Almacenamiento de energía térmica por calor latente en los edificios: bases para la optimización de aplicaciones pasivas, opacas y traslúcidas

La principal motivación para la elección del tema de la tesis es nuestra realidad energética y ambiental. Y más específicamente, la necesidad urgente de dar una respuesta a esta realidad desde el sector de la edificación. Por lo que, el trabajo parte de la búsqueda de soluciones pasivas que ayuden a la reducción del consumo energético y de las emisiones de C02 de los edificios, tanto nuevos como existentes. El objeto de estudio son aplicaciones innovadoras, basadas en el uso de materiales reactivos, con un efecto térmico de memoria bidireccional. La energía es un elemento imprescindible para el desarrollo. Sin embargo, el modelo energético predominante, basado principalmente en la utilización de combustibles de origen fósil, es uno de los importantes responsables del deterioro ambiental que sufre el planeta. Además, sus reservas son limitadas y están concentradas en unas pocas regiones del mundo, lo que genera problemas de dependencia, competitividad y de seguridad de suministro. Dado el gran potencial de ahorro energético del sector de la edificación, la Unión Europea en sus directivas enfatiza la necesidad de mejorar la eficiencia energética de los edificios. Añadiendo, además, la obligatoriedad de desarrollar edificios “energía casi nula”, cuyo prerrequisito es tener un muy alto rendimiento energético. En España, los edificios son responsables del 31% del consumo de energía primaria. La mayor parte de este consumo se relaciona a la utilización de sistemas activos de acondicionamiento. Una medida efectiva para reducir la demanda es mejorar la envolvente. Sin embargo, hay que buscar estrategias adicionales para aumentar aún más la eficiencia de los edificios nuevos y existentes. Para los climas de España, el uso de la inercia térmica ha probado ser una estrategia válida. Sin embargo, su funcionamiento está vinculado al peso y al volumen de los materiales utilizados. Esto limita sus posibilidades en la rehabilitación energética y en los nuevos edificios basados en la construcción ligera. Una alternativa es el uso de aplicaciones de almacenamiento térmico por calor latente, utilizando materiales de cambio de fase (PCM). Los PCM son sustancias con un muy alto calor de fusión, capaces de almacenar una gran cantidad de energía térmica sin requerir aumentos significativos de peso o volumen. Estas características los hacen idóneos para reducir el consumo relacionado con el acondicionamiento térmico, en edificios nuevos y existentes. En la parte preliminar de la investigación, se encontró que para lograr un aprovechamiento óptimo de las aplicaciones con PCM es necesario tener un conocimiento profundo de su funcionamiento y de las variables del sistema. De ahí que el objetivo principal de la presente tesis sea: establecer las bases para la optimizatión integral de las aplicaciones con almacenamiento de energía térmica por calor latente, identificando y validando sus variables más relevantes. La investigación consta de tres partes. La primera, documental, sistematizando y jerarquizando la información científica publicada; la segunda, numérica, basada en un análisis paramétrico de una aplicación con PCM, utilizando simulaciones térmicas; y la tercera, experimental, monitorizando el funcionamiento térmico y energético de diferentes aplicaciones con PCM en módulos a escala real. Los resultados brindan un más profundo entendimiento del funcionamiento de las aplicaciones evaluadas. Han permitido identificar sus variables relevantes, cuantificar su influencia, y determinar condiciones óptimas para su utilización así como situaciones en las que sería muy difícil justificar su uso. En el proceso, se realizó la caracterización térmica y energética de aplicaciones con PCM, tanto opacas como traslúcidas. Además, se ha encontrado que las aplicaciones con PCM son capaces de aumentar la eficiencia energética inclusive en recintos con diseños optimizados, demostrando ser una de las estrategias adecuadas para lograr el muy alto desempeño energético requerido en los edificios energía nula. ABSTRACT The main motivation for choosing the theme of the thesis is our energy and environmental reality. And more specifically, the urgent need to respond to this reality from the building sector. This is why, the work start with the search of passive solutions that help reduce energy consumption and C02 emissions of buildings, in both new and existing ones. The object of study is innovative applications based on the use of responsive materials, with bidirectional thermal memory. Energy is an essential element for development. However, the predominant energy model, based primarily on the use of fossil fuels, is one of the major responsible for the environmental deterioration of the planet, the cause of most of the CO2 emissions. Furthermore, reserves of fossil fuels are limited and are concentrated in a few regions of the world, which creates issues related to dependency, competitiveness, and security of supply. Given the large potential for energy savings in the building sector, the European Union in its directives emphasizes the need to improve energy efficiency in buildings. Also, adding the obligation to develop "nearly zero energy" buildings, whose first prerequisite is to achieve a very high energy efficiency. In Spain, buildings are responsible for 31% of primary energy consumption and most of this consumption is related to the used of HVAC systems. One of the most effective measures to reduce demand is to improve the envelope. However, it is necessary to look for additional strategies to further increase the efficiency of new and existing buildings. For the predominant climates in Spain, use of the thermal inertia may be a valid strategy. Nevertheless, its operation is linked to weight and volume of the materials used. This limits their possibilities in the existing buildings energy retrofitting and in the new buildings based on lightweight construction. An alternative is the use of latent heat thermal energy storage applications (LHTES), using phase change materials (PCM). PCM are substances with a high heat of fusion, capable of storing a large amount of thermal energy without requiring significant increases in weight or volume. These features make them ideal for reducing energy consumption associated with thermal conditioning in both new and existing buildings. In the preliminary part of the investigation, it was found that to get optimum utilization of the PCM applications is needed to have a deep understanding of its operation and, in particular, how the system variables affect its performance. Hence, the main objective of this thesis is: to establish the basis for the integral optimization of applications with latent heat thermal energy storage, identifying and validating the most relevant variables. The research comprises of three parts. The first, documentary, systematizing and prioritizing published scientific information. The second, numeric, based on a parametric analysis of an application PCM using thermal simulations. The third, experimental, monitoring the thermal and energy performance of different applications with PCM on real scale test cells. The results provide a complete understanding of the functioning of the evaluated LHTES application. They have allowed to identify their relevant variables, quantify their influence and determine optimum conditions for use as well as situations where it would be very difficult to justify its use. In the process, it was carried out the power and thermal characterization of various opaque and translucent PCM applications. Furthermore, it has been found that applications with PCM can increase the energy efficiency, even in buildings with optimized designs; proving to be one of the appropriate measures to achieve the high energy performance required in zero energy buildings.

Gene disruption of p27Kip1 allows cell proliferation in the postnatal and adult organ of Corti

Hearing loss is most often the result of hair-cell degeneration due to genetic abnormalities or ototoxic and traumatic insults. In the postembryonic and adult mammalian auditory sensory epithelium, the organ of Corti, no hair-cell regeneration has ever been observed. However, nonmammalian hair-cell epithelia are capable of regenerating sensory hair cells as a consequence of nonsensory supporting-cell proliferation. The supporting cells of the organ of Corti are highly specialized, terminally differentiated cell types that apparently are incapable of proliferation. At the molecular level terminally differentiated cells have been shown to express high levels of cell-cycle inhibitors, in particular, cyclin-dependent kinase inhibitors [Parker, S. B., et al. (1995) Science 267, 1024–1027], which are thought to be responsible for preventing these cells from reentering the cell cycle. Here we report that the cyclin-dependent kinase inhibitor p27Kip1 is selectively expressed in the supporting-cell population of the organ of Corti. Effects of p27Kip1-gene disruption include ongoing cell proliferation in postnatal and adult mouse organ of Corti at time points well after mitosis normally has ceased during embryonic development. This suggests that release from p27Kip1-induced cell-cycle arrest is sufficient to allow supporting-cell proliferation to occur. This finding may provide an important pathway for inducing hair-cell regeneration in the mammalian hearing organ.

Disease sequence from mutant rhodopsin allele to rod and cone photoreceptor degeneration in man

Mutations in the gene encoding rhodopsin, the visual pigment in rod photoreceptors, lead to retinal degeneration in species from Drosophila to man. The pathogenic sequence from rod cell-specific mutation to degeneration of rods and cones remains unclear. To understand the disease process in man, we studied heterozygotes with 18 different rhodopsin gene mutations by using noninvasive tests of rod and cone function and retinal histopathology. Two classes of disease expression were found, and there was allele-specificity. Class A mutants lead to severely abnormal rod function across the retina early in life; topography of residual cone function parallels cone cell density. Class B mutants are compatible with normal rods in adult life in some retinal regions or throughout the retina, and there is a slow stereotypical disease sequence. Disease manifests as a loss of rod photoreceptor outer segments, not singly but in microscopic patches that coalesce into larger irregular areas of degeneration. Cone outer segment function remains normal until >75% of rod outer segments are lost. The topography of cone loss coincides with that of rod loss. Most class B mutants show an inferior-nasal to superior-temporal retinal gradient of disease vulnerability associated with visual cycle abnormalities. Class A mutant alleles behave as if cytotoxic; class B mutants can be relatively innocuous and epigenetic factors may play a major role in the retinal degeneration.

Maternal Obesity During Pregnancy Associates With Premature Mortality and Major Cardiovascular Events in Later Life

Acknowledgements We thank Ms Katie Wilde, Data Management Team, University of Aberdeen and Lynsey Waugh, Information and Services Division of NHS Scotland for their help with data extraction and linkage. Funding sources This work was supported by funding from the Chief Scientist Office, Scotland. We also acknowledge support from Tommy’s and the British Heart Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. None of the authors are related to any of the funders

Phosphorylation of insulin receptor substrate 1 by glycogen synthase kinase 3 impairs insulin action

The phosphorylation of insulin receptor substrate 1 (IRS-1) on tyrosine residues by the insulin receptor (IR) tyrosine kinase is involved in most of the biological responses of insulin. IRS-1 mediates insulin signaling by recruiting SH2 proteins through its multiple tyrosine phosphorylation sites. The phosphorylation of IRS-1 on serine/threonine residues also occurs in cells; however, the particular protein kinase(s) promoting this type of phosphorylation are unknown. Here we report that glycogen synthase kinase 3 (GSK-3) is capable of phosphorylating IRS-1 and that this modification converts IRS-1 into an inhibitor of IR tyrosine kinase activity in vitro. Expression of wild-type GSK-3 or an “unregulated” mutant of the kinase (S9A) in CHO cells overexpressing IRS-1 and IR, resulted in increased serine phosphorylation levels of IRS-1, suggesting that IRS-1 is a cellular target of GSK-3. Furthermore, insulin-induced tyrosine phosphorylation of IRS-1 and IR was markedly suppressed in cells expressing wild-type or the S9A mutant, indicating that expression of GSK-3 impairs IR tyrosine kinase activity. Taken together, our studies suggest a new role for GSK-3 in attenuating insulin signaling via its phosphorylation of IRS-1 and may provide new insight into mechanisms important in insulin resistance.

A systematic review of the cost-effectiveness of non-surgical obesity interventions in men

Crown Copyright © 2015. Published by Elsevier Ltd. All rights reserved.

Altered regulation of platelet-derived growth factor receptor-α gene-transcription in vitro by spina bifida-associated mutant Pax1 proteins

Mouse models show that congenital neural tube defects (NTDs) can occur as a result of mutations in the platelet-derived growth factor receptor-α gene (PDGFRα). Mice heterozygous for the PDGFRα-mutation Patch, and at the same time homozygous for the undulated mutation in the Pax1 gene, exhibit a high incidence of lumbar spina bifida occulta, suggesting a functional relation between PDGFRα and Pax1. Using the human PDGFRα promoter linked to a luciferase reporter, we show in the present paper that Pax1 acts as a transcriptional activator of the PDGFRα gene in differentiated Tera-2 human embryonal carcinoma cells. Two mutant Pax1 proteins carrying either the undulated-mutation or the Gln → His mutation previously identified by us in the PAX1 gene of a patient with spina bifida, were not or less effective, respectively. Surprisingly, Pax1 mutant proteins appear to have opposing transcriptional activities in undifferentiated Tera-2 cells as well as in the U-2 OS osteosarcoma cell line. In these cells, the mutant Pax1 proteins enhance PDGFRα-promoter activity whereas the wild-type protein does not. The apparent up-regulation of PDGFRα expression in these cells clearly demonstrates a gain-of-function phenomenon associated with mutations in Pax genes. The altered transcriptional activation properties correlate with altered protein–DNA interaction in band-shift assays. Our data provide additional evidence that mutations in Pax1 can act as a risk factor for NTDs and suggest that the PDGFRα gene is a direct target of Pax1. In addition, the results support the hypothesis that deregulated PDGFRα expression may be causally related to NTDs.

Neuropeptide release by efficient recruitment of diffusing cytoplasmic secretory vesicles

Neuropeptides are slowly released from a limited pool of secretory vesicles. Despite decades of research, the composition of this pool has remained unknown. Endocrine cell studies support the hypothesis that a population of docked vesicles supports the first minutes of hormone release. However, it has been proposed that mobile cytoplasmic vesicles dominate the releasable neuropeptide pool. Here, to determine the cellular basis of the releasable pool, single green fluorescent protein-labeled secretory vesicles were visualized in neuronal growth cones with the use of an inducible construct or total internal reflection fluorescence microscopy. We report that vesicle movement follows the diffusion equation. Furthermore, rapidly moving secretory vesicles are used more efficiently than stationary vesicles near the plasma membrane to support stimulated release. Thus, randomly moving cytoplasmic vesicles participate in the first minutes of neuropeptide release. Importantly, the preferential recruitment of diffusing cytoplasmic secretory vesicles contributes to the characteristic slow kinetics and limited extent of sustained neuropeptide release.

DNA double-strand break repair proteins are required to cap the ends of mammalian chromosomes

Recent findings intriguingly place DNA double-strand break repair proteins at chromosome ends in yeast, where they help maintain normal telomere length and structure. In the present study, an essential telomere function, the ability to cap and thereby protect chromosomes from end-to-end fusions, was assessed in repair-deficient mouse cell lines. By using fluorescence in situ hybridization with a probe to telomeric DNA, spontaneously occurring chromosome aberrations were examined for telomere signal at the points of fusion, a clear indication of impaired end-capping. Telomeric fusions were not observed in any of the repair-proficient controls and occurred only rarely in a p53 null mutant. In striking contrast, chromosomal end fusions that retained telomeric sequence were observed in nontransformed DNA-PKcs-deficient cells, where they were a major source of chromosomal instability. Metacentric chromosomes created by telomeric fusion became even more abundant in these cells after spontaneous immortalization. Restoration of repair proficiency through transfection with a functional cDNA copy of the human DNA-PKcs gene reduced the number of fusions compared with a negative transfection control. Virally transformed cells derived from Ku70 and Ku80 knockout mice also displayed end-to-end fusions. These studies demonstrate that DNA double-strand break repair genes play a dual role in maintaining chromosomal stability in mammalian cells, the known role in repairing incidental DNA damage, as well as a new protective role in telomeric end-capping.

PDZ Motifs in PTP-BL and RIL Bind to Internal Protein Segments in the LIM Domain Protein RIL

The specificity of protein–protein interactions in cellular signaling cascades is dependent on the sequence and intramolecular location of distinct amino acid motifs. We used the two-hybrid interaction trap to identify proteins that can associate with the PDZ motif-rich segment in the protein tyrosine phosphatase PTP-BL. A specific interaction was found with the Lin-11, Isl-1, Mec-3 (LIM) domain containing protein RIL. More detailed analysis demonstrated that the binding specificity resides in the second and fourth PDZ motif of PTP-BL and the LIM domain in RIL. Immunohistochemistry on various mouse tissues revealed a submembranous colocalization of PTP-BL and RIL in epithelial cells. Remarkably, there is also an N-terminal PDZ motif in RIL itself that can bind to the RIL-LIM domain. We demonstrate here that the RIL-LIM domain can be phosphorylated on tyrosine in vitro and in vivo and can be dephosphorylated in vitro by the PTPase domain of PTP-BL. Our data point to the presence of a double PDZ-binding interface on the RIL-LIM domain and suggest tyrosine phosphorylation as a regulatory mechanism for LIM-PDZ associations in the assembly of multiprotein complexes. These findings are in line with an important role of PDZ-mediated interactions in the shaping and organization of submembranous microenvironments of polarized cells.

Role of metallothionein in nitric oxide signaling as revealed by a green fluorescent fusion protein

Although the function of metallothionein (MT), a 6- to 7-kDa cysteine-rich metal binding protein, remains unclear, it has been suggested from in vitro studies that MT is an important component of intracellular redox signaling, including being a target for nitric oxide (NO). To directly study the interaction between MT and NO in live cells, we generated a fusion protein consisting of MT sandwiched between two mutant green fluorescent proteins (GFPs). In vitro studies with this chimera (FRET-MT) demonstrate that fluorescent resonance energy transfer (FRET) can be used to follow conformational changes indicative of metal release from MT. Imaging experiments with live endothelial cells show that agents that increase cytoplasmic Ca2+ act via endogenously generated NO to rapidly and persistently release metal from MT. A role for this interaction in intact tissue is supported by the finding that the myogenic reflex of mesenteric arteries is absent in MT knockout mice (MT−/−) unless endogenous NO synthesis is blocked. These results are the first application of intramolecular green fluorescent protein (GFP)-based FRET in a native protein and demonstrate the utility of FRET-MT as an intracellular surrogate indicator of NO production. In addition, an important role of metal thiolate clusters of MT in NO signaling in vascular tissue is revealed.

Rapid restoration of visual pigment and function with oral retinoid in a mouse model of childhood blindness

Mutations in the retinal pigment epithelium gene encoding RPE65 are a cause of the incurable early-onset recessive human retinal degenerations known as Leber congenital amaurosis. Rpe65-deficient mice, a model of Leber congenital amaurosis, have no rod photopigment and severely impaired rod physiology. We analyzed retinoid flow in this model and then intervened by using oral 9-cis-retinal, attempting to bypass the biochemical block caused by the genetic abnormality. Within 48 h, there was formation of rod photopigment and dramatic improvement in rod physiology, thus demonstrating that mechanism-based pharmacological intervention has the potential to restore vision in otherwise incurable genetic retinal degenerations.