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.

Inherent rheology of a granular fluid in uniform shear flow.

Abstract: In contrast to normal fluids, a granular fluid under shear supports a steady state with uniform temperature and density since the collisional cooling can compensate locally for viscous heating. It is shown that the hydrodynamic description of this steady state is inherently non-Newtonian. As a consequence, the Newtonian shear viscosity cannot be determined from experiments or simulation of uniform shear flow. For a given degree of inelasticity, the complete nonlinear dependence of the shear viscosity on the shear rate requires the analysis of the unsteady hydrodynamic behavior. The relationship to the Chapman-Enskog method to derive hydrodynamics is clarified using an approximate Grad's solution of the Boltzmann kinetic equation.

Frontline employees’ collaboration in industrial service innovation: routes of co-creation’s effects on new service performance

Abstract: From a Service-Dominant Logic (S-DL) perspective, employees constitute operant resources that firms can draw to enhance the outcomes of innovation efforts. While research acknowledges that frontline employees (FLEs) constitute, through service encounters, a key interface for the transfer of valuable external knowledge into the firm, the range of potential benefits derived from FLE-driven innovation deserves more investigation. Using a sample of knowledge intensive business services firms (KIBS), this study examines how the collaboration with FLEs along the new service development (NSD) process, namely FLE co-creation, impacts on service innovation performance following two routes of different effects. Partial least squares structural equation modeling (PLS-SEM) results indicate that FLE co-creation benefits the NS success among FLEs and firm’s customers, the constituents of the resources route. FLE co-creation also has a positive effect on the NSD speed, which in turn enhances the NS quality. NSD speed and NS quality integrate the operational route, which proves to be the most effective path to impact the NS market performance. Accordingly, KIBS managers must value their FLEs as essential partners to achieve successful innovation from an internal and external perspective, and develop the appropriate mechanisms to guarantee their effective involvement along the NSD process.

Retinoic acid regulates programmed cell death through BMP signalling.

Abstract: rogrammed cell death by apoptosis is one of the major driving forces that shape and pattern the organs and tissues of a developing embryo. One of the best model systems for the study of apoptosis is the interdigital cell death (INZ) that occurs during the outgrowth of the vertebrate limb. However, although much has been learned about the cells involved in this process, the molecular mechanisms underlying INZ remain unclear. Retinoic acid (RA) and bone morphogenetic proteins (BMPs) are two of the signalling components known to be involved in INZ. However, the exact relationships between these two factors in controlling cell death remain unknown. Here we show that RA can control INZ by promoting BMP gene expression and simultaneously repressing the chondrogenic potential of BMPs. We found that RA-soaked beads implanted in the interdigital regions of the chick limb bud promoted apoptosis before the onset of physiological INZ (assessed by neutral red vital staining and TUNEL assay; Fig. 1a–c). Furthermore, interdigital web regression was accelerated (Fig. 1d,e). These effects were preceded by upregulation of different members of the BMP gene family (bmp-7, Fig. 1f,g and bmp-4, not shown). In accordance with these findings, the P

Is sustainable tourism an obstacle to the economic performance of the tourism industry? Evidence from an international empirical study

Abstract: Sustainability has become an important strategic objective for tourism destinations worldwide. All analytical tourism competitiveness models make direct or indirect positive references to sustainability. It is accepted that sustainable tourism can reduce resource costs and help create market differentiation. Nevertheless, it has traditionally been considered that, short term, sustainability measures can reduce profitability and compromise competitiveness. Debates on the progress, implications, and practicality of sustainable tourism remain open. The relationship between economic sustainability, and environmental and sociocultural sustainability, is a central but largely unresearched area for tourism scholars, especially at the macro level. This study explores that difficult but essential area, using the World Economic Forum's empirical evidence from 128 countries, backed by the economic data search tool of the World Travel & Tourism Council. It demonstrates that progress in tourism sustainability does not...

Inhibition of autophagy by TAB2 and TAB3

Abstract: Autophagic responses are coupled to the activation of the inhibitor of NF-κB kinase (IKK). Here, we report that the essential autophagy mediator Beclin 1 and TGFβ-activated kinase 1 (TAK1)-binding proteins 2 and 3 (TAB2 and TAB3), two upstream activators of the TAK1-IKK signalling axis, constitutively interact with each other via their coiled-coil domains (CCDs). Upon autophagy induction, TAB2 and TAB3 dissociate from Beclin 1 and bind TAK1. Moreover, overexpression of TAB2 and TAB3 suppresses, while their depletion triggers, autophagy. The expression of the C-terminal domain of TAB2 or TAB3 or that of the CCD of Beclin 1 competitively disrupts the interaction between endogenous Beclin 1, TAB2 and TAB3, hence stimulating autophagy through a pathway that requires endogenous Beclin 1, TAK1 and IKK to be optimally efficient. These results point to the existence of an autophagy-stimulatory ‘switch' whereby TAB2 and TAB3 abandon inhibitory interactions with Beclin 1 to engage in a stimulatory liaison with TAK1.