Efecto mediacional de las relaciones interpersonales y la autoestima sobre la relación entre gratitud y satisfacción vital

Un creciente campo de investigación pone de manifiesto que la gratitud es un predictor clave tanto del bienestar como de la vida social. Sin embargo, la mayoría de estos estudios se han basado principalmente en el diseño transversal, que no permite hacer ninguna inferencia causal entre variables. Objetivo: Este estudio exploratorio examina la influencia de la gratitud sobre la satisfacción vital, así como evaluar el efecto mediacional de las relaciones positivas y la autoestima en una muestra de universitarios con un diseño prospectivo. Este estudio utilizó un muestreo incidental no aleatorio con un diseño de corte longitudinal a ocho semanas, en una muestra de 228 estudiantes universitarios (77 hombres, 151 mujeres), con edades comprendidas entre los 18 y 52 años (M = 22), de un total de 563. Los participantes completaron voluntariamente un paquete de instrumentos compuestos por el cuestionario de gratitud (GQ-6) en tiempo 1 (T1), la dimensión de relaciones positivas de la escala de bienestar psicológico en T1, la escala de autoestima en T2 y la escala de satisfacción vital en T2. Utilizando un diseño prospectivo con efectos mediacionales, los resultados indicaron que la gratitud en T1 se asoció significativamente a las relaciones interpersonales positivas en T1, así como con la autoestima T2 y la satisfacción vital en T2. Además, las relaciones interpersonales positivas T1 se asociaron positivamente con la autoestima T2 y la satisfacción vital T2. Después de controlar las variables de edad y género en T1, la gratitud en T1 tuvo un efecto indirecto sobre la satisfacción vital en T2, a través de las relaciones interpersonales positivas y la autoestima

Victimización docente, agotamiento y engagement en el contexto de postpandemia: examinado el papel protector de la inteligencia emocional

Desde la teoría de Demandas y Recursos Laborales, estudios previos han analizado las relaciones entre las demandas del contexto docente y el bienestar ocupacional. Sin embargo, la evidencia acerca del impacto de las agresiones al profesorado sobre el agotamiento y el engagement laboral es limitada. La Inteligencia Emocional (IE) actúa como un recurso personal con relaciones consistentes con el burnout y el engagement laboral. En este trabajo se analiza el papel moderador de la IE en la relación entre las agresiones al profesorado, el agotamiento emocional y el engagement en una muestra de profesorado que ha sufrido agresiones por parte del alumnado. En este estudio transversal han participado un total de 253 profesionales docentes (153 mujeres) de Educación Primaria y Secundaria con una media de 44,28 años. Los participantes rellenaron una batería con cuestiones sociodemográficas y escalas validadas de las variables objeto de estudio. La recogida de datos se realizó mediante un muestro incidental no aleatorio y se contó con una muestra específica de docentes victimados, esto es, que informaban haber experimentado al menos un incidente de agresión en los últimos 15 días. Los resultados han mostrado que el agotamiento emocional mediaba totalmente la relación entre las agresiones y el engagement laboral controlando los efectos de la edad, el sexo y el nivel de especialidad. Además, se encontró significatividad para el papel moderador de la IE en la relación indirecta de las agresiones y el engagement a través del agotamiento emocional. Concretamente, la IE amortiguó la relación entre el agotamiento emocional y el engagement. A pesar de las limitaciones de este estudio, los resultados sugieren la necesidad de considerar posibles perfiles psicosociales de riesgo de la victimización docente y de su impacto sobre la motivación laboral.Este trabajo de investigación ha sido financiado por el Proyecto I+D+i en el marco del Programa Operativo FEDER Andalucía 2014-2020 (UMA18-FEDERJA-147), por el proyecto I+D+i en el marco de los programas estatales de generación del conocimiento del Ministerio de Ciencia e Innovación (PID2020-117006RB-I00) y por la Universidad de Málaga (grupo PAIDI CTS-1048). Además, la investigación ha sido financiada por la Universidad de Málaga (S.M.-L.). Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Programa de entrenamiento en gratitud y perdón para mujeres mayores de 50 con sintomatología depresiva.

En Andalucía, más de 3 millones de personas mayores de 50 años sufren depresión, siendo en la mayoría de los casos el tratamiento con medicación antidepresiva el único que se aplica. Sin embargo, son necesarias otras intervenciones que contribuyan no solo a reducir la sintomatología depresiva, sino que además fomenten el desarrollo de estados emocionales positivos e incrementen el bienestar. El objetivo general del trabajo ha sido comparar la eficacia diferencial de un programa centrado en las fortalezas de Gratitud y Perdón para reducir síntomas depresivos e incrementar bienestar, en comparación con un programa cognitivo conductual y un programa psicoeducativo. La muestra está constituida por mujeres con edades comprendidas entre 55 y 75 años, que presentan sintomatología depresiva, según los criterios diagnósticos del DSM-V y la puntuación de corte establecida para depresión moderada en el Inventario de Depresión de Beck-II. Las participantes cumplimentarán el Inventario de Depresión de Beck (BDI-II), la Escala de Satisfacción con la Vida (SWLS) de Diener et al. (1985), y la Escala de Bienestar de Ryff (PWB) antes del comienzo del entrenamiento, a la finalización del mismo y 3, 6 y 12 meses después de la conclusión del entrenamiento. Los programas de Fortalezas y Cognitivo-Conductual constarán de 6 sesiones grupales, de 1.5 horas de duración, mientras que el programa psicoeducativo constará de 4 sesiones de 1 hora. En la actualidad se están aplicando las intervenciones a subgrupos de participantes de cada grupo del estudio. Se espera disponer de algunos resultados preliminares para el mes de mayo

Preventive and Therapeutic Strategies for Bovine Leukemia Virus: Lessons for HTLV

Bovine leukemia virus (BLV) is a retrovirus closely related to the human T-lymphotropic virus type 1 (HTLV-1). BLV is a major animal health problem worldwide causing important economic losses. A series of attempts were developed to reduce prevalence, chiefly by eradication of infected cattle, segregation of BLV-free animals and vaccination. Although having been instrumental in regions such as the EU, these strategies were unsuccessful elsewhere mainly due to economic costs, management restrictions and lack of an efficient vaccine. This review, which summarizes the different attempts previously developed to decrease seroprevalence of BLV, may be informative for management of HTLV-1 infection. We also propose a new approach based on competitive infection with virus deletants aiming at reducing proviral loads

Association of Complement Factors With Disability Progression in Primary Progressive Multiple Sclerosis

Background and ObjectivesThe complement system is known to play a role in multiple sclerosis (MS) pathogenesis. However, its contribution to disease progression remains elusive. The study investigated the role of the complement system in disability progression of patients with primary progressive MS (PPMS).MethodsSixty-eight patients with PPMS from 12 European MS centers were included in the study. Serum and CSF levels of a panel of complement components (CCs) were measured by multiplex enzyme-linked immunosorbent assay at a baseline time point (i.e., sampling). Mean (SD) follow-up time from baseline was 9.6 (4.8) years. Only one patient (1.5%) was treated during follow-up. Univariable and multivariable logistic regressions adjusted for age, sex, and albumin quotient were performed to assess the association between baseline CC levels and disability progression in short term (2 years), medium term (6 years), and long term (at the time of the last follow-up).ResultsIn short term, CC played little or no role in disability progression. In medium term, an elevated serum C3a/C3 ratio was associated with a higher risk of disability progression (adjusted OR 2.30; 95% CI 1.17-6.03; p = 0.040). By contrast, increased CSF C1q levels were associated with a trend toward reduced risk of disability progression (adjusted OR 0.43; 95% CI 0.17-0.98; p = 0.054). Similarly, in long term, an elevated serum C3a/C3 ratio was associated with higher risk of disability progression (adjusted OR 1.81; 95% CI 1.09-3.40; p = 0.037), and increased CSF C1q levels predicted lower disability progression (adjusted OR 0.41; 95% CI 0.17-0.86; p = 0.025).DiscussionProteins involved in the activation of early complement cascades play a role in disability progression as risk (elevated serum C3a/C3 ratio) or protective (elevated CSF C1q) factors after 6 or more years of follow-up in patients with PPMS. The protective effects associated with C1q levels in CSF may be related to its neuroprotective and anti-inflammatory properties

Single hadron response measurement and calorimeter jet energy scale uncertainty with the ATLAS detector at the LHC

The uncertainty on the calorimeter energy response to jets of particles is derived for the ATLAS experiment at the Large Hadron Collider (LHC). First, the calorimeter response to single isolated charged hadrons is measured and compared to the Monte Carlo simulation using proton-proton collisions at centre-of-mass energies of sqrt(s) = 900 GeV and 7 TeV collected during 2009 and 2010. Then, using the decay of K_s and Lambda particles, the calorimeter response to specific types of particles (positively and negatively charged pions, protons, and anti-protons) is measured and compared to the Monte Carlo predictions. Finally, the jet energy scale uncertainty is determined by propagating the response uncertainty for single charged and neutral particles to jets. The response uncertainty is 2-5% for central isolated hadrons and 1-3% for the final calorimeter jet energy scale.Comment: 24 pages plus author list (36 pages total), 23 figures, 1 table, submitted to European Physical Journal

The Genome Sequence of the Grape Phylloxera Provides Insights into the Evolution, Adaptation, and Invasion Routes of an Iconic Pest

Background: Although native to North America, the invasion of the aphid-like grape phylloxera Daktulosphaira vitifoliae across the globe altered the course of grape cultivation. For the past 150 years, viticulture relied on grafting-resistant North American Vitis species as rootstocks, thereby limiting genetic stocks tolerant to other stressors such as pathogens and climate change. Limited understanding of the insect genetics resulted in successive outbreaks across the globe when rootstocks failed. Here we report the 294-Mb genome of D. vitifoliae as a basic tool to understand host plant manipulation, nutritional endosymbiosis, and enhance global viticulture. Results: Using a combination of genome, RNA, and population resequencing, we found grape phylloxera showed high duplication rates since its common ancestor with aphids, but similarity in most metabolic genes, despite lacking obligate nutritional symbioses and feeding from parenchyma. Similarly, no enrichment occurred in development genes in relation to viviparity. However, phylloxera evolved > 2700 unique genes that resemble putative effectors and are active during feeding. Population sequencing revealed the global invasion began from the upper Mississippi River in North America, spread to Europe and from there to the rest of the world. Conclusions: The grape phylloxera genome reveals genetic architecture relative to the evolution of nutritional endosymbiosis, viviparity, and herbivory. The extraordinary expansion in effector genes also suggests novel adaptations to plant feeding and how insects induce complex plant phenotypes, for instance galls. Finally, our understanding of the origin of this invasive species and its genome provide genetics resources to alleviate rootstock bottlenecks restricting the advancement of viticulture

Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets

Importance Substantial genome-wide association study (GWAS) work in Parkinson disease (PD) has led to the discovery of an increasing number of loci shown reliably to be associated with increased risk of disease. Improved understanding of the underlying genes and mechanisms at these loci will be key to understanding the pathogenesis of PD. / Objective To investigate what genes and genomic processes underlie the risk of sporadic PD. / Design and Setting This genetic association study used the bioinformatic tools Coloc and transcriptome-wide association study (TWAS) to integrate PD case-control GWAS data published in 2017 with expression data (from Braineac, the Genotype-Tissue Expression [GTEx], and CommonMind) and methylation data (derived from UK Parkinson brain samples) to uncover putative gene expression and splicing mechanisms associated with PD GWAS signals. Candidate genes were further characterized using cell-type specificity, weighted gene coexpression networks, and weighted protein-protein interaction networks. / Main Outcomes and Measures It was hypothesized a priori that some genes underlying PD loci would alter PD risk through changes to expression, splicing, or methylation. Candidate genes are presented whose change in expression, splicing, or methylation are associated with risk of PD as well as the functional pathways and cell types in which these genes have an important role. / Results Gene-level analysis of expression revealed 5 genes (WDR6 [OMIM 606031], CD38 [OMIM 107270], GPNMB [OMIM 604368], RAB29 [OMIM 603949], and TMEM163 [OMIM 618978]) that replicated using both Coloc and TWAS analyses in both the GTEx and Braineac expression data sets. A further 6 genes (ZRANB3 [OMIM 615655], PCGF3 [OMIM 617543], NEK1 [OMIM 604588], NUPL2 [NCBI 11097], GALC [OMIM 606890], and CTSB [OMIM 116810]) showed evidence of disease-associated splicing effects. Cell-type specificity analysis revealed that gene expression was overall more prevalent in glial cell types compared with neurons. The weighted gene coexpression performed on the GTEx data set showed that NUPL2 is a key gene in 3 modules implicated in catabolic processes associated with protein ubiquitination and in the ubiquitin-dependent protein catabolic process in the nucleus accumbens, caudate, and putamen. TMEM163 and ZRANB3 were both important in modules in the frontal cortex and caudate, respectively, indicating regulation of signaling and cell communication. Protein interactor analysis and simulations using random networks demonstrated that the candidate genes interact significantly more with known mendelian PD and parkinsonism proteins than would be expected by chance. / Conclusions and Relevance Together, these results suggest that several candidate genes and pathways are associated with the findings observed in PD GWAS studies

Regulatory sites for splicing in human basal ganglia are enriched for disease-relevant information

Genome-wide association studies have generated an increasing number of common genetic variants associated with neurological and psychiatric disease risk. An improved understanding of the genetic control of gene expression in human brain is vital considering this is the likely modus operandum for many causal variants. However, human brain sampling complexities limit the explanatory power of brain-related expression quantitative trait loci (eQTL) and allele-specific expression (ASE) signals. We address this, using paired genomic and transcriptomic data from putamen and substantia nigra from 117 human brains, interrogating regulation at different RNA processing stages and uncovering novel transcripts. We identify disease-relevant regulatory loci, find that splicing eQTLs are enriched for regulatory information of neuron-specific genes, that ASEs provide cell-specific regulatory information with evidence for cellular specificity, and that incomplete annotation of the brain transcriptome limits interpretation of risk loci for neuropsychiatric disease. This resource of regulatory data is accessible through our web server, http://braineacv2.inf.um.es/