University of Würzburg

About: University of Würzburg is a education organization based out in Wurzburg, Bayern, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 31437 authors who have published 62203 publications receiving 2337033 citations. The organization is also known as: Julius-Maximilians-Universität Würzburg & Würzburg University.

Supply chain coordination with emissions reduction incentives

Abstract: The European Union Emissions Trading System (EU-ETS) is considered one of the main legislative systems that are set up to reduce emissions and protect the environment. Most of the works in the literature approach this system from a legislation and/or global point of view. Little has been done to examine this system from the perspective of the user. This work is believed to be the first to consider the EU-ETS system in a supply chain and operations management context. A two-level (vendor–buyer) supply chain model with a coordination mechanism is presented while accounting for greenhouse gas (GHG) emissions from manufacturing processes. Different emissions trading schemes are considered, and possible combinations between these schemes are presented. The developed model could be found useful by mangers who wish to jointly minimise the inventory-related and GHG emissions costs of their supply chains when penalties for exceeding emissions limits are considered. Numerical examples are presented, and results are...

Collective cell movement in primary melanoma explants: Plasticity of cell-cell interaction, β1-integrin function, and migration strategies

Abstract: Collective cell movement represents an efficient dissemination strategy in neoplastic epithelial and mesenchymal cancer. In primary melanoma explants cultured in three-dimensional collagen lattices, invasive migration of multicellular clusters was dependent on the function of β1 integrins, as shown by preferential β1-integrin expression and clustering in a subset of promigratory cells at the leading edge (“guiding cells”) and the abrogation of multicellular migration by adhesion-perturbing anti-β1-integrin antibody. Interference with β1-integrin function induced complex changes in cluster polarity and cohesion, including development of two or several opposing leading edges, cluster disruption, and the detachment of individual cells followed by β1-integrin-independent “amoeboid” crawling and dissemination. The conversion from β1-integrin-dependent collective movement to β1-integrin-independent single-cell motility suggests efficient cellular and molecular plasticity in tumor cell migration strategies.

Organic Cation Transporters (OCTs, MATEs), In Vitro and In Vivo Evidence for the Importance in Drug Therapy

Abstract: Organic cation transporters (OCTs) of the solute carrier family (SLC) 22 and multidrug and toxin extrusion (MATE) transporters of the SLC47 family have been identified as uptake and efflux transporters, respectively, for xenobiotics including several clinically used drugs such as the antidiabetic agent metformin, the antiviral agent lamivudine, and the anticancer drug oxaliplatin. Expression of human OCT1 (SLC22A1) and OCT2 (SLC22A2) is highly restricted to the liver and kidney, respectively. By contrast, OCT3 (SLC22A3) is more widely distributed. MATEs (SLC47A1, SLC47A2) are predominantly expressed in human kidney. Data on in vitro studies reporting a large number of substrates and inhibitors of OCTs and MATEs are systematically summarized. Several genetic variants of human OCTs and in part of MATE1 have been reported, and some of them result in reduced in vitro transport activity corroborating data from studies with knockout mice. A comprehensive overview is given on currently known genotype-phenotype correlations for variants in OCTs and MATE1 related to protein expression, pharmacokinetics/-dynamics of transporter substrates, treatment outcome, and disease susceptibility.

Land-use intensification causes multitrophic homogenization of grassland communities

Abstract: Land-use intensification is a major driver of biodiversity loss. Alongside reductions in local species diversity, biotic homogenization at larger spatial scales is of great concern for conservation. Biotic homogenization means a decrease in β-diversity (the compositional dissimilarity between sites). Most studies have investigated losses in local (α)-diversity and neglected biodiversity loss at larger spatial scales. Studies addressing β-diversity have focused on single or a few organism groups (for example, ref. 4), and it is thus unknown whether land-use intensification homogenizes communities at different trophic levels, above- and belowground. Here we show that even moderate increases in local land-use intensity (LUI) cause biotic homogenization across microbial, plant and animal groups, both above- and belowground, and that this is largely independent of changes in α-diversity. We analysed a unique grassland biodiversity dataset, with abundances of more than 4,000 species belonging to 12 trophic groups. LUI, and, in particular, high mowing intensity, had consistent effects on β-diversity across groups, causing a homogenization of soil microbial, fungal pathogen, plant and arthropod communities. These effects were nonlinear and the strongest declines in β-diversity occurred in the transition from extensively managed to intermediate intensity grassland. LUI tended to reduce local α-diversity in aboveground groups, whereas the α-diversity increased in belowground groups. Correlations between the β-diversity of different groups, particularly between plants and their consumers, became weaker at high LUI. This suggests a loss of specialist species and is further evidence for biotic homogenization. The consistently negative effects of LUI on landscape-scale biodiversity underscore the high value of extensively managed grasslands for conserving multitrophic biodiversity and ecosystem service provision. Indeed, biotic homogenization rather than local diversity loss could prove to be the most substantial consequence of land-use intensification.