Mass-Transport Models with Multiple-Chipping Processes

We study mass-transport models with multiple-chipping processes. The rates of these processes are dependent on the chip size and mass of the fragmenting site. In this context, we consider k-chip moves (where k = 1, 2, 3, ....); and combinations of 1-chip, 2-chip and 3-chip moves. The corresponding mean-field (MF) equations are solved to obtain the steady-state probability distributions, P (m) vs. m. We also undertake Monte Carlo (MC) simulations of these models. The MC results are in excellent agreement with the corresponding MF results, demonstrating that MF theory is exact for these models.Comment: 18 pages, 4 figures, To appear in European Physical Journal

Revisiting the scaling of the specific heat of the three-dimensional random-field Ising model

We revisit the scaling behavior of the specific heat of the three-dimensional random-field Ising model with a Gaussian distribution of the disorder. Exact ground states of the model are obtained using graph-theoretical algorithms for different strengths = 268 3 spins. By numerically differentiating the bond energy with respect to h, a specific-heat-like quantity is obtained whose maximum is found to converge to a constant in the thermodynamic limit. Compared to a previous study following the same approach, we have studied here much larger system sizes with an increased statistical accuracy. We discuss the relevance of our results under the prism of a modified Rushbrooke inequality for the case of a saturating specific heat. Finally, as a byproduct of our analysis, we provide high-accuracy estimates of the critical field hc = 2.279(7) and the critical exponent of the correlation exponent ν = 1.37(1), in excellent agreement to the most recent computations in the literature

Human Immunodeficiency Virus (HIV)-1 viral protein R suppresses transcriptional activity of peroxisome proliferator-activated receptor γ and inhibits adipocyte differentiation: Implications for HIV-associated lipodystrophy

HIV-1-infected patients may develop lipodystrophy and insulin resistance. We investigated the effect of the HIV-1 accessory protein viral protein R (Vpr) on the activity of the peroxisome proliferator-activating receptor-γ (PPARγ), a key regulator of adipocyte differentiation and tissue insulin sensitivity. We studied expression of PPARγ-responsive reporter genes in 3T3-L1 mouse adipocytes. We investigated Vpr interaction with the PPAR/retinoid X receptor (RXR)-binding site of the c-Cbl-associating protein (CAP) gene using the chromatin immunoprecipitation assay as well as the interaction of Vpr and PPARγ using coimmunoprecipitation. Finally, we studied the ability of exogenous Vpr protein to enter cultured adipocytes and retard differentiation. We found that Vpr suppressed PPARγ-induced transactivation in both undifferentiated and differentiated 3T3-L1 cells. Transcriptional suppression by Vpr required an intact LXXLL coactivator motif. Vpr suppressed mRNA expression of PPARγ-responsive genes in undifferentiated 3T3-L1 cells and associated with the PPAR/ RXR-binding site located in the promoter region of the CAP gene. Vpr interacted with the ligand-binding domain of PPARγ in an agonist-dependent fashion in vitro. Vpr delivered either by an expression plasmid or as protein added to media suppressed PPARγ agonist-induced adipocyte differentiation, assessed as lipid accumulation and mRNA expression of the adipocyte differentiation marker adipocyte P2 in 3T3-L1 cells. In conclusion, circulating Vpr or, alternatively, Vpr produced as a consequence of direct infection of adipocytes could suppress in vivo differentiation of preadipocytes by acting as a corepressor of PPARγ-mediated gene transcription. Vpr may alter sensitivity to insulin and thereby contribute to the development of lipodystrophy and insulin resistance observed in HIV-1-infected patients. Copyright © 2008 by The Endocrine Society

Universality aspects of the trimodal random-field Ising model

We investigate the critical properties of the d = 3 random-field Ising model with an equal-weight trimodal distribution at zero temperature. By implementing suitable graph-theoretical algorithms, we compute large ensembles of ground states for several values of the disorder strength h and system sizes up to N = 1283. Using a new approach based on the sample-to-sample fluctuations of the order parameter of the system and proper finite-size scaling techniques we estimate the critical disorder strength hc = 2.747(3) and the critical exponents of the correlation length ν = 1.34(6) and order parameter β = 0.016(4). These estimates place the model into the universality class of the corresponding Gaussian random-field Ising model