Launch of sustainability labels : Effects of linking sustainability to major drivers for choice

Many food producers improve the sustainability of their products and look for ways of communicating the improvement. One approach is to launch a new sustainability label. However, little is known about how to launch new sustainability labels effectively. We suggest that such labels should not be launched in isolation, but rather linked to major drivers for choice, such as taste, convenience, or healthiness. We tested this prediction across three categories with different levels of sustainability, using a 2 (label communicated separately vs linked to driver for choice) x 3 (sustainability level of category: high/medium/low) betweensubjects design. The results provided partial support for the hypothesis that linking sustainability labels to major drivers for choice is more effective than a stand-alone launch of labels. The effect seems to be independent of the sustainability level of the product category.nhhma

The Kromosomer Project

This article is a reflection on the Kromosomer project, a storytell- ing performance held in the physical world and implemented through digital, virtual and social media. The motto was the traditional Norwegian legend characters that represent “the other”, the not “normal”. They were illustrated as avatars in the metaverse, where they were also distributed as unfinished arte- facts, open to mutation. We will describe and analyze the main work method used on this project, a shared creative process of collective and distributed creativity. We will also focus on how metaphors constitute them- selves as paramount to our way of working.info:eu-repo/semantics/publishedVersio

Kromosomer - an experience in shared creative work and expression

This article is a reflection on the Kromosomer project, a storytelling performance held in both physical and virtual worlds, which was implemented and disseminated through digital, virtual and social media. The aim of the whole project was to search for an expression that could combine physical experience with virtual world. The project was also looking at how to deal with social inclusion. The motto for this enterprise was the traditional Norwegian legend characters who represent “the other,” the “not-normal,” as a pretext to address the question of alterity. These legends’ characters were re-created as avatars in the metaverse, where they were also freely distributed in virtual installations as unfinished artifacts, open to mutation. In the Second Life virtual world, participants could pick up avatars and create their own stories through snapshots, machinima, etc. The physical performance later used these participants/produsers’ interpretations and narratives of the avatars in stage design and in the storytelling performance itself. We describe and analyse the main work method used for this project — a shared creative process of collective and distributed creativity. The project encompasses different forms of expression therefore we will also focus on how metaphors constitute themselves as paramount to our way of workin

Targeting determinants of dosage compensation in Drosophila

The dosage compensation complex (DCC) in Drosophila melanogaster is responsible for up-regulating transcription from the single male X chromosome to equal the transcription from the two X chromosomes in females. Visualization of the DCC, a large ribonucleoprotein complex, on male larval polytene chromosomes reveals that the complex binds selectively to many interbands on the X chromosome. The targeting of the DCC is thought to be in part determined by DNA sequences that are enriched on the X. So far, lack of knowledge about DCC binding sites has prevented the identification of sequence determinants. Only three binding sites have been identified to date, but analysis of their DNA sequence did not allow the prediction of further binding sites. We have used chromatin immunoprecipitation to identify a number of new DCC binding fragments and characterized them in vivo by visualizing DCC binding to autosomal insertions of these fragments, and we have demonstrated that they possess a wide range of potential to recruit the DCC. By varying the in vivo concentration of the DCC, we provide evidence that this range of recruitment potential is due to differences in affinity of the complex to these sites. We were also able to establish that DCC binding to ectopic high-affinity sites can allow nearby low-affinity sites to recruit the complex. Using the sequences of the newly identified and previously characterized binding fragments, we have uncovered a number of short sequence motifs, which in combination may contribute to DCC recruitment. Our findings suggest that the DCC is recruited to the X via a number of binding sites of decreasing affinities, and that the presence of high-and moderate-affinity sites on the X may ensure that lower-affinity sites are occupied in a context-dependent manner. Our bioinformatics analysis suggests that DCC binding sites may be composed of variable combinations of degenerate motifs

The story of Volund: a translation from the oral to the visual

The story of Volund from Norse poetry was the foundation of a large scaled installation in the spring of 2014 in the online virtual world of Second Life®. The installation was created in collaboration between a storyteller and a visual designer, who are also the authors of this text. This article will discuss how the principles of oral storytelling, agency and presence were woven together to bring about a ‘story-world’ in which visitors was able to become both protagonist and storyteller through various means and devices that were put at their disposal. This process – both the theoretical considerations that played a role during the formulation of the project, as well as the strategies employed during its building – will be examined through a literature review encompassing oral storytelling and its performative aspects, the extension of these into virtual environments, Joseph Campbell’s Hero with a Thousand Faces, and a discussion of the myth of Volund himself

«Why do some patients decline eating disorder treatment”?

Spiseforstyrrelser er en alvorlig psykisk lidelse med betydelige negative konsekvenser. På tross av dette lar mange være å oppsøke behandling, takker nei til, eller dropper ut av behandling. Kvantitative studier har undersøkt hvilke variabler som kan forklare den høye forekomsten av drop-out, uten konsekvente funn. Vi har derfor valgt et mixed methods design som kombinerer kvantitative og kvalitative data for å undersøke faktorer forbundet med å takke nei til behandling for spiseforstyrrelser. Registerdata fra Avdeling for spiseforstyrrelser ved Haukeland Universitetssykehus ble analysert for å undersøke om alder, BMI, alvorlighetsgrad av spiseforstyrrelsen og komorbide psykiske lidelser var ulik mellom pasienter som takket ja til behandling sammenlignet med de som takket nei. Pasientene som valgte å takke nei til behandling hadde signifikant lavere BMI enn pasientene som takket ja. Gjennom kvalitative intervjuer med fire av de tidligere pasientene har vi utforsket hvorfor de har valgt å takke nei til behandling og hvordan de opplever behandlingstilbudet. To hovedkategorier ble identifisert: aspekter ved spiseforstyrrelsen og forhold knyttet til behandlingstilbudet. Tema i førstnevnte kategori omhandlet manglende bevissthet rundt lidelsen, trygghet og mestring spiseforstyrrelsen gir, spiseforstyrrelsen som emosjonsregulerende mekanisme, håpløshet og tap, samt eierskap til spiseforstyrrelsen og behandlingen. Aspektene relatert til behandlingstilbudet omhandlet manglende fleksibilitet og et ønske om å jobbe for å finne motivasjon. Resultatene viste at deltakerne opplevde at aspekter ved spiseforstyrrelsen og dens funksjon gjorde det vanskelig å takke ja til behandling. På bakgrunn av resultatene foreslår vi at behandlere er spesielt oppmerksomme på ambivalens. Spesifikt fremstår det sentralt å validere spiseforstyrrelsens funksjon for den enkelte pasient, samtidig som en hjelper pasienten til å se og formulere tydelig for seg selv hvilke negative konsekvenser det har å leve med spiseforstyrrelsen.Eating disorders are considered a serious mental illness with severe negative consequences. Despite this, many do not seek treatment, decline treatment or drop out of treatment. Quantitative research has not succeeded in finding variables consistently explaining this high prevalence of drop-out before and during treatment. Therefore, we have chosen a mixed methods design combining quantitative and qualitative data to investigate factors associated with declining treatment for eating disorders. Register data from the Department of Eating Disorders at Haukeland University Hospital were analyzed to see if age, BMI, severity of the eating disorder or comorbid mental disorders were different for patients who agreed to treatment compared to those who declined. At a group level, patients who declined treatment had a significantly lower BMI compared to patients who accepted. Through qualitative in-depth interviews with four of the previous patients, we have explored why they chose to decline treatment and how they experience the current treatment offer. Two main categories of themes were identified, respectively aspects of the eating disorder, and conditions related to the treatment offer. Themes in the former relate to lack of awareness, the coping and security that the eating disorder provides, the eating disorder as a means to regulate emotions, hopelessness and loss, and the need for autonomy and ownership of the eating disorder. The aspects related to the treatment offer dealt with a lack of flexibility and a desire to work to find motivation. The results indicate that the participants experienced that the aspects and function of the eating disorder made it difficult to accept treatment. Based on the results, we suggest that therapists pay special attention to ambivalence in eating disorder treatment. Specifically, it is important to validate the eating disorder's function for the individual patient while at the same time helping the patient to see and formulate clearly for themselves what negative consequences living with the eating disorder has.Hovedoppgave psykologprogrammetPROPSY317PRPSY

Cumulative contributions of weak DNA determinants to targeting the Drosophila dosage compensation complex

Fine-tuning of X chromosomal gene expression in Drosophila melanogaster involves the selective interaction of the Dosage Compensation Complex (DCC) with the male X chromosome, in order to increase the transcription of many genes. However, the X chromosomal DNA sequences determining DCC binding remain elusive. By adapting a ‘one-hybrid’ assay, we identified minimal DNA elements that direct the interaction of the key DCC subunit, MSL2, in cells. Strikingly, several such novel MSL2 recruitment modules have very different DNA sequences. The assay revealed a novel, 40 bp DNA element that is necessary for recruitment of DCC to an autosomal binding site in flies in the context of a longer sequence and sufficient by itself to direct recruitment if trimerized. Accordingly, recruitment of MSL2 to the single 40 bp element in cells was weak, but as a trimer approached the power of the strongest DCC recruitment site known to date, the roX1 DH site. This element is the shortest MSL2 recruitment sequence known to date. The results support a model for MSL2 recruitment according to which several different, degenerate sequence motifs of variable affinity cluster and synergise to form a high affinity site

The DNA binding CXC domain of MSL2 is required for faithful targeting the Dosage Compensation Complex to the X chromosome

Dosage compensation in Drosophila melanogaster involves the selective targeting of the male X chromosome by the dosage compensation complex (DCC) and the coordinate, ∼2-fold activation of most genes. The principles that allow the DCC to distinguish the X chromosome from the autosomes are not understood. Targeting presumably involves DNA sequence elements whose combination or enrichment mark the X chromosome. DNA sequences that characterize ‘chromosomal entry sites’ or ‘high-affinity sites’ may serve such a function. However, to date no DNA binding domain that could interpret sequence information has been identified within the subunits of the DCC. Early genetic studies suggested that MSL1 and MSL2 serve to recognize high-affinity sites (HAS) in vivo, but a direct interaction of these DCC subunits with DNA has not been studied. We now show that recombinant MSL2, through its CXC domain, directly binds DNA with low nanomolar affinity. The DNA binding of MSL2 or of an MSL2–MSL1 complex does not discriminate between different sequences in vitro, but in a reporter gene assay in vivo, suggesting the existence of an unknown selectivity cofactor. Reporter gene assays and localization of GFP-fusion proteins confirm the important contribution of the CXC domain for DCC targeting in vivo

Global Analysis of the Relationship between JIL-1 Kinase and Transcription

The ubiquitous tandem kinase JIL-1 is essential for Drosophila development. Its role in defining decondensed domains of larval polytene chromosomes is well established, but its involvement in transcription regulation has remained controversial. For a first comprehensive molecular characterisation of JIL-1, we generated a high-resolution, chromosome-wide interaction profile of the kinase in Drosophila cells and determined its role in transcription. JIL-1 binds active genes along their entire length. The presence of the kinase is not proportional to average transcription levels or polymerase density. Comparison of JIL-1 association with elongating RNA polymerase and a variety of histone modifications suggests two distinct targeting principles. A basal level of JIL-1 binding can be defined that correlates best with the methylation of histone H3 at lysine 36, a mark that is placed co-transcriptionally. The additional acetylation of H4K16 defines a second state characterised by approximately twofold elevated JIL-1 levels, which is particularly prominent on the dosage-compensated male X chromosome. Phosphorylation of the histone H3 N-terminus by JIL-1 in vitro is compatible with other tail modifications. In vivo, phosphorylation of H3 at serine 10, together with acetylation at lysine 14, creates a composite histone mark that is enriched at JIL-1 binding regions. Its depletion by RNA interference leads to a modest, but significant, decrease of transcription from the male X chromosome. Collectively, the results suggest that JIL-1 participates in a complex histone modification network that characterises active, decondensed chromatin. We hypothesise that one specific role of JIL-1 may be to reinforce, rather than to establish, the status of active chromatin through the phosphorylation of histone H3 at serine 10

The Chromosomal High-Affinity Binding Sites for the Drosophila Dosage Compensation Complex

Dosage compensation in male Drosophila relies on the X chromosome–specific recruitment of a chromatin-modifying machinery, the dosage compensation complex (DCC). The principles that assure selective targeting of the DCC are unknown. According to a prevalent model, X chromosome targeting is initiated by recruitment of the DCC core components, MSL1 and MSL2, to a limited number of so-called “high-affinity sites” (HAS). Only very few such sites are known at the DNA sequence level, which has precluded the definition of DCC targeting principles. Combining RNA interference against DCC subunits, limited crosslinking, and chromatin immunoprecipitation coupled to probing high-resolution DNA microarrays, we identified a set of 131 HAS for MSL1 and MSL2 and confirmed their properties by various means. The HAS sites are distributed all over the X chromosome and are functionally important, since the extent of dosage compensation of a given gene and its proximity to a HAS are positively correlated. The sites are mainly located on non-coding parts of genes and predominantly map to regions that are devoid of nucleosomes. In contrast, the bulk of DCC binding is in coding regions and is marked by histone H3K36 methylation. Within the HAS, repetitive DNA sequences mainly based on GA and CA dinucleotides are enriched. Interestingly, DCC subcomplexes bind a small number of autosomal locations with similar features