Comment on "Probabilistic Quantum Memories"

This is a comment on two wrong Phys. Rev. Letters papers by C.A. Trugenberger. Trugenberger claimed that quantum registers could be used as exponentially large "associative" memories. We show that his scheme is no better than one where the quantum register is replaced with a classical one of equal size. We also point out that the Holevo bound and more recent bounds on "quantum random access codes" pretty much rule out powerful memories (for classical information) based on quantum states.Comment: REVTeX4, 1 page, published versio

Asymmetric exclusion process with next-nearest-neighbor interaction: some comments on traffic flow and a nonequilibrium reentrance transition

We study the steady-state behavior of a driven non-equilibrium lattice gas of hard-core particles with next-nearest-neighbor interaction. We calculate the exact stationary distribution of the periodic system and for a particular line in the phase diagram of the system with open boundaries where particles can enter and leave the system. For repulsive interactions the dynamics can be interpreted as a two-speed model for traffic flow. The exact stationary distribution of the periodic continuous-time system turns out to coincide with that of the asymmetric exclusion process (ASEP) with discrete-time parallel update. However, unlike in the (single-speed) ASEP, the exact flow diagram for the two-speed model resembles in some important features the flow diagram of real traffic. The stationary phase diagram of the open system obtained from Monte Carlo simulations can be understood in terms of a shock moving through the system and an overfeeding effect at the boundaries, thus confirming theoretical predictions of a recently developed general theory of boundary-induced phase transitions. In the case of attractive interaction we observe an unexpected reentrance transition due to boundary effects.Comment: 12 pages, Revtex, 7 figure

The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism

Although multiple reports show that defective genetic networks underlie the aetiology of autism, few have translated into pharmacotherapeutic opportunities. Since drugs compete with endogenous small molecules for protein binding, many successful drugs target large gene families with multiple drug binding sites. Here we search for defective gene family interaction networks (GFINs) in 6,742 patients with the ASDs relative to 12,544 neurologically normal controls, to find potentially druggable genetic targets. We find significant enrichment of structural defects (P≤2.40E-09, 1.8-fold enrichment) in the metabotropic glutamate receptor (GRM) GFIN, previously observed to impact attention deficit hyperactivity disorder (ADHD) and schizophrenia. Also, the MXD-MYC-MAX network of genes, previously implicated in cancer, is significantly enriched (P≤3.83E-23, 2.5-fold enrichment), as is the calmodulin 1 (CALM1) gene interaction network (P≤4.16E-04, 14.4-fold enrichment), which regulates voltage-independent calcium-activated action potentials at the neuronal synapse. We find that multiple defective gene family interactions underlie autism, presenting new translational opportunities to explore for therapeutic interventions