A Lorentz-violating low-energy model for the bilayer Graphene

In this work, we propose a model with Lorentz symmetry violation which describes the electronic low energy limit of the AA-bilayer graphene (BLG) system. The AA-type bilayer is known to preserve the linear dispersion relation of the graphene layer in the low energy limit. The theoretical model shows that in the BLG system, a time-like vector can be associated with the layer separation and contributes to the energy eigenstates. Based on these properties, we can describe in a $(2+1)$-dimensional space-time the fermionic quasi-particles that emerge in the low-energy limit with the introduction of a Lorentz-violating parameter, in analogy with the $(3 + 1)$-dimensional Standard Model Extension (SME). Moreover, we study the consequences of the coupling of these fermionic quasi-particles with the electromagnetic field, and we show via effective action that the low-energy photon acquires a massive spectrum. Finally, using the hydrodynamic approach in the collisionless limit, one finds that the LSV generates a new kind of anomalous thermal current to the vortexes of the system via coupling of the LSV vector.Comment: 13 pages, 4 figures, published version in EPJ Plu

Hamiltonian symplectic embedding of the massive noncommutative U(1) Theory

We show that the massive noncommutative U(1) theory is embedded in a gauge theory using an alternative systematic way, which is based on the symplectic framework. The embedded Hamiltonian density is obtained after a finite number of steps in the iterative symplectic process, oppositely to the result proposed using the BFFT formalism. This alternative formalism of embedding shows how to get a set of dynamically equivalent embedded Hamiltonian densities.Comment: 16 pages, no figures, revtex4, corrected version, references additione

Conhecimentos da silvicultura de Virola surinamensis para plantios em sistemas agroflorestais na Amazônia.

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A novel AhR ligand, 2AI, protects the retina from environmental stress.

Various retinal degenerative diseases including dry and neovascular age-related macular degeneration (AMD), retinitis pigmentosa, and diabetic retinopathy are associated with the degeneration of the retinal pigmented epithelial (RPE) layer of the retina. This consequently results in the death of rod and cone photoreceptors that they support, structurally and functionally leading to legal or complete blindness. Therefore, developing therapeutic strategies to preserve cellular homeostasis in the RPE would be a favorable asset in the clinic. The aryl hydrocarbon receptor (AhR) is a conserved, environmental ligand-dependent, per ARNT-sim (PAS) domain containing bHLH transcription factor that mediates adaptive response to stress via its downstream transcriptional targets. Using in silico, in vitro and in vivo assays, we identified 2,2'-aminophenyl indole (2AI) as a potent synthetic ligand of AhR that protects RPE cells in vitro from lipid peroxidation cytotoxicity mediated by 4-hydroxynonenal (4HNE) as well as the retina in vivo from light-damage. Additionally, metabolic characterization of this molecule by LC-MS suggests that 2AI alters the lipid metabolism of RPE cells, enhancing the intracellular levels of palmitoleic acid. Finally, we show that, as a downstream effector of 2AI-mediated AhR activation, palmitoleic acid protects RPE cells from 4HNE-mediated stress, and light mediated retinal degeneration in mice

Mechanisms of cisplatin resistance and targeting of cancer stem cells: Adding glycosylation to the equation

Cisplatin-based chemotherapeutic regimens are the most frequently used (neo)adjuvant treatments for the majority of solid tumors. While platinum-based chemotherapeutic regimens have proven effective against highly proliferative malignant tumors, significant relapse and progression rates as well as decreased overall survival are still observed. Currently, it is known that sub-populations of chemoresistant cells share biological properties with cancer stem cells (CSC), which are believed to be responsible for tumor relapse, invasion and ultimately disease dissemination through acquisition of mesenchymal cell traits. In spite of concentrated efforts devoted to decipher the mechanisms underlying CSC chemoresistance and to design targeted therapeutics to these cells, proteomics has failed to unveil molecular signatures capable of distinguishing between malignant and non-malignant stem cells. This has hampered substantial developments in this complex field. Envisaging a novel rationale for an effective therapy, the current review summarizes the main cellular and molecular mechanisms underlying cisplatin resistance and the impact of chemotherapy challenge in CSC selection and clinical outcome. It further emphasizes the growing amount of data supporting a role for protein glycosylation in drug resistance. The dynamic and context-dependent nature of protein glycosylation is also comprehensively discussed, hence highlighting its potentially important role as a biomarker of CSC. As the paradigm of cancer therapeutics shifts towards precision medicine and patient-tailored therapeutics, we bring into focus the need to introduce glycomics and glycoproteomics in holistic pan-omics models, in order to integrate diverse, multimodal and clinically relevant information towards more effective cancer therapeutics.This work was supported by European Union funds (FEDER/COMPETE) and by national funds (FCT, the Portuguese Foundation for Science and Technology) under the projects with the references FCOMP-01-0124-FEDER 028188 (PTDC/BBB-EBI/0786/2012) and PTDC/BBB-EBI/0567/2014. C.R. acknowledges the support by Gastric Glyco Explorer Initial Training Network (Seventh Framework Programme grant no. 316929). IPATIMUP integrates the i3S Research Unit, which is partially supported by FCT, (PEst-C/SAU/LA0003/2013). Grants were received from FCT: SFRH/BPD/111048/2015 to J.A.F and SFRH/BD/111242/2015 to A.P. FCT is co-financed by European Social Fund (ESF) under Human Potential Operation Programme (POPH) from National Strategic Reference Framework (NSRF)

Entropy of the Randall-Sundrum black brane world to all orders in the Planck length

We study the effects, to all orders in the Planck length from a generalized uncertainty principle (GUP), on the statistical entropy of massive scalar bulk fields in the Randall-Sundrum black brane world. We show that the Bekenstein-Hawking area law is not preserved, and contains small corrections terms proportional to the black hole inverse area.Comment: 19 pages, 1 figure. (v2): section 4 improve