Ursäkten hjälper ingen, åtgärden hjälper alla! - Kriskommunikation för ett återupprättat kundförtroende

Nyckelord: Skandal, ursäkt, ansvar, kundförtroende, åtgärd Syfte: Denna uppsats vill skapa en bättre förståelse för hur företag bör uttrycka sig i media efter en skandal, för att bättre möta det som konsumenterna efterfrågar av dessa uttalanden. Syftet med denna uppsats är därmed att hjälpa företag att förbättra sina uttalanden vid skandaler och därmed lyckas bättre med sin krishantering. Metod: Studien baseras på kvalitativa studier med en dokumentanalys av företags uttalanden i media, en ostrukturerad intervju samt tre stycken fokusgruppsintervjuer. Teori: Det teoretiska materialet som har använts har presenterat tidigare forskning som redogjort för hur företag bör uttala sig vid en skandal, för att återfå konsumenters förtroende. Det har även tagits upp teorier kring bland annat kriskommunikation, etik och kundlojalitet. Slutsats: Denna studie har tydliggjort när ursäkten är viktig i ett företags uttalande och vad som gör den trovärdig. Ursäktens betydelse har även ifrågasatts och det har framgått för den inte har lika stor påverkan på konsumenternas förtroende. Vikten av åtgärden, för att återfå konsumenternas förtroende har även belysts. Andra faktorer som kan påverka hur företags uttalanden mottas av konsumenterna har också framgått, som att planera uttalandet i förväg och att anpassa uttalandet efter det kundsegment företaget har. En annan faktor som har visat sig påverka hur uttalandena mottas av konsumenterna är hur pass hög moral de har, hur lojala de är samt hur känslomässigt nära de uppfattar problemet som orsakat skandalen

Vad styr anställdas ansträngningsnivå?- En kvantitativ undersökning inom den akademiska världen

Syfte: Undersöka lönens påverkan på agentens ansträngning beroende på agentens position i karriären. Hypoteser: 1: Det finns en negativ korrelation mellan lön och ansträngning. 2: Det finns en negativ korrelation mellan position i karriären och ansträngning. Metod: Studien har antagit en tvärsnittlig forskningsdesign genom en deduktiv ansats. Datainsamlingen har skett genom en enkätundersökning som bestod av 8 frågor och mätte relationen mellan lön, ansträngning och position i karriären samt hur respondenterna prioriterar vissa aspekter i sina liv. Resultatet analyserades genom korrelationstest och korstabeller. Teoretiskt perspektiv: Uppsatsen lägger ett kritiskt perspektiv på principal-agentteorin genom att ta hänsyn till andra aspekter än lön och ansträngning. Teori som tas upp behandlar kontrollfokus, jobbtillfredsställelse, inre och yttre motivation, förväntan, personliga aspekter samt framtida och föregående utdelning. Empiriskt område: Det empiriska området som valts till undersökningen är den akademiska världen. Urvalet har begränsats till doktorander, lektorer, docenter och professorer på två av Lunds universitets fakulteter. Valet av den akademiska världen grundades utifrån dess höga ansträngningsnivå i sitt arbete, samt att det finns tydliga karriärssteg i form av hierarkiska titlar. Slutsats: Uppsatsens båda hypoteser visar på en negativ korrelation, varav hypotes 1 är signifikant och hypotes 2 delvis är signifikant. Agenten styrs av både inre och yttre motivation vilket gör att crowding out uppstår som bidrar till att det skapas en negativ korrelation mellan lön och ansträngning. Uppsatsens andra hypotes, som består av tre dimensioner, kan accepteras utifrån ett tidsperspektiv. Således visar det på att det framförallt är agentens position i karriären ur ett tidsperspektiv, som styr agentens ansträngningsnivå.Purpose: Investigate the wage’s impact on the agent’s effort depending on the agent’s position in the career. Hypotheses: 1: There exists a negative correlation between wage and effort. 2: There exists a negative correlation between position in the career and effort. Methodology: The study used a cross-sectional research design in the form of a deductive approach. The data has been sampled through a survey. The questionnaire had 8 questions and measured the relation between wage, effort and position in the career, and how the respondents prioritise certain aspects in their lives. The result was examined by correlation tests and contingency tables. Theoretical perspectives: The essay has a critical perspective of Agency Theory, by not only looking at wage and effort, but by looking at other aspects as well. Other theories discuss locus of control, work satisfaction, intrinsic and extrinsic motivation, expectancy, aspects of one’s personality and forward and backward attribution. Empirical foundation: The empirical area we chose to examine is the academic world. The sample includes PhD students, lecturers, docents and professors from two faculties at Lund University. The academic world was chosen because of its high effort level at work, and its distinct career steps in the form of hierarchical titles. Conclusions: Both of the essay’s hypotheses shows a negative correlation: the first hypothesis being significant and the second hypothesis only partly significant. The agent is guided by both intrinsic and extrinsic motivation which creates a crowding out effect that contributes to create the negative correlation between wage and effort. The essay’s second hypothesis consists of three dimensions, where the hypothesis only can be accepted from a time perspective. Consequently this result shows that the agent’s position in the career, from a time perspective, influences the agent’s effort level

Impact of Birth Weight and Early Infant Weight Gain on Insulin Resistance and Associated Cardiovascular Risk Factors in Adolescence

BACKGROUND: Low birth weight followed by accelerated weight gain during early childhood has been associated with adverse metabolic and cardiovascular outcomes later in life. The aim of this study was to examine the impact of early infant weight gain on glucose metabolism and cardiovascular risk factors in adolescence and to study if the effect differed between adolescents born small for gestational age (SGA) vs. appropriate for gestational age (AGA). METHODOLOGY/PRINCIPAL FINDINGS: Data from 30 SGA and 57 AGA healthy young Danish adolescents were analysed. They had a mean age of 17.6 years and all were born at term. Data on early infant weight gain from birth to three months as well as from birth to one year were available in the majority of subjects. In adolescence, glucose metabolism was assessed by a simplified intravenous glucose tolerance test and body composition was assessed by dual-energy X-ray absorptiometry. Blood pressures as well as plasma concentrations of triglycerides and cholesterol were measured. Early infant weight gain from birth to three months was positively associated with the fasting insulin concentration, HOMA-IR, basal lipid levels and systolic blood pressure at 17 years. There was a differential effect of postnatal weight gain on HOMA-IR in AGA and SGA participants (P for interaction = 0.03). No significant associations were seen between postnatal weight gain and body composition or parameters of glucose metabolism assessed by the simplified intravenous glucose tolerance test. In subgroup analysis, all associations with early infant weight gain were absent in the AGA group, but the associations with basal insulin and HOMA-IR were still present in the SGA group. CONCLUSION: This study suggests that accelerated growth during the first three months of life may confer an increased risk of later metabolic disturbances--particularly of glucose metabolism--in individuals born SGA

Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation.

GWAS have identified a breast cancer susceptibility locus on 2q35. Here we report the fine mapping of this locus using data from 101,943 subjects from 50 case-control studies. We genotype 276 SNPs using the 'iCOGS' genotyping array and impute genotypes for a further 1,284 using 1000 Genomes Project data. All but two, strongly correlated SNPs (rs4442975 G/T and rs6721996 G/A) are excluded as candidate causal variants at odds against >100:1. The best functional candidate, rs4442975, is associated with oestrogen receptor positive (ER+) disease with an odds ratio (OR) in Europeans of 0.85 (95% confidence interval=0.84-0.87; P=1.7 × 10(-43)) per t-allele. This SNP flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5 (encoding insulin-like growth factor-binding protein 5) and displays allele-specific gene expression, FOXA1 binding and chromatin looping. Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5, a gene with known roles in breast cell biology

The impact of coding germline variants on contralateral breast cancer risk and survival

Evidence linking coding germline variants in breast cancer (BC)-susceptibility genes other than BRCA1, BRCA2, and CHEK2 with contralateral breast cancer (CBC) risk and breast cancer-specific survival (BCSS) is scarce. The aim of this study was to assess the association of protein-truncating variants (PTVs) and rare missense variants (MSVs) in nine known (ATM, BARD1, BRCA1, BRCA2, CHEK2, PALB2, RAD51C, RAD51D, and TP53) and 25 suspected BC-susceptibility genes with CBC risk and BCSS. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated with Cox regression models. Analyses included 34,401 women of European ancestry diagnosed with BC, including 676 CBCs and 3,449 BC deaths; the median follow-up was 10.9 years. Subtype analyses were based on estrogen receptor (ER) status of the first BC. Combined PTVs and pathogenic/likely pathogenic MSVs in BRCA1, BRCA2, and TP53 and PTVs in CHEK2 and PALB2 were associated with increased CBC risk [HRs (95% CIs): 2.88 (1.70–4.87), 2.31 (1.39–3.85), 8.29 (2.53–27.21), 2.25 (1.55–3.27), and 2.67 (1.33–5.35), respectively]. The strongest evidence of association with BCSS was for PTVs and pathogenic/likely pathogenic MSVs in BRCA2 (ER-positive BC) and TP53 and PTVs in CHEK2 [HRs (95% CIs): 1.53 (1.13–2.07), 2.08 (0.95–4.57), and 1.39 (1.13–1.72), respectively, after adjusting for tumor characteristics and treatment]. HRs were essentially unchanged when censoring for CBC, suggesting that these associations are not completely explained by increased CBC risk, tumor characteristics, or treatment. There was limited evidence of associations of PTVs and/or rare MSVs with CBC risk or BCSS for the 25 suspected BC genes. The CBC findings are relevant to treatment decisions, follow-up, and screening after BC diagnosis.</p

Modeling geographic vaccination strategies for COVID-19 in Norway.

Vaccination was a key intervention in controlling the COVID-19 pandemic globally. In early 2021, Norway faced significant regional variations in COVID-19 incidence and prevalence, with large differences in population density, necessitating efficient vaccine allocation to reduce infections and severe outcomes. This study explored alternative vaccination strategies to minimize health outcomes (infections, hospitalizations, ICU admissions, deaths) by varying regions prioritized, extra doses prioritized, and implementation start time. Using two models (individual-based and meta-population), we simulated COVID-19 transmission during the primary vaccination period in Norway, covering the first 7 months of 2021. We investigated alternative strategies to allocate more vaccine doses to regions with a higher force of infection. We also examined the robustness of our results and highlighted potential structural differences between the two models. Our findings suggest that early vaccine prioritization could reduce COVID-19 related health outcomes by 8% to 20% compared to a baseline strategy without geographic prioritization. For minimizing infections, hospitalizations, or ICU admissions, the best strategy was to initially allocate all available vaccine doses to fewer high-risk municipalities, comprising approximately one-fourth of the population. For minimizing deaths, a moderate level of geographic prioritization, with approximately one-third of the population receiving doubled doses, gave the best outcomes by balancing the trade-off between vaccinating younger people in high-risk areas and older people in low-risk areas. The actual strategy implemented in Norway was a two-step moderate level aimed at maintaining the balance and ensuring ethical considerations and public trust. However, it did not offer significant advantages over the baseline strategy without geographic prioritization. Earlier implementation of geographic prioritization could have more effectively addressed the main wave of infections, substantially reducing the national burden of the pandemic

Genome-wide meta-analyses reveal novel loci for verbal short-term memory and learning

Understanding the genomic basis of memory processes may help in combating neurodegenerative disorders. Hence, we examined the associations of common genetic variants with verbal short-term memory and verbal learning in adults without dementia or stroke (N = 53,637). We identified novel loci in the intronic region of CDH18, and at 13q21 and 3p21.1, as well as an expected signal in the APOE/APOC1/TOMM40 region. These results replicated in an independent sample. Functional and bioinformatic analyses supported many of these loci and further implicated POC1. We showed that polygenic score for verbal learning associated with brain activation in right parieto-occipital region during working memory task. Finally, we showed genetic correlations of these memory traits with several neurocognitive and health outcomes. Our findings suggest a role of several genomic loci in verbal memory processes.Peer reviewe

Association of the CHEK2 c.1100delC variant, radiotherapy, and systemic treatment with contralateral breast cancer risk and breast cancer-specific survival

Background: Breast cancer (BC) patients with a germline CHEK2 c.1100delC variant have an increased risk of contralateral BC (CBC) and worse BC-specific survival (BCSS) compared to non-carriers.Aim: To assessed the associations of CHEK2 c.1100delC, radiotherapy, and systemic treatment with CBC risk and BCSS.Methods: Analyses were based on 82,701 women diagnosed with a first primary invasive BC including 963 CHEK2 c.1100delC carriers; median follow-up was 9.1 years. Differential associations with treatment by CHEK2 c.1100delC status were tested by including interaction terms in a multivariable Cox regression model. A multi-state model was used for further insight into the relation between CHEK2 c.1100delC status, treatment, CBC risk and death. Results: There was no evidence for differential associations of therapy with CBC risk by CHEK2 c.1100delC status. The strongest association with reduced CBC risk was observed for the combination of chemotherapy and endocrine therapy [HR (95% CI): 0.66 (0.55-0.78)]. No association was observed with radiotherapy.Results from the multi-state model showed shorter BCSS for CHEK2 c.1100delC carriers versus non-carriers also after accounting for CBC occurrence [HR (95% CI): 1.30 (1.09-1.56)].Conclusion: Systemic therapy was associated with reduced CBC risk irrespective of CHEK2 c.1100delC status. Moreover, CHEK2 c.1100delC carriers had shorter BCSS, which appears not to be fully explained by their CBC risk.Peer reviewe

Evidence that the 5p12 Variant rs10941679 Confers Susceptibility to Estrogen Receptor-Positive Breast Cancer through FGF10 and MRPS30 Regulation

Genome-wide association studies (GWASs) have revealed increased breast cancer risk associated with multiple genetic variants at 5p12. Here, we report the fine mapping of this locus using data from 104,660 subjects from 50 case-control studies in the Breast Cancer Association Consortium (BCAC). With data for 3,365 genotyped and imputed SNPs across a 1 Mb region (positions 44,394,495–45,364,167; NCBI build 37), we found evidence for at least three independent signals: the strongest signal, consisting of a single SNP rs10941679, was associated with risk of estrogen receptor-positive (ER+) breast cancer (per-g allele OR ER+ = 1.15; 95% CI 1.13–1.18; p = 8.35 × 10−30). After adjustment for rs10941679, we detected signal 2, consisting of 38 SNPs more strongly associated with ER-negative (ER−) breast cancer (lead SNP rs6864776: per-a allele OR ER− = 1.10; 95% CI 1.05–1.14; p conditional = 1.44 × 10−12), and a single signal 3 SNP (rs200229088: per-t allele OR ER+ = 1.12; 95% CI 1.09–1.15; p conditional = 1.12 × 10−05). Expression quantitative trait locus analysis in normal breast tissues and breast tumors showed that the g (risk) allele of rs10941679 was associated with increased expression of FGF10 and MRPS30. Functional assays demonstrated that SNP rs10941679 maps to an enhancer element that physically interacts with the FGF10 and MRPS30 promoter regions in breast cancer cell lines. FGF10 is an oncogene that binds to FGFR2 and is overexpressed in ∼10% of human breast cancers, whereas MRPS30 plays a key role in apoptosis. These data suggest that the strongest signal of association at 5p12 is mediated through coordinated activation of FGF10 and MRPS30, two candidate genes for breast cancer pathogenesis

Rare germline copy number variants (CNVs) and breast cancer risk.

Funder: CIHRGermline copy number variants (CNVs) are pervasive in the human genome but potential disease associations with rare CNVs have not been comprehensively assessed in large datasets. We analysed rare CNVs in genes and non-coding regions for 86,788 breast cancer cases and 76,122 controls of European ancestry with genome-wide array data. Gene burden tests detected the strongest association for deletions in BRCA1 (P = 3.7E-18). Nine other genes were associated with a p-value < 0.01 including known susceptibility genes CHEK2 (P = 0.0008), ATM (P = 0.002) and BRCA2 (P = 0.008). Outside the known genes we detected associations with p-values < 0.001 for either overall or subtype-specific breast cancer at nine deletion regions and four duplication regions. Three of the deletion regions were in established common susceptibility loci. To the best of our knowledge, this is the first genome-wide analysis of rare CNVs in a large breast cancer case-control dataset. We detected associations with exonic deletions in established breast cancer susceptibility genes. We also detected suggestive associations with non-coding CNVs in known and novel loci with large effects sizes. Larger sample sizes will be required to reach robust levels of statistical significance