The electronic structure and reaction dynamics of molecular and cluster anions in the gas phase has been investigated using negative ion velocity-map imaging photoelectron spectrometer. Photoelectron images provide important information about both energies and symmetries of the parent anion orbitals from which photoelectron originates. The symmetry and the ordering of several low-lying electronic states of neutral nitromethane (X¹A′, a³A″, b³A″, and A¹A″) are assigned based on a group theoretical analysis of the transitions angular distributions and the results of DFT calculations. The through-bond electronic coherence in meta- and para-dinitrobenzene anions is explored by recording a series of photoelectron images in 532-266 nm wavelength range. Photoelectron angular distributions for both isomers exhibit oscillatory behavior characteristic of the quantum interference effect, suggesting that dinitrobenzene anions retain their high symmetry electronic structures in the gas phase. Photoelectron imaging experiments on [O(N₂O)(n)]⁻, n =0–9 at 266 and 355 nm provide clear evidence of a switch from the cova)lent NNO₂⁻ cluster core to the atomic O⁻ core occurring between n = 3 and 4. The experimental results and theoretical modeling indicate that despite the greater stability of NNO₂⁻ relative to the O⁻ + N₂O⁻ dissociation limit, an O⁻ cluster core becomes energetically favored over NNO₂⁻ for n > 3, due to the more efficient solvation of the atomic anion. The photodissociation dynamics of I₂⁻ and IBr⁻ anions on the respective A' excited-state anion potentials is effectively unraveled in 780 nm pump - 390 nm probe time-resolve experiments. The time-dependent photoelectron spectra and classical trajectory calculations of the IBr⁻ dissociation provide the first rigorous dynamical test of the recently calculated A′ potential for this system. The photoelectron anisotropy cyclic variation observed in photodissociation of I₂⁻ is interpreted in the context of dual-center quantum interference model. The 390 nm pump – 390 nm probe experimental data reveal fast (≤100 fs) and delayed (~ 700 fs) appearance of the I⁻ channel in the photodissociation of I₂Cl⁻ and BrICl⁻ anions respectively. The difference in the reaction time-scales is attributed to the distinct dissociation pathways available for the anions to form I⁻ product.

Engineered resistance mediated by RNA interference to control viral diseases in plants has shown great promise. However, the discovery that most known plant viruses encode RNAi suppressors which interfere with RNAi raised the issue to whether this type of engineered resistance can be durable in the presence of heterologous viruses in mixed infection. The overall goal of this study was to investigate the mechanism of suppression of RNAi-mediated resistance in transgenic plants in the presence of a virus carrying a strong suppressor of RNAi. Nicotiana benthamiana plants were transformed with a 1.2 kb from the 5' end of RCNMV RNA-1. Transgenic resistant lines were obtained. Resistance in two different transgenic lines was shown to be mediated by two different types of RNAi: constitutive RNAi in D2 line induced by doubles-stranded (ds) transgene transcripts and virus-induced RNAi in B1 line. We demonstrated that PVY differentially affected RNAi-mediated resistance in the two lines. D2 line is completely immune to RCNMV infection. D2 line contained multiple copies of the 1.2 kb transgene which are rearranged and produced dsRNAs. PVY did not break the resistance in this transgenic line however data showed that PVY interfered with RNAi which correlated to an increase of the 1.2 kb transgene mRNA. In addition, PVY infection induced accumulation of 21 nt siRNAs and did not alter the transcription of the transgene. In contrast, PVY infection suppressed resistance mediated by virus-induced RNAi in B1 line. B1 contains a single copy of the1.2 kb transgene and is initially susceptible to RCNMV infection however became resistant to RCNMV in newly merging leaves after 14 days post inoculation. PVY infection did not affect the accumulation of the 1.2 kb transgene mRNA nor the accumulation of 21 nt siRNA corresponding to the transgene. The differential effect of PVY infection on the two RNAi-mediated resistances in the two transgenic lines suggests that properly designed resistant plants might withstand mixed virus infections and the presence of a strong suppressor of RNAi. In addition, the differential effect of PVY on RNAi suggests that parallel but distinct pathways are involved in dsRNA-induced, virus-induced, and sense RNAi.

Influenza virus is a globally significant infectious agent with the potential to cause catastrophic pandemic outbreaks. Present treatment of influenza infections is restricted to only four anti-viral drugs, but there are increasing global reports of anti-viral resistance in several seasonal strains and also the 2009 pandemic swine-origin influenza virus H1N1. Possible future pandemic outbreaks, emerging new strains and drug resistance underscore the need to understand this complex virus and its pathogenicity with the goal that novel targets can be uncovered for future therapeutic development. Extensive lung tissue damage during influenza virus infection is proposed to contribute to the development of aberrant host immune responses. Strong evidence now demonstrates the significance of the cellular death pathway in promoting efficient influenza virus replication and disease progression. Viruses rely heavily on the machinery of their host for productive replication, which is also an Achilles’ heel that could be targeted for treatment. In pursuit of unraveling the complex nature of influenza virus replication, I carried out a global shRNA screen to identify specific host factors and signaling pathways that are involved in influenza-induced cell death and replication. In this study I identified 138 genes required for influenza viruses to induce infected host cell death. These genes were found to be involved in Protein Kinase A, NF-kB and PI3K signaling cascades. These signaling pathways are well known regulators of cell death and survival, which suggests influenza viruses may carefully regulate these pathways to reach a balance that suit their requirements for efficient proliferation, eventually at the cost of the host cell. I chose five candidate genes—BAD, MxB, TNFSF12-13,TNFSF13, and USP47—that were associated with apoptosis and the major signaling pathways determined in my network analysis to further verify the genome-wide screen as well as elucidate the role of these potentially novel host factors in influenza virus replication. I show in my study that influenza virus-induced cytopathology and cell death are considerably inhibited in BAD knockdown cells and both virus replication and viral protein production also are dramatically reduced. I also report here that MxB depletion protected cells from virus-mediated cytopathology and resulted in significant inhibition of influenza virus replication for H1N1 and H3N2 subtypes. Additionally, I report that TNFSF12-13, TFNSF13, and USP47, similarly, are required for efficient influenza virus replication and induction of cell death. Depletion of these proteins resulted in significant inhibition of viral propagation and conferred protection of host cells to virus killing. Overall, my study has provided a list of novel host factors that play significant roles during influenza virus infection. Further studies on these potential genes and their encoded protein products may uncover possible new targets for drug development for future therapeutic treatment. In addition to providing greater understanding of influenza virus infection, these studies will also highlight important fundamentals of cellular processes that may be broadly applicable to other fields of research.

The use of relay nodes to improve the performance of broadband wireless access (BWA) networks has been the subject of intense research activities in recent years. Relay enhanced BWA networks are anticipated to support multimedia traffic (i.e., voice, video, and data traffic). In order to guarantee service to network users, efficient resource distribution is imperative. Wireless multihop networks are characterized by two inherent dynamic characteristics: 1) the existence of wireless interference and 2) mobility of user nodes. Both mobility and interference greatly influence the ability of users to obtain the necessary resources for service. In this dissertation we conduct a comprehensive research study on the topic of resource allocation in the presence of interference and mobility. Specifically, this dissertation investigates the impact interference and mobility have on various aspects of resource allocation, ranging from fairness to spectrum utilization. We study four important resource allocation algorithms for relay enhanced BWA networks. The problems and our research achievements are briefly outlined as follows. First, we propose an interference aware rate adaptive subcarrier and power allocation algorithm using maximum multicommodity flow optimization. We consider the impact of the wireless interference constraints using Signal to Interference Noise Ratio (SINR). We exploit spatial reuse to allocate subcarriers in the network and show that an intelligent reuse of resources can improve throughput while mitigating the impact of interference. We provide a sub-optimal heuristic to solve the rate adaptive resource allocation problem. We demonstrate that aggressive spatial reuse and fine tuned-interference modeling garner advantages in terms of throughput, end-to-end delay and power distribution. Second, we investigate the benefits of decoupled optimization of interference aware routing and scheduling using SINR and spatial reuse to improve the overall achievable throughput. We model the routing optimization problem as a linear program using maximum concurrent flows. We develop an optimization formulation to schedule the link traffic such that interference is mitigated and time slots are reused appropriately based on spatial TDMA (STDMA). The scheduling problem is shown to be NP-hard and is solved using the column generation technique. We compare our formulations to conventional counterparts in the literature and show that our approach guarantees higher throughput by mitigating the effect of interference effectively. Third, we investigate the problem of multipath flow routing and fair bandwidth allocation under interference constraints for multihop wireless networks. We first develop a novel isotonic routing metric, RI3M, considering the influence of interflow and intraflow interference. Second, in order to ensure QoS, an interference-aware max-min fair bandwidth allocation algorithm, LMX:M3F, is proposed where the lexicographically largest bandwidth allocation vector is found among all optimal allocation vectors while considering constraints of interference on the flows. We compare with various interference based routing metrics and interference aware bandwidth allocation algorithms established in the literature to show that RI3M and LMX:M3F succeed in improving network performance in terms of delay, packet loss ratio and bandwidth usage. Lastly, we develop a user mobility prediction model using the Hidden Markov Model(HMM) in which prediction control is transferred to the various fixed relay nodes in the network. Given the HMM prediction model, we develop a routing protocol which uses the location information of the mobile user to determine the interference level on links in its surrounding neighborhood. We use SINR as the routing metric to calculate the interference on a specific link (link cost). We minimize the total cost of routing as a cost function of SINR while guaranteeing that the load on each link does not exceed its capacity. The routing protocol is formulated and solved as a minimum cost flow optimization problem. We compare our SINR based routing algorithm with conventional counterparts in the literature and show that our algorithm reinforces routing paths with high link quality and low latency, therefore improving overall system throughput. The research solutions obtained in this dissertation improve the service reliability and QoS assurance of emerging BWA networks.

Remediation of DNAPL contaminated sites in fractured rock has proven to be very difficult. No current technology can be used to remediate such sites in a timely and economic manner due to the inherent heterogeneity of fractured rock and back diffusion of contaminants stored in the rock matrix. This study was conducted in order to evaluate the viability of biostimulation of native biofilm as a means to control flow and back diffusion at fractured rock sites. A field trial was conducted at an uncontaminated site in southern Ontario. The site is underlain by dolomites of the Lockport formation. Three major fracture zones have been identified in the study area. Two closely spaced (5.04 m) boreholes were used to isolate a fracture zone at a depth of 17 m with straddle packers. These boreholes were used to create an injection-withdrawal system with recirculation, which was used for tracer injection in order to load the rock matrix with a conservative dye tracer and to inject nutrients for 21 days in order to stimulate the growth of biofilm in the fracture. Evaluation of the ability of the biofilm to control flow through the fracture was conducted through pulse interference tests. Pulse interference tests were conducted before and after the injection of nutrients. The results from the pulse interference tests showed a maximum 65% reduction in transmissivity, which is equivalent to a 28% reduction in fracture aperture shortly after the cessation of biostimulation. In order to investigate the effect of the biofilm stimulation on matrix diffusion the rock matrix was loaded with Lissamine, a conservative fluorescent dye tracer prior to biostimulation and its concentration was monitored at injection and withdrawal wells. The effect that biostimulation had on matrix diffusion was determined by comparing field concentration measurements with a model that simulates a system unaffected by biofilm stimulation. The biostimulation lowered the concentration of tracer attributable to back diffusion at the withdrawal well by about 20% for approximately 30 days following the cessation of biostimulation. It is also thought that large amounts of tracer might have been trapped in the biofilm as it formed and was then released back into the fracture as the biofilm deteriorated. / Thesis (Master, Civil Engineering) -- Queen's University, 2009-08-11 19:27:44.232

No description available.

Influenza virus is a globally significant infectious agent with the potential to cause catastrophic pandemic outbreaks. Present treatment of influenza infections is restricted to only four anti-viral drugs, but there are increasing global reports of anti-viral resistance in several seasonal strains and also the 2009 pandemic swine-origin influenza virus H1N1. Possible future pandemic outbreaks, emerging new strains and drug resistance underscore the need to understand this complex virus and its pathogenicity with the goal that novel targets can be uncovered for future therapeutic development. Extensive lung tissue damage during influenza virus infection is proposed to contribute to the development of aberrant host immune responses. Strong evidence now demonstrates the significance of the cellular death pathway in promoting efficient influenza virus replication and disease progression. Viruses rely heavily on the machinery of their host for productive replication, which is also an Achilles’ heel that could be targeted for treatment. In pursuit of unraveling the complex nature of influenza virus replication, I carried out a global shRNA screen to identify specific host factors and signaling pathways that are involved in influenza-induced cell death and replication. In this study I identified 138 genes required for influenza viruses to induce infected host cell death. These genes were found to be involved in Protein Kinase A, NF-kB and PI3K signaling cascades. These signaling pathways are well known regulators of cell death and survival, which suggests influenza viruses may carefully regulate these pathways to reach a balance that suit their requirements for efficient proliferation, eventually at the cost of the host cell. I chose five candidate genes—BAD, MxB, TNFSF12-13,TNFSF13, and USP47—that were associated with apoptosis and the major signaling pathways determined in my network analysis to further verify the genome-wide screen as well as elucidate the role of these potentially novel host factors in influenza virus replication. I show in my study that influenza virus-induced cytopathology and cell death are considerably inhibited in BAD knockdown cells and both virus replication and viral protein production also are dramatically reduced. I also report here that MxB depletion protected cells from virus-mediated cytopathology and resulted in significant inhibition of influenza virus replication for H1N1 and H3N2 subtypes. Additionally, I report that TNFSF12-13, TFNSF13, and USP47, similarly, are required for efficient influenza virus replication and induction of cell death. Depletion of these proteins resulted in significant inhibition of viral propagation and conferred protection of host cells to virus killing. Overall, my study has provided a list of novel host factors that play significant roles during influenza virus infection. Further studies on these potential genes and their encoded protein products may uncover possible new targets for drug development for future therapeutic treatment. In addition to providing greater understanding of influenza virus infection, these studies will also highlight important fundamentals of cellular processes that may be broadly applicable to other fields of research.

Kochia and biennial wormwood are two weeds sometimes found growing in sunflower fields that may be difficult to control. Weed management in sunflowers is usually conducted using a combination of herbicides and mechanical weed control methods. Some farmers are growing sunflowers in reduced tillage systems, which may rely solely on herbicides to manage weeds; however, the spectrum of broadleaf weeds that can be controlled with herbicides is limited. Field experiments were conducted across southern Manitoba to determine the effect of kochia and biennial wormwood density and relative time of weed seedling recruitment on sunflower growth and development, yield and seed quality and to determine action thresholds for each weed. Early emerging kochia (plants that emerged at about the same time as the sunflowers) reduced sunflower yield by as much as 82%, which was greater than early emerging biennial wormwood plants, which reduced yield by as much as 27%. At low weed densities, each kochia plant reduced sunflower yield by 0.52% and each biennial wormwood plant reduced sunflower yield by 0.17%. As the density of early emerging kochia plants increased, sunflower height, stem diameter, leaf counts and head diameter were reduced in some of the experiments. Increasing densities of early emerging biennial wormwood plants had minimal effect on sunflower growth and development. Early emerging kochia and biennial wormwood plants both had the potential to reduce sunflower seed size and seed weight, while late emerging kochia and biennial wormwood (plants that emerged after the 4-leaf stage of the sunflowers) did not affect sunflower seed quality. The action threshold (5% sunflower yield loss) for early emerging kochia was 10 plants per metre square and the action threshold for early emerging biennial wormwood was 36 plants per square metre in the combined site-year analysis. Kochia or biennial wormwood plants that recruited after the 4-leaf stage of the sunflower crop did not affect sunflower yield, or seed quality.

No description available.

Wireless sensor networks are used to collect sensor data in different applications such as environmental monitoring, smart building control, and health care applications. Wireless sensor nodes used are typically small, low-cost, and battery powered. The nodes are often hard to access after deployment, for example when they are in remote  locations. Another property of wireless sensor networks is that their operation is dependent on the environment they operate in, both due to the specific sensor readings but also due to the effects on communication by factors such as fading and radio interference. This makes it important to evaluate a wireless sensor network in its intendent target environment before final deployment. To enable experiments with wireless sensor networks in their target environment, we have designed and implemented a testbed called Sensei-UU. It is designed to allow WSN experiments to be repeated in different locations, thus exposing effects caused by the environment. To allow this, the testbed is designed to be easily moved between experimental sites. One type of WSN applications Sensei-UU is aimed to evaluate is protocols where nodes are mobile. Mobile testbed nodes are low-cost robots which follow a tape track on the floor. The localization accuracy of the robot approach is evaluated and is accurate enough to expose a protocol to fading phenoma in a repeatable manner. Sensei-UU has helped us develop a lightweight interference classification approach, SoNIC, which runs on standard motes. The approach only use information from a standard cc2420 chipset available when packets are received. We believe that the classification accuracy is good enough to motivate specific transmission techniques avoiding interference. / WISENET