Constraints on the χ_(c1) versus χ_(c2) polarizations in proton-proton collisions at √s = 8 TeV

The polarizations of promptly produced χ_(c1) and χ_(c2) mesons are studied using data collected by the CMS experiment at the LHC, in proton-proton collisions at √s=8  TeV. The χ_c states are reconstructed via their radiative decays χ_c → J/ψγ, with the photons being measured through conversions to e⁺e⁻, which allows the two states to be well resolved. The polarizations are measured in the helicity frame, through the analysis of the χ_(c2) to χ_(c1) yield ratio as a function of the polar or azimuthal angle of the positive muon emitted in the J/ψ → μ⁺μ⁻ decay, in three bins of J/ψ transverse momentum. While no differences are seen between the two states in terms of azimuthal decay angle distributions, they are observed to have significantly different polar anisotropies. The measurement favors a scenario where at least one of the two states is strongly polarized along the helicity quantization axis, in agreement with nonrelativistic quantum chromodynamics predictions. This is the first measurement of significantly polarized quarkonia produced at high transverse momentum

La sustitución C>A en el NT 46 en la región 3’ UTR (Alfa Complex Protected Region) del gen ALFA 1 de globina ¿mutación o polimorfismo?

PC-048 Antecedentes: Las regiones no traducidas [UnTranslated Region (UTR)] desempeñan un papel crucial en la regulación postranscripcional de la expresión génica, incluida la modulación del transporte de ARNm fuera del núcleo, la eficacia de la traducción, la localización subcelular y la estabilidad. La estabilidad del ARNm es un factor decisivo para el desarrollo y funcionamiento normal de los glóbulos rojos. En el caso del ARNm de a-globina, los principales determinantes de la estabilidad se localizan en el extremo 3’ UTR; en concreto, se han identificado 3 áreas discontinuas ricas en citosina (C) ubicadas entre los nucleótidos (nt) 25 y 70 corriente abajo del codon de parada. Estas áreas ricas en C son responsables de atraer a una ribonucleoproteína (RNP) llamada a-globina poli (C) de unión o a-complejo proteína (aCP) para estabilizar la molécula de ARNm. Wagoner et al. demostraron a través del análisis in vitro que cualquier mutación en estos elementos ricos en C dificulta la unión del ARNm de a-globina con el aCP y desestabiliza al ARNm. Objetivos: Presentamos 15 pacientes con la sustitución C>A en el extremo 3’UTR del gen a1 de globina, localizada en la región del complejo a (aCP), la cual podría causar a-talasemia no deleción al afectar a la estabilidad postranscripcional (estabilidad del ARNm) o tratarse de un polimorfismo. Métodos: Se han estudiado 15 pacientes pertenecientes a 12 familias, todas de origen español excepto dos, una procedente de Rumanía y otra de Marruecos. Las edades estuvieron comprendidas entre 2 y 67 años. Todos fueron estudiados por presentar microcitosis e hipocromía sin ..

Patterns of HIV-1 Protein Interaction Identify Perturbed Host-Cellular Subsystems

Human immunodeficiency virus type 1 (HIV-1) exploits a diverse array of host cell functions in order to replicate. This is mediated through a network of virus-host interactions. A variety of recent studies have catalogued this information. In particular the HIV-1, Human Protein Interaction Database (HHPID) has provided a unique depth of protein interaction detail. However, as a map of HIV-1 infection, the HHPID is problematic, as it contains curation error and redundancy; in addition, it is based on a heterogeneous set of experimental methods. Based on identifying shared patterns of HIV-host interaction, we have developed a novel methodology to delimit the core set of host-cellular functions and their associated perturbation from the HHPID. Initially, using biclustering, we identify 279 significant sets of host proteins that undergo the same types of interaction. The functional cohesiveness of these protein sets was validated using a human protein-protein interaction network, gene ontology annotation and sequence similarity. Next, using a distance measure, we group host protein sets and identify 37 distinct higher-level subsystems. We further demonstrate the biological significance of these subsystems by cross-referencing with global siRNA screens that have been used to detect host factors necessary for HIV-1 replication, and investigate the seemingly small intersect between these data sets. Our results highlight significant host-cell subsystems that are perturbed during the course of HIV-1 infection. Moreover, we characterise the patterns of interaction that contribute to these perturbations. Thus, our work disentangles the complex set of HIV-1-host protein interactions in the HHPID, reconciles these with siRNA screens and provides an accessible and interpretable map of infection