Peeling Bifurcations of Toroidal Chaotic Attractors

Chaotic attractors with toroidal topology (van der Pol attractor) have counterparts with symmetry that exhibit unfamiliar phenomena. We investigate double covers of toroidal attractors, discuss changes in their morphology under correlated peeling bifurcations, describe their topological structures and the changes undergone as a symmetry axis crosses the original attractor, and indicate how the symbol name of a trajectory in the original lifts to one in the cover. Covering orbits are described using a powerful synthesis of kneading theory with refinements of the circle map. These methods are applied to a simple version of the van der Pol oscillator.Comment: 7 pages, 14 figures, accepted to Physical Review

Metastability and Nucleation for the Blume-Capel Model. Different mechanisms of transition

We study metastability and nucleation for the Blume-Capel model: a ferromagnetic nearest neighbour two-dimensional lattice system with spin variables taking values in -1,0,+1. We consider large but finite volume, small fixed magnetic field h and chemical potential "lambda" in the limit of zero temperature; we analyze the first excursion from the metastable -1 configuration to the stable +1 configuration. We compute the asymptotic behaviour of the transition time and describe the typical tube of trajectories during the transition. We show that, unexpectedly, the mechanism of transition changes abruptly when the line h=2*lambda is crossed.Comment: 96 pages, 44 tex-figures, 7 postscript figure

Amplification of simian retroviral sequences from human recipients of baboon liver transplants

Investigations into the use of baboons as organ donors for human transplant recipients, a procedure called xenotransplantation, have raised the specter of transmitting baboon viruses to humans and possibly establishing new human infectious diseases. Retrospective analysis of tissues from two human transplant recipients with end-stage hepatic disease who died 70 and 27 days after the transplantation of baboon livers revealed the presence of two simian retroviruses of baboon origin, simian foamy virus (SFV) and baboon endogenous virus (BaEV), in multiple tissue compartments. The presence of baboon mitochondrial DNA was also detected in these same tissues, suggesting that xenogeneic 'passenger leukocytes' harboring latent or active viral infections had migrated from the xenografts to distant sites within the human recipients. The persistence of SFV and BaEV in human recipients throughout the posttransplant period underscores the potential infectious risks associated with xenotransplantation

Remarks on Shannon's Statistical Inference and the Second Law in Quantum Statistical Mechanics

We comment on a formulation of quantum statistical mechanics, which incorporates the statistical inference of Shannon. Our basic idea is to distinguish the dynamical entropy of von Neumann, $H = -k Tr \hat{\rho}\ln\hat{\rho}$, in terms of the density matrix $\hat{\rho}(t)$, and the statistical amount of uncertainty of Shannon, $S= -k \sum_{n}p_{n}\ln p_{n}$, with $p_{n}=$ in the representation where the total energy and particle numbers are diagonal. These quantities satisfy the inequality $S\geq H$. We propose to interprete Shannon's statistical inference as specifying the {\em initial conditions} of the system in terms of $p_{n}$. A definition of macroscopic observables which are characterized by intrinsic time scales is given, and a quantum mechanical condition on the system, which ensures equilibrium, is discussed on the basis of time averaging. An interesting analogy of the change of entroy with the running coupling in renormalization group is noted. A salient feature of our approach is that the distinction between statistical aspects and dynamical aspects of quantum statistical mechanics is very transparent.Comment: 16 pages. Minor refinement in the statements in the previous version. This version has been published in Journal of Phys. Soc. Jpn. 71 (2002) 6

Hepatitis C Virus Indirectly Disrupts DNA Damage-Induced p53 Responses by Activating Protein Kinase R

ABSTRACT Many DNA tumor viruses promote cellular transformation by inactivating the critically important tumor suppressor protein p53. In contrast, it is not known whether p53 function is disrupted by hepatitis C virus (HCV), a unique, oncogenic RNA virus that is the leading infectious cause of liver cancer in many regions of the world. Here we show that HCV-permissive, liver-derived HepG2 cells engineered to constitutively express microRNA-122 (HepG2/miR-122 cells) have normal p53-mediated responses to DNA damage and that HCV replication in these cells potently suppresses p53 responses to etoposide, an inducer of DNA damage, or nutlin-3, an inhibitor of p53 degradation pathways. Upregulation of p53-dependent targets is consequently repressed within HCV-infected cells, with potential consequences for cell survival. Despite this, p53 function is not disrupted by overexpression of the complete HCV polyprotein, suggesting that altered p53 function may result from the host response to viral RNA replication intermediates. Clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9-mediated ablation of double-stranded RNA (dsRNA)-activated protein kinase R (PKR) restored p53 responses while boosting HCV replication, showing that p53 inhibition results directly from viral activation of PKR. The hepatocellular abundance of phosphorylated PKR is elevated in HCV-infected chimpanzees, suggesting that PKR activation and consequent p53 inhibition accompany HCV infection in vivo . These findings reveal a feature of the host response to HCV infection that may contribute to hepatocellular carcinogenesis. IMPORTANCE Chronic infection with hepatitis C virus (HCV) is the leading cause of liver cancer in most developed nations. However, the mechanisms whereby HCV infection promotes carcinogenesis remain unclear. Here, we demonstrate that HCV infection inhibits the activation of p53 following DNA damage. Contrary to previous reports, HCV protein expression is insufficient to inhibit p53. Rather, p53 inhibition is mediated by cellular protein kinase R (PKR), which is activated by HCV RNA replication and subsequently suppresses global protein synthesis. These results redefine our understanding of how HCV infection influences p53 function. We speculate that persistent disruption of p53-mediated DNA damage responses may contribute to hepatocellular carcinogenesis in chronically infected individuals

Critical droplets in Metastable States of Probabilistic Cellular Automata

We consider the problem of metastability in a probabilistic cellular automaton (PCA) with a parallel updating rule which is reversible with respect to a Gibbs measure. The dynamical rules contain two parameters $\beta$ and $h$ which resemble, but are not identical to, the inverse temperature and external magnetic field in a ferromagnetic Ising model; in particular, the phase diagram of the system has two stable phases when $\beta$ is large enough and $h$ is zero, and a unique phase when $h$ is nonzero. When the system evolves, at small positive values of $h$, from an initial state with all spins down, the PCA dynamics give rise to a transition from a metastable to a stable phase when a droplet of the favored $+$ phase inside the metastable $-$ phase reaches a critical size. We give heuristic arguments to estimate the critical size in the limit of zero ``temperature'' ($\beta\to\infty$), as well as estimates of the time required for the formation of such a droplet in a finite system. Monte Carlo simulations give results in good agreement with the theoretical predictions.Comment: 5 LaTeX picture

Kinetic hierarchy and propagation of chaos in biological swarm models

We consider two models of biological swarm behavior. In these models, pairs of particles interact to adjust their velocities one to each other. In the first process, called 'BDG', they join their average velocity up to some noise. In the second process, called 'CL', one of the two particles tries to join the other one's velocity. This paper establishes the master equations and BBGKY hierarchies of these two processes. It investigates the infinite particle limit of the hierarchies at large time-scale. It shows that the resulting kinetic hierarchy for the CL process does not satisfy propagation of chaos. Numerical simulations indicate that the BDG process has similar behavior to the CL process