642 research outputs found

    SU(2) Flux Distributions on Finite Lattices

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    We studied SU(2) flux distributions on four dimensional euclidean lattices with one dimension very large. By choosing the time direction appropriately we can study physics in two cases: one is finite volume in the zero temperature limit, another is finite temperature in the the intermediate to large volume limit. We found that for cases of beta > beta crit there is no intrinsic string formation. Our lattices with beta > beta crit belong to intermediate volume region, and the string tension in this region is due to finite volume effects. In large volumes we found evidence for intrinsic string formation.Comment: 21 pages text, 12 pages of postscript figure

    Dual function of rare earth carboxylate compounds on the barrier properties and active corrosion inhibition of epoxy coatings on mild steel

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    In this work, two rare earth carboxylate compounds, lanthanum 4-hydroxycinnamate (La(4-OHcin)3) and yttrium 3-(4-methylbenzoyl)propanoate (Y(mbp)3), were incorporated into bisphenol-based epoxy resin to investigate their effectiveness in coating barrier properties and active corrosion inhibition. EIS results showed that the incorporation of rare earth carboxylate inhibitors significantly improved corrosion resistance compared to the inhibitor free coating, with the global impedance modulus remaining at a level higher than 1 GΩ cm2 after 219 days immersion. Following EIS experiments, cross-sectional views of the coatings exhibited a pore-plugging behavior by rare earth containing precipitates, which reinforced the coating barrier properties and delayed the electrolyte diffusion process. These effects were also reflected from the electrochemical parameters extracted from breakpoint frequency analysis and equivalent circuit modelling. Filiform corrosion experiments for artificially scratched coatings suggest that the addition of rare earth carboxylates effectively suppressed the initiation and growth of filaments as well as the development of the coating delamination front. The active corrosion inhibition is possibly related to the formation of a surface protective film consisting of bimetallic complexes and rare earth metal rich precipitates. The electrochemical measurements and surface analyses evidence the dual function of rare earth carboxylate species for enhancing coating barrier properties against electrolyte penetration and providing active corrosion inhibition for the underlying AS1020 mild steel

    Geochemical analysis of bulk marine sediment by Inductively Coupled Plasma–Atomic Emission Spectroscopy on board the JOIDES Resolution

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    Geochemical analyses on board the JOIDES Resolution have been enhanced with the addition of a Jobin-Yvon Ultrace inductively coupled plasma-atomic emission spectrometer (ICP-AES) as an upgrade from the previous X-ray fluorescence facility. During Leg 199, we sought to both challenge and utilize the capabilities of the ICP-AES in order to provide an extensive bulk-sediment geochemical database during the cruise. These near real-time analyses were then used to help characterize the recovered sedimentary sequences, calculate mass accumulation rates of the different sedimentary components, and assist with cruise and postcruise sampling requests. The general procedures, sample preparation techniques, and basic protocol for ICP-AES analyses on board ship are outlined by Murray et al. (2000) in Ocean Drilling Program Tech Note, 29. We expand on those concepts and offer suggestions for ICP-AES methodology, calibration by standard reference materials, data reduction procedures, and challenges that are specific to the analysis of bulk-sediment samples. During Leg 199, we employed an extensive bulk-sediment analytical program of ~600 samples of varying lithologies, thereby providing several opportunities for refinement of techniques. We also discuss some difficulties and challenges that were faced and suggest how to alleviate such occurrences for sedimentary chemical analyses during future legs

    Chemotherapy-induced CDA expression renders resistant non-small cell lung cancer cells sensitive to 5'-deoxy-5-fluorocytidine (5'-DFCR).

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    Pemetrexed (MTA) plus cisplatin combination therapy is considered the standard of care for patients with advanced non-small-cell lung cancer (NSCLC). However, in advanced NSCLC, the 5-year survival rate is below 10%, mainly due to resistance to therapy. We have previously shown that the fraction of mesenchymal-like, chemotherapy-resistant paraclone cells increased after MTA and cisplatin combination therapy in the NSCLC cell line A549. Cytidine deaminase (CDA) and thymidine phosphorylase (TYMP) are key enzymes of the pyrimidine salvage pathway. 5'-deoxy-5-fluorocytidine (5'-DFCR) is a cytidine analogue (metabolite of capecitabine), which is converted by CDA and subsequently by TYMP into 5-fluorouracil, a chemotherapeutic agent frequently used to treat solid tumors. The aim of this study was to identify and exploit chemotherapy-induced metabolic adaptations to target resistant cancer cells. Cell viability and colony formation assays were used to quantify the efficacy of MTA and cisplatin treatment in combination with schedule-dependent addition of 5'-DFCR on growth and survival of A549 paraclone cells and NSCLC cell lines. CDA and TYMP protein expression were monitored by Western blot. Finally, flow cytometry was used to analyze the EMT phenotype, DNA damage response activation and cell cycle distribution over time after treatment. CDA expression was measured by immunohistochemistry in tumor tissues of patients before and after neoadjuvant chemotherapy. We performed a small-scale screen of mitochondrial metabolism inhibitors, which revealed that 5'-DFCR selectively targets chemotherapy-resistant A549 paraclone cells characterized by high CDA and TYMP expression. In the cell line A549, CDA and TYMP expression was further increased by chemotherapy in a time-dependent manner, which was also observed in the KRAS-addicted NSCLC cell lines H358 and H411. The addition of 5'-DFCR on the second day after MTA and cisplatin combination therapy was the most efficient treatment to eradicate chemotherapy-resistant NSCLC cells. Moreover, recovery from treatment-induced DNA damage was delayed and accompanied by senescence induction and acquisition of a hybrid-EMT phenotype. In a subset of patient tumors, CDA expression was also increased after treatment with neoadjuvant chemotherapy. Chemotherapy increases CDA and TYMP expression thereby rendering resistant lung cancer cells susceptible to subsequent 5'-DFCR treatment

    A microsatellite marker for yellow rust resistance in wheat

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    Bulk segregant analysis (BSA) was used to identify molecular markers associated with yellow rust disease resistance in wheat (Triticum aestivum L.). DNAs isolated from the selected yellow rust tolerant and susceptible F-2 individuals derived from a cross between yellow rust resistant and susceptible wheat genotypes were used to established a "tolerant" and a "susceptible" DNA pool. The BSA was then performed on these DNA pools using 230 markers that were previously mapped onto the individual wheat chromosomes. One of the SSR markers (Xgwm382) located on chromosome group 2 (A, B, D genomes) was present in the resistant parent and the resistant bulk but not in the susceptible parent and the susceptible bulk, suggesting that this marker is linked to a yellow rust resistance gene. The presence of Xgwm382 was also tested in 108 additional wheat genotypes differing in yellow rust resistance. This analysis showed that 81% of the wheat genotypes known to be yellow rust resistant had the Xgwm382 marker, further suggesting that the presence of this marker correlates with yellow rust resistance in diverse wheat germplasm. Therefore, Xgwm382 could be useful for marker assisted selection of yellow rust resistances genotypes in wheat breeding programs

    Enhancement of the magnetic anisotropy of nanometer-sized Co clusters: influence of the surface and of the inter-particle interactions

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    We study the magnetic properties of spherical Co clusters with diameters between 0.8 nm and 5.4 nm (25 to 7500$ atoms) prepared by sequential sputtering of Co and Al2O3. The particle size distribution has been determined from the equilibrium susceptibility and magnetization data and it is compared to previous structural characterizations. The distribution of activation energies was independently obtained from a scaling plot of the ac susceptibility. Combining these two distributions we have accurately determined the effective anisotropy constant Keff. We find that Keff is enhanced with respect to the bulk value and that it is dominated by a strong anisotropy induced at the surface of the clusters. Interactions between the magnetic moments of adjacent layers are shown to increase the effective activation energy barrier for the reversal of the magnetic moments. Finally, this reversal is shown to proceed classically down to the lowest temperature investigated (1.8 K).Comment: 13 figures submitted to Phys. Rev.

    Observing Long Colour Flux Tubes in SU(2) Lattice Gauge Theory

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    We present results of a high statistics study of the chromo field distribution between static quarks in SU(2) gauge theory on lattices of volumes 16^4, 32^4, and 48^3*64, with physical extent ranging from 1.3 fm up to 2.7 fm at beta=2.5, beta=2.635, and beta=2.74. We establish string formation over physical distances as large as 2 fm. The results are tested against Michael's sum rules. A detailed investigation of the transverse action and energy flux tube profiles is provided. As a by-product, we obtain the static lattice potential in unpreceded accuracy.Comment: 66 pages, 29 figures, uuencoded latex file with epsfigures (450 K), supplementary full colour figures are available via ftp, CERN-TH.7413/94 (extended version

    MEK1 drives oncogenic signaling and interacts with PARP1 for genomic and metabolic homeostasis in malignant pleural mesothelioma.

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    Malignant pleural mesothelioma (MPM) is a lethal malignancy etiologically caused by asbestos exposure, for which there are few effective treatment options. Although asbestos carcinogenesis is associated with reactive oxygen species (ROS), the bona fide oncogenic signaling pathways that regulate ROS homeostasis and bypass ROS-evoked apoptosis in MPM are poorly understood. In this study, we demonstrate that the mitogen-activated protein kinase (MAPK) pathway RAS-RAF-MEK-ERK is hyperactive and a molecular driver of MPM, independent of histological subtypes and genetic heterogeneity. Suppression of MAPK signaling by clinically approved MEK inhibitors (MEKi) elicits PARP1 to protect MPM cells from the cytotoxic effects of MAPK pathway blockage. Mechanistically, MEKi induces impairment of homologous recombination (HR) repair proficiency and mitochondrial metabolic activity, which is counterbalanced by pleiotropic PARP1. Consequently, the combination of MEK with PARP inhibitors enhances apoptotic cell death in vitro and in vivo that occurs through coordinated upregulation of cytotoxic ROS in MPM cells, suggesting a mechanism-based, readily translatable strategy to treat this daunting disease. Collectively, our studies uncover a previously unrecognized scenario that hyperactivation of the MAPK pathway is an essential feature of MPM and provide unprecedented evidence that MAPK signaling cooperates with PARP1 to homeostatically maintain ROS levels and escape ROS-mediated apoptosis
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