The art of recontextualisation: How firms make sense of the European ecolabel

 The globalisation of markets and gradual depletion of natural resources not only gave rise to fiercer competition, but also emphasised the need for sustainable production processes and business solutions (Golden, 2010, p. 10). Initially, legislators sought to tackle environmental issues by directly regulating the market through command-and-control instruments such as hard law, albeit with mixed success (Jordan et al., 2003, p. 562). The main criticism of command-and-control mechanisms lies in the fact that these often undermine a firm’s competitive advantage (p. 564). As a response, legislative instruments have taken on a more market-based character, developed as a result of negotiations between policy makers, scientific experts, non-governmental organisations (NGO) and firms. The soft-law approach is considered more effective as it better reflects the interest of a firm; however, its environmental benefits remain a matter of debate (Iraldo, Testa, Melis & Frey, 2011, p. 213). The European Union (EU), one of the leading economies in the world, adopted such a market-based policy instrument in shape of the EU ecolabel. The ecolabel was created as a voluntary scheme motivating firms to produce environmentally friendlier products and services (European Commission, 2011b). The label is awarded to a wide array of products, however, only if – after careful examination – they have met the ecological criteria agreed upon at the EU level (Locret & de Roo, 2004, p. 3). Besides the protection of the environment, ideally this approach also creates trust for the consumers and a competitive advantage for the firm (European Commission, 2011b). While at the EU level various stakeholders standardise criteria to ensure their widespread applicability for many economic sectors and products, the national competent authorities (NCAs) have to interpret the legislation in such a way as to ensure their practical use at the local level. Subsequently, firms that apply for the ecolabel have to re-interpret the legislation and adapt their resource selection, production, and distribution accordingly. This process – in this chapter referred to as the recontextualisation of standards – creates a tension between the European and the local level

A rare differential diagnosis to occupational neck pain: bilateral stylohyoid syndrome

Chronic neck pain is widely prevalent and a common source of disability in the working-age population. Etiology of chronic neck pain includes neck sprain, mechanical or muscular neck pain, myofascial pain syndrome, postural neck pain as well as pain due to degenerative changes. We report the case of a 42 year old secretary, complaining about a longer history of neck pain and limited movement of the cervical spine. Surprisingly, the adequate radiologic examination revealed a bilateral ossification of the stylohyoid ligament complex. Her symptoms remained intractable from conservative treatment consisting of anti-inflammatory medication as well as physical therapy. Hence the patient was admitted to surgical resection of the ossified stylohyoid ligament complex. Afterwards she was free of any complaints and went back to work. Therefore, ossification of the stylohyoid ligament complex causing severe neck pain and movement disorder should be regarded as a rare differential diagnosis of occupational related neck pain

Preface and acknowledgements

This collection is the outcome of a Maastricht Research Based Learning Project (MARBLE) that took place at the Faculty of Arts and Social Sciences at Maastricht University in spring 2011. Under the guidance of Jens Lachmund (who is a lecturer at that faculty) a group of nine students worked on eight distinct case-studies on the culture and politics of product labelling

Resonant helical deformations in nonhomogeneous Kirchhoff filaments

We study the three-dimensional static configurations of nonhomogeneous Kirchhoff filaments with periodically varying Young's modulus. This type of variation may occur in long tandemly repeated sequences of DNA. We analyse the effects of the Young's modulus frequence and amplitude of oscillation in the stroboscopic maps, and in the regular (non chaotic) spatial configurations of the filaments. Our analysis shows that the tridimensional conformations of long filaments may depend critically on the Young's modulus frequence in case of resonance with other natural frequencies of the filament. As expected, far from resonance the shape of the solutions remain very close to that of the homogeneous case. In the case of biomolecules, it is well known that various other elements, besides sequence-dependent effects, combine to determine their conformation, like self-contact, salt concentration, thermal fluctuations, anisotropy and interaction with proteins. Our results show that sequence-dependent effects alone may have a significant influence on the shape of these molecules, including DNA. This could, therefore, be a possible mechanical function of the ``junk'' sequences.Comment: 18 pages (twocolumn), 5 figures Revised manuscrip

CD95 co-stimulation blocks activation of naive T cells by inhibiting T cell receptor signaling

CD95 is a multifunctional receptor that induces cell death or proliferation depending on the signal, cell type, and cellular context. Here, we describe a thus far unknown function of CD95 as a silencer of T cell activation. Naive human T cells triggered by antigen-presenting cells expressing a membrane-bound form of CD95 ligand (CD95L) or stimulated by anti-CD3 and -CD28 antibodies in the presence of recombinant CD95L had reduced activation and proliferation, whereas preactivated, CD95-sensitive T cells underwent apoptosis. Triggering of CD95 during T cell priming interfered with proximal T cell receptor signaling by inhibiting the recruitment of ζ-chain–associated protein of 70 kD, phospholipase-γ, and protein kinase C-θ into lipid rafts, thereby preventing their mutual tyrosine protein phosphorylation. Subsequently, Ca2+ mobilization and nuclear translocation of transcription factors NFAT, AP1, and NF-κB were strongly reduced, leading to impaired cytokine secretion. CD95-mediated inhibition of proliferation in naive T cells could not be reverted by the addition of exogenous interleukin-2 and T cells primed by CD95 co-stimulation remained partially unresponsive upon secondary T cell stimulation. HIV infection induced CD95L expression in primary human antigeen-presenting cells, and thereby suppressed T cell activation, suggesting that CD95/CD95L-mediated silencing of T cell activation represents a novel mechanism of immune evasion

Adhesion Class GPCRs (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Adhesion GPCRs are structurally identified on the basis of a large extracellular region, similar to the Class B GPCR, but which is linked to the 7TM region by a GPCR autoproteolysis-inducing (GAIN) domain [8] containing a GPCR proteolytic site. The N-terminus often shares structural homology with adhesive domains (e.g. cadherins, immunolobulin, lectins) facilitating inter- and matricellular interactions and leading to the term adhesion GPCR [82, 332]. Several receptors have been suggested to function as mechanosensors [254, 234, 315, 32]. The nomenclature of these receptors was revised in 2015 as recommended by NC-IUPHAR and the Adhesion GPCR Consortium [100]

Adhesion Class GPCRs in GtoPdb v.2023.1

Adhesion GPCRs are structurally identified on the basis of a large extracellular region, similar to the Class B GPCR, but which is linked to the 7TM region by a GPCR autoproteolysis-inducing (GAIN) domain [10] containing a GPCR proteolysis site (GPS). The N-terminal extracellular region often shares structural homology with adhesive domains (e.g. cadherins, immunolobulin, lectins) facilitating inter- and matricellular interactions and leading to the term adhesion GPCR [104, 418]. Several receptors have been suggested to function as mechanosensors [320, 288, 396, 38]. Cryo-EM structures of the 7-transmembrane domain of several adhesion GPCRs have been determined recently [292, 21, 403, 212, 300, 302, 431, 293]. The nomenclature of these receptors was revised in 2015 as recommended by NC-IUPHAR and the Adhesion GPCR Consortium [125]

Adhesion Class GPCRs in GtoPdb v.2021.3

Adhesion GPCRs are structurally identified on the basis of a large extracellular region, similar to the Class B GPCR, but which is linked to the 7TM region by a GPCR autoproteolysis-inducing (GAIN) domain [9] containing a GPCR proteolytic site. The N-terminus often shares structural homology with adhesive domains (e.g. cadherins, immunolobulin, lectins) facilitating inter- and matricellular interactions and leading to the term adhesion GPCR [101, 403]. Several receptors have been suggested to function as mechanosensors [309, 280, 383, 35]. The nomenclature of these receptors was revised in 2015 as recommended by NC-IUPHAR and the Adhesion GPCR Consortium [122]

Identification of a BRCA2-Specific modifier locus at 6p24 related to breast cancer risk

Common genetic variants contribute to the observed variation in breast cancer risk for BRCA2 mutation carriers; those known to date have all been found through population-based genome-wide association studies (GWAS). To comprehensively identify breast cancer risk modifying loci for BRCA2 mutation carriers, we conducted a deep replication of an ongoing GWAS discovery study. Using the ranked P-values of the breast cancer associations with the imputed genotype of 1.4 M SNPs, 19,029 SNPs were selected and designed for inclusion on a custom Illumina array that included a total of 211,155 SNPs as part of a multi-consortial project. DNA samples from 3,881 breast cancer affected and 4,330 unaffected BRCA2 mutation carriers from 47 studies belonging to the Consortium of Investigators of Modifiers of BRCA1/2 were genotyped and available for analysis. We replicated previously reported breast cancer susceptibility alleles in these BRCA2 mutation carriers and for several regions (including FGFR2, MAP3K1, CDKN2A/B, and PTHLH) identified SNPs that have stronger evidence of association than those previously published. We also identified a novel susceptibility allele at 6p24 that was inversely associated with risk in BRCA2 mutation carriers (rs9348512; per allele HR = 0.85, 95% CI 0.80-0.90, P = 3.9×10−8). This SNP was not associated with breast cancer risk either in the general population or in BRCA1 mutation carriers. The locus lies within a region containing TFAP2A, which encodes a transcriptional activation protein that interacts with several tumor suppressor genes. This report identifies the first breast cancer risk locus specific to a BRCA2 mutation background. This comprehensive update of novel and previously reported breast cancer susceptibility loci contributes to the establishment of a panel of SNPs that modify breast cancer risk in BRCA2 mutation carriers. This panel may have clinical utility for women with BRCA2 mutations weighing options for medical prevention of breast cancer