Multiple-Input Multiple-Output (MIMO) systems have gained an enormous amount of attention as one of the most promising research areas in wireless communications. However, while MIMO systems have been extensively explored over the past decade, few schemes acknowledge the nonlinearity caused by the use of high power amplifiers (HPAs) in the communication chain. When HPAs operate near their saturation points, nonlinear distortions are introduced in the transmitted signals, and the resulting MIMO channel will be nonlinear. The nonlinear distortion is further exacerbated by the fading caused by the propagation channel. The goal of this thesis is: 1) to use neural networks (NNs) to model and identify nonlinear MIMO channels; and 2) to employ the proposed NN model in designing efficient detection techniques for these types of MIMO channels. In the first part of the thesis, we follow a previous work on modeling and identification of nonlinear MIMO channels, where it has been shown that a proposed block-oriented NN scheme allows not only good identification of the overall MIMO input-output transfer function but also good characterization of each component of the system. The proposed scheme employs an ordinary gradient descent based algorithm to update the NN weights during the learning process and it assumes only real-valued inputs. In this thesis, natural gradient (NG) descent is used for training the NN. Moreover, we derive an improved variation of the previously proposed NN scheme to avoid the input type restriction and allow for complex modulated inputs as well. We also investigate the scheme tracking capabilities of time-varying nonlinear MIMO channels. Simulation results show that NG descent learning significantly outperforms the ordinary gradient descent in terms of convergence speed, mean squared error (MSE) performance, and nonlinearity approximation. Moreover, the NG descent based NN provides better tracking capabilities than the previously proposed NN. The second part of the thesis focuses on signal detection. We propose a receiver that employs the neural network channel estimator (NNCE) proposed in part one, and uses the Zero-Forcing Vertical Bell Laboratories Layered Space-Time (ZF V-BLAST) detection algorithm to retrieve the transmitted signals. Computer simulations show that in slow time-varying environments the performance of our receiver is close to the ideal V-BLAST receiver in which the channel is perfectly known. We also present a NN based linearization technique for HPAs, which takes advantage of the channel information provided by the NNCE. Such linearization technique can be used for adaptive data predistortion at the transmitter side or adaptive nonlinear equalization at the receiver side. Simulation results show that, when higher modulation schemes (>16-QAM) are used, the nonlinear distortion caused by the use of HPAs is greatly minimized by our proposed NN predistorter and the performance of the communication system is significantly improved. / Thesis (Master, Electrical & Computer Engineering) -- Queen's University, 2007-08-08 14:55:50.489

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In septic shock (SS), hydrogen peroxide (H2O2) and other reactive oxygen species (ROS) are released by inflammatory cells and have been implicated in tissue damage and inflammation. Recently, H2O2 has been established as an important signaling molecule and an important component of SS. The pathways involved in this process are not completely understood, but the formation of hydroperoxides (HPs), arachidonic acid (AA) metabolites and potassium (K+) channels have been implicated. In this study, we used a canine carotid ring preparation as a bioassay to determine the role of peroxyacetic acid (POX), a hydroperoxide (HP), in causing vasodilation and elucidate the subsequent pathways involved. We removed internal carotid artery segments from dogs and placed them in an organ bath. The segments were preconstricted after which we added POX to the preparation. We found that POX produced an endothelium and nitric oxide independent vasodilation in the carotid artery ring preparation. This decrease in tension could be prevented by high concentrations of K+ in the bath. This suggested that K+ channels were involved in POX’s action. Further investigation showed that the particular K+ channels implicated were the combination of small (SKCa) and intermediate conductance calcium activated K+ channels (IKCa). In addition we found that the prostaglandin H synthase (PGHS) inhibitor, indomethacin, could block POX’s mechanism of action. This finding indicates that PGHS takes part in the vasodilation caused by POX. Our results suggest that HPs that are released from inflammatory cells in sepsis could stimulate the PGHS pathway leading to prostaglandin synthesis and subsequently activating SKCa and IKCa to produce vasodilation. Inhibition of this pathway may be important component in the treatment of SS.

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Glutamate-gated chloride channels (GluCl) belong to then icotinic ligand-gated ion channel family and are thus assumed to be heteropentamers. Each subunit contains a large extracellular N-terminal domain, four transmembrane domains (TM1--TM4), and an extracellular C terminal. Caenorhabditis elegans expresses various GluCl channels formed by alpha1, alpha2, alpha3, alpha4 and beta subunits. The best understood GluCl channel is expressed in pharyngeal muscle cells where it mediates response to the M3 motor neuron. alpha2 forms this channel, probably in association with beta. The alpha2 mutant lacks M3 neurotransmission which can be rescued by pharynx-specific alpha2 expression. My results show that alpha1 and alpha3 subunits cannot substitute for alpha2. Formation of chimeric constructs of alpha1, alpha2 and alpha3 pinpoints the M1--M3 transmembrane region of alpha2 as the minimal rescuing domain. This region may therefore be important for localization or, in association with another subunit, in the formation of the active channel.