Nuevas tecnologías y redes sociales en la investigación en Humanidades

Uno de los aspectos más fascinantes de la World Wide Web es que hace el mundo al mismo tiempo asequible e impredecible. En este sentido, los ámbitos de interés y el conocimiento general de las personas han avanzado hacia nuevas expectativas. Este contexto digital ofrece múltiples posibilidades al investigador y a la comunidad científica que estén dispuestos a explorar estas herramientas. El trabajo colaborativo, la extensión de las redes de investigación, la visibilidad y los actuales cauces de comunicación y conversación, son algunas de las ideas que debemos plantearnos y tener presentes en la aplicación de las nuevas tecnologías y de las redes sociales a la investigación en Humanidades. El presente trabajo aporta algunas reflexiones sobre esta cuestión y trata de mostrar formas concretas en las que seguir avanzando a la hora de incorporar las posibilidades que las novedades técnicas nos ofrecen. One of the most fascinating aspects about the World Wide Web is its ambiguous essence of both making the world miraculously accessible and at the same time empirically serendipitous. In this realm, the fact is that the general interest and the common knowledge of the average person had risen into new dimensions. This digital context paves a path of new possibilities to the ones that are ready to embrace these exciting tools and possibilities to the scientific community. Collaborative work, extended research network, visibility and existing communication and conversation channels are some of the ideas that we must favor and take under consideration in applying new technologies and social networks to research in Humanities. This paper provides some reflections on this issue and is to show specific ways in which further progress is possible when we incorpo-rate the meaningful technical advances

Literatura y propaganda en tiempo de Quevedo: guerras y plumas contra Francia, Cataluña y Portugal [RESEÑA]

Reseña de Arredondo, María Soledad Literatura y propaganda en tiempo de Quevedo: guerras y plumas contra Francia, Cataluña y Portugal. Madrid: Iberoamericana/Frankfurt: Vervuert, 2011. 378 pp. (ISBN: 978-84-8489-549-7, Iberoamericana; ISBN: 978-3-86527-615-5, Vervuert

“Callando pasan los ligeros años...”: el Lope de Vega joven y el teatro antes de 1609. [RESEÑA]

Brioso Santos, Héctor, y Alexandra Chereches, eds. “Callando pasan los ligeros años...”: el Lope de Vega joven y el teatro antes de 1609. Madrid: Liceus, 2012. 220 pp. (ISBN: 978- 84-9714-033-1

Limited path percolation in complex networks

We study the stability of network communication after removal of $q=1-p$ links under the assumption that communication is effective only if the shortest path between nodes $i$ and $j$ after removal is shorter than $a\ell_{ij} (a\geq1)$ where $\ell_{ij}$ is the shortest path before removal. For a large class of networks, we find a new percolation transition at $\tilde{p}_c=(\kappa_o-1)^{(1-a)/a}$, where $\kappa_o\equiv /$ and $k$ is the node degree. Below $\tilde{p}_c$, only a fraction $N^{\delta}$ of the network nodes can communicate, where $\delta\equiv a(1-|\log p|/\log{(\kappa_o-1)}) < 1$, while above $\tilde{p}_c$, order $N$ nodes can communicate within the limited path length $a\ell_{ij}$. Our analytical results are supported by simulations on Erd\H{o}s-R\'{e}nyi and scale-free network models. We expect our results to influence the design of networks, routing algorithms, and immunization strategies, where short paths are most relevant.Comment: 11 pages, 3 figures, 1 tabl

Membrane-Anchored HIV-1 N-Heptad Repeat Peptides Are Highly Potent Cell Fusion Inhibitors via an Altered Mode of Action

Peptide inhibitors derived from HIV-gp41 envelope protein play a pivotal role in deciphering the molecular mechanism of HIV-cell fusion. According to accepted models, N-heptad repeat (NHR) peptides can bind two targets in an intermediate fusion conformation, thereby inhibiting progression of the fusion process. In both cases the orientation towards the endogenous intermediate conformation should be important. To test this, we anchored NHR to the cell membrane by conjugating fatty acids with increasing lengths to the N- or C-terminus of N36, as well as to two known N36 mutants; one that cannot bind C-heptad repeat (CHR) but can bind NHR (N36 MUTe,g), and the second cannot bind to either NHR or CHR (N36 MUTa,d). Importantly, the IC50 increased up to 100-fold in a lipopeptide-dependent manner. However, no preferred directionality was observed for the wild type derived lipopeptides, suggesting a planar orientation of the peptides as well as the endogenous NHR region on the cell membrane. Furthermore, based on: (i) specialized analysis of the inhibition curves, (ii) the finding that N36 conjugates reside more on the target cells that occupy the receptors, and (iii) the finding that N36 MUTe,g acts as a monomer both in its soluble form and when anchored to the cell membrane, we suggest that anchoring N36 to the cell changes the inhibitory mode from a trimer which can target both the endogenous NHR and CHR regions, to mainly monomeric lipopetides that target primarily the internal NHR. Besides shedding light on the mode of action of HIV-cell fusion, the similarity between functional regions in the envelopes of other viruses suggests a new approach for developing potent HIV-1 inhibitors

HIV-1 gp41 and TCRα Trans-Membrane Domains Share a Motif Exploited by the HIV Virus to Modulate T-Cell Proliferation

Viruses have evolved several strategies to modify cellular processes and evade the immune response in order to successfully infect, replicate, and persist in the host. By utilizing in-silico testing of a transmembrane sequence library derived from virus protein sequences, we have pin-pointed a nine amino-acid motif shared by a group of different viruses; this motif resembles the transmembrane domain of the α-subunit of the T-cell receptor (TCRα). The most striking similarity was found within the immunodeficiency virus (SIV and HIV) glycoprotein 41 TMD (gp41 TMD). Previous studies have shown that stable interactions between TCRα and CD3 are localized to this nine amino acid motif within TCRα, and a peptide derived from it (TCRα TMD, GLRILLLKV) interfered and intervened in the TCR function when added exogenously. We now report that the gp41 TMD peptide co-localizes with CD3 within the TCR complex and inhibits T cell proliferation in vitro. However, the inhibitory mechanism of gp41 TMD differs from that of the TCRα TMD and also from the other two known immunosuppressive regions within gp41

Identification of Genes that Elicit Disuse Muscle Atrophy via the Transcription Factors p50 and Bcl-3

Skeletal muscle atrophy is a debilitating condition associated with weakness, fatigue, and reduced functional capacity. Nuclear factor-kappaB (NF-κB) transcription factors play a critical role in atrophy. Knockout of genes encoding p50 or the NF-κB co-transactivator, Bcl-3, abolish disuse atrophy and thus they are NF-κB factors required for disuse atrophy. We do not know however, the genes targeted by NF-κB that produce the atrophied phenotype. Here we identify the genes required to produce disuse atrophy using gene expression profiling in wild type compared to Nfkb1 (gene encodes p50) and Bcl-3 deficient mice. There were 185 and 240 genes upregulated in wild type mice due to unloading, that were not upregulated in Nfkb1−/− and Bcl-3−/− mice, respectively, and so these genes were considered direct or indirect targets of p50 and Bcl-3. All of the p50 gene targets were contained in the Bcl-3 gene target list. Most genes were involved with protein degradation, signaling, translation, transcription, and transport. To identify direct targets of p50 and Bcl-3 we performed chromatin immunoprecipitation of selected genes previously shown to have roles in atrophy. Trim63 (MuRF1), Fbxo32 (MAFbx), Ubc, Ctsl, Runx1, Tnfrsf12a (Tweak receptor), and Cxcl10 (IP-10) showed increased Bcl-3 binding to κB sites in unloaded muscle and thus were direct targets of Bcl-3. p50 binding to the same sites on these genes either did not change or increased, supporting the idea of p50:Bcl-3 binding complexes. p65 binding to κB sites showed decreased or no binding to these genes with unloading. Fbxo9, Psma6, Psmc4, Psmg4, Foxo3, Ankrd1 (CARP), and Eif4ebp1 did not show changes in p65, p50, or Bcl-3 binding to κB sites, and so were considered indirect targets of p50 and Bcl-3. This work represents the first study to use a global approach to identify genes required to produce the atrophied phenotype with disuse