A dual null formalism for the collapse of fluids in a cosmological background

In this work we revisit the definition of Matter Trapping Surfaces (MTS) introduced in previous investigations and show how it can be expressed in the so-called dual null formalism developed for Trapping Horizons (TH). With the aim of unifying both approaches, we construct a 2+2 threading from the 1+3 flow, and thus isolate one prefered spatial direction, that allows straightforward translation into a dual nul subbasis, and to deduce the geometric apparatus that follows. We remain as general as possible, reverting to spherical symmetry only when needed, and express the MTS conditions in terms of 2-expansion of the flow, then in purely geometric form of the dual null expansions. The Raychadhuri equations that describe both MTS and TH are written and interpreted using the previously defined gTOV (generalized Tolman-Oppenheimer-Volkov) functional introduced in previous work. Further using the Misner-Sharp mass and its previous perfect fluid definition, we relate the spatial 2-expansion to the fluid pressure, density and acceleration. The Raychaudhuri equations also allows us to define the MTS dynamic condition with first order differentials so the MTS conditions are now shown to be all first order differentials. This unified formalism allows one to realise that the MTS can only exist in normal regions, and so it can exist only between black hole horizons and cosmological horizons. Finally we obtain a relation yielding the sign, on a TH, of the non-vanishing null expansion which determines the nature of the TH from fluid content, and flow characteristics. The 2+2 unified formalism here investigated thus proves a powerful tool to reveal, in the future extensions, more of the very rich and subtle relations between MTS and TH.Comment: 10pp 1 fig. corrected for equation labels, cross listing correcte

Radio source evolution on galactic scales

There is mounting evidence that mechanical radio source feedback is important in galaxy evolution and in order to quantify this feedback, detailed models of radio source evolution are required. We present an extension to current analytic models that encompasses young radio sources with physical sizes on sub-kiloparsec scales. This work builds on an existing young source dynamical model to include radiative losses in a flat environment, and as such, is the best physically-motivated Compact Symmetric Object model to date. Results predict that young radio sources experience significant radiative loss on length scales and spectral scales consistent with observed Compact Steep-Spectrum sources. We include full expressions for the transition to self-similar expansion and present this complete model of radio source evolution from first cocoon formation to end of source lifetime around 108 years within the context of a simplified King profile external atmosphere.T.M. thanks the Marshall Aid Commemoration Commission and St John’s College, Cambridge for PhD research funding.This is the final version of the article. It first appeared from Oxford University Press via http://dx.doi.org/10.1093/mnras/stu111

Chromatin remodeling and neuronal function: exciting links

Regulation of gene expression occurs at different levels, from DNA to protein, and through various mechanisms. One of them is modification of the chromatin structure, which is involved in the definition of transcriptional active and inactive regions of the chromosomes. These phenomena are associated with reversible chemical modifications of the genetic material rather than with variability within the DNA sequences inherited by the individual and are therefore called 'epigenetic' modifications. Ablation of the molecular players responsible for epigenetic modifications often gives rise to neurological and behavioral phenotypes in humans and in mouse models, suggesting a relevant function for chromatin remodeling in central nervous system function, particularly in the adaptive response of the brain to stimuli. We will discuss several human disorders that are due to altered epigenetic mechanisms, with special focus on Rett syndrome.Mónica Santos and Paula A. Coelho are supported by Fundação para a Ciência e Tecnologia (FCT, Portugal) with the PhD fellowship SFRH/BD/9111/2002 and SFRH/BPD/20360/2004, respectively. Research in Rett syndrome is supported by the FSE/ FEDER and the FCT, grant POCTI 41416/200

Witnessed entanglement and the geometric measure of quantum discord

We establish relations between geometric quantum discord and entanglement quantifiers obtained by means of optimal witness operators. In particular, we prove a relation between negativity and geometric discord in the Hilbert-Schmidt norm, which is slightly different from a previous conjectured one [Phys. Rev. A 84, 052110 (2011)].We also show that, redefining the geometric discord with the trace norm, better bounds can be obtained. We illustrate our results numerically.Comment: 8 pages + 3 figures. Revised version with erratum for PRA 86, 024302 (2012). Simplified proof that discord is bounded by entanglement in any nor

Viable entanglement detection of unknown mixed states in low dimensions

We explore procedures to detect entanglement of unknown mixed states, which can be experimentally viable. The heart of the method is a hierarchy of simple feasibility problems, which provides sufficient conditions to entanglement. Our numerical investigations indicate that the entanglement is detected with a cost which is much lower than full state tomography. The procedure is applicable to both free and bound entanglement, and involves only single copy measurements.Comment: 8 pages, 9 figures, 4 table

Melhoramento de espécies aquícolas com foco na resistência a doenças.

Introdução. Aspectos a serem considerados no melhoramento genético com foco em doenças. Estimativas de herdabilidade e de correlações genéticas entre resistência a doenças e outras características. Cuidados no desenho experimental dos desafios para a fenotipagem de animais. Considerações finais. Referências.bitstream/item/136151/1/CNPASA2015doc17.pd

Molecular genetics of intellectual disability

The goal of this chapter is to review the current knowledge of the genetic causes of intellectual disability, focusing on alterations at the chromosomal and single gene level, with particular mention to the new technological developments, including array technologies and next-generation sequencing, which allowed an enormous increase in yield from genetic studies. The cellular and physiological pathways that seem to be most affected in intellectual disability will also be addressed. Finally, a brief analysis of the contribution of the genetically modified animal models for the study of the pathogenesis of intellectual disability and for the development and testing of novel therapeutic approaches, with unexpectedly good results, previously thought to be impossible to achieve. The chapter will close with some considerations on the relevance and future perspectives of genetic testing in patients with intellectual disability