Electrostatics of electron-hole interactions in van der Waals heterostructures

The role of dielectric screening of electron-hole interaction in van der Waals heterostructures is theoretically investigated. A comparison between models available in the literature for describing these interactions is made and the limitations of these approaches are discussed. A simple numerical solution of Poissons equation for a stack of dielectric slabs based on a transfer matrix method is developed, enabling the calculation of the electron-hole interaction potential at very low computational cost and with reasonable accuracy. Using different potential models, direct and indirect exciton binding energies in these systems are calculated within Wannier-Mott theory, and a comparison of theoretical results with recent experiments on excitons in two-dimensional materials is discussed.Comment: 10 pages, 8 figure

Microfenótipos e proteínas associados à expressão da resistência durável à ferrugem da folha do trigo.

Editores técnicos: Joseani Mesquita Antunes, Ana Lídia Variani Bonato, Márcia Barrocas Moreira Pimentel

Detection of very-high-energy gamma-ray emission from the vicinity of PSR B1706-44 with H.E.S.S

The energetic pulsar PSR B1706-44 and the adjacent supernova remnant (SNR) candidate G 343.1-2.3 were observed by H.E.S.S. during a dedicated observational campaign in 2007. A new source of very-high-energy (VHE; E > 100 GeV) gamma-ray emission, HESS J1708-443, was discovered with its centroid at RA(J2000) = 17h08m10s and Dec(J2000) = -44d21', with a statistical error of 3 arcmin on each axis. The VHE gamma-ray source is significantly more extended than the H.E.S.S. point-spread function, with an intrinsic Gaussian width of 0.29 +/- 0.04 deg. Its energy spectrum can be described by a power law with a photon index Gamma = 2.0 +/- 0.1 (stat) +/- 0.2 (sys). The integral flux measured between 1-10 TeV is ~17% of the Crab Nebula flux in the same energy range. The possible associations with PSR B1706-44 and SNR G343.1-2.3 are discussed.Comment: 4+ pages, 2 figures; v1 submitted to ICRC Proceedings on 15 May 2009; v2 has additional references and minor change

The corticotrophin-releasing factor/urocortin system regulates white fat browning in mice through paracrine mechanisms

Objectives: The corticotrophin-releasing factor (CRF)/urocortin system is expressed in the adipose tissue of mammals, but its functional role in this tissue remains unknown. Methods: Pharmacological manipulation of the activity of CRF receptors, CRF1 and CRF2, was performed in 3T3L1 white pre-adipocytes and T37i brown pre-adipocytes during in vitro differentiation. The expression of genes of the CRF/urocortin system and of markers of white and brown adipocytes was evaluated along with mitochondrial biogenesis and cellular oxygen consumption. Metabolic evaluation of corticosterone-deficient or supplemented Crhr1-null (Crhr1−/−) mice and their wild-type controls was performed along with gene expression analysis carried out in white (WAT) and brown (BAT) adipose tissues. Results: Peptides of the CRF/urocortin system and their cognate receptors were expressed in both pre-adipocyte cell lines. In vitro pharmacological studies showed an inhibition of the expression of the CRF2 pathway by the constitutive activity of the CRF1 pathway. Pharmacological activation of CRF2 and, to a lesser extent, inhibition of CRF1 signaling induced molecular and functional changes indicating transdifferentiation of white pre-adipocytes and differentiation of brown pre-adipocytes. Crhr1−/− mice showed increased expression of CRF2 and its agonist Urocortin 2 in adipocytes that was associated to brown conversion of WAT and activation of BAT. Crhr1−/− mice were resistant to diet-induced obesity and glucose intolerance. Restoring physiological circulating corticosterone levels abrogated molecular changes in adipocytes and the favorable phenotype of Crhr1−/− mice. Conclusions: Our findings suggest the importance of the CRF2 pathway in the control of adipocyte plasticity. Increased CRF2 activity in adipocytes induces browning of WAT, differentiation of BAT and is associated with a favorable metabolic phenotype in mice lacking CRF1. Circulating corticosterone represses CRF2 activity in adipocytes and may thus regulate adipocyte physiology through the modulation of the local CRF/urocortin system. Targeting CRF receptor signaling specifically in the adipose tissue may represent a novel approach to tackle obesity