The Least-core and Nucleolus of Path Cooperative Games

Cooperative games provide an appropriate framework for fair and stable profit distribution in multiagent systems. In this paper, we study the algorithmic issues on path cooperative games that arise from the situations where some commodity flows through a network. In these games, a coalition of edges or vertices is successful if it enables a path from the source to the sink in the network, and lose otherwise. Based on dual theory of linear programming and the relationship with flow games, we provide the characterizations on the CS-core, least-core and nucleolus of path cooperative games. Furthermore, we show that the least-core and nucleolus are polynomially solvable for path cooperative games defined on both directed and undirected network

Online Makespan Minimization with Parallel Schedules

In online makespan minimization a sequence of jobs $\sigma = J_1,..., J_n$ has to be scheduled on $m$ identical parallel machines so as to minimize the maximum completion time of any job. We investigate the problem with an essentially new model of resource augmentation. Here, an online algorithm is allowed to build several schedules in parallel while processing $\sigma$. At the end of the scheduling process the best schedule is selected. This model can be viewed as providing an online algorithm with extra space, which is invested to maintain multiple solutions. The setting is of particular interest in parallel processing environments where each processor can maintain a single or a small set of solutions. We develop a (4/3+\eps)-competitive algorithm, for any 0<\eps\leq 1, that uses a number of 1/\eps^{O(\log (1/\eps))} schedules. We also give a (1+\eps)-competitive algorithm, for any 0<\eps\leq 1, that builds a polynomial number of (m/\eps)^{O(\log (1/\eps) / \eps)} schedules. This value depends on $m$ but is independent of the input $\sigma$. The performance guarantees are nearly best possible. We show that any algorithm that achieves a competitiveness smaller than 4/3 must construct $\Omega(m)$ schedules. Our algorithms make use of novel guessing schemes that (1) predict the optimum makespan of a job sequence $\sigma$ to within a factor of 1+\eps and (2) guess the job processing times and their frequencies in $\sigma$. In (2) we have to sparsify the universe of all guesses so as to reduce the number of schedules to a constant. The competitive ratios achieved using parallel schedules are considerably smaller than those in the standard problem without resource augmentation

Resource Competition on Integral Polymatroids

We study competitive resource allocation problems in which players distribute their demands integrally on a set of resources subject to player-specific submodular capacity constraints. Each player has to pay for each unit of demand a cost that is a nondecreasing and convex function of the total allocation of that resource. This general model of resource allocation generalizes both singleton congestion games with integer-splittable demands and matroid congestion games with player-specific costs. As our main result, we show that in such general resource allocation problems a pure Nash equilibrium is guaranteed to exist by giving a pseudo-polynomial algorithm computing a pure Nash equilibrium.Comment: 17 page

Soluble CD44 Interacts with Intermediate Filament Protein Vimentin on Endothelial Cell Surface

CD44 is a cell surface glycoprotein that functions as hyaluronan receptor. Mouse and human serum contain substantial amounts of soluble CD44, generated either by shedding or alternative splicing. During inflammation and in cancer patients serum levels of soluble CD44 are significantly increased. Experimentally, soluble CD44 overexpression blocks cancer cell adhesion to HA. We have previously found that recombinant CD44 hyaluronan binding domain (CD44HABD) and its non-HA-binding mutant inhibited tumor xenograft growth, angiogenesis, and endothelial cell proliferation. These data suggested an additional target other than HA for CD44HABD. By using non-HA-binding CD44HABD Arg41Ala, Arg78Ser, and Tyr79Ser-triple mutant (CD443MUT) we have identified intermediate filament protein vimentin as a novel interaction partner of CD44. We found that vimentin is expressed on the cell surface of human umbilical vein endothelial cells (HUVEC). Endogenous CD44 and vimentin coprecipitate from HUVECs, and when overexpressed in vimentin-negative MCF-7 cells. By using deletion mutants, we found that CD44HABD and CD443MUT bind vimentin N-terminal head domain. CD443MUT binds vimentin in solution with a Kd in range of 12–37 nM, and immobilised vimentin with Kd of 74 nM. CD443MUT binds to HUVEC and recombinant vimentin displaces CD443MUT from its binding sites. CD44HABD and CD443MUT were internalized by wild-type endothelial cells, but not by lung endothelial cells isolated from vimentin knock-out mice. Together, these data suggest that vimentin provides a specific binding site for soluble CD44 on endothelial cells

Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury

Severe pulmonary infection or vigorous cyclic deformation of the alveolar epithelial type I (AT I) cells by mechanical ventilation leads to massive extracellular ATP release. High levels of extracellular ATP saturate the ATP hydrolysis enzymes CD39 and CD73 resulting in persistent high ATP levels despite the conversion to adenosine. Above a certain level, extracellular ATP molecules act as danger-associated molecular patterns (DAMPs) and activate the pro-inflammatory response of the innate immunity through purinergic receptors on the surface of the immune cells. This results in lung tissue inflammation, capillary leakage, interstitial and alveolar oedema and lung injury reducing the production of surfactant by the damaged AT II cells and deactivating the surfactant function by the concomitant extravasated serum proteins through capillary leakage followed by a substantial increase in alveolar surface tension and alveolar collapse. The resulting inhomogeneous ventilation of the lungs is an important mechanism in the development of ventilation-induced lung injury. The high levels of extracellular ATP and the upregulation of ecto-enzymes and soluble enzymes that hydrolyse ATP to adenosine (CD39 and CD73) increase the extracellular adenosine levels that inhibit the innate and adaptive immune responses rendering the host susceptible to infection by invading microorganisms. Moreover, high levels of extracellular adenosine increase the expression, the production and the activation of pro-fibrotic proteins (such as TGF-β, α-SMA, etc.) followed by the establishment of lung fibrosis