Backscatter Communication: Design and Optimisation For Emerging Use-Cases

Backscatter communication (BackCom) holds significant potential to improve the pervasiveness and energy efficiency of future wireless networks, through its passive modulation and reuse of existing radiofrequency signals. In order to function as a key technology under the Internet of Things paradigm, issues relating to BackCom, such as its limited coverage and deployment flexibility, low data rates, and the difficulty of channel estimation, need to be addressed. To complement this, a wider range of use-cases and deployment scenarios also need to be established. This thesis focuses on addressing these issues inherent to BackCom, by exploring a series of system setups which push the boundaries in terms of coverage and flexible deployment, and then future-proofs BackCom through the study of the assistance from another emerging technology, the intelligent reflecting surface (IRS). The first half of the thesis focuses on the coverage and deployment flexibility of BackCom devices under conventional wireless communication settings. First, we study a novel use-case in which BackCom devices replace conventional, actively transmitting relays to assist an information transmission from a source to a destination. We introduce the decode-and-forward (DF) BackCom relaying scheme and perform a detailed bit error rate (BER) characterisation of the DF BackCom scheme alongside the amplify-and-forward (AF) BackCom 'reflection' scheme. The feasibility and practical range of the BackCom relay is demonstrated through a case study, and our findings indicate that with careful selection of relay parameters, the DF scheme can improve the functionality of BackCom relays through the decoding operation, while resulting in minimal BER differences compared to the AF 'reflection' scheme. Second, we study the coverage maximisation of bistatic BackCom systems in wide-area environmental monitoring applications through judicious power beacon (PB) placement. We propose a straightforward metric to characterise coverage, the guaranteed coverage distance (GCD), to overcome the complex shape of each PB's coverage area when the performance of the BackCom link is dependent on the strength of the energy transfer link. We find that a single-tier symmetric deployment of PBs performs favourably under a practical number (24 or less) of PBs, with a GCD of more than 100m being readily achievable. The second half of the thesis studies the incorporation of the IRS into BackCom systems, with the aim of improving BackCom performance. The IRS-assisted bistatic BackCom system is studied first, where we solve a transmit power minimisation problem at the carrier emitter involving the joint optimisation of the transmit and receive beamforming, the IRS phase shifts and the BackCom splitting coefficients. We present a unique signal model arising from this system, where a signal originating from the carrier emitter may be reflected by the IRS twice before reaching the reader, and account for this added complexity in our algorithm design. Our results indicate that transmit power savings of over 6 dB may be achieved with a moderately-sized IRS, which may be converted to nearly 50m of range increase. Then, we study the use of the IRS in an ambient BackCom system, with the goal of reducing direct-link interference and improving detection performance. We assume the absence of all ambient signal and channel knowledge, which is a practical assumption given the passively reflecting nature of both BackCom devices and IRSs. We propose a deep reinforcement learning (DRL)-based algorithm which maximises the backscatter channel difference (that is, the ratio of the energies of the direct-link interference and overall received signal) based on instantaneous signal samples, which may be converted to BER reductions. We find that the DRL approach with no channel knowledge can achieve a backscatter channel difference within 25% of that obtained using benchmarks with full channel knowledge

The Role of Immune Response and Microbiota on Campylobacteriosis

Million cases of campylobacteriosis and complications of post-Campylobacter jejuni infection occur every year around the world with huge life losses and economic burdens of billions of dollars. Few therapy options, such as antibiotics, are available to relieve severe cases of the enteritis. The slow progression on new intervention discovery and application is partially resulted from limited mechanistic understanding on campylobacteriosis pathogenesis. As a type of intestinal disorders, campylobacteriosis shares many common features with other intestinal diseases such as inflammatory bowel diseases (IBD) and Clostridium difficile infection. In pace with the advancement of the gastroenterology field, a large body of knowledge is accumulating on the factors influencing campylobacteriosis onset, development, and outcomes, including host immune response, intestinal microbiota, and its metabolites. In this chapter, we review the intestinal immune system, intestinal microbiome, and microbiome modulation of inflammation in the development of campylobacteriosis. The interplay between immunity, microbiota, and its metabolites may play essential roles on campylobacteriosis pathogenesis and the finding on the interaction may lead to new prevention and treatment options. The purpose of this chapter is to provide updated knowledge on the role of host–microbe interaction and the therapeutic potential on campylobacteriosis

Natural Compound Resveratrol Attenuates TNF-Alpha-Induced Vascular Dysfunction in Mice and Human Endothelial Cells: The Involvement of the NF-κB Signaling Pathway

Resveratrol, a natural compound in grapes and red wine, has drawn attention due to potential cardiovascular-related health benefits. However, its effect on vascular inflammation at physiologically achievable concentrations is largely unknown. In this study, resveratrol in concentrations as low as 1 μm suppressed TNF-α-induced monocyte adhesion to human EA.hy926 endothelial cells (ECs), a key event in the initiation and development of atherosclerosis. Low concentrations of resveratrol (0.25–2 μm) also significantly attenuated TNF-α-stimulated mRNA expressions of MCP-1/CCL2 and ICAM-1, which are vital mediators of EC-monocyte adhesion molecules and cytokines for cardiovascular plaque formation. Additionally, resveratrol diminished TNF-α-induced IκB-α degradation and subsequent nuclear translocation of NF-κB p65 in ECs. In the animal study, resveratrol supplementation in diet significantly diminished TNF-α-induced increases in circulating levels of adhesion molecules and cytokines, monocyte adhesion to mouse aortic ECs, F4/80-positive macrophages and VCAM-1 expression in mice aortas and restored the disruption in aortic elastin fiber caused by TNF-α treatment. The animal study also confirmed that resveratrol blocks the activation of NF-κB In Vivo. In conclusion, resveratrol at physiologically achievable concentrations displayed protective effects against TNF-α-induced vascular endothelial inflammation in vitro and In Vivo. The ability of resveratrol in reducing inflammation may be associated with its role as a down-regulator of the NF-κB pathway

Triterpenoid CDDO-IM protects against lipopolysaccharide-induced inflammatory response and cytotoxicity in macrophages: The involvement of the NF-κB signaling pathway

Lipopolysaccharide (LPS), also known as endotoxin, can trigger septic shock, a severe form of inflammation-mediated sepsis with a very high mortality rate. However, the precise mechanisms underlying this endotoxin remain to be defined and detoxification of LPS is yet to be established. Macrophages, a type of immune cells, initiate a key response responsible for the cascade of events leading to the surge in inflammatory cytokines and immunopathology of septic shock. This study was undertaken to determine whether the LPS-induced inflammation in macrophage cells could be ameliorated via CDDO-IM (2-cyano-3,12 dioxooleana-1,9 dien-28-oyl imidazoline), a novel triterpenoid compound. Data from this study show that gene expression levels of inflammatory cytokine genes such as interleukin-1 beta (IL-1β), interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) were considerably increased by treatment with LPS in macrophages differentiated from ML-1 monocytes. Interestingly, LPS-induced increase in expression of pro-inflammatory cytokine levels is reduced by CDDO-IM. In addition, endogenous upregulation of a series of antioxidant molecules by CDDO-IM provided protection against LPS-induced cytotoxicity in macrophages. LPS-mediated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) transcriptional activity was also noted to decrease upon treatment with CDDO-IM in macrophages suggesting the involvement of the NF-κB signaling. This study would contribute to improve our understanding of the detoxification of endotoxin LPS by the triterpenoid CDDO-IM

Targeting glutathione with the triterpenoid CDDO-Im protects against benzo-a-pyrene-1,6-quinone-induced cytotoxicity in endothelial cells

Epidemiological studies have exhibited a strong correlation between exposure to air pollution and deaths due to vascular diseases such as atherosclerosis. Benzo-a-pyrene-1,6-quinone (BP-1,6-Q) is one of the components of air pollution This study was to examine the role of GSH in BP-1,6-Q mediated cytotoxicity in human EA.hy96 endothelial cells and demonstrated that induction of cellular glutathione by a potent triterpenoid, CDDO-Im (1-[2-cyano-3-,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole), protects cells against BP-1,6-Q induced protein and lipid damage. Incubation of EA.hy926 endothelial cells with BP-1,6-Q caused a significant increase in dose-dependent cytotoxicity as measured by LDH release assay and both apoptotic and necrotic cell deaths as measured by flow cytometric analysis. Incubation of EA.hy926 endothelial cells with BP-1,6-Q also caused a significant decrease in cellular GSH levels. The diminishment of cellular GSH by buthionine sulfoximine (BSO) potentiated BP-1,6-Q-induced toxicity significantly suggesting a critical involvement of GSH in BP-1,6-Q induced cellular toxicity. GSH-induction by CDDO-Im significantly protects cells against BP-1,6-Q induced protein and lipid damage as measured by protein carbonyl (PC) assay and thiobarbituric acid reactive substances (TBARS) assay, respectively. However, the co-treatment of cells with CDDO-Im and BSO reversed the cytoprotective effect of CDDO-Im on BP-1,6-Q-mediated lipid peroxidation and protein oxidation. These results suggest that induction of GSH by CDDO-Im might be the important cellular defense against BP-1,6-Q induced protein and lipid damage. These findings would contribute to better understand the action of BP-1,6-Q and may help to develop novel therapies to protect against BP-1,6-Q-induced atherogenesis