1,053 research outputs found

    L’ampliació del temps d’aprenentatge, una pràctica inclusiva que millora el rendiment acadèmic de tot l’alumnat

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    La recerca R+D «Formas de agrupación del alumnado y su relación con el éxito escolar: ‘mixture’, ‘streaming’ e inclusión (2009-2011)» ha realitzat una anàlisi quantitativa i una de qualitativa sobre la presència d’aquestes modalitats d’agrupació en els centres d’educació primària i secundària de l’Estat espanyol. Els resultats quantitatius reflecteixen que l’ampliació del temps d’aprenentatge és la pràctica inclusiva més implementada en els centres educatius. Una pràctica que pot suposar una alternativa a la separació per nivells de l’alumnat, que es dóna dins de la modalitat de streaming, i que ajuda a millorar aquells alumnes que tenen un nivell més baix. L’estudi qualitatiu mostra diferents formes de com s’aplica aquesta pràctica i com els centres que les vinculen més directament als continguts instrumentals, a la vegada que aprofiten per al seu desenvolupament els recursos disponibles, tant de l’administració com de la comunitat, aconsegueixen una incidència més gran en la millora acadèmica de l’alumnat

    Rcor2 underexpression in senescent mice: a target for inflammaging?

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    BACKGROUND: Aging is characterized by a low-grade systemic inflammation that contributes to the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). However, little knowledge is currently available on the molecular processes leading to chronic neuroinflammation. In this context, recent studies have described the role of chromatin regulators in inflammation and longevity including the REST corepressor (Rcor)-2 factor, which seems to be involved in an inflammatory suppressive program. METHODS: To assess the impact of Rcor2 in age-related inflammation, gene expression levels were quantified in different tissues and ages of the spontaneous senescence-accelerated P8 mouse (P8) using the SAMR1 mouse (R1) as a control. Specific siRNA transfection in P8 and R1 astrocyte cultures was used to determine Rcor2 involvement in the modulation of neuroinflammation. The effect of lipopolysaccharide (LPS) treatment on Rcor2 levels and neuroinflammation was analyzed both in vivo and in vitro. RESULTS: P8 mice presented a dramatic decrease in Rcor2 gene expression compared with R1 controls in splenocytes, an alteration also observed in the brain cortex, hippocampus and primary astrocytes of these mice. Rcor2 reduction in astrocytes was accompanied by an increased basal expression of the interleukin (Il)-6 gene. Strikingly, intraperitoneal LPS injection in R1 mice downregulated Rcor2 in the hippocampus, with a concomitant upregulation of tumor necrosis factor (Tnf-α), Il1-β and Il6 genes. A negative correlation between Rcor2 and Il6 gene expression was also verified in LPS-treated C6 glioma cells. Knock down of Rcor2 by siRNA transfection (siRcor2) in R1 astrocytes upregulated Il6 gene expression while siRcor2 further increased Il6 expression in P8 astrocytes. Moreover, LPS activation provoked a further downregulation of Rcor2 and an amplified induction of Il6 in siRcor2-tranfected astrocytes. CONCLUSIONS: Data presented here show interplay between Rcor2 downregulation and increased inflammation and suggest that Rcor2 may be a key regulator of inflammagin

    Systemic and Pulmonary Vascular Remodelling in Chronic Obstructive Pulmonary Disease

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    Background: Chronic Obstructive Pulmonary Disease (COPD) is associated with subclinical systemic atherosclerosis and pulmonary vascular remodelling characterized by intimal hyperplasia and luminal narrowing. We aimed to determine differences in the intimal thickening of systemic and pulmonary arteries in COPD subjects and smokers. Secondary aims include comparisons with a non-smokers group; determining the clinical variables associated with systemic and pulmonary intimal thickening, and the correlations between systemic and pulmonary remodelling changes. Methods: All consecutive subjects undergoing lung resection were included and divided into 3 groups: 1) COPD, 2) smokers, and 3) non-smokers. Sections of the 5th intercostal artery and muscular pulmonary arteries were measured by histo-morphometry. Four parameters of intimal thickening were evaluated: 1) percentage of intimal area (%IA), 2) percentage of luminal narrowing, 3) intimal thickness index, and 4) intima-to-media ratio. Results: In the adjusted analysis, the systemic arteries of COPD subjects showed greater intimal thickening (%IA) than those of smokers (15.6 +/- 1.5% vs. 14.2 +/- 1.6%, p = 0.038). In the pulmonary arteries, significant differences were observed for % IA between the 2 groups (37.3 +/- 2.2% vs. 29.3 +/- 2.3%, p = 0.016). Among clinical factors, metabolic syndrome, gender and COPD status were associated with the systemic intimal thickening, while only COPD status was associated with pulmonary intimal thickening. A correlation between the % IA of the systemic and pulmonary arteries was observed (Spearman's rho = 0.46, p = 0.008). Conclusions: Greater intimal thickening in systemic and pulmonary arteries is observed in COPD patients than in smokers. There is a correlation between systemic and pulmonary vascular remodelling in the overall population

    Lung fibrotic tenascin-C upregulation is associated with other extracellular matrix proteins and induced by TGFβ1

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    Background Idiopathic pulmonary fibrosis (IPF) is a progressive parenchymal lung disease of unknown aetiology and poor prognosis, characterized by altered tissue repair and fibrosis. The extracellular matrix (ECM) is a critical component in regulating cellular homeostasis and appropriate wound healing. The aim of our study was to determine the expression profile of highlighted ECM proteins in IPF lungs. Methods ECM gene and protein expression was analyzed by cDNA microarrays, rt-PCR, immunohistochemistry and western-blot in lungs from idiopathic pulmonary fibrosis (IPF), hypersensitivity pneumonitis (HP), categorized as chronic (cHP) and subacute (saHP), and healthy lung tissue. Primary fibroblast cultures from normal subjects and fibrotic patients were studied to evaluate tenascin-C (TNC) synthesis. Results A total of 20 ECM proteins were upregulated and 6 proteins downregulated in IPF. TNC was almost undetected in normal lungs and significantly upregulated in fibrotic lungs (IPF and cHP) compared to saHP. Furthermore, it was located specifically in the fibroblastic foci areas of the fibrotic lung with a subepithelial gradient pattern. TNC levels were correlated with fibroblastic foci content in cHP lungs. Versican and fibronectin glycoproteins were associated with TNC, mainly in fibroblastic foci of fibrotic lungs. Fibroblasts from IPF patients constitutively synthesized higher levels of TNC than normal fibroblasts. TNC and α-sma was induced by TGF-β1 in both fibrotic and normal fibroblasts. TNC treatment of normal and fibrotic fibroblasts induced a non-significant increased α-sma mRNA. Conclusions The difference in ECM glycoprotein content in interstitial lung diseases could contribute to the development of lung fibrosis. The increase of TNC in interstitial areas of fibrotic activity could play a key role in the altered wound healing

    A new set of estimated cardiorespiratory fitness equations are associated with cognitive performance in older adults

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    This study aimed to develop new equations to estimate cardiorespiratory fitness specifically for older adults and, secondly, to analyze the associations of cardiorespiratory fitness, both objectively measured and estimated using new equations, with cognitive performance. Ninety-two older adults (41 females, 65-75years) from baseline data of a randomized controlled trial were analyzed ("ClinicalTrials.gov" Identifier: NCT03923712). Participants completed 4 measurement sessions including (i) physiological and health indicators in a laboratory setting, (ii) field-based fitness tests, (iii) sociodemographic and physical activity questionnaires, and (iv) a battery of neuropsychological tests to evaluate cognitive performance. The main findings were as follows: (i) a set of new equations with good predictive value for estimated cardiorespiratory fitness were developed (74-87%), using different scenarios of complexity and/or equipment requirements, and (ii) higher estimated cardiorespiratory fitness, even using its simplest equation (eCRF=-1261.99+1.97*6min walking test (m)+1.12*bioimpedance basal metabolic rate (kcal/day)+5.25*basal heart rate (bpm)), was associated with better cognitive performance evaluated by several neuropsychological tests (i.e., language, cognitive flexibility, fluency, attention, and working memory), similar to using objectively measured cardiorespiratory fitness. In summary, a new set of estimated cardiorespiratory fitness equations have been developed with predictive values ranging from 74 to 87% that could be used based on necessity, availability of equipment, resources, or measurement context. Moreover, similar to objectively measured cardiorespiratory fitness, this measure of estimated cardiorespiratory fitness was positively associated with performance on language, fluency, cognitive flexibility, attention, and working memory, independently of sex, age, and education level. © 2023. The Author(s)

    Resemblance of the human liver sinusoid in a fluidic device with biomedical and pharmaceutical applications

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    Maintenance of the complex phenotype of primary hepatocytes in vitro represents a limitation for developing liver support systems and reliable tools for biomedical research and drug screening. We herein aimed at developing a biosystem able to preserve human and rodent hepatocytes phenotype in vitro based on the main characteristics of the liver sinusoid: unique cellular architecture, endothelial biodynamic stimulation, and parenchymal zonation. Primary hepatocytes and liver sinusoidal endothelial cells (LSEC) were isolated from control and cirrhotic human or control rat livers and cultured in conventional in vitro platforms or within our liver-resembling device. Hepatocytes phenotype, function, and response to hepatotoxic drugs were analyzed. Results evidenced that mimicking the in vivo sinusoidal environment within our biosystem, primary human and rat hepatocytes cocultured with functional LSEC maintained morphology and showed high albumin and urea production, enhanced cytochrome P450 family 3 subfamily A member 4 (CYP3A4) activity, and maintained expression of hepatocyte nuclear factor 4 alpha (hnf4α) and transporters, showing delayed hepatocyte dedifferentiation. In addition, differentiated hepatocytes cultured within this liver-resembling device responded to acute treatment with known hepatotoxic drugs significantly different from those seen in conventional culture platforms. In conclusion, this study describes a new bioengineered device that mimics the human sinusoid in vitro, representing a novel method to study liver diseases and toxicology

    Cómo elaborar, tutorizar y evaluar un trabajo de fin de máster

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    Podeu consultar la versió en català a: http://hdl.handle.net/2445/48356Los estudios de nivel superior en el marco de la Unión Europea se componen del Grado y del Postgrado (Másters y doctorados). Los Másters son titulaciones producto de una formación avanzada, multidisciplinar o especializada, dirigida a la consecución de logros académicos en profundidad, de especialidades profesionales o de iniciación a la investigación. Los estudios de Master exigen la evaluación continua del proceso de aprendizaje que se concreta finalmente en el denominado Trabajo de Fin de Máster, verdadera piedra angular de la formación del estudiante. Ese trabajo final está pensado para evidenciar las competencias adquiridas a lo largo de todo el programa formativo y para demostrar el logro de los objetivos globales del aprendizaje. Es la prueba definitiva de la madurez y de la profesionalidad de una carrera hecha a conciencia..

    Com elaborar, tutoritzar i avaluar um treball de fi de màster

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    Podeu consultar la versió en castellà a: http://hdl.handle.net/2445/48357Els estudis de nivell superior en el marc de la Unió Europea es componen del Grau i del Postgrau (Màsters i Doctorats). Els Màsters són titulacions producte d’una formació avançada, multidisciplinària o especialitzada, dirigida a la consecució d’assoliments acadèmics en profunditat, d’especialitats professionals o d’iniciació a la recerca. Els estudis de Màster exigeixen l’avaluació continuada del procés d’aprenentatge que es concreta finalment en el denominat Treball de Fi de Màster (TFM), vertadera pedra angular de la formació de l’estudiant. Aquest treball final està pensat per evidenciar les competències adquirides al llarg de tot el programa formatiu i demostrar l’assoliment dels objectius globals de l’aprenentatge. És la prova definitiva de la maduresa i de la professionalitat d’una carrera feta a consciència..

    Reverberation Mapping of the Seyfert 1 Galaxy NGC 7469

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    A large reverberation mapping study of the Seyfert 1 galaxy NGC 7469 has yielded emission-line lags for Hbeta 4861 and He II 4686 and a central black hole mass measurement of about 10 million solar masses, consistent with previous measurements. A very low level of variability during the monitoring campaign precluded meeting our original goal of recovering velocity-delay maps from the data, but with the new Hbeta measurement, NGC 7469 is no longer an outlier in the relationship between the size of the Hbeta-emitting broad-line region and the AGN luminosity. It was necessary to detrend the continuum and Hbeta and He II 4686 line light curves and those from archival UV data for different time-series analysis methods to yield consistent results.Comment: 9 Pages, 7 figures, 6 tables. Accepted for publication in The Astrophysical Journa

    MYH10 activation rescues contractile defects in arrhythmogenic cardiomyopathy (ACM).

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    The most prevalent genetic form of inherited arrhythmogenic cardiomyopathy (ACM) is caused by mutations in desmosomal plakophilin-2 (PKP2). By studying pathogenic deletion mutations in the desmosomal protein PKP2, here we identify a general mechanism by which PKP2 delocalization restricts actomyosin network organization and cardiac sarcomeric contraction in this untreatable disease. Computational modeling of PKP2 variants reveals that the carboxy-terminal (CT) domain is required for N-terminal domain stabilization, which determines PKP2 cortical localization and function. In mutant PKP2 cells the expression of the interacting protein MYH10 rescues actomyosin disorganization. Conversely, dominant-negative MYH10 mutant expression mimics the pathogenic CT-deletion PKP2 mutant causing actin network abnormalities and right ventricle systolic dysfunction. A chemical activator of non-muscle myosins, 4-hydroxyacetophenone (4-HAP), also restores normal contractility. Our findings demonstrate that activation of MYH10 corrects the deleterious effect of PKP2 mutant over systolic cardiac contraction, with potential implications for ACM therapy.This study was supported by MCIU grant BFU2016-75144-R and PID2020- 116935RB-I00, and by a “la Caixa” Banking Foundation grant under the project code HR18-00304” to J.A.B.; The study was also supported by the “Ayudas a la Investigación Cátedra Real Madrid-Universidad Europea” (2017/RM01). C.M.-L. and S.S. hold MCIU predoctoral contracts BES-2017-079715, and BES-2017-079707 respectively. R.G. acknowledges funding from the European Research Council under grant ERCAG-340177 (3DNanoMech) and from the MCIU under grant MAT2016- 76507-R. The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación (MCIN) and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence, grant CEX2020-001041-S funded by MICIN/AEI/10.13039/501100011033. The microscopy experiments were carried out at the Dynamic Microscopy and Image Unit, CNIC, ICTS-ReDib, co-financed by MCIN/AEI /10.13039/ 501100011033 and FEDER “A way of making Europe” (#ICTS-2018-04- CNIC-16). Imaris full analysis were carried out at the Microscopy & Dynamic Imaging, CNIC, ICTS-ReDib, co-funded by MCIN/AEI /10.13039/501100011033. Biomedical Imaging has been conducted at the Advanced Imaging Unit of the CNIC (Centro Nacional de Investigaciones Cardiovasculares Carlos III), Madrid, Spain. This project used the ReDIB ICTS infrastructure TRIMA@CNIC, Ministerio de Ciencia e Innovación (MCIN).S
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