Fuzzy Bigraphs: An Exercise in Fuzzy Communicating Agents

Bigraphs and their algebra is a model of concurrency. Fuzzy bigraphs are a generalization of birgraphs intended to be a model of concurrency that incorporates vagueness. More specifically, this model assumes that agents are similar, communication is not perfect, and, in general, everything is or happens to some degree.Comment: 11 pages, 3 figure

Prehension and perception of size in left visual neglect

Right hemisphere damaged patients with and without left visual neglect, and age-matched controls had objects of various sizes presented within left or right body hemispace. Subjects were asked to estimate the objects’ sizes or to reach out and grasp them, in order to assess visual size processing in perceptual-experiential and action-based contexts respectively. No impairments of size processing were detected in the prehension performance of the neglect patients but a generalised slowing of movement was observed, associated with an extended deceleration phase. Additionally both patient groups reached maximum grip aperture relatively later in the movement than did controls. For the estimation task it was predicted that the left visual neglect group would systematically underestimate the sizes of objects presented within left hemispace but no such abnormalities were observed. Possible reasons for this unexpected null finding are discussed

Measurement of kinematic and nuclear dependence of R = σ_L/σ_T in deep inelastic electron scattering

We report results on a precision measurement of the ratio R=σ_L/σ_T in deep inelastic electron-nucleon scattering in the kinematic range 0.2≤x≤0.5 and 1≤Q^2≤10 (GeV/c)^2. Our results show, for the first time, a clear falloff of R with increasing Q^2. Our R results are in agreement with QCD predictions only when corrections for target mass effects and some additional higher twist effects are included. At small x, the data on R favor structure functions with a large gluon contribution. We also report results on the differences R_A-R_D and the cross section ratio σ^A/σ^D between Fe and Au nuclei and the deuteron. Our results for R_A-R_D are consistent with zero for all x, Q^2 indicating that possible contributions to R from nuclear higher twist effects and spin-0 constituents in nuclei are not different from those in nucleons. The ratios σ^A/σ^D from all recent experiments, at all x, Q^2 values, are now in agreement

Measurement of the Difference in R=σ_L/σ_T and of σ^A/σ^D in Deep-Inelastic e-D, e-Fe, and e-Au Scattering

We measured the differences in R=σ_L/σ_T and the cross-section ratio σA/σD in deep-inelastic electron scattering from D, Fe, and Au nuclei in the kinematic range 0.2≤x≤0.5 and 1≤Q^2≤5 (Gev/c)^2. Our results for R^A-R^D are consistent with zero for all x and Q^2, indicating that possible contributions to R from nuclear higher-twist effects and spin-0 constituents in nuclei are not different from those in nucleons. The European Muon Collaboration effect is reconfirmed, and the low-x data from all recent experiments, at all Q^2, are now in agreement

Radiative corrections for (e,e′p) reactions at GeV energies

A general framework for applying radiative corrections to (e,e′p) coincidence reactions at GeV energies is presented, with special emphasis to higher-order bremsstrahlung effects, radiation from the scattered hadron, and the validity of peaking approximations. The sensitivity to the assumptions made in practically applying radiative corrections to (e,e′p) data is extensively discussed. The general framework is tested against experimental data of the 1H(e,e′p) reaction at momentum transfer values larger than 1.0 (GeV/c)^2, where radiative processes become a dominant source of uncertainty. The formulas presented here can easily be modified for any other electron-induced coincidence reaction

Rate-Based Transition Systems for Stochastic Process Calculi

A variant of Rate Transition Systems (RTS), proposed by Klin and Sassone, is introduced and used as the basic model for defining stochastic behaviour of processes. The transition relation used in our variant associates to each process, for each action, the set of possible futures paired with a measure indicating their rates. We show how RTS can be used for providing the operational semantics of stochastic extensions of classical formalisms, namely CSP and CCS. We also show that our semantics for stochastic CCS guarantees associativity of parallel composition. Similarly, in contrast with the original definition by Priami, we argue that a semantics for stochastic π-calculus can be provided that guarantees associativity of parallel composition

Identification of LDH-A as a therapeutic target for cancer cell killing via (i) p53/NAD(H)-dependent and (ii) p53 independent pathways

Most cancer cells use aerobic glycolysis to fuel their growth. The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer’s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD þ ) from reduced nicotinamide adenine dinucleotide (NADH) necessary to sustain glycolysis. As such, LDH-A is a promising target for anticancer therapy. Here we ask if the tumour suppressor p53, a major regulator of cellular metabolism, influences the response of cancer cells to LDH-A suppression. LDH-A knockdown by RNA interference (RNAi) induced cancer cell death in p53 wild-type, mutant and p53-null human cancer cell lines, indicating that endogenous LDH-A promotes cancer cell survival irrespective of cancer cell p53 status. Unexpectedly,however,weuncoveredanovelroleforp53intheregulationofcancercellNADþ anditsreducedformNADH.Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratioofNADH:NADþ.Thiseffectwasspecificforp53þ/þ cancercellsandcorrelatedwith(i)reducedactivityofNADþ-dependent deacetylase sirtuin 1 (SIRT1) and (ii) an increase in acetylated p53, a known target of SIRT1 deacetylation activity. In addition, activation of the redox-sensitive anticancer drug EO9 was enhanced selectively in p53 þ / þ cancer cells, attributable to increased activity of NAD(P)H-dependent oxidoreductase NQO1 (NAD(P)H quinone oxidoreductase 1). Suppressing LDH-A increased EO9-inducedDNAdamageinp53þ/þ cancercells,butimportantlyhadnoadditiveeffectinnon-cancercells.Ourresultsidentifya unique strategy by which the NADH/NADþ cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes. To summarise, this work indicates two distinct mechanisms by which suppressing LDH-A could potentially be used to kill cancer cells selectively, (i) through induction of apoptosis, irrespective of cancer cell p53 status and (ii) as a part of a combinatorial approach with redox-sensitive anticancer drugs via a novel p53/NAD(H)-dependent mechanism