This thesis focuses on designing Low-Density Parity-Check (LDPC) codes for forward-error-correction. The target application is real-time multimedia communications over packet networks. We investigate two code design issues, which are important in the target application scenarios, designing LDPC codes with low decoding latency, and constructing capacity-approaching LDPC codes with very low error probabilities. On designing LDPC codes with low decoding latency, we present a framework for optimizing the code parameters so that the decoding can be fulfilled after only a small number of iterative decoding iterations. The brute force approach for such optimization is numerical intractable, because it involves a difficult discrete optimization programming. In this thesis, we show an asymptotic approximation to the number of decoding iterations. Based on this asymptotic approximation, we propose an approximate optimization framework for finding near-optimal code parameters, so that the number of decoding iterations is minimized. The approximate optimization approach is numerically tractable. Numerical results confirm that the proposed optimization approach has excellent numerical properties, and codes with excellent performance in terms of number of decoding iterations can be obtained. Our results show that the numbers of decoding iterations of the codes by the proposed design approach can be as small as one-fifth of the numbers of decoding iterations of some previously well-known codes. The numerical results also show that the proposed asymptotic approximation is generally tight for even non-extremely limiting cases. On constructing capacity-approaching LDPC codes with very low error probabilities, we propose a new LDPC code construction scheme based on $2$-lifts. Based on stopping set distribution analysis, we propose design criteria for the resulting codes to have very low error floors. High error floors are the main problems of previously constructed capacity-approaching codes, which prevent them from achieving very low error probabilities. Numerical results confirm that codes with very low error floors can be obtained by the proposed code construction scheme and the design criteria. Compared with the codes by the previous standard construction schemes, which have error floors at the levels of $10^{-3}$ to $10^{-4}$, the codes by the proposed approach do not have observable error floors at the levels higher than $10^{-7}$. The error floors of the codes by the proposed approach are also significantly lower compared with the codes by the previous approaches to constructing codes with low error floors.

This thesis focuses on designing Low-Density Parity-Check (LDPC) codes for forward-error-correction. The target application is real-time multimedia communications over packet networks. We investigate two code design issues, which are important in the target application scenarios, designing LDPC codes with low decoding latency, and constructing capacity-approaching LDPC codes with very low error probabilities. On designing LDPC codes with low decoding latency, we present a framework for optimizing the code parameters so that the decoding can be fulfilled after only a small number of iterative decoding iterations. The brute force approach for such optimization is numerical intractable, because it involves a difficult discrete optimization programming. In this thesis, we show an asymptotic approximation to the number of decoding iterations. Based on this asymptotic approximation, we propose an approximate optimization framework for finding near-optimal code parameters, so that the number of decoding iterations is minimized. The approximate optimization approach is numerically tractable. Numerical results confirm that the proposed optimization approach has excellent numerical properties, and codes with excellent performance in terms of number of decoding iterations can be obtained. Our results show that the numbers of decoding iterations of the codes by the proposed design approach can be as small as one-fifth of the numbers of decoding iterations of some previously well-known codes. The numerical results also show that the proposed asymptotic approximation is generally tight for even non-extremely limiting cases. On constructing capacity-approaching LDPC codes with very low error probabilities, we propose a new LDPC code construction scheme based on $2$-lifts. Based on stopping set distribution analysis, we propose design criteria for the resulting codes to have very low error floors. High error floors are the main problems of previously constructed capacity-approaching codes, which prevent them from achieving very low error probabilities. Numerical results confirm that codes with very low error floors can be obtained by the proposed code construction scheme and the design criteria. Compared with the codes by the previous standard construction schemes, which have error floors at the levels of $10^{-3}$ to $10^{-4}$, the codes by the proposed approach do not have observable error floors at the levels higher than $10^{-7}$. The error floors of the codes by the proposed approach are also significantly lower compared with the codes by the previous approaches to constructing codes with low error floors.

Receptors that transport vitellogenin into oocytes are of vital importance to egg-laying species because they promote oocyte development. In this study, we describe the cloning of the first hymenopteran vitellogenin receptor (VgR) cDNA. Using reverse transcription polymerase chain reaction (RT-PCR) and both 5’- and 3’- rapid amplification of cDNA ends (RACE), cDNA fragments encompassing the entire coding region of a putative VgR from fire ant (= SiVgR) were cloned and sequenced. The complete SiVgR cDNA has a length of 5764 bp encoding a 1782-residue protein with a predicted molecular mass of 201.3 kDa. The deduced amino acid sequence of the SiVgR revealed that it encoded a protein belonging to the low-density lipoprotein receptor superfamily. The number and arrangement of modular domains of SiVgR are the same as those of mosquito and fruit fly VgRs, except there are only four Class A cysteine-rich repeats in the first ligand binding domain of SiVgR compared to five in the mosquito and fruit fly. The deduced amino acid sequence of the SiVgR exhibited 35% and 31% identity to those of the mosquito and fruit fly VgRs, respectively. Northern blot analysis demonstrated that the 7.4-kb SiVgR mRNA was present only in Northern blot analysis demonstrated that the 7.4-kb SiVgR mRNA was present only in ovaries of reproductive females − both alates (virgins) and queens (mated) and was more abundant in alates. The developmental profile of transcriptional expression was determined by semiquantitative RT-PCR. It showed that the SiVgR transcript increased 6-fold from 0- to 10-days after mating, then remained constant through 30 days. It also showed that the SiVgR transcripts increased with age in alate virgin females. The transcriptional expression of the SiVgR was up-regulated more than two-fold by methoprene, a juvenile hormone analog, as determined by using an in vitro system. This suggested the SiVgR gene is JH regulated.

dsc-4(qm182), a mutation that suppresses the lengthened defecation cycle of clk-1 also suppresses the delay in germline development. dsc-4 encodes a putative orthologue of microsomal triglyceride transfer protein (MTP), a protein essential for the assembly and secretion of apo-B-containing low density lipoproteins (LDL). The effect of dsc-4 on clk-1(qm30), coupled to studies of apoB homologues in worms led to a model suggesting the possibility of using C. elegans in the study of LDL-like lipoprotein particles. The impact of the level of lipoproteins is particularly evident in the germline developmental rate of the worms. / We report here a further elucidation of clk-1 mutants in the study of the biology of LDL-like particles. In particular, we investigated the effect of targeting LDL receptor-like genes by RNA interference (RNAi) on the egg laying rate of clk-1(qm30). We find positive modulating effects by disruption of these putative LDL receptors. In confirmation of our model of lipoprotein metabolism in clk-1 mutants, we find that disruption of these putative LDL receptors produces strikingly different effects in wild-type, clk-1(qm30) or clk-1(qm30); dsc-4(qm182) animals. / In addition, we report unexpected effects of various clk-1 alleles on the phenotypes of animals in which lrp-1 and rme-2 are disrupted. Specifically, we observe an allele specific amelioration of the phenotypes associated with disruption of these genes (abnormal molting and sterility, respectively). We discuss the possible significance of these findings. (Abstract shortened by UMI.)

Erratum final three leaves of thesis. / Includes bibliographical references (leaves 266-288). / xvi, 288, [3] leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Demonstrates that fatty acids and antioxidants can regulate the low density lipoprotein (LDL) receptor at the level of gene transcription in cultured liver cells. EPA and linoleic acid (PUFAs) are specifically shown to downregulate the LDL receptor compared to saturated and monosaturated fatty acids in the presence or absence of cholesterol. The experiments lead to the discovery that antioxidants can upregulate the LDL receptor in the human HepG2 cells. / Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 1996

Includes bibliographical references (34 leaves). / xxi, 204 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Investigates the in vitro antioxidant properties of red wine containing polphends and the isoflavone genistein. Subsequently the effect of red wine on low density lipoprotein oxidation and fatty streak lesion development in cholesterol-fed rabbits was examined. / Thesis (Ph.D.)--University of Adelaide, Dept. of Clinical and Experimental Pharmacology, 1998

Any lipoproteins and cells present in the inflammatory environment of atherosclerotic plaques are likely to be exposed to high levels of oxidative stress. As 7,8-dihydroneopterin (7,8-NP) is synthesized by interferon-γ (IFN-γ)-activated macrophages, this pteridine is also thought to exist at sites of inflammation. 7,8-NP s in vivo role remains controversial, but numerous in vitro studies have identified a radical scavenging activity. The possibility of 7,8-NP protecting against oxidative damage in inflammatory environments like plaque was investigated in this thesis. Both human monocyte-derived macrophages (HMDMs) and low density lipoprotein (LDL) were used as substrates. The extent of protein hydroperoxide formation in each model, and 7,8-NP s effect on this process, were specifically studied since most previous research has focussed on lipid rather than protein peroxidation. For the first time, neopterin (including oxidized 7,8-NP) was also directly detected by high performance liquid chromatography in the inflammatory environments of 19 pus and two atherosclerotic plaque samples. Peak concentrations even reached the low micromolar range. The positive correlation identified in the pus between neopterin and a well known antioxidant, vitamin E, further hinted at a potential antioxidant function. However, no significant association was noted between neopterin and markers of protein or lipid oxidation. Exposure of HMDMs to the AAPH peroxyl radical generator resulted in significant quantities of lipid hydroperoxides but not protein hydroperoxides, as detected by the FOX assays. This is likely due to the large accumulation of polyunsaturated fatty acidrich lipid in the primary HMDMs during differentiation in 10% human serum and is of relevance to atherosclerotic plaque, where macrophages also become lipid-loaded. The addition of up to 200μM 7,8-NP failed to prevent AAPH-induced lipid peroxidation and was also unable to inhibit a loss of cellular thiols or viability. This lack of effect suggests the damaging peroxyl radicals are not being scavenged by 7,8-NP. The high lipid content of HMDM cells appears to cause the AAPH and/or 7,8-NP to localize to a cellular site, where they are unable to interact. Macrophage-mediated oxidation of LDL in iron(II)-supplemented Hams F10 was associated with the formation of 30-40 moles of protein hydroperoxides per mole of LDL. The close parallel between protein and lipid peroxidation supports the theory that lipid-derived radicals are involved in protein hydroperoxide formation on LDL and indicates that protein hydroperoxides are an early product of LDL oxidation. Their detection during exposure of LDL to both the THP-1 macrophage cell line and primary HMDM cells confirms that protein hydroperoxides are also a normal consequence of macrophage-mediated LDL oxidation. Incubation of LDL with micromolar 7,8-NP prevented macrophage-mediated protein hydroperoxide formation in a concentration-dependent manner. Lipid oxidation and vitamin E loss were similarly inhibited by 7,8-NP during the cell-mediated attack of LDL. Kinetic analysis revealed protection due to extension of the lag phase, with 7,8-NP depletion and initiation of the propagation phase coinciding. This supports a radical scavenging activity for 7,8-NP, resulting in protection of the entire LDL particle. By contrast, the release of nanomolar quantities of 7,8-NP by IFN-γ-stimulated THP-1 macrophages failed to prevent LDL oxidation. HMDMs activated by IFN-γ did significantly inhibit LDL oxidation, including protein hydroperoxide formation, for up to 48 hours but this antioxidant effect was not due to the de novo synthesis of 7,8-NP. These results indicate that both the prevalence of protein hydroperoxides, and the ability of 7,8-NP to act as an antioxidant, depend on the system under investigation. Neopterin exists in inflammatory environments but, considering the lack of protection against AAPH-mediated HMDM oxidation and the 7,8-NP concentration required to inhibit macrophage-mediated LDL oxidation, strong evidence for an antioxidant activity of 7,8-NP in atherosclerotic plaque is currently lacking.

Universiẗat, Diss.--Heidelberg, 1997.

Thesis (Ph. D.)--University of Canterbury, 2008. / Typescript (photocopy). Includes bibliographical references (p. 211-250). Also available via the World Wide Web.

Thesis (Ph.D.)--University of Alberta, 2009. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy, Department of Cell Biology. Title from pdf file main screen (viewed on October 18, 2009). Accompanied by four supplementary video recording files. Includes bibliographical references.