University of Extremadura

About: University of Extremadura is a education organization based out in Badajoz, Spain. It is known for research contribution in the topics: Population & Hyperspectral imaging. The organization has 7856 authors who have published 18299 publications receiving 396126 citations. The organization is also known as: Universidad de Extremadura.

On the Role of Weight Restrictions in Data Envelopment Analysis

Abstract: This paper examines the role that weight restrictions play in Data Envelopment Analysis (DEA). It is argued that the decision to include a factor (input or output) in a DEA model represents an implicit judgement that the factor has a non-trivial weight. It therefore seems perverse to allow DEA to assign a trivial weight to that factor in assessing the efficiency of a unit. There is therefore a strong case for imposing restrictions on factor weights. However, many existing methods of weight restriction are in practice unwieldy. This paper proposes an alternative approach we term contingent weight restriction which is both practical and intellectually consistent with the DEA philosophy. The paper explores the implications of alternative methods of weight restriction using simulated data from a well known production process.

p38γ regulates the localisation of SAP97 in the cytoskeleton by modulating its interaction with GKAP

Abstract: Activation of the p38 MAP kinase pathways is crucial for the adaptation of mammalian cells to changes in the osmolarity of the environment. Here we identify SAP97/hDlg, the mammalian homologue of the Drosophila tumour suppressor Dlg, as a physiological substrate for the p38γ MAP kinase (SAPK3/p38γ) isoform. SAP97/hDlg is a scaffold protein that forms multiprotein complexes with a variety of proteins and is targeted to the cytoskeleton by its association with the protein guanylate kinase-associated protein (GKAP). The SAPK3/p38γ-catalysed phosphorylation of SAP97/hDlg triggers its dissociation from GKAP and therefore releases it from the cytoskeleton. This is likely to regulate the integrity of intercellular–junctional complexes, and cell shape and volume in response to osmotic stress.

Seismic Sources on the Iberia-African Plate Boundary and their Tectonic Implications

Abstract: The plate boundary between Iberia and Africa has been studied using data on seismicity and focal mechanisms The region has been divided into three areas: A; the Gulf of Cadiz; B, the Betics, Alboran Sea and northern Morocco; and C, Algeria Seismicity shows a complex behavior, large shallow earthquakes (h < 30 km) occur in areas A and C and moderate shocks in area B; intermediate-depth activity (30 < h < 150 km) is located in area B; the depth earthquakes (h = 650 km) are located to the south of Granada Moment rate, slip velocity andhvalues have been estimated for shallow shocks, and show similar characteristics for the Gulf of Cadiz and Algeria, and quite different ones for the central region Focal mechanisms of 80 selected shallow earthquakes (8 ? mb? 4) show thrust faulting in the Gulf of Cadiz and Algeria with horizontal NNW-SSE compression, and normal faulting in the Alboran Sea with E-W extension Focal mechanisms of 26 intermediate-depth earthquakes in the Alboran Sea display vertical motions, with a predominant plane trending E-W Solutions for very deep shocks correspond to vertical dip-slip along N-S trends Frohlich diagrams and seismic moment tensors show different behavior in the Gulf of Cadiz, Betic-Alboran Sea and northern Morocco, and northern Algeria for shallow events The stress pattern of intermediate-depth and very deep earthquakes has different directions: vertical extension in the NW-SE direction for intermediate depth earthquakes, and tension and pressure axes dipping about 45 o for very deep earthquakes Regional stress pattern may result from the collision between the African plate and Iberia, with extension and subduction of lithospheric material in the Alboran Sea at intermediate depth The very deep seismicity may be correlated with older subduction processes

Mitochondrial DNA Mutations Induce Mitochondrial Dysfunction, Apoptosis and Sarcopenia in Skeletal Muscle of Mitochondrial DNA Mutator Mice

Abstract: Background: Aging results in a progressive loss of skeletal muscle, a condition known as sarcopenia. Mitochondrial DNA (mtDNA) mutations accumulate with aging in skeletal muscle and correlate with muscle loss, although no causal relationship has been established. Methodology/Principal Findings: We investigated the relationship between mtDNA mutations and sarcopenia at the gene expression and biochemical levels using a mouse model that expresses a proofreading-deficient version (D257A) of the mitochondrial DNA Polymerase c, resulting in increased spontaneous mtDNA mutation rates. Gene expression profiling of D257A mice followed by Parametric Analysis of Gene Set Enrichment (PAGE) indicates that the D257A mutation is associated with a profound downregulation of gene sets associated with mitochondrial function. At the biochemical level, sarcopenia in D257A mice is associated with a marked reduction (35–50%) in the content of electron transport chain (ETC) complexes I, III and IV, all of which are partly encoded by mtDNA. D257A mice display impaired mitochondrial bioenergetics associated with compromised state-3 respiration, lower ATP content and a resulting decrease in mitochondrial membrane potential (Dym). Surprisingly, mitochondrial dysfunction was not accompanied by an increase in mitochondrial reactive oxygen species (ROS) production or oxidative damage. Conclusions/Significance: These findings demonstrate that mutations in mtDNA can be causal in sarcopenia by affecting the assembly of functional ETC complexes, the lack of which provokes a decrease in oxidative phosphorylation, without an increase in oxidative stress, and ultimately, skeletal muscle apoptosis and sarcopenia.

Clinical implications of a staging model for bipolar disorders

Abstract: A model of staging in the field of bipolar disorder (BD) should offer a means for clinicians to predict response to treatment and more general outcome measures, such as the level of functioning and autonomy. The present staging model emphasizes the assessment of patients in the interepisodic period and includes: latent phase: individuals who present mood and anxiety symptoms and increased risk for developing threshold BD; Stage I - patients with BD who present well established periods of euthymia and absence of overt psychiatric morbidity between episodes; Stage II - patients who present rapid cycling or current axis I or II comorbidities; Stage III - patients who present a clinically relevant pattern of cognitive and functioning deterioration, as well as altered biomarkers; and Stage IV - patients who are unable to live autonomously and present altered brain scans and biomarkers. Such a model implies a longitudinal appraisal of clinical variables, as well as assessment of neurocognition and biomarkers in the interepisodic period. Staging facilitates understanding of the mechanisms underlying progression of the disorder, assists in treatment planning and prognosis and, finally, underscores the imperative for early intervention.