180 research outputs found

    Bibliografía usada en la formación matemática del profesorado de infantil

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    Para realizar el estudio se escogió una muestra de 13 universidades españolas en las que se imparte la titulación y cuyas guías docentes son accesibles desde sus páginas webs. Se descargaron todas las guías docentes y se pasó la información a una base de datos ad hoc. Se realizó un proceso de estandarización de los nombres y de las referencias porque para cada asignatura utilizan formatos distintos incluso en la misma universidad. Se obtuvieron 493 referencias, que se presentan como bibliografía básica, específica, recomendada o complementaria. Posteriormente se hicieron conteos de frecuencias de cada autor, referencia y año para determinar la antigüedad de las mismas

    A novel selective 11β-hydroxysteroid dehydrogenase type 1 inhibitor prevents human adipogenesis

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    Glucocorticoid excess increases fat mass, preferentially within omental depots; yet circulating cortisol concentrations are normal in most patients with metabolic syndrome (MS). At a pre-receptor level, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activates cortisol from cortisone locally within adipose tissue, and inhibition of 11β-HSD1 in liver and adipose tissue has been proposed as a novel therapy to treat MS by reducing hepatic glucose output and adiposity. Using a transformed human subcutaneous preadipocyte cell line (Chub-S7) and human primary preadipocytes, we have defined the role of glucocorticoids and 11β-HSD1 in regulating adipose tissue differentiation. Human cells were differentiated with 1·0 μM cortisol (F), or cortisone (E) with or without 100 nM of a highly selective 11β-HSD1 inhibitor PF-877423. 11β-HSD1 mRNA expression increased across adipocyte differentiation (P<0·001, n=4), which was paralleled by an increase in 11β-HSD1 oxo-reductase activity (from nil on day 0 to 5·9±1.9 pmol/mg per h on day 16, P<0·01, n=7). Cortisone enhanced adipocyte differentiation; fatty acid-binding protein 4 expression increased 312-fold (P<0·001) and glycerol-3-phosphate dehydrogenase 47-fold (P<0·001) versus controls. This was abolished by co-incubation with PF-877423. In addition, cellular lipid content decreased significantly. These findings were confirmed in the primary cultures of human subcutaneous preadipocytes. The increase in 11β-HSD1 mRNA expression and activity is essential for the induction of human adipogenesis. Blocking adipogenesis with a novel and specific 11β-HSD1 inhibitor may represent a novel approach to treat obesity in patients with MS

    Plasmonically-enhanced all-optical integrated phase-change memory

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    This is the final version. Available on open access from the Optical Society of America via the DOI in this record.Integrated phase-change photonic memory devices offer a novel route to non-volatile storage and computing that can be carried out entirely in the optical domain, obviating the necessity for time and energy consuming opto-electrical conversions. Such memory devices generally consist of integrated waveguide structures onto which are fabricated small phase-change memory cells. Switching these cells between their amorphous and crystalline states modifies significantly the optical transmission through the waveguide, so providing memory, and computing, functionality. To carry out such switching, optical pulses are sent down the waveguide, coupling to the phase-change cell, heating it up, and so switching it between states. While great strides have been made in the development of integrated phase-change photonic devices in recent years, there is always a pressing need for faster switching times, lower energy consumption and a smaller device footprint. In this work, therefore, we propose the use of plasmonic enhancement of the light-matter interaction between the propagating waveguide mode and the phase-change cell as a means to faster, smaller and more energy-efficient devices. In particular, we propose a form of plasmonic dimer nanoantenna of significantly sub-micron size that, in simulations, offers significant improvements in switching speeds and energies. Write/erase speeds in the range 2 to 20 ns and write/erase energies in the range 2 to 15 pJ were predicted, representing improvements of one to two orders of magnitude when compared to conventional device architectures.Engineering and Physical Sciences Research Council (EPSRC

    Asymmetric Organocatalysis in Deep Eutectic Solvents

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    The recent advances in asymmetric organocatalysis using eutectic mixtures as a reaction medium are revised in this mini‐review. In addition, the first enantioselective transformations using chiral eutectic solvents, which play the role of a green medium and organocatalyst, are described. In this mini‐review we intend to deepen not only in the synthetic aspects of asymmetric organocatalysis in eutectic mixtures, but also in the fundamental issues that seem to be essential for a successful development of this promising, and at the same time challenging, methodology.This work was supported by the Spanish Ministerio de Ciencia, Innovación y Universidades (MICINN, PGC2018-096616-B-I00), the University of Alicante (VIGROB-173 and VIGROB-316FI), and the University of Pisa (PRA_2018_36)

    The Spatial Distribution of LGR5+ Cells Correlates With Gastric Cancer Progression

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    In this study we tested the prevalence, histoanatomical distribution and tumour biological significance of the Wnt target protein and cancer stem cell marker LGR5 in tumours of the human gastrointestinal tract. Differential expression of LGR5 was studied on transcriptional (real-time polymerase chain reaction) and translational level (immunohistochemistry) in malignant and corresponding non-malignant tissues of 127 patients comprising six different primary tumour sites, i.e. oesophagus, stomach, liver, pancreas, colon and rectum. The clinico-pathological significance of LGR5 expression was studied in 100 patients with gastric carcinoma (GC). Non-neoplastic tissue usually harboured only very few scattered LGR5+ cells. The corresponding carcinomas of the oesophagus, stomach, liver, pancreas, colon and rectum showed significantly more LGR5+ cells as well as significantly higher levels of LGR5-mRNA compared with the corresponding non-neoplastic tissue. Double staining experiments revealed a coexpression of LGR5 with the putative stem cell markers CD44, Musashi-1 and ADAM17. Next we tested the hypothesis that the sequential changes of gastric carcinogenesis, i.e. chronic atrophic gastritis, intestinal metaplasia and invasive carcinoma, are associated with a reallocation of the LGR5+ cells. Interestingly, the spatial distribution of LGR5 changed: in non-neoplastic stomach mucosa, LGR5+ cells were found predominantly in the mucous neck region; in intestinal metaplasia LGR5+ cells were localized at the crypt base, and in GC LGR5+ cells were present at the luminal surface, the tumour centre and the invasion front. The expression of LGR5 in the tumour centre and invasion front of GC correlated significantly with the local tumour growth (T-category) and the nodal spread (N-category). Furthermore, patients with LGR5+ GCs had a shorter median survival (28.0±8.6 months) than patients with LGR5− GCs (54.5±6.3 months). Our results show that LGR5 is differentially expressed in gastrointestinal cancers and that the spatial histoanatomical distribution of LGR5+ cells has to be considered when their tumour biological significance is sought

    MMP-8 Deficiency Increases TLR/RAGE Ligands S100A8 and S100A9 and Exacerbates Lung Inflammation during Endotoxemia

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    Matrix metalloproteinase-8, released mainly from neutrophils, is a critical regulator of the inflammatory response by its ability to cleave multiple mediators. Herein, we report the results of a model of endotoxemia after intraperitoneal LPS injection in mice lacking MMP-8 and their wildtype counterparts. Control, saline-treated animals showed no differences between genotypes. However, there was an increased lung inflammatory response, with a prominent neutrophilic infiltration in mutant animals after LPS treatment. Using a proteomic approach, we identify alarmins S100A8 and S100A9 as two of the main differences between genotypes. Mice lacking MMP-8 showed a significant increase in these two molecules in lung homogenates, but not in spleen and serum. Mice lacking MMP-8 also showed an increase in MIP-1α levels and a marked activation of the non-canonical NF-κB pathway, with no differences in CXC-chemokines such as MIP-2 or LIX. These results show that MMP-8 can modulate the levels of S100A8 and S100A9 and its absence promotes the lung inflammatory response during endotoxemia

    The Evolution of Extracellular Matrix

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    We present a perspective on the molecular evolution of the extracellular matrix (ECM) in metazoa that draws on research publications and data from sequenced genomes and expressed sequence tag libraries. ECM components do not function in isolation, and the biological ECM system or “adhesome” also depends on posttranslational processing enzymes, cell surface receptors, and extracellular proteases. We focus principally on the adhesome of internal tissues and discuss its origins at the dawn of the metazoa and the expansion of complexity that occurred in the chordate lineage. The analyses demonstrate very high conservation of a core adhesome that apparently evolved in a major wave of innovation in conjunction with the origin of metazoa. Integrin, CD36, and certain domains predate the metazoa, and some ECM-related proteins are identified in choanoflagellates as predicted sequences. Modern deuterostomes and vertebrates have many novelties and elaborations of ECM as a result of domain shuffling, domain innovations and gene family expansions. Knowledge of the evolution of metazoan ECM is important for understanding how it is built as a system, its roles in normal tissues and disease processes, and has relevance for tissue engineering, the development of artificial organs, and the goals of synthetic biology
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