Random Matching and assignment under dichotomous preferences

We consider bilateral matching problems where each person views those on the other side of the market as either acceptable or unacceptable: an acceptable mate is preferred to remaining single, and the latter to an unacceptable mate all acceptable mates are welfare-wise identical. Using randomization, many efficient and fair matching methods define strategyproof revelation mechanisms. Randomly selecting a priority ordering of the participants gives a simple example. Equalizing as much as possible the probability of getting an acceptable mate accross all participants stands out for its normative and incentives properties: the profile of probabilities is Lorenz dominant, and the revelation mechanism is groupstrategyproof for each side of the market. Our results apply to the random assignment problem as well.

Competitive division of a mixed manna

A mixed manna contains goods (that everyone likes) and bads (that everyone dislikes), as well as items that are goods to some agents, but bads or satiated to others. If all items are goods and utility functions are homogeneous of degree 1 and concave (and monotone), the competitive division maximizes the Nash product of utilities (Gale–Eisenberg): hence it is welfarist (determined by the set of feasible utility profiles), unique, continuous, and easy to compute. We show that the competitive division of a mixed manna is still welfarist. If the zero utility profile is Pareto dominated, the competitive profile is strictly positive and still uniquely maximizes the product of utilities. If the zero profile is unfeasible (for instance, if all items are bads), the competitive profiles are strictly negative and are the critical points of the product of disutilities on the efficiency frontier. The latter allows for multiple competitive utility profiles, from which no single-valued selection can be continuous or resource monotonic. Thus the implementation of competitive fairness under linear preferences in interactive platforms like SPLIDDIT will be more difficult when the manna contains bads that overwhelm the goods

Decentralized Pricing in Minimum Cost Spanning Trees

In the minimum cost spanning tree model we consider decentralized pricing rules, i.e. rules that cover at least the efficient cost while the price charged to each user only depends upon his own connection costs. We define a canonical pricing rule and provide two axiomatic characterizations. First, the canonical pricing rule is the smallest among those that improve upon the Stand Alone bound, and are either superadditive or piece-wise linear in connection costs. Our second, direct characterization relies on two simple properties highlighting the special role of the source cost.pricing rules; minimum cost spanning trees; canonical pricing rule; stand-alone cost; decentralization

Les risques liés aux embâcles de bois dans les cours d'eau : état des connaissances et principes de gestion

Wood trapped in rivers can obstruct infrastructures such as the bridges, and contribute to undermine them but also to increase the flooding and bank erosion frequency. In order to manage these risks, a set of actions can be promoted: a) maintain the channel and the riparian vegetation based on clear objectives in order to preserve wood jams which are ecologically interesting, b) build retention structures and adapt existing infrastructures to wood transfers, c) improve citizen environmental knowledge in order to help them to positively consider these natural elements.Le bois mort aggrave les conséquences des crues en s'accumulant au droit d'ouvrages, mais aussi en favorisant les sapements de berge et les débordements sur les propriétés riveraines. Face à ces problèmes, les gestionnaires préconisent un entretien sectorisé reposant des objectifs clairs afin de préserver les embâcles là où ils sont écologiquement intéressants. La construction d'ouvrages de rétention, lorsque des enjeux aval existent, ainsi que l'adaptation des infrastructures au transfert de flottants peuvent également être préconisés. Une campagne de sensibilisation des citoyens pourrait être aussi effectuée afin que ceux-ci perçoivent plus positivement ces structures naturelles

Highly pathogenic avian influenza virus H5N1 controls type I IFN induction in chicken macrophage HD-11 cells: a polygenic trait that involves NS1 and the polymerase complex

<p>Abstract</p> <p>Background</p> <p>Influenza A viruses are well characterized to antagonize type I IFN induction in infected mammalian cells. However, limited information is available for avian cells. It was hypothesised that avian influenza viruses (AIV) with distinct virulence may interact differently with the avian innate immune system. Therefore, the type I IFN responses induced by highly virulent and low virulent H5N1 AIV and reassortants thereof were analysed in chicken cells.</p> <p>Results</p> <p>The highly pathogenic (HP) AIV A/chicken/Yamaguchi/7/04 (H5N1) (Yama) did not induce type I IFN in infected chicken HD-11 macrophage-like cells. This contrasted with an NS1 mutant Yama virus (Yama-NS1^A144V) and with the attenuated H5N1 AIV A/duck/Hokkaido/Vac-1/04 (Vac) carrying the haemagglutinin (HA) of the Yama virus (Vac-Yama/HA), that both induced type I IFN in these cells. The substitution of the NS segment from Yama with that from Vac in the Yama backbone resulted in induction of type I IFN secretion in HD-11 cells. However, vice versa, the Yama NS segment did not prevent type I IFN induction by the Vac-Yama/HA virus. This was different with the PB1/PB2/PA segment reassortant Yama and Vac-Yama/HA viruses. Whereas the Yama virus with the Vac PB1/PB2/PA segments induced type I IFN in HD-11 cells, the Vac-Yama/HA virus with the Yama PB1/PB2/PA segments did not. As reported for mammalian cells, the expression of H5N1 PB2 inhibited the activation of the IFN-β promoter in chicken DF-1 fibroblast cells. Importantly, the Yama PB2 was more potent at inhibiting the IFN-β promoter than the Vac PB2.</p> <p>Conclusions</p> <p>The present study demonstrates that the NS1 protein and the polymerase complex of the HPAIV Yama act in concert to antagonize chicken type I IFN secretion in HD-11 cells. PB2 alone can also exert a partial inhibitory effect on type I IFN induction. In conclusion, the control of type I IFN induction by H5N1 HPAIV represents a complex phenotype that involves a particular viral gene constellation rather than a single viral protein. Collectively, these findings contribute to understand the high virulence of HPAIV H5N1 viruses observed in the chicken host.</p

On guarantees, vetoes and random dictators

A mechanism guarantees a certain welfare level to its agents, if each of them can secure that level against unanimously adversarial others. How high can such a guarantee be, and what type of mechanism achieves it? In the n-person probabilistic voting/bargaining model with p deterministic outcomes a guarantee takes the form of a probability distribution over the ranks from 1 to p. If n ≥ p, the uniform lottery is shown to be the only maximal (unimprovable) guarantee. If n &lt; p, combining (variants of) the familiar random dictator and voting by veto mechanisms yields a large family of maximal guarantees: it is exhaustive if n = 2 and almost so if p ≤ 2n. Voting rules à la Condorcet or Borda, even in probabilistic form, are ruled out by our worst case viewpoint

High interferon type I responses in the lung, plasma and spleen during highly pathogenic H5N1 infection of chicken

This study shows that high pathogenic H5N1 influenza virus infection of chicken induced high levels of bioactive interferon type I in the lung (4.3 × 105 U/mg tissue), plasma (1.1 × 105 U/mL), and spleen (9.1 × 105 U/mg tissue). In contrast, a low pathogenic attenuated H5N1 vaccine strain only induced approximately 24 times less IFN in the lung, 441 times less in the spleen and 649 less in the plasma. This was in the same range as a reassortant carrying the HA from the vaccine strain and the remaining genes from the high pathogenic virus. On the other hand, a reassortant virus with the HA from the high pathogenic H5N1 with the remaining genes from the vaccine strain had intermediate levels of IFN. The level of interferon responses related to the viral load, and those in the spleen and blood to the spread of virus to lymphoid tissue, as well as disease severity. In vitro, the viruses did not induce interferon in chicken embryonic fibroblasts, but high levels in splenocytes, with not clear relationship to pathogenicity and virulence. This, and the responses also with inactivated viruses imply the presence of plasmacytoid dendritic cell-like leukocytes within the chicken immune system, possibly responsible for the high interferon responses during H5N1 infection. Our data also indicate that the viral load as well as the cleavability of the HA enabling systemic spread of the virus are two major factors controlling systemic IFN responses in chicken