the apelin receptor play different roles in signal transduction

The apelin and Elabela proteins constitute a spatiotemporal double-ligand system that controls apelin receptor (APJ) signal transduction. Phosphorylation of multiple sites within the C-terminus of APJ is essential for the recruitment of β-arrestins. We sought to determine the precise mechanisms by which apelin and Elabela promote APJ phosphorylation, and to elucidate the influence of β-arrestin phosphorylation on G-protein-coupled receptor (GPCR)/β-arrestin-dependent signaling. We used techniques including mass spectrometry (MS), mutation analysis, and bioluminescence resonance energy transfer (BRET) to evaluate the role of phosphorylation sites in APJ-mediated G-protein-dependent and β-dependent signaling. Phosphorylation of APJ occurred at five serine residues in the C-terminal region (Ser335, Ser339, Ser345, Ser348 and Ser369). We also identified two phosphorylation sites in β-arrestin1 and three in β-arrestin2, including three previously identified residues (Ser412, Ser361, and Thr383) and two new sites, Tyr47 in β-arrestin1 and Tyr48 in β-arrestin2. APJ mutations did not affect the phosphorylation of β-arrestins, but it affects the β-arrestin signaling pathway, specifically Ser335 and Ser339. Mutation of Ser335 decreased the ability of the receptor to interact with β-arrestin1/2 and AP2, indicating that APJ affects the β-arrestin signaling pathway by stimulating Elabela. Mutation of Ser339 abolished the capability of the receptor to interact with GRK2 and β-arrestin1/2 upon stimulation with apelin-36, and disrupted receptor internalization and β-arrestin-dependent ERK1/2 activation. Five peptides act on distinct phosphorylation sites at the APJ C-terminus, differentially regulating APJ signal transduction and causing different biological effects. These findings may facilitate screening for drugs to treat cardiovascular and metabolic diseases

MiR-27b-3p Inhibition Enhances Browning of Epididymal Fat in High-Fat Diet Induced Obese Mice

Objective: Long-term dysregulation of energy balance is the key component of the obesity epidemic. Given the harm of central obesity and the discovery that beige cells appear within white adipose tissue (WAT), enhancing the energy-expending or “browning” ability of visceral adipose tissue (VAT) has become of therapeutic interest. In this study, we focused on the regulating role of microRNA (miRNA)-27b-3p in mice epididymal white adipose tissue (eWAT) browning.Methods: High-fat diet (HFD) induced obese mice model was constructed. Expression of miR-27b-3p and Ucp1 in eWAT was measured during the course of HFD. Through tail vein injection of antimiR-27b-3p, miR-27b-3p expression was inhibited to analyze the potential role of miR-27b-3p in fat browning and metabolism.Results: miR-27b-3p was predominantly expressed in eWAT and browning ability of eWAT in HFD induced obese mice was impaired. Inhibition of miR-27b-3p enhanced browning capacity of eWAT in mice fed an HFD and led to weight loss and insulin sensitivity improvement.Conclusions: High expression of miR-27b-3p in eWAT inhibits browning ability and leads to visceral fat accumulation. It is suggested miR-27b-3p may become a potential therapeutic option for visceral obesity and its associated diseases