Impact-parameter dependent nuclear parton distribution functions: EPS09s and EKS98s and their applications in nuclear hard processes

We determine the spatial (impact parameter) dependence of nuclear parton distribution functions (nPDFs) using the $A$-dependence of the spatially independent (averaged) global fits EPS09 and EKS98. We work under the assumption that the spatial dependence can be formulated as a power series of the nuclear thickness functions $T_A$. To reproduce the $A$-dependence over the entire $x$ range we need terms up to $[T_A]^4$. As an outcome, we release two sets, EPS09s (LO, NLO, error sets) and EKS98s, of spatially dependent nPDFs for public use. We also discuss the implementation of these into the existing calculations. With our results, the centrality dependence of nuclear hard-process observables can be studied consistently with the globally fitted nPDFs for the first time. As an application, we first calculate the LO nuclear modification factor $R^{1jet}_{AA}$ for primary partonic-jet production in different centrality classes in Au+Au collisions at RHIC and Pb+Pb collisions at LHC. Also the corresponding central-to-peripheral ratios $R_{CP}^{1jet}$ are studied. We also calculate the LO and NLO nuclear modification factors for single inclusive neutral pion production, $R_{dAu}^{\pi^0}$, at mid- and forward rapidities in different centrality classes in d+Au collisions at RHIC. In particular, we show that our results are compatible with the PHENIX mid-rapidity data within the overall normalization uncertainties given by the experiment. Finally, we show our predictions for the corresponding modifications $R_{pPb}^{\pi^0}$ in the forthcoming p+Pb collisions at LHC.Comment: 36 page

Ecological equivalence: a realistic assumption for niche theory as a testable alternative to neutral theory

Hubbell's 2001 neutral theory unifies biodiversity and biogeography by modelling steady-state distributions of species richness and abundances across spatio-temporal scales. Accurate predictions have issued from its core premise that all species have identical vital rates. Yet no ecologist believes that species are identical in reality. Here I explain this paradox in terms of the ecological equivalence that species must achieve at their coexistence equilibrium, defined by zero net fitness for all regardless of intrinsic differences between them. I show that the distinction of realised from intrinsic vital rates is crucial to evaluating community resilience. An analysis of competitive interactions reveals how zero-sum patterns of abundance emerge for species with contrasting life-history traits as for identical species. I develop a stochastic model to simulate community assembly from a random drift of invasions sustaining the dynamics of recruitment following deaths and extinctions. Species are allocated identical intrinsic vital rates for neutral dynamics, or random intrinsic vital rates and competitive abilities for niche dynamics either on a continuous scale or between dominant-fugitive extremes. Resulting communities have steady-state distributions of the same type for more or less extremely differentiated species as for identical species. All produce negatively skewed log-normal distributions of species abundance, zero-sum relationships of total abundance to area, and Arrhenius relationships of species to area. Intrinsically identical species nevertheless support fewer total individuals, because their densities impact as strongly on each other as on themselves. Truly neutral communities have measurably lower abundance/area and higher species/abundance ratios. Neutral scenarios can be parameterized as null hypotheses for testing competitive release, which is a sure signal of niche dynamics. Ignoring the true strength of interactions between and within species risks a substantial misrepresentation of community resilience to habitat los

Modeling a bacterial ecosystem through chemotaxis simulation of a single cell

International audienceWe present in this paper an artificial life ecosystem in which bacteria are evolved to perform chemotaxis. In this system, surviving bacteria have to overcome the problems of detecting resources (or sensing the environment), modulating their motion to generate a foraging behavior, and communicating with their kin to produce more sophisticated behaviors. A cell’s chemotactic pathway is modulated by a hybrid approach that uses an algebraic model for the receptor clusters activity, an ordinary differential equation for the adaptation dynamics, and a metabolic model that converts nutrients into biomass. The results show some analysis of the motion obtained from some bacteria and their effects on the evolved population behavior. The evolutionary process improves the bacteria’s ability to react to their environment, enhancing their growth and allowing them to better survive. As future work, we propose to investigate the effect of emergent bacterial communication as new species arise, and to explore the dynamics of colonies

Stochastic population growth in spatially heterogeneous environments

Classical ecological theory predicts that environmental stochasticity increases extinction risk by reducing the average per-capita growth rate of populations. To understand the interactive effects of environmental stochasticity, spatial heterogeneity, and dispersal on population growth, we study the following model for population abundances in $n$ patches: the conditional law of $X_{t+dt}$ given $X_t=x$ is such that when $dt$ is small the conditional mean of $X_{t+dt}^i-X_t^i$ is approximately $[x^i\mu_i+\sum_j(x^j D_{ji}-x^i D_{ij})]dt$, where $X_t^i$ and $\mu_i$ are the abundance and per capita growth rate in the $i$-th patch respectivly, and $D_{ij}$ is the dispersal rate from the $i$-th to the $j$-th patch, and the conditional covariance of $X_{t+dt}^i-X_t^i$ and $X_{t+dt}^j-X_t^j$ is approximately $x^i x^j \sigma_{ij}dt$. We show for such a spatially extended population that if $S_t=(X_t^1+...+X_t^n)$ is the total population abundance, then $Y_t=X_t/S_t$, the vector of patch proportions, converges in law to a random vector $Y_\infty$ as $t\to\infty$, and the stochastic growth rate $\lim_{t\to\infty}t^{-1}\log S_t$ equals the space-time average per-capita growth rate \sum_i\mu_i\E[Y_\infty^i] experienced by the population minus half of the space-time average temporal variation \E[\sum_{i,j}\sigma_{ij}Y_\infty^i Y_\infty^j] experienced by the population. We derive analytic results for the law of $Y_\infty$, find which choice of the dispersal mechanism $D$ produces an optimal stochastic growth rate for a freely dispersing population, and investigate the effect on the stochastic growth rate of constraints on dispersal rates. Our results provide fundamental insights into "ideal free" movement in the face of uncertainty, the persistence of coupled sink populations, the evolution of dispersal rates, and the single large or several small (SLOSS) debate in conservation biology.Comment: 47 pages, 4 figure

Haloperidol differentially modulates prepulse inhibition and p50 suppression in healthy humans stratified for low and high gating levels

Schizophrenia patients exhibit deficits in sensory gating as indexed by reduced prepulse inhibition (PPI) and P50 suppression, which have been linked to psychotic symptom formation and cognitive deficits. Although recent evidence suggests that atypical antipsychotics might be superior over typical antipsychotics in reversing PPI and P50 suppression deficits not only in schizophrenia patients, but also in healthy volunteers exhibiting low levels of PPI, the impact of typical antipsychotics on these gating measures is less clear. To explore the impact of the dopamine D2-like receptor system on gating and cognition, the acute effects of haloperidol on PPI, P50 suppression, and cognition were assessed in 26 healthy male volunteers split into subgroups having low vs high PPI or P50 suppression levels using a placebo-controlled within-subject design. Haloperidol failed to increase PPI in subjects exhibiting low levels of PPI, but attenuated PPI in those subjects with high sensorimotor gating levels. Furthermore, haloperidol increased P50 suppression in subjects exhibiting low P50 gating and disrupted P50 suppression in individuals expressing high P50 gating levels. Independently of drug condition, high PPI levels were associated with superior strategy formation and execution times in a subset of cognitive tests. Moreover, haloperidol impaired spatial working memory performance and planning ability. These findings suggest that dopamine D2-like receptors are critically involved in the modulation of P50 suppression in healthy volunteers, and to a lesser extent also in PPI among subjects expressing high sensorimotor gating levels. Furthermore, the results suggest a relation between sensorimotor gating and working memory performance

Nonlinear Supersymmetry as a Hidden Symmetry

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