Dinámicas espaciales de ocupación de suelo en torno a la burbuja inmobiliaria española (1990-2012)

Although the recent housing boom & bust in Spain has triggered significant transformations in its urban fabric, the geographical dimensions of this economic phenomenon and its spatial impacts on the local urban structure have not yet been described in depth. Following the latest published data from CORINE Land cover (2012), this study undertakes a dynamic multi-scale spatial analysis of data representing urban land cover over a 22-year span, contributing to the understanding of four main issues: (i) the total amount of change, (ii) its proportion in comparison with the initial stage of geographical distribution, and the (iv) the implications for the metropolitan and regional urban layout. This quantification describes the outlying regional structure of Spain’s urbanization process during the last decades in Europe, showing great acceleration and a significant transformation in land use patterns, as well as major differences in rates and components on smaller scales, using an integrated growth index.Utilizando los datos de ocupación de suelo de CORINE Land Cover (2012), este trabajo propone un análisis multiescalar, cuantitativo y espacial de las dinámicas de urbanización antes, durante y después de la burbuja inmobiliaria española, aportando una visión inédita del fenómeno en cuatro aspectos interrelacionados: (i) la magnitud absoluta del cambio, (ii) su proporción respecto al estado inicial, (iii) su variación temporal respecto a los usos del suelo, y (iv) sus implicaciones para los distintos componentes del sistema urbano español. El estudio precisa el lugar destacado del caso español en el continente europeo, y evidencia, a nivel provincial, una fuerte transformación del modelo de ocupación del territorio o las desigualdades en el ritmo y componentes del proceso, mediante la utilización de un índice integrado de crecimiento

Desarrollos urbanos y transporte público ferroviario : el caso en la región metropolitana de Madrid: TODs, TADs y TJDs

Este artículo se centra en los modelos de ciudad que tratan de favorecer una movilidad más eficiente, como son la planificación y el diseño urbano que favorecen el transporte colectivo en plataforma reservada (metro, ferrocarril, BRT) y, de modo subsidiario, la movilidad peatonal. Se analiza en el caso de la aglomeración madrileña la aplicación del conocido concepto TOD, "Transit Oriented Development" (Desarrollo Urbano Orientado al Transporte Público), diferenciándolo de otros más recientes como los denominados TAD, "Transit Adjcent Development" (Desarrollos junto al transporte público pero que no tienen una planificación coordinada) o los TJD, "Transit Joint Development" (Desarrollo conjunto urbano-infraestructura de transporte).Aquest article se centra en els models de ciutat que tracten d'afavorir una mobilitat més eficient, com són la planificació i el disseny urbà que afavoreixen el transport col·lectiu en plataforma reservada (metro, ferrocarril, BRT) i, de manera subsidiària, la mobilitat de vianants. S'analitza en el cas de l'aglomeració madrilenya l'aplicació del conegut concepte TOD, "Transit Oriented Development" (Desenvolupament Urbà Orientat al Transport Públic), diferenciant-lo d'altres més recents com els denominats TAD, "Transit Adjcent Development" (Desenvolupaments al costat del transport públic però que no tenen una planificació coordinada) o els TJD, "Transit Joint Development" (Desenvolupament conjunt urbà-infraestructura de transport)

Microbial volatile emissions promote accumulation of exceptionally high levels of starch in leaves in mono- and di-cotyledonous plants

Trabajo presentado en la X Reunión de Biología Molecular de plantas, celebrada en Valencia del 8 al 10 de julio de 2010.Peer Reviewe

Ectopic expression of the AtCDF1 transcription factor in potato enhances tuber starch and amino acid contents and yield under open field conditions

Introduction Cycling Dof transcription factors (CDFs) have been involved in different aspects of plant growth and development. In Arabidopsis and tomato, one member of this family (CDF1) has recently been associated with the regulation of primary metabolism and abiotic stress responses, but their roles in crop production under open field conditions remain unknown. Methods In this study, we compared the growth, and tuber yield and composition of plants ectopically expressing the CDF1 gene from Arabidopsis under the control of the 35S promoter with wild-type (WT) potato plants cultured in growth chamber and open field conditions. Results In growth chambers, the 35S::AtCDF1 plants showed a greater tuber yield than the WT by increasing the biomass partition for tuber development. Under field conditions, the ectopic expression of CDF1 also promoted the sink strength of the tubers, since 35S::AtCDF1 plants exhibited significant increases in tuber size and weight resulting in higher tuber yield. A metabolomic analysis revealed that tubers of 35S::AtCDF1 plants cultured under open field conditions accumulated higher levels of glucose, starch and amino acids than WT tubers. A comparative proteomic analysis of tubers of 35S::AtCDF1 and WT plants cultured under open field conditions revealed that these changes can be accounted for changes in the expression of proteins involved in energy production and different aspects of C and N metabolism. Discussion The results from this study advance our collective understanding of the role of CDFs and are of great interest for the purposes of improving the yield and breeding of crop plants

DYRK1A genetic variants are not linked to Alzheimer's disease in a Spanish case-control cohort

<p>Abstract</p> <p>Background</p> <p>As dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) has been implicated in the abnormal hyperphosphorylation of tau in Alzheimer's disease (AD) brain, and the development of neurofibrillary tangles, we examined the contribution of this gene to the susceptibility for AD.</p> <p>Methods</p> <p>We examined genetic variations of DYRK1A by genotyping haplotype tagging SNPs (htSNPs) (rs11701483, rs2835740, rs1137600, rs2835761, rs2835762, rs2154545 and rs8132976) in a group of 634 Spanish AD cases and 733 controls.</p> <p>Results</p> <p>There were no differences in the genotypic, allelic or haplotypic distributions between cases and controls in the overall analysis or after stratification by APOE ε4 allele.</p> <p>Conclusion</p> <p>Our negative findings in the Spanish population argue against the hypothesis that DYRK1A genetic variations are causally related to AD risk. Still, additional studies using different sets of patients and control subjects deserve further attention, since supporting evidence for association between DYRK1A gene and AD risk in the Japanese population exists.</p

Detection of early Alzheimer's disease in MCI patients by the combination of MMSE and an episodic memory test

BACKGROUND: Mild cognitive impairment (MCI) is a heterogeneous clinical entity that comprises the prodromal phase of Alzheimer's disease (Pr-AD). New biomarkers are useful in detecting Pr-AD, but they are not universally available. We aimed to investigate baseline clinical and neuropsychological variables that might predict progression from MCI to AD dementia. METHODS: All patients underwent a complete clinical and neuropsychological evaluation at baseline and every 6 months during a two-year follow-up period, with 54 out of 109 MCI patients progressing to dementia (50 of them progressed to AD dementia), and 55 remaining as stable MCI (S-MCI). RESULTS: A combination of MMSE and California Verbal Learning Test Long Delayed Total Recall (CVLT-LDTR) constituted the best predictive model: subjects scoring above 26/30 on MMSE and 4/16 on CVLT-LDTR had a negative predictive value of 93.93% at 2 years, whereas those subjects scoring below both of these cut-off scores had a positive predictive value of 80.95%. CONCLUSIONS: Pr-AD might be distinguished from S-MCI at baseline using the combination of MMSE and CVLT-LDTR. These two neuropsychological predictors are relatively brief and may be readily completed in non-specialist clinical settings

Genetic variation in the tau protein phosphatase-2A pathway is not associated with Alzheimer's disease risk

<p>Abstract</p> <p>Background</p> <p>Tau abnormal hyperphosphorylation and the formation of neurofibrillary tangles in AD brain is the result of upregulation of tau kinases and downregulation of tau phosphatases.</p> <p>Methods</p> <p>In a group of 729 Spanish late-onset Alzheimer's disease (AD) patients and 670 healthy controls, we examined variations into a set of candidate genes (PPP2CA, PPP2R2A, ANP32A, LCMT1, PPME1 and PIN1) in the tau protein phosphatase-2A (PP2A) pathway, to address hypotheses of genetic variation that might influence AD risk.</p> <p>Results</p> <p>There were no differences in the genotypic, allelic or haplotypic distributions between cases and controls in the overall analysis or after stratification by age, gender or APOE ε4 allele.</p> <p>Conclusion</p> <p>Our negative findings in the Spanish population argue against the hypothesis that genetic variation in the tau protein phosphatase-2A (PP2A) pathway is causally related to AD risk</p

Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model

Calbindin-D28k (CB), one of the major calcium-binding and buffering proteins, has a critical role in preventing a neuronal death as well as maintaining calcium homeostasis. Although marked reductions of CB expression have been observed in the brains of mice and humans with Alzheimer disease (AD), it is unknown whether these changes contribute to AD-related dysfunction. To determine the pathogenic importance of CB depletions in AD models, we crossed 5 familial AD mutations (5XFAD; Tg) mice with CB knock-out (CBKO) mice and generated a novel line CBKO·5XFAD (CBKOTg) mice. We first identified the change of signaling pathways and differentially expressed proteins globally by removing CB in Tg mice using mass spectrometry and antibody microarray. Immunohistochemistry showed that CBKOTg mice had significant neuronal loss in the subiculum area without changing the magnitude (number) of amyloid β-peptide (Aβ) plaques deposition and elicited significant apoptotic features and mitochondrial dysfunction compared with Tg mice. Moreover, CBKOTg mice reduced levels of phosphorylated mitogen-activated protein kinase (extracellular signal-regulated kinase) 1/2 and cAMP response element-binding protein at Ser-133 and synaptic molecules such as N-methyl-D-aspartate receptor 1 (NMDA receptor 1), NMDA receptor 2A, PSD-95 and synaptophysin in the subiculum compared with Tg mice. Importantly, this is the first experimental evidence that removal of CB from amyloid precursor protein/presenilin transgenic mice aggravates AD pathogenesis, suggesting that CB has a critical role in AD pathogenesis

Genome-Wide Screening of Genes Whose Enhanced Expression Affects Glycogen Accumulation in Escherichia coli

Using a systematic and comprehensive gene expression library (the ASKA library), we have carried out a genome-wide screening of the genes whose increased plasmid-directed expression affected glycogen metabolism in Escherichia coli. Of the 4123 clones of the collection, 28 displayed a glycogen-excess phenotype, whereas 58 displayed a glycogen-deficient phenotype. The genes whose enhanced expression affected glycogen accumulation were classified into various functional categories including carbon sensing, transport and metabolism, general stress and stringent responses, factors determining intercellular communication, aggregative and social behaviour, nitrogen metabolism and energy status. Noteworthy, one-third of them were genes about which little or nothing is known. We propose an integrated metabolic model wherein E. coli glycogen metabolism is highly interconnected with a wide variety of cellular processes and is tightly adjusted to the nutritional and energetic status of the cell. Furthermore, we provide clues about possible biological roles of genes of still unknown functions

Rho GTPases as therapeutic targets in Alzheimer’s disease

The progress we have made in understanding Alzheimer’s disease (AD) pathogenesis has led to the identification of several novel pathways and potential therapeutic targets. Rho GTPases have been implicated as critical components in AD pathogenesis, but their various functions and interactions make understanding their complex signaling challenging to study. Recent advancements in both the field of AD and Rho GTPase drug development provide novel tools for the elucidation of Rho GTPases as a viable target for AD. Herein, we summarize the fluctuating activity of Rho GTPases in various stages of AD pathogenesis and in several in vitro and in vivo AD models. We also review the current pharmacological tools such as NSAIDs, RhoA/ROCK, Rac1, and Cdc42 inhibitors used to target Rho GTPases and their use in AD-related studies. Finally, we summarize the behavioral modifications following Rho GTPase modulation in several AD mouse models. As key regulators of several AD-related signals, Rho GTPases have been studied as targets in AD. However, a consensus has yet to be reached regarding the stage at which targeting Rho GTPases would be the most beneficial. The studies discussed herein emphasize the critical role of Rho GTPases and the benefits of their modulation in AD