51 research outputs found

    Constructing universal graphs for induced-hereditary graph properties

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    Rado constructed a (simple) denumerable graph R with the positive integers as vertex set with the following edges: For given m and n with m < n, m is adjacent to n if n has a 1 in the m'th position of its binary expansion. It is well known that R is a universal graph in the set Ic of all countable graphs (since every graph in Ic is isomorphic to an induced subgraph of R). In this paper we construct graphs which are universal in or for P for di erent inducedhereditary properties P of countable graphs. Constructions of universal graphs for the graph properties containing all graphs with colouring-number at most k+1 and k-degenerate graphs are obtained by restricting the edges of R. Results on the properties of these graphs are given and relationships between them are explored. This is followed by a general recursive construction which proves the existence of a countable universal graph for any induced-hereditary property of countable general graphs. A general construction of universal graphs for products of properties of graphs is also presented. The paper is concluded by a comparison between the two types of constructions of universal graphs.Research of the third author was supported by VEGA Grant No. 2/0194/10.http://link.springer.com/journal/12175hb201

    Роль социологических опросов в изучении водопотребления населения

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    Доказано, що соціологічні опитування є важливим інструментам формування програм соціальної та екологічної скерованості. Вони дозволяють отримати не лише суб'єктивну, але і об'єктивну оцінку стану довкілля, інформацію про ефективність муніципальних та державних програм, можуть бути використані для проведення маркетингових досліджень.It is shown that sociological questionnaire are the important tool at formation of the programs of a social and ecological orientation, allow to receive not only subjective, but also objective estimation of a condition of an environment, allow to receive the information not only about efficiency of the municipal and state programs, but also to be used for realization of marketing researches

    Two canine CD1a proteins are differentially expressed in skin

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    Lipid antigens are presented to T cells by the CD1 family of proteins. In this study, we characterize the complete dog (Canis familiaris) CD1 locus, which is located on chromosome 38. The canine locus contains eight CD1A genes (canCD1A), of which five are pseudogenes, one canCD1B, one canCD1C, one canCD1D, and one canCD1E gene. In vivo expression of canine CD1 proteins was shown for canCD1a6, canCD1a8, and canCD1b, using a panel of anti-CD1 monoclonal antibodies (mAbs). CanCD1a6 and canCD1a8 are recognized by two distinct mAbs. Furthermore, we show differential transcription of the three canCD1A genes in canine tissues. In canine skin, the transcription level of canCD1A8 was higher than that of canCD1A6, and no transcription of canCD1A2 was detected. Based on protein modeling and protein sequence alignment, we predict that both canine CD1a proteins can bind different glycolipids in their groove. Besides differences in ectodomain structure, we observed the unique presence of three types of cytoplasmic tails encoded by canCD1A genes. cDNA sequencing and expressed sequence tag sequences confirmed the existence of a short, human CD1a-like cytoplasmic tail of four amino acids, of an intermediate length form of 15 amino acids, and of a long form of 31 amino acids

    IL-10 Is Critically Involved in Mycobacterial HSP70 Induced Suppression of Proteoglycan-Induced Arthritis

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    BACKGROUND: The anti-inflammatory capacity of heat shock proteins (HSP) has been demonstrated in various animal models of inflammatory diseases and in patients. However, the mechanisms underlying this anti-inflammatory capacity are poorly understood. Therefore, the possible protective potential of HSP70 and its mechanisms were studied in proteoglycan (PG) induced arthritis (PGIA), a chronic and relapsing, T cell mediated murine model of arthritis. METHODOLOGY/PRINCIPAL FINDINGS: HSP70 immunization, 10 days prior to disease induction with PG, inhibited arthritis both clinically and histologically. In addition, it significantly reduced PG-specific IgG2a but not IgG1 antibody production. Furthermore, IFN-gamma and IL-10 production upon in vitro restimulation with HSP70 was indicative of the induction of an HSP70-specific T cell response in HSP70 immunized mice. Remarkably, HSP70 treatment also modulated the PG-specific T cell response, as shown by the increased production of IL-10 and IFN-gamma upon in vitro PG restimulation. Moreover, it increased IL-10 mRNA expression in CD4+CD25+ cells. HSP70 vaccination did not suppress arthritis in IL-10(-/-) mice, indicating the crucial role of IL-10 in the protective effect. CONCLUSIONS/SIGNIFICANCE: In conclusion, a single mycobacterial HSP70 immunization can suppress inflammation and tissue damage in PGIA and results in an enhanced regulatory response as shown by the antigen-specific IL-10 production. Moreover, HSP70 induced protection is critically IL-10 dependent

    The HMGB1/RAGE axis triggers neutrophil-mediated injury amplification following necrosis

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    In contrast to microbially triggered inflammation, mechanisms promoting sterile inflammation remain poorly understood. Damage-associated molecular patterns (DAMPs) are considered key inducers of sterile inflammation following cell death, but the relative contribution of specific DAMPs, including high–mobility group box 1 (HMGB1), is ill defined. Due to the postnatal lethality of Hmgb1-knockout mice, the role of HMGB1 in sterile inflammation and disease processes in vivo remains controversial. Here, using conditional ablation strategies, we have demonstrated that epithelial, but not bone marrow–derived, HMGB1 is required for sterile inflammation following injury. Epithelial HMGB1, through its receptor RAGE, triggered recruitment of neutrophils, but not macrophages, toward necrosis. In clinically relevant models of necrosis, HMGB1/RAGE-induced neutrophil recruitment mediated subsequent amplification of injury, depending on the presence of neutrophil elastase. Notably, hepatocyte-specific HMGB1 ablation resulted in 100% survival following lethal acetaminophen intoxication. In contrast to necrosis, HMGB1 ablation did not alter inflammation or mortality in response to TNF- or FAS-mediated apoptosis. In LPS-induced shock, in which HMGB1 was considered a key mediator, HMGB1 ablation did not ameliorate inflammation or lethality, despite efficient reduction of HMGB1 serum levels. Our study establishes HMGB1 as a bona fide and targetable DAMP that selectively triggers a neutrophil-mediated injury amplification loop in the setting of necrosis

    Tandem repeats modify the structure of the canine CD1D gene

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    Among the CD1 proteins that present lipid antigens to T cells, CD1d is the only one that stimulates a population of T cells with an invariant T-cell receptor known as NKT cells. Sequencing of a 722 nucleotide gap in the dog (Canis lupus familiaris) genome revealed that the canine CD1D gene lacks a sequence homologous to exon 2 of human CD1D, coding for the start codon and signal peptide. Also, the canine CD1D gene contains three different short tandem repeats that disrupt the expected gene structure. Because canine CD1D cDNA lacks sequences homologous to human exon 2 and 3, the functionality of canine CD1d protein may be affected, and this could have consequences for the development and activation of canine NKT cells.IVR was supported by an NWO Meervoud subsidy; Netherlands.FALVB was supported by Royal Canin, France.http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2052hb201

    Status of Muon Collider Research and Development and Future Plans

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    The status of the research on muon colliders is discussed and plans are outlined for future theoretical and experimental studies. Besides continued work on the parameters of a 3-4 and 0.5 TeV center-of-mass (CoM) energy collider, many studies are now concentrating on a machine near 0.1 TeV (CoM) that could be a factory for the s-channel production of Higgs particles. We discuss the research on the various components in such muon colliders, starting from the proton accelerator needed to generate pions from a heavy-Z target and proceeding through the phase rotation and decay (πμνμ\pi \to \mu \nu_{\mu}) channel, muon cooling, acceleration, storage in a collider ring and the collider detector. We also present theoretical and experimental R & D plans for the next several years that should lead to a better understanding of the design and feasibility issues for all of the components. This report is an update of the progress on the R & D since the Feasibility Study of Muon Colliders presented at the Snowmass'96 Workshop [R. B. Palmer, A. Sessler and A. Tollestrup, Proceedings of the 1996 DPF/DPB Summer Study on High-Energy Physics (Stanford Linear Accelerator Center, Menlo Park, CA, 1997)].Comment: 95 pages, 75 figures. Submitted to Physical Review Special Topics, Accelerators and Beam

    Criteria for of the existence of uniquely partitionable graphs with respect to additive induced-hereditary properties

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    Let ₁,₂,...,ₙ be graph properties, a graph G is said to be uniquely (₁,₂, ...,ₙ)-partitionable if there is exactly one (unordered) partition {V₁,V₂,...,Vₙ} of V(G) such that G[Vi]iG[V_i] ∈ _i for i = 1,2,...,n. We prove that for additive and induced-hereditary properties uniquely (₁,₂,...,ₙ)-partitionable graphs exist if and only if i_i and j_j are either coprime or equal irreducible properties of graphs for every i ≠ j, i,j ∈ {1,2,...,n}

    The order of uniquely partitionable graphs

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    Let ₁,...,ₙ be properties of graphs. A (₁,...,ₙ)-partition of a graph G is a partition {V₁,...,Vₙ} of V(G) such that, for each i = 1,...,n, the subgraph of G induced by ViV_i has property i_i. If a graph G has a unique (₁,...,ₙ)-partition we say it is uniquely (₁,...,ₙ)-partitionable. We establish best lower bounds for the order of uniquely (₁,...,ₙ)-partitionable graphs, for various choices of ₁,...,ₙ

    Partition problems and kernels of graphs

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