The Editors

Luxury industry and Corporate Social Responsibility (CSR) activates are generally considered as incompatible concepts by consumers. This because luxury is generally related to hedonism, excess, and ostentation, while CSR is generally based on sobriety, moderation and ethics. However, nowadays more and more luxury companies seem highly committed toward sustainability. For example, Tiffany started certifying its diamonds as “conflict free”, Chanel incorporated “earthy materials” in its 2016 collection, and Bulgari has recently funded restoration of Rome's Spanish Steps. Therefore, it seems plausible the presence of a certain compatibility degree between luxury and CSR activities. However, this issue has received very limited empirical investigation from marketing literature. As a consequence, the present research aims to empirically test whether and under what conditions consumers react to different kinds of luxury companies’ CSR initiatives. Using the Carroll’s four dimensions model of internal vs. external CSR, we argue and demonstrated that luxury companies’ internal (versus external) CSR initiatives increase willingness to buy luxury products, but mainly for those customers who buy luxury for internal motivations and not for status ostentation, as for example individual style and personal taste

Target genes, variants, tissues and transcriptional pathways influencing human serum urate levels.

Elevated serum urate levels cause gout and correlate with cardiometabolic diseases via poorly understood mechanisms. We performed a trans-ancestry genome-wide association study of serum urate in 457,690 individuals, identifying 183 loci (147 previously unknown) that improve the prediction of gout in an independent cohort of 334,880 individuals. Serum urate showed significant genetic correlations with many cardiometabolic traits, with genetic causality analyses supporting a substantial role for pleiotropy. Enrichment analysis, fine-mapping of urate-associated loci and colocalization with gene expression in 47 tissues implicated the kidney and liver as the main target organs and prioritized potentially causal genes and variants, including the transcriptional master regulators in the liver and kidney, HNF1A and HNF4A. Experimental validation showed that HNF4A transactivated the promoter of ABCG2, encoding a major urate transporter, in kidney cells, and that HNF4A p.Thr139Ile is a functional variant. Transcriptional coregulation within and across organs may be a general mechanism underlying the observed pleiotropy between urate and cardiometabolic traits.The Genotype-Tissue Expression (GTEx) Project was supported by the Common Fund of the Office of the Director of the National Institutes of Health, and by NCI, NHGRI, NHLBI, NIDA, NIMH, and NINDS. Variant annotation was supported by software resources provided via the Caché Campus program of the InterSystems GmbH to Alexander Teumer