Sliding blocks with random friction and absorbing random walks

With the purpose of explaining recent experimental findings, we study the distribution $A(\lambda)$ of distances $\lambda$ traversed by a block that slides on an inclined plane and stops due to friction. A simple model in which the friction coefficient $\mu$ is a random function of position is considered. The problem of finding $A(\lambda)$ is equivalent to a First-Passage-Time problem for a one-dimensional random walk with nonzero drift, whose exact solution is well-known. From the exact solution of this problem we conclude that: a) for inclination angles $\theta$ less than \theta_c=\tan(\av{\mu}) the average traversed distance \av{\lambda} is finite, and diverges when $\theta \to \theta_c^{-}$ as \av{\lambda} \sim (\theta_c-\theta)^{-1}; b) at the critical angle a power-law distribution of slidings is obtained: $A(\lambda) \sim \lambda^{-3/2}$. Our analytical results are confirmed by numerical simulation, and are in partial agreement with the reported experimental results. We discuss the possible reasons for the remaining discrepancies.Comment: 8 pages, 8 figures, submitted to Phys. Rev.

Production of Υ(nS) mesons in Pb+Pb and pp collisions at 5.02 TeV

A measurement of the production of vector bottomonium states, Υ ( 1S ) , Υ ( 2S ) , and Υ ( 3S ) , in Pb + Pb and p p collisions at a center-of-mass energy per nucleon pair of 5.02 TeV is presented. The data correspond to integrated luminosities of 1.38 nb − 1 of Pb + Pb data collected in 2018, 0.44 nb − 1 of Pb + Pb data collected in 2015, and 0.26 fb − 1 of p p data collected in 2017 by the ATLAS detector at the Large Hadron Collider. The measurements are performed in the dimuon decay channel for transverse momentum p μ μ T < 30 GeV , absolute rapidity | y μ μ | < 1.5 , and Pb + Pb event centrality 0–80%. The production rates of the three bottomonium states in Pb + Pb collisions are compared with those in p p collisions to extract the nuclear modification factors as functions of event centrality, p μ μ T , and | y μ μ | . In addition, the suppression of the excited states relative to the ground state is studied. The results are compared with theoretical model calculations

Role of prostacyclin versus peroxisome proliferator-activated receptor beta receptors in prostacyclin sensing by lung fibroblasts.

Prostacyclin and its mimetics are used therapeutically for the treatment of pulmonary hypertension. These drugs act via cell surface prostacyclin receptors (IP receptors); however, some of them can also activate the nuclear receptor peroxisome proliferator-activated receptor beta (PPARbeta). We examined the possibility that PPARbeta is a therapeutic target for the treatment of pulmonary hypertension. Using the newly approved (for pulmonary hypertension) prostacyclin mimetic treprostinil sodium, reporter gene assays for PPARbeta activation and measurement of lung fibroblast proliferation were analyzed. Treprostinil sodium was found to activate PPARbeta in reporter gene assays and to inhibit proliferation of human lung fibroblasts at concentrations consistent with an effect on PPARs but not on IP receptors. The effects of treprostinil sodium on human lung cell proliferation are mimicked by those of the highly selective PPARbeta ligand GW0742. There are no receptor antagonists for PPARbeta or for IP receptors, but by using lung fibroblasts cultured from mice lacking PPARbeta (PPARbeta-/-) or IP (IP-/-), we demonstrate that the antiproliferative effects of treprostinil sodium are mediated by PPARbeta and not IP in lung fibroblasts. These observations suggest that some of the local, longer-term benefits of treprostinil sodium on reducing the remodeling associated with pulmonary hypertension may be mediated by PPARbeta. This study is the first to identify PPARbeta as a potential therapeutic target for the treatment of pulmonary hypertension, which is important because orally active PPARbeta ligands have been developed for the treatment of dyslipidemia