901 resultados para Iterative determinant maximization
Resumo:
Orthogonal frequency division multiplexing (OFDM) requires an expensive linear amplifier at the transmitter due to its high peak-to-average power ratio (PAPR). Single carrier with cyclic prefix (SC-CP) is a closely related transmission scheme that possesses most of the benefits of OFDM but does not have the PAPR problem. Although in a multipath environment, SC-CP is very robust to frequency-selective fading, it is sensitive to the time-selective fading characteristics of the wireless channel that disturbs the orthogonality of the channel matrix (CM) and increases the computational complexity of the receiver. In this paper, we propose a time-domain low-complexity iterative algorithm to compensate for the effects of time selectivity of the channel that exploits the sparsity present in the channel convolution matrix. Simulation results show the superior performance of the proposed algorithm over the standard linear minimum mean-square error (L-MMSE) equalizer for SC-CP.
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The convergence of the iterative identification algorithm for a general Hammerstein system has been an open problem for a long time. In this paper, it is shown that the convergence can be achieved by incorporating a regularization procedure on the nonlinearity in addition to a normalization step on the parameters.
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Suppose C is a bounded chain complex of finitely generated free modules over the Laurent polynomial ring L = R[x,x -1]. Then C is R-finitely dominated, i.e. homotopy equivalent over R to a bounded chain complex of finitely generated projective R-modules if and only if the two chain complexes C ? L R((x)) and C ? L R((x -1)) are acyclic, as has been proved by Ranicki (A. Ranicki, Finite domination and Novikov rings, Topology 34(3) (1995), 619–632). Here R((x)) = R[[x]][x -1] and R((x -1)) = R[[x -1]][x] are rings of the formal Laurent series, also known as Novikov rings. In this paper, we prove a generalisation of this criterion which allows us to detect finite domination of bounded below chain complexes of projective modules over Laurent rings in several indeterminates.
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This paper compares the Random Regret Minimization and the Random Utility Maximization models for determining recreational choice. The Random Regret approach is based on the idea that, when choosing, individuals aim to minimize their regret – regret being defined as what one experiences when a non-chosen alternative in a choice set performs better than a chosen one in relation to one or more attributes. The Random Regret paradigm, recently developed in transport economics, presents a tractable, regret-based alternative to the dominant choice paradigm based on Random Utility. Using data from a travel cost study exploring factors that influence kayakers’ site-choice decisions in the Republic of Ireland, we estimate both the traditional Random Utility multinomial logit model (RU-MNL) and the Random Regret multinomial logit model (RR-MNL) to gain more insights into site choice decisions. We further explore whether choices are driven by a utility maximization or a regret minimization paradigm by running a binary logit model to examine the likelihood of the two decision choice paradigms using site visits and respondents characteristics as explanatory variables. In addition to being one of the first studies to apply the RR-MNL to an environmental good, this paper also represents the first application of the RR-MNL to compute the Logsum to test and strengthen conclusions on welfare impacts of potential alternative policy scenarios.
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The rejoining kinetics of double-stranded DNA fragments, along with measurements of residual damage after postirradiation incubation, are often used as indicators of the biological relevance of the damage induced by ionizing radiation of different qualities. Although it is widely accepted that high-LET radiation-induced double-strand breaks (DSBs) tend to rejoin with kinetics slower than low-LET radiation-induced DSBs, possibly due to the complexity of the DSB itself, the nature of a slowly rejoining DSB-containing DNA lesion remains unknown. Using an approach that combines pulsed-field gel electrophoresis (PFGE) of fragmented DNA from human skin fibroblasts and a recently developed Monte Carlo simulation of radiation-induced DNA breakage and rejoining kinetics, we have tested the role of DSB-containing DNA lesions in the 8-kbp-5.7-Mbp fragment size range in determining the DSB rejoining kinetics. It is found that with low-LET X rays or high LET alpha particles, DSB rejoining kinetics data obtained with PFGE can be computer-simulated assuming that DSB rejoining kinetics does not depend on spacing of breaks along the chromosomes. After analysis of DNA fragmentation profiles, the rejoining kinetics of X-ray-induced DSBs could be fitted by two components: a fast component with a half-life of 0.9 +/- 0.5 h and a slow component with a half-life of 16 +/- 9 h. For a particles, a fast component with a half-life of 0.7 +/- 0.4 h and a slow component with a half-life of 12 5 h along with a residual fraction of unrepaired breaks accounting for 8% of the initial damage were observed. In summary, it is shown that genomic proximity of breaks along a chromosome does not determine the rejoining kinetics, so the slowly rejoining breaks induced with higher frequencies after exposure to high-LET radiation (0.37 +/- 0.12) relative to low-LET radiation (0.22 +/- 0.07) can be explained on the basis of lesion complexity at the nanometer scale, known as locally multiply damaged sites. (c) 2005 by Radiation Research Society.
Resumo:
Chemotherapy response rates for advanced colorectal cancer remain disappointingly low, primarily because of drug resistance, so there is an urgent need to improve current treatment strategies. To identify novel determinants of resistance to the clinically relevant drugs 5-fluorouracil (5-FU) and SN38 (the active metabolite of irinotecan), transcriptional profiling experiments were carried out on pretreatment metastatic colorectal cancer biopsies and HCT116 parental and chemotherapy-resistant cell line models using a disease-specific DNA microarray. To enrich for potential chemoresistance-determining genes, an unsupervised bioinformatics approach was used, and 50 genes were selected and then functionally assessed using custom-designed short interfering RNA(siRNA) screens. In the primary siRNA screen, silencing of 21 genes sensitized HCT116 cells to either 5-FU or SN38 treatment. Three genes (RAPGEF2, PTRF, and SART1) were selected for further analysis in a panel of 5 colorectal cancer cell lines. Silencing SART1 sensitized all 5 cell lines to 5-FU treatment and 4/5 cell lines to SN38 treatment. However, silencing of RAPGEF2 or PTRF had no significant effect on 5-FU or SN38 sensitivity in the wider cell line panel. Further functional analysis of SART1 showed that its silencing induced apoptosis that was caspase-8 dependent. Furthermore, silencing of SART1 led to a downregulation of the caspase-8 inhibitor, c-FLIP, which we have previously shown is a key determinant of drug resistance in colorectal cancer. This study shows the power of systems biology approaches for identifying novel genes that regulate drug resistance and identifies SART1 as a previously unidentified regulator of c-FLIP and drug-induced activation of caspase-8. Mol Cancer Ther; 11(1); 119-31. (C) 2011 AACR.
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The Burkholderia cepacia complex (Bcc) is a group of genetically related environmental bacteria that can cause chronic opportunistic infections in patients with cystic fibrosis (CF) and other underlying diseases. These infections are difficult to treat due to the inherent resistance of the bacteria to antibiotics. Bacteria can spread between CF patients through social contact and sometimes cause cepacia syndrome, a fatal pneumonia accompanied by septicemia. Burkholderia cenocepacia has been the focus of attention because initially it was the most common Bcc species isolated from patients with CF in North America and Europe. Today, B. cenocepacia, along with Burkholderia multivorans, is the most prevalent Bcc species in patients with CF. Given the progress that has been made in our understanding of B. cenocepacia over the past decade, we thought that it was an appropriate time to review our knowledge of the pathogenesis of B. cenocepacia, paying particular attention to the characterization of virulence determinants and the new tools that have been developed to study them. A common theme emerging from these studies is that B. cenocepacia establishes chronic infections in immuno-compromised patients, which depend more on determinants mediating host niche adaptation than those involved directly in host cells and tissue damage.
Resumo:
Wzz is a membrane protein that determines the chain length distribution of the O-antigen lipopolysaccharide by an unknown mechanism. Wzz proteins consist of two transmembrane helices separated by a large periplasmic loop. The periplasmic loop of Escherichia coli K-12 Wzz (244 amino acids from K65 to A308) was purified and found to be a monomer with an extended conformation, as determined by gel filtration chromatography and analytical ultracentrifugation. Circular dichroism showed that the loop has a 60% helical content. The Wzz periplasmic loop also contains three regions with predicted coiled coils. To probe the function of the predicted coiled coils, we constructed amino acid replacement mutants of the E. coli K-12 Wzz protein, which were designed so that the coiled coils could be separate without compromising the helicity of the individual molecules. Mutations in one of the regions, spanning amino acids 108 to 130 (region I), were associated with a partial defect in O-antigen chain length distribution, while mutants with mutations in the region spanning amino acids 209 to 223 (region III) did not have an apparent functional defect. In contrast, mutations in the region spanning amino acids 153 to 173 (region II) eliminated the Wzz function. This phenotype was associated with protein instability, most likely due to conformational changes caused by the amino acid replacements, which was confirmed by limited trypsin proteolysis. Additional mutagenesis based on a three-dimensional model of region I demonstrated that the amino acids implicated in function are all located at the same face of a predicted alpha-helix, suggesting that a coiled coil actually does not exist in this region. Together, our results suggest that the regions predicted to be coiled coils are important for Wzz function because they maintain the native conformation of the protein, although the existence of coiled coils could not be demonstrated experimentally.