Prioritized Repairing and Consistent Query Answering in Relational Databases

A consistent query answer in an inconsistent database is an answer obtained in every (minimal) repair. The repairs are obtained by resolving all conflicts in all possible ways. Often, however, the user is able to provide a preference on how conflicts should be resolved. We investigate here the framework of preferred consistent query answers, in which user preferences are used to narrow down the set of repairs to a set of preferred repairs. We axiomatize desirable properties of preferred repairs. We present three different families of preferred repairs and study their mutual relationships. Finally, we investigate the complexity of preferred repairing and computing preferred consistent query answers.Comment: Accepted to the special SUM'08 issue of AMA

Rainbow domination and related problems on some classes of perfect graphs

Let $k \in \mathbb{N}$ and let $G$ be a graph. A function $f: V(G) \rightarrow 2^{[k]}$ is a rainbow function if, for every vertex $x$ with $f(x)=\emptyset$, $f(N(x)) =[k]$. The rainbow domination number $\gamma_{kr}(G)$ is the minimum of $\sum_{x \in V(G)} |f(x)|$ over all rainbow functions. We investigate the rainbow domination problem for some classes of perfect graphs

Ground state properties of a Tonks-Girardeau Gas in a periodic potential

In this paper, we investigate the ground-state properties of a bosonic Tonks-Girardeau gas confined in a one-dimensional periodic potential. The single-particle reduced density matrix is computed numerically for systems up to $N=265$ bosons. Scaling analysis of the occupation number of the lowest orbital shows that there are no Bose-Einstein Condensation(BEC) for the periodically trapped TG gas in both commensurate and incommensurate cases. We find that, in the commensurate case, the scaling exponents of the occupation number of the lowest orbital, the amplitude of the lowest orbital and the zero-momentum peak height with the particle numbers are 0, -0.5 and 1, respectively, while in the incommensurate case, they are 0.5, -0.5 and 1.5, respectively. These exponents are related to each other in a universal relation.Comment: 9 pages, 10 figure

Alternative splicing of MALT1 controls signalling and activation of CD4+ T cells

MALT1 channels proximal T-cell receptor (TCR) signalling to downstream signalling pathways. With MALT1A and MALT1B two conserved splice variants exist and we demonstrate here that MALT1 alternative splicing supports optimal T-cell activation. Inclusion of exon7 in MALT1A facilitates the recruitment of TRAF6, which augments MALT1 scaffolding function, but not protease activity. Naive CD4+ T cells express almost exclusively MALT1B and MALT1A expression is induced by TCR stimulation. We identify hnRNP U as a suppressor of exon7 inclusion. Whereas selective depletion of MALT1A impairs T-cell signalling and activation, downregulation of hnRNP U enhances MALT1A expression and T-cell activation. Thus, TCR-induced alternative splicing augments MALT1 scaffolding to enhance downstream signalling and to promote optimal T-cell activation

Extension of Some Edge Graph Problems: Standard and Parameterized Complexity

Le PDF est une version auteur non publiée.We consider extension variants of some edge optimization problems in graphs containing the classical Edge Cover, Matching, and Edge Dominating Set problems. Given a graph G=(V,E) and an edge set U⊆E, it is asked whether there exists an inclusion-wise minimal (resp., maximal) feasible solution E′ which satisfies a given property, for instance, being an edge dominating set (resp., a matching) and containing the forced edge set U (resp., avoiding any edges from the forbidden edge set E∖U). We present hardness results for these problems, for restricted instances such as bipartite or planar graphs. We counter-balance these negative results with parameterized complexity results. We also consider the price of extension, a natural optimization problem variant of extension problems, leading to some approximation results

Roquin Paralogs 1 and 2 Redundantly Repress the Icos and Ox40 Costimulator mRNAs and Control Follicular Helper T Cell Differentiation

SummaryThe Roquin-1 protein binds to messenger RNAs (mRNAs) and regulates gene expression posttranscriptionally. A single point mutation in Roquin-1, but not gene ablation, increases follicular helper T (Tfh) cell numbers and causes lupus-like autoimmune disease in mice. In T cells, we did not identify a unique role for the much lower expressed paralog Roquin-2. However, combined ablation of both genes induced accumulation of T cells with an effector and follicular helper phenotype. We showed that Roquin-1 and Roquin-2 proteins redundantly repressed the mRNA of inducible costimulator (Icos) and identified the Ox40 costimulatory receptor as another shared mRNA target. Combined acute deletion increased Ox40 signaling, as well as Irf4 expression, and imposed Tfh differentiation on CD4+ T cells. These data imply that both proteins maintain tolerance by preventing inappropriate T cell activation and Tfh cell differentiation, and that Roquin-2 compensates in the absence of Roquin-1, but not in the presence of its mutated form

The prolyl-isomerase PIN1 is essential for nuclear Lamin-B structure and function and protects heterochromatin under mechanical stress

Chromatin organization plays a crucial role in tissue homeostasis. Heterochromatin relaxation and consequent unscheduled mobilization of transposable elements (TEs) are emerging as key contributors of aging and aging-related pathologies, including Alzheimer's disease (AD) and cancer. However, the mechanisms governing heterochromatin maintenance or its relaxation in pathological conditions remain poorly understood. Here we show that PIN1, the only phosphorylation-specific cis/trans prolyl isomerase, whose loss is associated with premature aging and AD, is essential to preserve heterochromatin. We demonstrate that this PIN1 function is conserved from Drosophila to humans and prevents TE mobilization-dependent neurodegeneration and cognitive defects. Mechanistically, PIN1 maintains nuclear type-B Lamin structure and anchoring function for heterochromatin protein 1\u3b1 (HP1\u3b1). This mechanism prevents nuclear envelope alterations and heterochromatin relaxation under mechanical stress, which is a key contributor to aging-related pathologies