Unified description of the dc conductivity of monolayer and bilayer graphene at finite densities based on resonant scatterers

We show that a coherent picture of the dc conductivity of monolayer and bilayer graphene at finite electronic densities emerges upon considering that strong short-range potentials are the main source of scattering in these two systems. The origin of the strong short-range potentials may lie in adsorbed hydrocarbons at the surface of graphene. The equivalence among results based on the partial-wave description of scattering, the Lippmann-Schwinger equation, and the T-matrix approach is established. Scattering due to resonant impurities close to the neutrality point is investigated via a numerical computation of the Kubo formula using a kernel polynomial method. We find that relevant adsorbate species originate impurity bands in monolayer and bilayer graphene close to the Dirac point. In the midgap region, a plateau of minimum conductivity of about $e^2/h$ (per layer) is induced by the resonant disorder. In bilayer graphene, a large adsorbate concentration can develop an energy gap between midgap and high-energy states. As a consequence, the conductivity plateau is supressed near the edges and a "conductivity gap" takes place. Finally, a scattering formalism for electrons in biased bilayer graphene, taking into account the degeneracy of the spectrum, is developed and the dc conductivity of that system is studied.Comment: 25 pages, 13 figures. published version: appendixes improved, references added, abstract and title slightly changed, plus other minor revision

Resolution of inflammation: a new therapeutic frontier

Dysregulated inflammation is a central pathological process in diverse disease states. Traditionally, therapeutic approaches have sought to modulate the pro- or anti-inflammatory limbs of inflammation, with mixed success. However, insight into the pathways by which inflammation is resolved has highlighted novel opportunities to pharmacologically manipulate these processes — a strategy that might represent a complementary (and perhaps even superior) therapeutic approach. This Review discusses the state of the art in the biology of resolution of inflammation, highlighting the opportunities and challenges for translational research in this field

Resolvins suppress tumor growth and enhance cancer therapy

National Cancer Institute grants RO1 01CA170549-02 (to D. Panigrahy and C.N. Serhan), ROCA148633-01A4 (to D. Panigrahy), and GM095467 (to C.N. Serhan); the Stop and Shop Pediatric Brain Tumor Fund (to M.W. Kieran); the CJ Buckley Pediatric Brain Tumor Fund (to M.W. Kieran); Alex Lemonade Stand (to M.W. Kieran); Molly’s Magic Wand for Pediatric Brain Tumors (to M.W. Kieran); the Markoff Foundation Art-In-Giving Foundation (to M.W. Kieran); the Kamen Foundation (to M.W. Kieran); Jared Branfman Sunflowers for Life (to M.W.K.); and The Wellcome Trust program 086867/Z/08 (to M. Perretti)

Changing glucocorticoid action:11β-hydroxysteroid dehydrogenase type 1 in acute and chronic inflammation

AbstractSince the discovery of cortisone in the 1940s and its early success in treatment of rheumatoid arthritis, glucocorticoids have remained the mainstay of anti-inflammatory therapies. However, cortisone itself is intrinsically inert. To be effective, it requires conversion to cortisol, the active glucocorticoid, by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Despite the identification of 11β-HSD in liver in 1953 (which we now know to be 11β-HSD1), its physiological role has been little explored until recently. Over the past decade, however, it has become apparent that 11β-HSD1 plays an important role in shaping endogenous glucocorticoid action. Acute inflammation is more severe with 11β-HSD1-deficiency or inhibition, yet in some inflammatory settings such as obesity or diabetes, 11β-HSD1-deficiency/inhibition is beneficial, reducing inflammation. Current evidence suggests both beneficial and detrimental effects may result from 11β-HSD1 inhibition in chronic inflammatory disease. Here we review recent evidence pertaining to the role of 11β-HSD1 in inflammation.This article is part of a Special Issue entitled ‘CSR 2013’