New analyticity constraints on the high energy behavior of hadron-hadron cross sections

We here comment on a series of recent papers by Igi and Ishida[K. Igi and M. Ishida, Phys. Lett B 622, 286 (2005)] and Block and Halzen[M. M. Block and F. Halzen, Phys. Rev D 72, 036006 (2005)] that fit high energy $pp$ and $\bar pp$ cross section and $\rho$-value data, where $\rho$ is the ratio of the real to the imaginary portion of the forward scattering amplitude. These authors used Finite Energy Sum Rules and analyticity consistency conditions, respectively, to constrain the asymptotic behavior of hadron cross sections by anchoring their high energy asymptotic amplitudes--even under crossing--to low energy experimental data. Using analyticity, we here show that i) the two apparently very different approaches are in fact equivalent, ii) that these analyticity constraints can be extended to give new constraints, and iii) that these constraints can be extended to crossing odd amplitudes. We also apply these extensions to photoproduction. A new interpretation of duality is given.Comment: 9 pages, 1 postscript figure; redone for clarity, removal of typos, changing reference; figure replace

What Is Wrong with the No-Report Paradigm and How to Fix It

Is consciousness based in prefrontal circuits involved in cognitive processes like thought, reasoning, and memory or, alternatively, is it based in sensory areas in the back of the neocortex? The no-report paradigm has been crucial to this debate because it aims to separate the neural basis of the cognitive processes underlying post-perceptual decision and report from the neural basis of conscious perception itself. However, the no-report paradigm is problematic because, even in the absence of report, subjects might engage in post-perceptual cognitive processing. Therefore, to isolate the neural basis of consciousness, a no-cognition paradigm is needed. Here, I describe a no-cognition approach to binocular rivalry and outline how this approach can help resolve debates about the neural basis of consciousness

Decoupling the coupled DGLAP evolution equations: an analytic solution to pQCD

Using Laplace transform techniques, along with newly-developed accurate numerical inverse Laplace transform algorithms, we decouple the solutions for the singlet structure function $F_s(x,Q^2)$ and $G(x,Q^2)$ of the two leading-order coupled singlet DGLAP equations, allowing us to write fully decoupled solutions: F_s(x,Q^2)={\cal F}_s(F_{s0}(x), G_0(x)), G(x,Q^2)={\cal G}(F_{s0}(x), G_0(x)). Here ${\cal F}_s$ and $\cal G$ are known functions---found using the DGLAP splitting functions---of the functions $F_{s0}(x) \equiv F_s(x,Q_0^2)$ and $G_{0}(x) \equiv G(x,Q_0^2)$, the chosen starting functions at the virtuality $Q_0^2$. As a proof of method, we compare our numerical results from the above equations with the published MSTW LO gluon and singlet $F_s$ distributions, starting from their initial values at $Q_0^2=1 GeV^2$. Our method completely decouples the two LO distributions, at the same time guaranteeing that both distributions satisfy the singlet coupled DGLAP equations. It furnishes us with a new tool for readily obtaining the effects of the starting functions (independently) on the gluon and singlet structure functions, as functions of both $Q^2$ and $Q_0^2$. In addition, it can also be used for non-singlet distributions, thus allowing one to solve analytically for individual quark and gluon distributions values at a given $x$ and $Q^2$, with typical numerical accuracies of about 1 part in $10^5$, rather than having to evolve numerically coupled integral-differential equations on a two-dimensional grid in $x, Q^2$, as is currently done.Comment: 6 pages, 2 figure

Evidence for the saturation of the Froissart bound

It is well known that fits to high energy data cannot discriminate between asymptotic ln(s) and ln^2(s) behavior of total cross section. We show that this is no longer the case when we impose the condition that the amplitudes also describe, on average, low energy data dominated by resonances. We demonstrate this by fitting real analytic amplitudes to high energy measurements of the gamma p total cross section, for sqrt(s) > 4 GeV. We subsequently require that the asymptotic fit smoothly join the sqrt(s) = 2.01 GeV cross section described by Dameshek and Gilman as a sum of Breit-Wigner resonances. The results strongly favor the high energy ln^2(s) fit of the form sigma_{gamma p} = c_0 + c_1 ln(nu/m) + c_2 ln^2(nu/m) + beta_{P'}/sqrt(nu/m), basically excluding a ln(s) fit of the form sigma_{\gamma p} = c_0 + c_1 ln(nu/m) + beta_P'/sqrt(\nu/m), where nu is the laboratory photon energy. This evidence for saturation of the Froissart bound for gamma p interactions is confirmed by applying the same analysis to pi p data using vector meson dominance.Comment: 7 pages, Latex2e, 4 postscript figures, uses epsf.st

NADPH oxidase as a therapeutic target in Alzheimer\u27s disease

At present, available treatments for Alzheimer\u27s disease (AD) are largely unable to halt disease progression. Microglia, the resident macrophages in the brain, are strongly implicated in the pathology and progressively degenerative nature of AD. Specifically, microglia are activated in response to both β amyloid (Aβ) and neuronal damage, and can become a chronic source of neurotoxic cytokines and reactive oxygen species (ROS). NADPH oxidase is a multi-subunit enzyme complex responsible for the production of both extracellular and intracellular ROS by microglia. Importantly, NADPH oxidase expression is upregulated in AD and is an essential component of microglia-mediated Aβ neurotoxicity. Activation of microglial NADPH oxidase causes neurotoxicity through two mechanisms: 1) extracellular ROS produced by microglia are directly toxic to neurons; 2) intracellular ROS function as a signaling mechanism in microglia to amplify the production of several pro-inflammatory and neurotoxic cytokines (for example, tumor necrosis factor-α, prostaglandin E2, and interleukin-1β). The following review describes how targeting NADPH oxidase can reduce a broad spectrum of toxic factors (for example, cytokines, ROS, and reactive nitrogen species) to result in inhibition of neuronal damage from two triggers of deleterious microglial activation (Aβ and neuron damage), offering hope in halting the progression of AD