Trading interactions for topology in scale-free networks

Scale-free networks with topology-dependent interactions are studied. It is shown that the universality classes of critical behavior, which conventionally depend only on topology, can also be explored by tuning the interactions. A mapping, $\gamma' = (\gamma - \mu)/(1-\mu)$, describes how a shift of the standard exponent $\gamma$ of the degree distribution $P(q)$ can absorb the effect of degree-dependent pair interactions $J_{ij} \propto (q_iq_j)^{-\mu}$. Replica technique, cavity method and Monte Carlo simulation support the physical picture suggested by Landau theory for the critical exponents and by the Bethe-Peierls approximation for the critical temperature. The equivalence of topology and interaction holds for equilibrium and non-equilibrium systems, and is illustrated with interdisciplinary applications.Comment: 4 pages, 5 figure

CLINICAL TRIAL PARTICIPATION AFTER ACUTE CORONARY SYNDROME AND ASSOCIATED OUTCOMES: INSIGHT FROM THE ACTION REGISTRY-GWTG

Background/Aims: In liver diseases, reactive oxygen species (ROS) are involved in cell death and liver injury, but the mechanisms are not completely elucidated. To elucidate the mechanisms of hepatocyte cell death induced by the ROS superoxide anions and hydrogen peroxide, primary cultures of hepatocytes were exposed to the superoxide anion donor menadione (10-50 mu mol/L) or H(2)O(2) (1-5 mmol/L). Hepatocytes were also treated with caspases and MAPKs inhibitors, superoxide dismutase (PEG-SOD) and SNAP, a nitric oxide donor. Apoptosis was determined by measuring caspase-9, -6, -3 activation and cleaved PARP, and necrotic cell death by Sytox Green staining. Results: (1) Menadione (50 mu mol/L) induces JNK phosphorylation, caspase-9, -6, -3 activation, PARP cleavage and apoptosis. Superoxide anions-induced apoptosis is dependent on JNK activity. Menadione (50 mu mol/L) induces the phosphorylation of ERK1/2 and this attenuates cell death. (2) H(2)O(2) increases necrotic cell death at high concentration or when H(2)O(2) detoxification is impaired. H202 does not activate MAPKs signalling. (3) PEG-SOD prevents ERK1/2-, JNK- phosphorylation, caspase activation and apoptosis induced by menadione. Glutathione depletion increases menadione-induced apoptosis. (4) SNAP abolishes menadione-induced apoptosis but increases necrotic cell death. Conclusions: In normal hepatocytes, superoxide anions-induced caspase activation and apoptosis is dependent on JNK activity and totally abolished by superoxide scavengers. (c) 2005 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved