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Lleida, Spain

The University of Lleida is a university based in Lleida , Spain. It was the first university in Catalonia and the whole Crown of Aragon. It was founded between 1297 and 1301, probably with the name of Estudi General in the style of other Universities founded at that time , and closed down through a royal law or "Real Cédula" in 1717 along with the banning of the rest of Catalan Universities and the original political institutions of Catalonia. Felipe V founded a university in Cervera, a town 70 km. east of Lleida whose authorities had supported his side in the Spanish War of Succession in 1713, which replaced all Catalan universities.It was refounded on December 12, 1991 after a few hundred years parentheses by a law passed by the Catalan Parliament, and since then, besides the historical central edification located in Rambla d'Aragó, in what is nowadays the town district called Universitat, new buildings have been added to it. Wikipedia.

Chemisana D.,University of Lleida
Renewable and Sustainable Energy Reviews | Year: 2011

For building integration, Concentrating Photovoltaic (CPV) systems can offer a host of advantages over conventional flat panel devices, the most notable being: a higher electrical conversion efficiency in the PV cells, better use of space, ease of recycling of constituent materials, and reduced use of toxic products involved in the PV cells' production process. However, the viability of Building-Integrated Concentrating PV (BICPV) systems is dependent on their ability to offer a comparative economic advantage over flat panel photovoltaic technologies whose market prices are decreasing from day to day and which offer other advantages such as ease of replacement of structural elements. A comparative analysis is presented of the main existing CPV systems' suitability for use in buildings, in which the different challenges specific to integration of each system are discussed. The systems are categorized by type of concentration technology and concentration factor. © 2010 Elsevier Ltd.

The interest in incorporating carotenoids, such as β-carotene, into foods and beverages is growing due to their potential health benefits. However, the poor water-solubility and low bioavailability of carotenoids is currently a challenge to their incorporation into many foods. The aim of this work was to study the influence of particle size on lipid digestion and β-carotene bioaccessibility using corn oil-in-water emulsions with different initial droplet diameters: large (d43≈23μm); medium (d43≈0.4μm); and small (d43≈0.2μm). There was a progressive increase in the mean particle size of all the emulsions as they passed through a simulated gastrointestinal tract (GIT) consisting of mouth, stomach, and small intestine phases, which was attributed to droplet coalescence, flocculation, and digestion. The electrical charge on all the lipid particles became highly negative after passage through the GIT due to accumulation of anionic bile salts, phospholipids, and free fatty acids at their surfaces. The rate and extent of lipid digestion increased with decreasing mean droplet diameter (small≈medium≫large), which was attributed to the increase in lipid surface area exposed to pancreatic lipase with decreasing droplet size. There was also an appreciable increase in β-carotene bioaccessibility with decreasing droplet diameter (small>medium>large). These results provide useful information for designing emulsion-based delivery systems for carotenoids for food and pharmaceutical uses. Copyright © 2013 Elsevier Ltd. All rights reserved.

Dusso A.S.,University of Lleida
Kidney International Supplements | Year: 2011

A normal vitamin D status is essential for human health. Vitamin D deficiency is a recognized risk factor for all-cause mortality in normal individuals and in chronic kidney disease (CKD) patients. The link between vitamin D deficiency and death is a defective activation of the vitamin D receptor (VDR) by 1,25-dihydroxyvitamin D (calcitriol, the vitamin D hormone) to induce/repress genes that maintain mineral homeostasis and skeletal integrity, and prevent secondary hyperparathyroidism, hypertension, immune disorders, and renal and cardiovascular (CV) damage. The kidney is the main site for the conversion of 25-hydroxyvitamin D (25D) to circulating calcitriol, and therefore essential for the health benefits of endocrine VDR activation. The kidney is also essential for the uptake of 25D from the glomerular ultrafiltrate for its recycling to the circulation to maintain serum 25D levels, extrarenal calcitriol synthesis, and the prosurvival benefits of autocrine/paracrine VDR activation. Indeed, both calcitriol and vitamin D deficiency increase progressively in the course of CKD, and associate directly with accelerated disease progression and death. Therefore, the safe correction of calcitriol and vitamin D deficiency/insufficiency is becoming a high priority among nephrologists. This review updates the pathophysiology behind 25D and calcitriol deficiency and impaired VDR activation in CKD, the adequacy of current recommendations for vitamin D supplementation, and potential markers of the efficacy of therapy to prevent or slow the development of renal and CV lesions unrelated to parathyroid hormone suppression, a knowledge required for the design of trials to obtain evidence-based recommendations for vitamin D and calcitriol replacement at all stages of CKD.

Porcel J.M.,University of Lleida
Clinics in Chest Medicine | Year: 2013

Although distinguishing transudates from exudates through the Light criteria is still considered a pragmatic first step in the diagnostic work-up of pleural effusions, the measurement of various pleural fluid biomarkers may aid in the identification of common and specific entities, such as heart failure (natriuretic peptides), tuberculosis (adenosine deaminase), malignancy (mesothelin, fibulin-3, immunocytochemical stains), or bacterial pleural infections (C-reactive protein). The use of these biomarkers is currently encouraged as a routine diagnostic procedure. © 2013 Elsevier Inc.

Garcera A.,University of Lleida
Cell death & disease | Year: 2013

Spinal muscular atrophy (SMA) is a genetic disorder characterized by degeneration of spinal cord motoneurons (MNs), resulting in muscular atrophy and weakness. SMA is caused by mutations in the Survival Motor Neuron 1 (SMN1) gene and decreased SMN protein. SMN is ubiquitously expressed and has a general role in the assembly of small nuclear ribonucleoproteins and pre-mRNA splicing requirements. SMN reduction causes neurite degeneration and cell death without classical apoptotic features, but the direct events leading to SMN degeneration in SMA are still unknown. Autophagy is a conserved lysosomal protein degradation pathway whose precise roles in neurodegenerative diseases remain largely unknown. In particular, it is unclear whether autophagosome accumulation is protective or destructive, but the accumulation of autophagosomes in the neuritic beadings observed in several neurite degeneration models suggests a close relationship between the autophagic process and neurite collapse. In the present work, we describe an increase in the levels of the autophagy markers including autophagosomes, Beclin1 and light chain (LC)3-II proteins in cultured mouse spinal cord MNs from two SMA cellular models, suggesting an upregulation of the autophagy process in Smn (murine survival motor neuron protein)-reduced MNs. Overexpression of Bcl-xL counteracts LC3-II increase, contributing to the hypothesis that the protective role of Bcl-xL observed in some SMA models may be mediated by its role in autophagy inhibition. Our in vitro experimental data indicate an upregulation in the autophagy process and autophagosome accumulation in the pathogenesis of SMA, thus providing a valuable clue in understanding the mechanisms of axonal degeneration and a possible therapeutic target in the treatment of SMA.

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