3,772 research outputs found

    Interpretations of Presburger Arithmetic in Itself

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    Presburger arithmetic PrA is the true theory of natural numbers with addition. We study interpretations of PrA in itself. We prove that all one-dimensional self-interpretations are definably isomorphic to the identity self-interpretation. In order to prove the results we show that all linear orders that are interpretable in (N,+) are scattered orders with the finite Hausdorff rank and that the ranks are bounded in terms of the dimension of the respective interpretations. From our result about self-interpretations of PrA it follows that PrA isn't one-dimensionally interpretable in any of its finite subtheories. We note that the latter was conjectured by A. Visser.Comment: Published in proceedings of LFCS 201

    Quantum cohomology of flag manifolds and Toda lattices

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    We discuss relations of Vafa's quantum cohomology with Floer's homology theory, introduce equivariant quantum cohomology, formulate some conjectures about its general properties and, on the basis of these conjectures, compute quantum cohomology algebras of the flag manifolds. The answer turns out to coincide with the algebra of regular functions on an invariant lagrangian variety of a Toda lattice.Comment: 35 page

    The Context-Freeness Problem Is coNP-Complete for Flat Counter Systems

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    International audienceBounded languages have recently proved to be an important class of languages for the analysis of Turing-powerful models. For instance, bounded context-free languages are used to under-approximate the behav-iors of recursive programs. Ginsburg and Spanier have shown in 1966 that a bounded language L ⊆ a * 1 · · · a * d is context-free if, and only if, its Parikh image is a stratifiable semilinear set. However, the question whether a semilinear set is stratifiable, hereafter called the stratifiability problem, was left open, and remains so. In this paper, we give a partial answer to this problem. We focus on semilinear sets that are given as finite systems of linear inequalities, and we show that stratifiability is coNP-complete in this case. Then, we apply our techniques to the context-freeness problem for flat counter systems, that asks whether the trace language of a counter system intersected with a bounded regular language is context-free. As main result of the paper, we show that this problem is coNP-complete

    Lysophosphatides enhance superoxide responses of stimulated human neutrophils

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    Human neutrophils which are pretreated with subtoxic concentrations of a variety of lysophosphatides (lysophosphatidytcholine, lysophosphatidylcholine oleoyl, lysophosphatidylcholine myrioyl, lysophosphatidylcholine stearoyl, lysophosphatidylcholine gamma- O -hexadecyl, lysophosphatidylinositol, and lysophosphatidylglycerol) act synergistically with neutrophil agonists phorbol myristate acetate, immune complexes, poly- L -histidine, phytohemagglutinin, and N -formyl methionyl-leucyl-phenyalanine to cause enhanced generation of superoxide (O 2 − ). None of the lyso compounds by themselves caused generation of O 2 − . The lyso compounds strongly bound to the neutrophils and could not be washed away. All of the lyso compounds that collaborated with agonists to stimulate O 2 − generation were hemolytic for human red blood cells. On the other hand, lyso compounds that were nonhemolytic for red blood cells (lysophosphatidylcholine caproate, lysophosphatidylcholine decanoyl, lysophosphatidylethanolamine, lysophosphatidylserine) failed to collaborate with agonists to generate synergistic amounts of O 2 − . However, in the presence of cytochalasin B, both lysophosphatidyiethanolamine and lysophosphatidylserine also markedly enhanced O 2 − generation induced by immune complexes. O 2 − generation was also very markedly enhanced when substimulatory amounts of arachidonic acid or eicosapentanoic acid were added to PMNs in the presence of a variety of agonists. On the other hand, neither phospholipase C, streptolysin S (highly hemolytic), phospholipase A 2 , phosphatidylcholine, nor phosphatidylcholine dipalmitoyl (all nonhemolytic) had the capacity to synergize with any of the agonists tested to generate enhanced amounts of O 2 − . The data suggest that in addition to long-chain fatty acids, only those lyso compounds that possess fatty acids with more than 10 carbons and that are also highly hemolytic can cause enhanced generation of O 2 − in stimulated PMNs.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44499/1/10753_2004_Article_BF00924787.pd

    Chemiluminescence in activated human neutrophils

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    Human neutrophils (PMNs) suspended in Hanks' balanced salt solution (HBSS), which are stimulated either by polycation-opsonized streptococci or by phorbol myristate acetate (PMA), generate nonamplified (CL), luminol-dependent (LDCL), and lucigenin-dependent chemiluminescence (LUCDCL). Treatment of activated PMNs with azide yielded a very intense CL response, but only a small LDCL or LUCDCL responses, when horse radish peroxidase (HRP) was added. Both CL and LDCL depend on the generation of Superoxide and on myeloperoxidase (MPO). Treatment of PMNs with azide followed either by dimethylthiourea (DMTU), deferoxamine, EDTA, or detapac generated very little CL upon addition of HRP, suggesting that CL is the: result of the interaction among H 2 O 2 , a peroxidase, and trace metals. In a cell-free system practically no CL was generated when H 2 O 2 was mixed with HRP in distilled water (DW). On the other hand significant CL was generated when either HBSS or RPMI media was employed. In both cases CL was markedly depressed either by deferoxamine or by EDTA, suggesting that these media might be contaminated by trace metals, which catalyzed a Fenton-driven reaction. Both HEPES and Tris buffers, when added to DW, failed to support significant HRP-induced CL. Nitrilotriacetate (NTA) chelates of Mn 2+ , Fe 2+ , Cu 2+ , and Co 2+ very markedly enhanced CL induced by mixtures of H 2 O 2 and HRP when distilled water was the supporting medium. Both HEPES and Tris buffer when added to DW strongly quenced NTA-metal-catalyzed CL. None of the NTA-metal chelates could boost CL generation by activated PMNs, because the salts in HBSS and RPMI interfered with the activity of the added metals. CL and LDCL of activated PMNs was enhanced by aminotriazole, but strongly inhibited by diphenylene iodonium (an inhibitor of NADPH oxidase) by azide, sodium cyanide (CN), cimetidine, histidine, benzoate, DMTU and moderately by Superoxide dismutase (SOD) and by deferoxamine. LUCDCL was markedly inhibited only by SOD but was boosted by CN. Taken together, it is suggested that CL generated by stimulated PMNs might be the result of the interactions among, NADPH oxidase, (inhibitable by diphenylene iodonium), MPO (inhibitable by sodium azide), H 2 O 2 probably of intracellular origin (inhibitable by DMTU but not by catalase), and trace metals that contaminate salt solutions. The nature of the salt solutions employed to measure CL in activated PMNs is critical.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44510/1/10753_2004_Article_BF00918987.pd

    Genome‐wide studies of von Willebrand factor propeptide identify loci contributing to variation in propeptide levels and von Willebrand factor clearance

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134219/1/jth13401-sup-0001-FigS1-S7.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134219/2/jth13401.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134219/3/jth13401_am.pd

    Forward Analysis and Model Checking for Trace Bounded WSTS

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    We investigate a subclass of well-structured transition systems (WSTS), the bounded---in the sense of Ginsburg and Spanier (Trans. AMS 1964)---complete deterministic ones, which we claim provide an adequate basis for the study of forward analyses as developed by Finkel and Goubault-Larrecq (Logic. Meth. Comput. Sci. 2012). Indeed, we prove that, unlike other conditions considered previously for the termination of forward analysis, boundedness is decidable. Boundedness turns out to be a valuable restriction for WSTS verification, as we show that it further allows to decide all ω\omega-regular properties on the set of infinite traces of the system

    Palaeontological data about the climatic trends from Chattian to present along the Northeastern Atlantic frontage

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    Climatic changes that affected the Northeastern Atlantic frontage are analyzed on the basis of the evolution of faunas and floras from the late Oligocene onwards. The study deals with calcareous nannoplankton, marine micro- and macrofaunas, some terrestrial vertebrates and vegetal assemblages. The climate, first tropical, underwent a progressive cooling (North-South thermic gradient). Notable climatic deteriorations (withdrawal towards the South or disappearance of taxa indicative of warm climate and appearance of "cold" taxa) are evidenced mainly during the Middle Miocene and the late Pliocene. Faunas and floras of modern pattern have regained, after the Pleistocene glaciations, a new climatic ranging of a temperate type in the northern part

    Socioeconomic inequalities in cancer mortality between and within countries in Europe: a population-based study

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    Background: Reducing socioeconomic inequalities in cancer is a priority for the public health agenda. A systematic assessment and benchmarking of socioeconomic inequalities in cancer across many countries and over time in Europe is not yet available. Methods: Census-linked, whole-of-population cancer-specific mortality data by socioeconomic position, as measured by education level, and sex were collected, harmonized, analysed, and compared across 18 countries during 1990–2015, in adults aged 40–79. We computed absolute and relative educational inequalities; temporal trends using estimated-annual-percentage-changes; the share of cancer mortality linked to educational inequalities. Findings: Everywhere in Europe, lower-educated individuals have higher mortality rates for nearly all cancer-types relative to their more highly-educated counterparts, particularly for tobacco/infection-related cancers [relative risk of lung cancer mortality for lower- versus higher-educated = 2.4 (95% confidence intervals: 2.1–2.8) among men; = 1.8 (95% confidence intervals: 1.5–2.1) among women]. However, the magnitude of inequalities varies greatly by country and over time, predominantly due to differences in cancer mortality among lower-educated groups, as for many cancer-types higher-educated have more similar (and lower) rates, irrespective of the country. Inequalities were generally greater in Baltic/Central/East-Europe and smaller in South-Europe, although among women large and rising inequalities were found in North–Europe (relative risk of all cancer mortality for lower- versus higher-educated ≥1.4 in Denmark, Norway, Sweden, Finland and the England/Wales). Among men, rate differences (per 100,000 person-years) in total-cancer mortality for lower-vs-higher-educated groups ranged from 110 (Sweden) to 559 (Czech Republic); among women from approximately null (Slovenia, Italy, Spain) to 176 (Denmark). Lung cancer was the largest contributor to inequalities in total-cancer mortality (between-country range: men, 29–61%; women, 10–56%). 32% of cancer deaths in men and 16% in women (but up to 46% and 24%, respectively in Baltic/Central/East-Europe) were associated with educational inequalities. Interpretation: Cancer mortality in Europe is largely driven by levels and trends of cancer mortality rates in lower-education groups. Even Nordic-countries, with a long-established tradition of equitable welfare and social justice policies, witness increases in cancer inequalities among women. These results call for a systematic measurement, monitoring and action upon the remarkable socioeconomic inequalities in cancer existing in Europe. Funding: This study was done as part of the LIFEPATH project, which has received financial support from the European Commission (Horizon 2020 grant number 633666), and the DEMETRIQ project, which received support from the European Commission (grant numbers FP7-CP-FP and 278511). SV and WN were supported by the French Institut National du Cancer (INCa) (Grant number 2018-116). PM was supported by the Academy of Finland (#308247, # 345219) and the European Research Council under the European Union's Horizon 2020 research and innovation programme (grant agreement No 101019329). The work by Mall Leinsalu was supported by the Estonian Research Council (grant PRG722)

    Interaction of mammalian cells with polymorphonuclear leukocytes: Relative sensitivity to monolayer disruption and killing

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    Monolayers of murine fibrosarcoma cells that had been treated either with histone-opsonized streptococci, histone-opsonized Candida globerata , or lipoteichoic acid-anti-lipoteichoic acid complexes underwent disruption when incubated with human polymorphonuclear leukocytes (PMNs). Although the architecture of the monolayers was destroyed, the target cells were not killed. The destruction of the monolayers was totally inhibited by proteinase inhibitors, suggesting that the detachment of the cells from the monolayers and aggregation in suspension were induced by proteinases released from the activated PMNs. Monolayers of normal endothelial cells and fibroblasts were much more resistant to the monolayer-disrupting effects of the PMNs than were the fibrosarcoma cells. Although the fibrosarcoma cells were resistant to killing by PMNs, killing was promoted by the addition of sodium azide (a catalase inhibitor). This suggests that the failure of the PMNs to kill the target cells was due to catalase inhibition of the hydrogen peroxide produced by the activated PMNs. Target cell killing that occurred in the presence of sodium azide was reduced by the addition of a “cocktail” containing methionine, histidine, and deferoxamine mesylate, suggesting that hydroxyl radicals but not myeloperoxidase-catalayzed products were responsible for cell killing. The relative ease with which the murine fibrosarcoma cells can be released from their substratum by the action of PMNs, coupled with their insensitivity to PMN-mediated killing, may explain why the presence of large numbers of PMNs at the site of tumors produced in experimental animals by the fibrosarcoma cells is associated with an unfavorable outcome.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44503/1/10753_2004_Article_BF00916759.pd
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