The Price of Anarchy in Cooperative Network Creation Games

In general, the games are played on a host graph, where each node is a selfish independent agent (player) and each edge has a fixed link creation cost \alpha. Together the agents create a network (a subgraph of the host graph) while selfishly minimizing the link creation costs plus the sum of the distances to all other players (usage cost). In this paper, we pursue two important facets of the network creation game. First, we study extensively a natural version of the game, called the cooperative model, where nodes can collaborate and share the cost of creating any edge in the host graph. We prove the first nontrivial bounds in this model, establishing that the price of anarchy is polylogarithmic in n for all values of α in complete host graphs. This bound is the first result of this type for any version of the network creation game; most previous general upper bounds are polynomial in n. Interestingly, we also show that equilibrium graphs have polylogarithmic diameter for the most natural range of \alpha (at most n polylg n). Second, we study the impact of the natural assumption that the host graph is a general graph, not necessarily complete. This model is a simple example of nonuniform creation costs among the edges (effectively allowing weights of \alpha and \infty). We prove the first assemblage of upper and lower bounds for this context, stablishing nontrivial tight bounds for many ranges of \alpha, for both the unilateral and cooperative versions of network creation. In particular, we establish polynomial lower bounds for both versions and many ranges of \alpha, even for this simple nonuniform cost model, which sharply contrasts the conjectured constant bounds for these games in complete (uniform) graphs

Probabilistic computing with future deep sub-micrometer devices: a modelling approach

An approach is described that investigates the potential of probabilistic "neural" architectures for computation with deep sub-micrometer (DSM) MOSFETs. Initially, noisy MOSFET models are based upon those for a 0.35 /spl mu/m MOS technology with an exaggerated 1/f characteristic. We explore the manifestation of the 1/f characteristic at the output of a 2-quadrant multiplier when the key n-channel MOSFETs are replaced by "noisy" MOSFETs. The stochastic behavior of this noisy multiplier has been mapped on to a software (Matlab) model of a continuous restricted Boltzmann machine (CRBM) - an analogue-input stochastic computing structure. Simulation of this DSM CRBM implementation shows little degradation from that of a "perfect" CRBM. This paper thus introduces a methodology for a form of "technology-downstreaming" and highlights the potential of probabilistic architectures for DSM computation

Biotin Supplementation Ameliorates Murine Colitis by Preventing NF-κB Activation.

Background & aimsBiotin is a water-soluble vitamin that is indispensable for human health. Biotin deficiency can cause failure-to-thrive, immunodeficiency, alopecia, dermatitis, and conjunctivitis. We previously reported that biotin deficiency also can lead to severe colitis in mice, which is completely reversed with supplementation. Our aim in this study was to determine if high-dose biotin supplementation can provide a therapeutic benefit in a preclinical model for inflammatory bowel disease (IBD) and to identify the molecular mechanism by which this occurs.MethodsMice were challenged with dextran sodium sulfate to induce colitis and were treated with 1 mmol/L biotin to induce or maintain remission. Clinical response was monitored by the Disease Activity Index and fecal calprotectin levels. The colon tissue was investigated for histology, length, as well as expression of inflammatory cytokines (interleukin 6, tumor necrosis factor-α, interleukin 1β), intestinal permeability, tight junctions (zonula occludens-1 and claudin-2), and the transcription factor nuclear factor-κB (NF-κB).ResultsBiotin therapy led to delayed onset and severity of colitis as well as accelerated healing. There was improvement in the Disease Activity Index, fecal calprotectin levels, colon length, and histology. In addition, biotin-treated mice had reduced expression of inflammatory cytokines, reduced intestinal permeability, and reduced activation of NF-κB.ConclusionsOral supplementation with biotin provides benefit for maintenance and induction of remission in the dextran sodium sulfate preclinical model for IBD. Biotin does this by reducing the activation of NF-κB, which prevents the production of inflammatory cytokines and helps maintain the integrity of the intestinal barrier. Clinically, the NF-κB pathway is important in the development of IBD and this finding suggests that biotin may have therapeutic potential for patients with IBD

High-Reynolds-number turbulence in complex fluids

International audienceWe here examine the structure of turbulence in the case of a complex fluid made up of water and surfactants. This fluid has the particular property of shear thickening when driven at shear rates above a certain threshold. Through a study of the spectral properties and the structure function scalings, important differences arise with respect to the reference case, i.e., water. The surfactant solution shows strong intermittency at small scales. The large scales are, on the other hand, free of intermittency. While this transition is observed in the structure function scalings, no sign of this transition is seen in the power spectrum of velocity fluctuations which shows a single scaling range. The strongly intermittent small-scale region, despite the scaling of the power spectrum, exhibits properties reminiscent of the near-dissipative range