899 resultados para Target costing


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BIOMECANBICA DE LA ESGRIMA

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Analysis of low initial aspect ratio direct-drive target designs is carried out by varying the implosion velocity and the fuel mass. Starting from two different spherical targets with a given 300?g-DT mass, optimization of laser pulse and drive power allows to obtain a set of target seeds referenced by their peak implosion velocities and initial aspect ratio (A = 3 and A = 5). Self-ignition is achieved with higher implosion velocity for A = 5-design than for A = 3-design. Then, rescaling is done to extend the set of designs to a huge amount of mass, peak kinetic energies and peak areal densities. Self-ignition kinetic energy threshold Ek is characterized by a dependance of Ek ? v? with ?-values which depart from self-ignition models. Nevertheless, self-ignition energy is seen lower for smaller initial aspect ratio. An analysis of Two-Plasmons Decay threshold and Rayleigh?Taylor instability e-folding is carried out and it is shown that two-plasmon decay threshold is always overpassed for all designs. The hydrodynamic stability analysis is performed by embedded models to deal with linear and non-linear regime. It is found that the A = 5-designs are always at the limit of disruption of the shell.

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A numerical method providing the optimal laser intensity profiles for a direct-drive inertial confinement fusion scheme has been developed. The method provides an alternative approach to phase-space optimization studies, which can prove computationally expensive. The method applies to a generic irradiation configuration characterized by an arbitrary number NB of laser beams provided that they irradiate the whole target surface, and thus goes beyond previous analyses limited to symmetric configurations. The calculated laser intensity profiles optimize the illumination of a spherical target. This paper focuses on description of the method, which uses two steps: first, the target irradiation is calculated for initial trial laser intensities, and then in a second step the optimal laser intensities are obtained by correcting the trial intensities using the calculated illumination. A limited number of example applications to direct drive on the Laser MegaJoule (LMJ) are described.

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Smart and green cities are hot topics in current research because people are becoming more conscious about their impact on the environment and the sustainability of their cities as the population increases. Many researchers are searching for mechanisms that can reduce power consumption and pollution in the city environment. This paper addresses the issue of public lighting and how it can be improved in order to achieve a more energy efficient city. This work is focused on making the process of turning the streetlights on and off more intelligent so that they consume less power and cause less light pollution. The proposed solution is comprised of a radar device and an expert system implemented on a low-cost platform based on a DSP. By analyzing the radar echo in both the frequency and time domains, the system is able to detect and identify objects moving in front of it. This information is used to decide whether or not the streetlight should be turned on. Experimental results show that the proposed system can provide hit rates over 80%, promising a good performance. In addition, the proposed solution could be useful in kind of other applications such as intelligent security and surveillance systems and home automation.

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The study of service quality and its implication for transport contracts has several approaches in research and practical applications, where the main emphasis is the consideration of quality from the user's point of view, thus obtaining a customer satisfaction index as a measurement of the overall quality with no further implications for service providers. The main aim of this paper is to estimate the real economic impact of improving quality attributes for a bus operator. An application of the activity-based costing methodology is developed for a bus contract in Madrid, using quality data from surveys together with economic and performance information, and focusing on headway as a quality variable. Results show the consistency and practicality of this methodology, overcoming simplifications from traditional procedures. This method is a powerful tool in quality-based contracting as well as for effective investment in transport quality under poverty funding constraints

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This paper discusses the target localization problem in wireless visual sensor networks. Additive noises and measurement errors will affect the accuracy of target localization when the visual nodes are equipped with low-resolution cameras. In the goal of improving the accuracy of target localization without prior knowledge of the target, each node extracts multiple feature points from images to represent the target at the sensor node level. A statistical method is presented to match the most correlated feature point pair for merging the position information of different sensor nodes at the base station. Besides, in the case that more than one target exists in the field of interest, a scheme for locating multiple targets is provided. Simulation results show that, our proposed method has desirable performance in improving the accuracy of locating single target or multiple targets. Results also show that the proposed method has a better trade-off between camera node usage and localization accuracy.

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Initiation factor eIF4G is an essential protein required for initiation of mRNA translation via the 5′ cap-dependent pathway. It interacts with eIF4E (the mRNA 5′ cap-binding protein) and serves as an anchor for the assembly of further initiation factors. With treatment of Saccharomyces cerevisiae with rapamycin or with entry of cells into the diauxic phase, eIF4G is rapidly degraded, whereas initiation factors eIF4E and eIF4A remain stable. We propose that nutritional deprivation or interruption of the TOR signal transduction pathway induces eIF4G degradation.

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Unique, small sequences (sequence tag sites) have been identified at the 3′ ends of most human genes that serve as landmarks in genome mapping. We investigated whether a single copy gene could be isolated directly from total human DNA by transformation-associated recombination (TAR) cloning in yeast using a short, 3′ unique target. A TAR cloning vector was constructed that, when linearized, contained a small amount (381 bp) of 3′ hypoxanthine phosphoribosyltransferase (HPRT) sequence at one end and an 189-bp Alu repeat at the other end. Transformation with this vector along with human DNA led to selective isolations of the entire HPRT gene as yeast artificial chromosomes (YACs) that extended from the 3′ end sequence to various Alu positions as much as 600 kb upstream. These YACs were retrofitted with a NeoR and a bacterial artificial chromosome (BAC) sequence to transfer the YACs to bacteria and subsequently the BACs to mouse cells by using a Neo selection. Most of the HPRT isolates were functional, demonstrating that TAR cloning retains the functional integrity of the isolated material. Thus, this modified version of TAR cloning, which we refer to as radial TAR cloning, can be used to isolate large segments of the human genome accurately and directly with only a small amount of sequence information.

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ALL1, the human homologue of Drosophila trithorax, is directly involved in human acute leukemias associated with abnormalities at 11q23. Using the differential display method, we isolated a gene that is down-regulated in All1 double-knockout mouse embryonic stem (ES) cells. The gene, designated ARP1 (also termed RIEG, Ptx2, or Otlx2), is a member of a family of homeotic genes containing a short motif shared with several homeobox genes. Using a bacterially synthesized All1 polypeptide encompassing the AT-hook motifs, we identified a 0.5-kb ARP1 DNA fragment that preferentially bound to the polypeptide. Within this DNA, a region of ≈100 bp was protected by the polypeptide from digestion with ExoIII and DNase I. Whole-mount in situ hybridization to early mouse embryos of 9.5–10.5 days indicated a complex pattern of Arp1 expression spatially overlapping with the expression of All1. Although the ARP1 gene is expressed strongly in bone marrow cells, no transcripts were detected in six leukemia cell lines with 11q23 translocations. These results suggest that ARP1 is up-regulated by the All1 protein, possibly through direct interaction with an upstream DNA sequence of the former. The results are also consistent with the suggestion that ALL1 chimeric proteins resulting from 11q23 abnormalities act in a dominant negative fashion.

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The effects of insulin on the mammalian target of rapamycin, mTOR, were investigated in 3T3-L1 adipocytes. mTOR protein kinase activity was measured in immune complex assays with recombinant PHAS-I as substrate. Insulin-stimulated kinase activity was clearly observed when immunoprecipitations were conducted with the mTOR antibody, mTAb2. Insulin also increased by severalfold the 32P content of mTOR that was determined after purifying the protein from 32P-labeled adipocytes with rapamycin⋅FKBP12 agarose beads. Insulin affected neither the amount of mTOR immunoprecipitated nor the amount of mTOR detected by immunoblotting with mTAb2. However, the hormone markedly decreased the reactivity of mTOR with mTAb1, an antibody that activates the mTOR protein kinase. The effects of insulin on increasing mTOR protein kinase activity and on decreasing mTAb1 reactivity were abolished by incubating mTOR with protein phosphatase 1. Interestingly, the epitope for mTAb1 is located near the COOH terminus of mTOR in a 20-amino acid region that includes consensus sites for phosphorylation by protein kinase B (PKB). Experiments were performed in MER-Akt cells to investigate the role of PKB in controlling mTOR. These cells express a PKB-mutant estrogen receptor fusion protein that is activated when the cells are exposed to 4-hydroxytamoxifen. Activating PKB with 4-hydroxytamoxifen mimicked insulin by decreasing mTOR reactivity with mTAb1 and by increasing the PHAS-I kinase activity of mTOR. Our findings support the conclusion that insulin activates mTOR by promoting phosphorylation of the protein via a signaling pathway that contains PKB.

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A vestigial, nonphotosynthetic plastid has been identified recently in protozoan parasites of the phylum Apicomplexa. The apicomplexan plastid, or “apicoplast,” is indispensable, but the complete sequence of both the Plasmodium falciparum and Toxoplasma gondii apicoplast genomes has offered no clue as to what essential metabolic function(s) this organelle might perform in parasites. To investigate possible functions of the apicoplast, we sought to identify nuclear-encoded genes whose products are targeted to the apicoplast in Plasmodium and Toxoplasma. We describe here nuclear genes encoding ribosomal proteins S9 and L28 and the fatty acid biosynthetic enzymes acyl carrier protein (ACP), β-ketoacyl-ACP synthase III (FabH), and β-hydroxyacyl-ACP dehydratase (FabZ). These genes show high similarity to plastid homologues, and immunolocalization of S9 and ACP verifies that the proteins accumulate in the plastid. All the putatively apicoplast-targeted proteins bear N-terminal presequences consistent with plastid targeting, and the ACP presequence is shown to be sufficient to target a recombinant green fluorescent protein reporter to the apicoplast in transgenic T. gondii. Localization of ACP, and very probably FabH and FabZ, in the apicoplast implicates fatty acid biosynthesis as a likely function of the apicoplast. Moreover, inhibition of P. falciparum growth by thiolactomycin, an inhibitor of FabH, indicates a vital role for apicoplast fatty acid biosynthesis. Because the fatty acid biosynthesis genes identified here are of a plastid/bacterial type, and distinct from those of the equivalent pathway in animals, fatty acid biosynthesis is potentially an excellent target for therapeutics directed against malaria, toxoplasmosis, and other apicomplexan-mediated diseases.

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The egr-type zinc-finger transcription factor encoded by the Drosophila gene stripe (sr) is expressed in a subset of epidermal cells to which muscles attach during late stages of embryogenesis. We report loss-of-function and gain-of-function experiments indicating that sr activity provides ectodermal cells with properties required for the establishment of a normal muscle pattern during embryogenesis and for the differentiation of tendon-like epidermal muscle attachment sites (EMA). Our results show that sr encodes a transcriptional activator which acts as an autoregulated developmental switch gene. sr activity controls the expression of EMA-specific target genes in cells of ectodermal but not of mesodermal origin. sr-expressing ectodermal cells generate long-range signals that interfere with the spatial orientation of the elongating myotubes.

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Aflatoxin B1 (AFB1) is a potent human carcinogen implicated in the etiology of hepatocellular carcinoma. Upon metabolic activation to the reactive epoxide, AFB1 forms DNA adducts primarily at the N7 position of guanines. To elucidate more fully the molecular mechanism of AFB1-induced mutagenesis, an intercalation inhibitor was designed to probe the effects of intercalation by AFB1 epoxide on its reaction with DNA. DNA duplexes were prepared consisting of a target strand containing multiple potentially reactive guanines and a nontarget strand containing a cis-syn thymidine-benzofuran photoproduct. Because the covalently linked benzofuran moiety physically occupies an intercalation site, we reasoned that such a site would be rendered inaccessible to AFB1 epoxide. By strategic positioning of this intercalation inhibitor in the intercalation site 5′ to a specific guanine, the adduct yield at that site was greatly diminished, indicating that intercalation by AFB1 epoxide contributes favorably to adduct formation. Using this approach it has been possible to simplify the production of site-specifically modified oligonucleotides containing AFB1 adducts in the sequence context of a p53 mutational hotspot. Moreover, we report herein isolation of site-specifically AFB1-modified oligonucleotides in sequences containing multiple guanines. Use of intercalation inhibitors will facilitate both investigation of the ability of other carcinogens to intercalate into DNA and the synthesis of specific carcinogen-DNA adducts.

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This research was supported by the James S. McDonnell Foundation (ARH). Early version was supported by EPSRC grants EP/F02553X/1 and EP/D059364/1.

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FUNDING This work was supported by the Biotechnology and Biological Sciences Research Council [BB/I003746/1 to S.H., BB/M001695/1 to S.H and Y.N]