Theoretical analysis of thin-wire elliptic antennas

In this communication we extend the state-of-the art by providing closed-form equations for thin-wire elliptical antennas with arbitrary current distributions, valid from low frequencies to the infrared regime. To this end, we derive an electric-field integral equation (EFIE) for imperfectly conducting wires and elliptical geometries. Using this formulation, we obtain unknown arbitrary current distributions through a modal expansion, enabling thus the calculation of far-fields and other radiation parameters. Results shown not only achieve remarkable but also to show the superior design possibilities of elliptical geometries in comparison to the classical circular loops, which may be considered just a particular case of the methodology here presented. Special attention is paid to mathematical details of electric farfield equations, thus providing guidelines to produce efficient codes

A Computationally Efficient Method for Simulating Metal-Nanowire Dipole Antennas at Infrared and Longer Visible Wavelengths

This paper presents a numerically efficient approach for simulating nanowires at infrared and long optical wavelengths. A computationally efficient circuit-equivalent modeling approach based on the electric-field integral-equation (EFIE) formulation is employed to simulate the highly dispersive behavior of nanowires at short wavelengths. The proposed approach can be used both for frequency-domain and for time-domain EFIE formulations. In comparison with widely used full-wave solutions achieved through the finite-difference time-domain method, the circuit-based EFIE formulation results in a sharp reduction of the computational resources while retaining high accuracy.This work was supported in part by the Spanish Ministry of Education under Project PR2009-0443, in part by the Penn State MRSEC under NSF Grant 0213623, in part by the EU FP7/2007-2013 under Grant GA 205294 (HIRF SE project), in part by the Spanish National Projects TEC2010-20841- C04-04, CSD200800068, and DEX-5300002008105, and in part by the Junta de Andalucia Project P09-TIC5327

Multiobjective-Optimized Design of a New UWB Antenna for UWB Applications

A multiobjective genetic algorithm has been applied to design a new printed, bow-tie antenna for ultrawideband applications, that is, ground penetrating radar, short range and high data rate communications, and so forth. The ultrawideband performance with respect to antenna impedance and gain is achieved by an optimized resistive loading profile and flare angle. A low-cost prototype is manufactured and numerical simulations are validated with measurements

SIVA UAV: A Case Study for the EMC Analysis of Composite Air Vehicles

[EN] The increased use of carbon-fiber composites in unmanned aerial vehicles is a challenge for their EMC assessment by numerical solvers. For accurate and reliable simulations, numerical procedures should be tested not only for individual components, but also within the framework of complete systems. With this aim, this paper presents a benchmark test case based on experimental measurements coming from direct-current injection tests in the SIVA unmanned air vehicle, reproduced by a numerical finite-difference-time-domain solver that employs a new subgridding scheme to treat lossy composite thin panels. Validation was undertaken by applying the feature selective validation method, which quantifies the agreement between experimental and numerical data.This work was supported by the Projects TEC2013-48414C3-{ 1,2,3}-R, TEC2016-79214-C3-{1,2,3}-R, and TEC2015-68766-REDC (Spanish MINECO, EU FEDER), P12-TIC-1442 (J. de Andalucia, Spain), Alhambra-UGRFDTD (AIRBUS DS), and by the CSIRC alhambra.ugr.es supercomputing center.Cabello, MR.; Fernández, S.; Pous, M.; Pascual-Gil, E.; Angulo, LD.; López, P.; Riu, PJ.... (2017). SIVA UAV: A Case Study for the EMC Analysis of Composite Air Vehicles. IEEE Transactions on Electromagnetic Compatibility. 59(4):1103-1113. https://doi.org/10.1109/TEMC.2017.2648507S1103111359

Selective small molecule induced degradation of the BET bromodomain protein BRD4

The Bromo- and Extra-Terminal (BET) proteins BRD2, BRD3, and BRD4 play important roles in transcriptional regulation, epigenetics, and cancer and are the targets of pan-BET selective bromodomain inhibitor JQ1. However, the lack of intra-BET selectivity limits the scope of current inhibitors as probes for target validation and could lead to unwanted side effects or toxicity in a therapeutic setting. We designed Proteolysis Targeted Chimeras (PROTACs) that tether JQ1 to a ligand for the E3 ubiquitin ligase VHL, aimed at triggering the intracellular destruction of BET proteins. Compound MZ1 potently and rapidly induces reversible, long-lasting, and unexpectedly selective removal of BRD4 over BRD2 and BRD3. The activity of MZ1 is dependent on binding to VHL but is achieved at a sufficiently low concentration not to induce stabilization of HIF-1α. Gene expression profiles of selected cancer-related genes responsive to JQ1 reveal distinct and more limited transcriptional responses induced by MZ1, consistent with selective suppression of BRD4. Our discovery opens up new opportunities to elucidate the cellular phenotypes and therapeutic implications associated with selective targeting of BRD4

Giant tortoise genomes provide insights into longevity and age-related disease

© 2018, The Author(s), under exclusive licence to Springer Nature Limited. Giant tortoises are among the longest-lived vertebrate animals and, as such, provide an excellent model to study traits like longevity and age-related diseases. However, genomic and molecular evolutionary information on giant tortoises is scarce. Here, we describe a global analysis of the genomes of Lonesome George—the iconic last member of Chelonoidis abingdonii—and the Aldabra giant tortoise (Aldabrachelys gigantea). Comparison of these genomes with those of related species, using both unsupervised and supervised analyses, led us to detect lineage-specific variants affecting DNA repair genes, inflammatory mediators and genes related to cancer development. Our study also hints at specific evolutionary strategies linked to increased lifespan, and expands our understanding of the genomic determinants of ageing. These new genome sequences also provide important resources to help the efforts for restoration of giant tortoise populations

A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection

There are two major and alternative pathways to repair DNA double-strand breaks: non-homologous end-joining and homologous recombination. Here we identify and characterize novel factors involved in choosing between these pathways; in this study we took advantage of the SeeSaw Reporter, in which the repair of double-strand breaks by homology-independent or -dependent mechanisms is distinguished by the accumulation of green or red fluorescence, respectively. Using a genome-wide human esiRNA (endoribonuclease- prepared siRNA) library, we isolate genes that control the recombination/endjoining ratio. Here we report that two distinct sets of genes are involved in the control of the balance between NHEJ and HR: those that are required to facilitate recombination and those that favour NHEJ. This last category includes CCAR2/DBC1, which we show inhibits recombination by limiting the initiation and the extent of DNA end resection, thereby acting as an antagonist of CtIP

Myc Stimulates Cell Cycle Progression Through the Activation of Cdk1 and Phosphorylation of p27

Cell cycle stimulation is a major transforming mechanism of Myc oncoprotein. This is achieved through at least three concomitant mechanisms: upregulation of cyclins and Cdks, downregulation of the Cdk inhibitors p15 and p21 and the degradation of p27. The Myc-p27 antagonism has been shown to be relevant in human cancer. To be degraded, p27 must be phosphorylated at Thr-187 to be recognized by Skp2, a component of the ubiquitination complex. We previously described that Myc induces Skp2 expression. Here we show that not only Cdk2 but Cdk1 phosphorylates p27 at the Thr-187. Moreover, Myc induced p27 degradation in murine fibroblasts through Cdk1 activation, which was achieved by Myc-dependent cyclin A and B induction. In the absence of Cdk2, p27 phosphorylation at Thr-187 was mainly carried out by cyclin A2-Cdk1 and cyclin B1-Cdk1. We also show that Cdk1 inhibition was enough for the synthetic lethal interaction with Myc. This result is relevant because Cdk1 is the only Cdk strictly required for cell cycle and the reported synthetic lethal interaction between Cdk1 and Myc.The work was supported by grant SAF2017-88026-R from MINECO, Spanish Government, to JL and MDD (partially funded by FEDER program from European Union). L.G.G. was recipient of FPI fellowship from Spanish Government. We are grateful Sandra Zunzunegui for technical assistance and John Sedivy and M. Dolores Delgado for helpful discussion

p21 as a Transcriptional Co-Repressor of S-Phase and Mitotic Control Genes

It has been previously described that p21 functions not only as a CDK inhibitor but also as a transcriptional co-repressor in some systems. To investigate the roles of p21 in transcriptional control, we studied the gene expression changes in two human cell systems. Using a human leukemia cell line (K562) with inducible p21 expression and human primary keratinocytes with adenoviral-mediated p21 expression, we carried out microarray-based gene expression profiling. We found that p21 rapidly and strongly repressed the mRNA levels of a number of genes involved in cell cycle and mitosis. One of the most strongly down-regulated genes was CCNE2 (cyclin E2 gene). Mutational analysis in K562 cells showed that the N-terminal region of p21 is required for repression of gene expression of CCNE2 and other genes. Chromatin immunoprecipitation assays indicated that p21 was bound to human CCNE2 and other p21-repressed genes gene in the vicinity of the transcription start site. Moreover, p21 repressed human CCNE2 promoter-luciferase constructs in K562 cells. Bioinformatic analysis revealed that the CDE motif is present in most of the promoters of the p21-regulated genes. Altogether, the results suggest that p21 exerts a repressive effect on a relevant number of genes controlling S phase and mitosis. Thus, p21 activity as inhibitor of cell cycle progression would be mediated not only by the inhibition of CDKs but also by the transcriptional down-regulation of key genes