No description available.

No description available.

This research thesis is focussed on the development of a novel low density explosive composition whose main application is wall control in open pit mining. The product has, however, the potential to be used in a variety of applications and rock conditions where customization of the explosive’s energy output is required. Experimental observations on the novel low density explosive showed that the product is capable of initiating and sustaining stable detonations at densities as low as 0.10 g/cm3. Given the extreme low densities at which the novel product maintains its detonating characteristics, it will be appropriate to treat it as a reactive bulking agent, hence its name: Low Density Reactive Agent or LDRA for short. When mixed with standard ANFO prills, the reactive nature of the LDRA ensures a detonable mixture regardless of the final dilution sought or the degree of segregation eventually produced during mixing and loading. If operational constraints are such that a lower energy is required, the LDRA can then be used on a stand‐alone basis, without mixing it with other explosive compositions, such as ANFO or emulsions. The detonation characteristics of the LDRA at a target density of 0.15 g/cm3 were evaluated, with particular effort placed on measuring the detonation and explosion pressures, parameters having the greatest influence on damage. The effects of diameter, confinement and primer on LDRA performance were evaluated through velocity of detonation (VOD) measurements. In addition, VOD experiments were conducted in the LDRA to evaluate the stability of propagation in longer columns, the behaviour in a decking configuration and the ability to initiate and be initiated by a column of ANFO. The low pressure regimes characterizing the LDRA provided the opportunity to investigate the full pressure history of the detonation gases by designing experiments of a non‐destructive nature that allowed the repetition of tests under different loading scenarios. Following the characterization stage, the opportunity to test the LDRA as a damage control tool under a true operational scenario arose at the Chuquicamata Mine, in northern Chile. The project provided important input as to the feasibility of manufacturing the LDRA at a semi‐industrial scale and to evaluate the performance of the product in the large diameter blastholes used at the mine / Thesis (Ph.D, Mining Engineering) -- Queen's University, 2007-11-09 12:19:49.747

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Thesis (M.S.)--Northern Michigan University, 2006. / Bibliography: leaves 70-72.

A family of low-density lattice codes (LDLC) is studied based on Construction-A for lattices. The family of Construction-A codes is already known to contain a large capacity-achieving subset. Parallels are drawn between coset non-binary low-density parity-check (LDPC) codes and nested low-density Construction-A lattices codes. Most of the related research in LDPC domain assumes optimal power allocation to encoded codeword. The source coding problem of mapping message to power optimal codeword for any LDPC code is in general, NP-hard. In this thesis, we present a novel method for encoding and decoding lattice based on non-binary LDPC codes using message-passing algorithms. / text

Zellproliferation stellt einen integralen Bestandteil der Plaqueentstehung und somit der Atherosklerose dar. Zahlreiche Studien belegen, daß oxidativ verändertes LDL eine Schlüsselrolle in diesem Pathomechanismus spielt. Neben einer Reihe von proatherogenen Eigenschaften, vermag oxLDL die Zellzyklusregulation insbesondere über den Zyklinkinaseinhibitors p27kip1 zu beeinflussen. Als wichtigen Regulator der Zellproliferation wurde die kleine GTPase RhoA identifiziert. Vor diesem Hintergrund sollte in der vorliegenden Arbeit die oxLDL induzierte Expressionsminderung des Zyklinkinaseinhibitors p27kip1 sowie Zellproliferation über eine Aktivierung des RhoA/Rho-Kinase Signalwegs untersucht werden. Die Aktivierung von RhoA in HUVEC durch oxLDL sollte mittels immunhistochemischem Nachweisverfahren sichtbar gemacht werden. Weiterhin war interessant welche Rolle RhoA in der Signaltransduktion von oxLDL-Wirkungen spielt. Aus diesem Grund und um die Wirkung von RhoA analysieren zu können verwendeten wir die inaktive RhoA N19-Mutante und untersuchten sowohl die Auswirkung der RhoA-Hemmung auf die oxLDL induzierte Zellproliferation als auch auf die oxLDL induzierte p27kip1 Suppression. Zusätzlich sollten die Auswirkungen der Hemmung des nachgeschalteten Effektorproteins von RhoA nämlich Rho-Kinase mittels Y27632 auf die oxLDL-vermittelte Zellproliferation dargestellt werden. Es konnte gezeigt werden, daß oxLDL RhoA zu stimulieren vermag, indem die Translokation von RhoA aus dem Zytosol in die Plasmamembran, als Marker für die Aktivierung von RhoA nach oxLDL Stimulation sichtbar gemacht werden konnte. Die deutlichste Translokation von RhoA wurde nach 5 minütiger oxLDL Inkubation nachgewiesen. Die Hemmung der RhoA Aktivierung durch Transfektion einer dominant negativen RhoA N19 Mutante verdeutlichte, daß sowohl die oxLDL induzierte p27Kip1 Suppression in HUVEC als auch die oxLDL induzierte Proliferation auf die oxLDL vermittelte RhoA Aktivierung angewiesen sind. In Endothelzellen, welche nur mit dem Leervektor pcDNA3 transfiziert waren (Kontrolle), bestätigte sich nach einer vierstündigen oxLDL Inkubation wie in den früheren Untersuchungen eine signifikante Expressionsverminderung von p27Kip1 um ca. 66%. Im Gegensatz dazu konnte in Zellen, die mit der dominant-negativen RhoA N19 Mutante transfiziert waren keine p27Kip1 Suppression festgestellt werden. Ebenso zeigte sich in MTT-Assays bei Zellen mit der inaktiven RhoA N19 Mutante eine nahezu vollständig fehlende Proliferationsantwort. Im Anschluß daran, wurde in weiteren MTT-Assays die oxLDL induzierte Proliferation unter der Verwendung des Rho-Kinase Inhibitors Y27632 untersucht und eine signifikant reduzierte Proliferationsrate von 166 + 19 % im Vergleich zu Kontrollzellen 200 + 12 % nachgewiesen. Dieses Ergebnis könnte dadurch erklärt werden, daß neben dem nachgeschaltetem Effektorprotein Rho-Kinase, die Phosphatidylinositol 3-Kinase (PI3K) in der RhoA vermittelten p27Kip1 Suppression und Zellzyklusprogression eine zusätzliche Rolle zu spielen scheint. Zusammenfassend läßt sich sagen, daß sowohl die oxLDL induzierte Expressionsverminderung von p27Kip1 in HUVEC und somit die Zellprogression als auch die oxLDL induzierte Endothelproliferation auf die oxLDL vermittelte RhoA Aktivierung angewiesen ist. Diese Ergebnisse aus der vorliegenden Arbeit untermauern, daß der RhoA/Rho-Kinase Signalweg ein neuer therapeutischer bzw. medikamentöser Ansatz bei kardiovaskulären Erkrankungen sein könnte. / A typical feature of atherosclerotic plaques is increased cellular turnover, with the parallel existence of cell proliferation and cell death. Oxodized LDL plays a key role in its pathogenesis. Oxidized LDL induces proliferation in HUVEC. The influence of oxLDL on the cyclin-dependent kinase inhibitor p27Kip1, on the activity of small GTPase RhoA as a known regulator of p27Kip1, and on the resulting cell proliferation was studied. RhoA stimulation was assessed by means of its translocation from the cytosolic to the particulate fraction, an effect that is associated with RhoA activation. After oxLDL stimulation the translocation of RhoA to the cell membrane was visible after 1 min and peaked after 5 min of stimulation. We next investigated the influence of RhoA activation on oxLDL induced downregulation of p27Kip1 expression and proliferation. RhoA activity was inhibited in HUVEC by transfection with dominant inhibitory RhoA N19 mutant before stimulation with oxLDL. In cells that were transfected with dominant negative RhoA, the effect of oxLDL on p27Kip1 expression and on cellular proliferation was abolished. HUVEC that were preincubated with the Rho-kinase inhibitor Y27632 also showed a significantly decreased proliferative response to oxLDL stimulation. In summary, oxLDL induced cell-cycle progression via regulation of p27Kip1 expression, resulting in cellular proliferation, involving activation of RhoA. This results confirm, that the Rho/Rho signaling pathway could be a new target for the treatment of vascular disease.

In wireless networks, it has always been a challenge to satisfy high traffic throughput demands, due to limited spectrum resources. In past decades, various techniques, including cooperative communications, have been developed to achieve higher communication rates. This thesis addresses the challenges imposed by cooperative wireless networks, in particular focusing on practical code constructions and designs for wireless relay networks. The thesis is divided into the following four topics: 1) constructing and designing low-density parity-check (LDPC) codes for half-duplex three-phase two-way relay channels, 2) extending LDPC code constructions to half-duplex three-way relay channels, 3) proposing maximum-rate relay selection algorithms and LDPC code constructions for the broadcast problem in wireless relay networks, and 4) proposing an iterative hard interference cancellation decoder for LDPC codes in 2-user multiple-access channels. Under the first topic, we construct codes for half-duplex three-phase two-way relay channels where two terminal nodes exchange information with the help of a relay node. Constructing codes for such channels is challenging, especially when messages are encoded into multiple streams and a destination node receives signals from multiple nodes. We first prove an achievable rate region by random coding. Next, a systematic LDPC code is constructed at the relay node where relay bits are generated from two source codewords. At the terminal nodes, messages are decoded from signals of the source node and the relay node. To analyze the performance of the codes, discretized density evolution is derived. Based on the discretized density evolution, degree distributions are optimized by iterative linear programming in three steps. The optimized codes obtained are 26% longer than the theoretic ones. For the second topic, we extend LDPC code constructions from half-duplex three-phase two-way relay channels to half-duplex three-way relay channels. An achievable rate region of half-duplex three-way relay channels is first proved. Next, LDPC codes for each sub-region of the achievable rate region are constructed, where relay bits can be generated only from a received codeword or from both the source codeword and received codewords. Under the third topic, we study relay selection and code constructions for the broadcast problem in wireless relay networks. We start with the system model, followed by a theorem stating that a node can decode a message by jointly decoding multiple blocks of received signals. Next, the maximum rate is given when a message is decoded hop-by-hop or decoded by a set of nodes in a transmission phase. Furthermore, optimal relay selection algorithms are proposed for the two relay schemes. Finally, LDPC codes are constructed for the broadcast problem in wireless relay networks. For the fourth topic, an iterative hard interference cancellation decoder for LDPC codes in 2-user multiple-access channels is proposed. The decoder is based on log-likelihood ratios (LLRs). Interference is estimated, quantized and subtracted from channel outputs. To analyze the codes, density evolution is derived. We show that the required signal-to-noise ratio (SNR) for the proposed low-complexity decoder is 0.2 dB higher than that for an existing sub-optimal belief propagation decoder at code rate 1/3.

Thesis (Ph. D.)--University of Sydney, 2005. / Title from title screen (viewed 19 May 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Heart Research Institute, Faculty of Medicine. Degree awarded 2005; thesis submitted 2004. Includes bibliographical references. Also available in print form.

Zugl.: Ulm, Univ., Diss., 2008