REFLEXIONES SOBRE EL LIDERAZGO INSTITUCIONAL COMO ESTRATEGIA COMPETITIVA PARA EL DESARROLLO ORGANIZACIONAL DE LAS UNIVERSIDADES DEL ECUADOR

REFLECTIONS ON INSTITUTIONAL LEADERSHIP AS A COMPETITIVE STRATEGY FOR THE ORGANIZATIONAL DEVELOPMENT OF THE UNIVERSITIES OF ECUADOR RESUMEN La investigación realizada se desarrolló con el objetivo de determinar los factores influyentes del liderazgo, los que se presentan desde un enfoque estratégico competitivo, con una valoración histórica del mismo y de las diferentes teorías y posturas de autores, donde es percibido como un factor preponderante. El estudio se dimensionó hacia una aproximación de su implementación en las unidades administrativas de la Universidad Técnica de Babahoyo, en este sentido, y por tratarse de un análisis descriptivo, se realiza a través de una revisión bibliográfica, cuyos propósitos son tendientes a relacionar las bases teóricas indagadas para la construcción del estado del arte. Como conclusión se afirma, que el liderazgo institucional concebido como una estrategia competitiva, se convierte en un factor agente de cambio dentro de las universidades que buscan la excelencia. PALABRAS CLAVE: Liderazgo; organización;, desarrollo institucional; estrategia competitiva; agente de cambio. ABSTRACT The research carried out was developed in order to determine the influential factors of leadership, which are presented from a competitive strategic approach, with a historical assessment of it and the different theories and positions of authors, where it is perceived as a preponderant factor. The study was dimensioned towards an approximation of its implementation in the administrative units of the Technical University of Babahoyo, in this sense, and because it is a descriptive analysis, it is done through a bibliographic review, whose purposes are tending to relate the bases Theoretical questions for the construction of the state of the art. In conclusion, it is affirmed that institutional leadership conceived as a competitive strategy, becomes an agent of change within universities that seek excellence. KEYWORDS: Leadership; organization; institutional development; competitive strategy; agent of change

Mendelian Randomisation Confirms the Role of Y-Chromosome Loss in Alzheimer’s Disease Aetiopathogenesis in Men

Mosaic loss of chromosome Y (mLOY) is a common ageing-related somatic event and has been previously associated with Alzheimer’s disease (AD). However, mLOY estimation from genotype microarray data only reflects the mLOY degree of subjects at the moment of DNA sampling. Therefore, mLOY phenotype associations with AD can be severely age-confounded in the context of genome-wide association studies. Here, we applied Mendelian randomisation to construct an age-independent mLOY polygenic risk score (mloy-PRS) using 114 autosomal variants. The mloy-PRS instrument was associated with an 80% increase in mLOY risk per standard deviation unit (p = 4.22 × 10−20) and was orthogonal with age. We found that a higher genetic risk for mLOY was associated with faster progression to AD in men with mild cognitive impairment (hazard ratio (HR) = 1.23, p = 0.01). Importantly, mloy-PRS had no effect on AD conversion or risk in the female group, suggesting that these associations are caused by the inherent loss of the Y chromosome. Additionally, the blood mLOY phenotype in men was associated with increased cerebrospinal fluid levels of total tau and phosphorylated tau181 in subjects with mild cognitive impairment and dementia. Our results strongly suggest that mLOY is involved in AD pathogenesis.P.G.-G. (Pablo García-González) is supported by CIBERNED employment plan CNV-304-PRF-866. CIBERNED is integrated into ISCIII (Instituto de Salud Carlos III). I.d.R is supported by a national grant from the Instituto de Salud Carlos III FI20/00215. A.C. (Amanda Cano) acknowledges the support of the Spanish Ministry of Science, Innovation, and Universities under the grant Juan de la Cierva (FJC2018-036012-I). M.B. (Mercé Boada) and A.R. (Agustín Ruiz) are also supported by national grants PI13/02434, PI16/01861, PI17/01474, PI19/01240, and PI19/01301. The Genome Research @ Fundació ACE project (GR@ACE) is supported by Grifols SA, Fundación bancaria “La Caixa”, Fundació ACE, and CIBERNED. Acción Estratégica en Salud is integrated into the Spanish National R + D + I Plan and funded by ISCIII (Instituto de Salud Carlos III)—Subdirección General de Evaluación—and the Fondo Europeo de Desarrollo Regional (FEDER—“Una manera de hacer Europa”). Genotyping of the ACE MCI-EADB samples was performed in the context of EADB (European Alzheimer DNA biobank) funded by the JPco-fuND FP-829-029 (ZonMW project number 733051061). This work was supported by a grant (European Alzheimer DNA BioBank, EADB) from the EU Joint Program—Neurodegenerative Disease Research (JPND). Partial funding for open access charge: Universidad de Málag

Multiomics integrative analysis identifies APOE allele-specific blood biomarkers associated to Alzheimer's disease etiopathogenesis

Alzheimer’s disease (AD) is the most common form of dementia, currently affecting 35 million people worldwide. Apolipoprotein E (APOE) ε4 allele is the major risk factor for sporadic, late-onset AD (LOAD), which comprises over 95% of AD cases, increasing the risk of AD 4-12 fold. Despite this, the role of APOE in AD pathogenesis is still a mystery. Aiming for a better understanding of APOE-specific effects, the ADAPTED consortium analysed and integrated publicly available data of multiple OMICS technologies from both plasma and brain stratified by APOE haplotype (APOE2, APOE3 and APOE4). Combining genome-wide association studies (GWAS) with differential mRNA and protein expression analyses and single-nuclei transcriptomics, we identified genes and pathways contributing to AD in both APOE dependent and independent fashion. Interestingly, we characterised a set of biomarkers showing plasma and brain consistent protein profiles and opposite trends in APOE2 and APOE4 AD cases that could constitute screening tools for a disease that lacks specific blood biomarkers. Beside the identification of APOE-specific signatures, our findings advocate that this novel approach, based on the concordance across OMIC layers and tissues, is an effective strategy for overcoming the limitations of often underpowered single-OMICS studies

Frecuencia de Alteraciones Dentales de Tamaño, Número, Forma y Estéticas en Pacientes con Capacidades Especiales.

Este artículo presenta la frecuencia de alteraciones dentales de tamaño, número, forma y estética en pacientes especiales (pacientes con retraso mental, síndrome Down y parálisis cerebral) del Hogar del Niño Minusválido Abandonado "Padre Vito Guarato". Se trabajó con una población de 200 pacientes (4688 piezas dentales). Los resultados muestran que del total de piezas evaluadas (4688); 2.5% (117) presentaron alteraciones de tamaño, 0.79% (37) presentaron alteraciones en cuanto a número , 3.14% (147) presentaron alteraciones de forma, 6.44% (302) presentaron alteraciones estéticas y 87.14 (4085) no presentaron alteraciones dentales

Frecuencia de Alteraciones Dentales de Tamaño, Numero, Forma y Estéticas en Pacientes con Capacidad Especiales

Las alteraciones dentales tienen estrecha relación con los diversos síndromes que presentan los pacientes con capacidades esenciales; por lo tanto, es preciso determinar la frecuencia de las alteraciones dentales de tamaño, número, forma y estéticas en pacientes especiale

IL-7R is essential for leukemia-initiating cell activity of T-cell acute lymphoblastic leukemia

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy resulting from the dysregulation of signaling pathways that control intrathymic T-cell development. Relapse rates are still significant, and prognosis is particularly bleak for relapsed patients. Therefore, development of novel therapies specifically targeting pathways controlling leukemia-initiating cell (LIC) activity is mandatory for fighting refractory T-ALL. The interleukin-7 receptor (IL-7R) is a crucial T-cell developmental pathway that is commonly expressed in T-ALL and has been implicated in leukemia progression; however, the significance of IL-7R/IL-7 signaling in T-ALL pathogenesis and its contribution to disease relapse remain unknown. To directly explore whether IL-7R targeting may be therapeutically efficient against T-ALL relapse, we focused on a known Notch1-induced T-ALL model, because a majority of T-ALL patients harbor activating mutations in NOTCH1, which is a transcriptional regulator of IL-7R expression. Using loss-of-function approaches, we show that Il7r-deficient, but not wild-type, mouse hematopoietic progenitors transduced with constitutively active Notch1 failed to generate leukemia upon transplantation into immunodeficient mice, thus providing formal evidence that IL-7R function is essential for Notch1-induced T-cell leukemogenesis. Moreover, we demonstrate that IL-7R expression is an early functional biomarker of T-ALL cells with LIC potential and report that impaired IL-7R signaling hampers engraftment and progression of patient-derived T-ALL xenografts. Notably, we show that IL-7R–dependent LIC activity and leukemia progression can be extended to human B-cell acute lymphoblastic leukemia (B-ALL). These results have important therapeutic implications, highlighting the relevance that targeting normal IL-7R signaling may have in future therapeutic interventions, particularly for preventing T-ALL (and B-ALL) relapse.This work was supported in part by funds from Plan Nacional, Ministerio de Ciencia, Innovacion y Universidades SAF2013-44857-R and SAF2016- ´ 75442-R (Agencia Estatal de Investigacion/European Regional Devel- ´ opment Fund, European Union), Fundacion Asociaci ´ on Española Contra ´ el Cancer (AECC CI13131229, CICPF18030TORI), Fundaci ´ on Uno Entre ´ Cien Mil, and Fundacion Lair. Institutional grants from the Fundaci ´ on´ Ramon Areces and Banco de Santander to the Centro de Biolog ´ ´ıa Molecular Severo Ochoa are also acknowledged.Peer reviewe

Investigando juegos alternativos

Investigación y recopilación de juegos alternativos del entorno y de otras culturas presentes en el centro para utilizarlos didácticamente. Los objetivos son: conocer y valorar los juegos musulmanes, sudamericanos, europeos y de las distintas Comunidades españolas; utilizar diferentes fuentes para compilar los juegos; conocer los juegos en función de las diferentes estaciones o fiestas señaladas, con la colaboración de las abuelas y abuelos de Fuenlabrada; fomentar la aceptación de reglas comunes compartidas, trabajando estrategias más participativas y autónomas; facilitar la integración social y el desarrollo de la sociabilidad del alumando, familias y profesorado del centro. Se elaboran materiales para los juegos y fichas desciptivas y valorativas de los juegos clasificados por: edades materiales, canciones, etc. Se evalúa los nuevos aprendizajes sobre los juegos y actitudes del alumnado, las estrategias didácticas aprendidas por el profesorado, y el nivel de participación de las familias a partir de reuniones o informes por equipos.MadridMadrid (Comunidad Autónoma). Subdirección General de Formación del Profesorado. CRIF Las Acacias; General Ricardos 179 - 28025 Madrid; Tel. + 34915250893ES

Mendelian randomisation confirms the role of Y-chromosome loss in Alzheimer's disease aetiopathogenesis in men

Mosaic loss of chromosome Y (mLOY) is a common ageing-related somatic event and has been previously associated with Alzheimer's disease (AD). However, mLOY estimation from genotype microarray data only reflects the mLOY degree of subjects at the moment of DNA sampling. Therefore, mLOY phenotype associations with AD can be severely age-confounded in the context of genome-wide association studies. Here, we applied Mendelian randomisation to construct an age-independent mLOY polygenic risk score (mloy-PRS) using 114 autosomal variants. The mloy-PRS instrument was associated with an 80% increase in mLOY risk per standard deviation unit (p = 4.22 × 10-²⁰) and was orthogonal with age. We found that a higher genetic risk for mLOY was associated with faster progression to AD in men with mild cognitive impairment (hazard ratio (HR) = 1.23, p = 0.01). Importantly, mloy-PRS had no effect on AD conversion or risk in the female group, suggesting that these associations are caused by the inherent loss of the Y chromosome. Additionally, the blood mLOY phenotype in men was associated with increased cerebrospinal fluid levels of total tau and phosphorylated tau181 in subjects with mild cognitive impairment and dementia. Our results strongly suggest that mLOY is involved in AD pathogenesis.Funding: P.G.-G. (Pablo García-González) is supported by CIBERNED employment plan CNV-304- PRF-866. CIBERNED is integrated into ISCIII (Instituto de Salud Carlos III). I.d.R is supported by a national grant from the Instituto de Salud Carlos III FI20/00215. A.C. (Amanda Cano) acknowledges the support of the Spanish Ministry of Science, Innovation, and Universities under the grant Juan de la Cierva (FJC2018-036012-I). M.B. (Mercé Boada) and A.R. (Agustín Ruiz) are also supported by national grants PI13/02434, PI16/01861, PI17/01474, PI19/01240, and PI19/01301. The Genome Research @ Fundació ACE project (GR@ACE) is supported by Grifols SA, Fundación bancaria “La Caixa”, Fundació ACE, and CIBERNED. Acción Estratégica en Salud is integrated into the Spanish National R + D + I Plan and funded by ISCIII (Instituto de Salud Carlos III)—Subdirección General de Evaluación—and the Fondo Europeo de Desarrollo Regional (FEDER—“Una manera de hacer Europa”). Genotyping of the ACE MCI-EADB samples was performed in the context of EADB (European Alzheimer DNA biobank) funded by the JPco-fuND FP-829-029 (ZonMW project number 733051061). This work was supported by a grant (European Alzheimer DNA BioBank, EADB) from the EU Joint Program—Neurodegenerative Disease Research (JPND). Acknowledgments: We would like to thank patients and controls who participated in this project. The present work has been performed as part of the doctoral thesis of P.G.-G. (Pablo García-González) at the University of Barcelona (Barcelona, Spain). Some control samples and data from patients included in this study were provided in part by the National DNA Bank Carlos III (www.bancoadn. org, University of Salamanca, Spain) and Hospital Universitario Virgen de Valme (Sevilla, Spain); they were processed following standard operating procedures with the appropriate approval of the Ethical and Scientific Committee