To Touch a Story: Crisis and Textual Textures in Argentine Queer Writing

This essay examines two queer literary chapbooks published by art gallery/press Belleza y Felicidad (ByF) in the context of the Argentine 2001 social and economic crisis to show that these texts imagine reading as a performance which entails doing, touching, and being touched back. Through their visual, verbal, and material elements, these works imagine new relations between literature and everyday life and practices in a period in which those practices were dramatically altered. Offering a verbal/visual platform from where to reflect on the deployment of touch and the haptic beyond strictly visual or filmic disciplinary realms, these writings exploit their material dimensions to build specifically literary, historically located "textual textures". This article argues that textual textures contribute to shed light on how these works resonate with, register, and critically intervene in the crisis context

Daemonic Ergotropy: Enhanced Work Extraction from Quantum Correlations

We investigate how the presence of quantum correlations can influence work extraction in closed quantum systems, establishing a new link between the field of quantum non-equilibrium thermodynamics and the one of quantum information theory. We consider a bipartite quantum system and we show that it is possible to optimise the process of work extraction, thanks to the correlations between the two parts of the system, by using an appropriate feedback protocol based on the concept of ergotropy. We prove that the maximum gain in the extracted work is related to the existence of quantum correlations between the two parts, quantified by either quantum discord or, for pure states, entanglement. We then illustrate our general findings on a simple physical situation consisting of a qubit system.Comment: 7 pages, 3 figures; RevTeX

Work statistics, irreversible heat and correlations build-up in joining two spin chains

We investigate the influences of quantum many-body effects, such as criticality and the existence of factorisation fields, in the thermodynamic cost of establishing a bonding link between two independent quantum spin chains. We provide a physical interpretation of the behavior of irreversible work spent in such process by linking the phenomenology of such quantities to the properties of the spectrum of the systemComment: 9 pages, 8 figures. Contribution to the FQMT13 special volum

A Study of the Ebola Virus Glycoprotein: Disruption of Host Surface Protein Function and Evasion of Immune Responses

The Ebola virus (EBOV) is a member of the family, Filoviridae, and is the etiological agent of Ebola hemorrhagic fever (EHF). This disease causes significant morbidity and mortality in humans and non-human primates, with human fatality rates reaching 90% during outbreaks of the Zaire subtype. Currently, there are no licensed vaccines or antivirals for EBOV and our understanding of viral pathogenesis is limited. Therefore, further studies examining the pathogenic mechanisms of EBOV are necessary to fully understand and effectively treat EHF. The main Ebola virus glycoprotein (GP) is the only viral protein found on the surface of the Ebola virion and is therefore responsible for mediating attachment and entry of the virus into host cells. However, expression of GP independently of other viral proteins induces dramatic morphological changes including cell rounding and detachment in those cells expressing GP. This phenomenon is referred to as GP-mediated cytopathology and is the focus of the work described herein. We have undertaken studies to identify the mucin domain, a highly glycosylated domain within GP, as sufficient to cause this cytopathology. We then have used a cell-biological approach to elucidate the mechanism by which this cytopathology occurs. The mucin domain forms a glycan shield at the plasma membrane, disrupting the function of host proteins in the vicinity of GP. We then show that GP-mediated shielding of major histocompatibility complex class I at the cell surface prevents the activation of CD 8+ T cells. Additionally, GP can sterically shield its own epitopes at the cell surface. This model of steric hindrance was also found to apply to the surface of pseudoviral particles, where access to a neutralizing epitope on GP is affected. Our data indicate that the EBOV GP forms a glycan shield with the ability to block antibody binding and disrupt protein function at the cell and virion surface. This study describes a novel viral mechanism for the disruption of surface protein function and suggests a possible mechanism for the evasion of host humoral and cellular immune responses