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The unprecedented access to consumer information through digital technologies seems to have had two unrelated consequences on markets for final goods. It has been used to enhance product innovation and accelerate commodity circulation. Building on a multi-disciplinary literature on these phenomena, from marketing and management to industrial economics, this article proposes to model them as "feedback processes" that complement one another to allow markets to expand and profit to be accumulated. We explore this hypothesis in a qualitative study of the beauty market, which shows the tight relationship between devices operationalizing innovation and circulation. [ABSTRACT FROM AUTHOR]

Introduction: We have reanalyzed the genomic data from the International Collaboration for the Genomics of HIV (ICGH), focusing on HIV-1 Elite Controllers (EC). Methods: A genome-wide association study (GWAS) was performed, comparing 543 HIV-1 EC individuals with 3,272 uninfected controls (CTR) of European ancestry. 8 million single nucleotide polymorphisms (SNPs) and HLA class I and class II gene alleles were imputed to compare EC and CTR. Results: Two thousand six hundred twenty-six SNPs were associated with EC (p<5.10-8), all located within the Major Histocompatibility Complex (MHC) region. Stepwise regression analysis narrowed this list to 17 SNPs. In parallel, 22 HLA class I and II alleles were associated with EC. Through meticulous mapping of the LD between all identified signals and employing reciprocal covariate analyses, we delineated a final set of 6 independent SNPs and 3 HLA class I gene alleles that accounted for most of the associations observed with EC. Our study revealed the presence of cumulative haploblock effects (SNP rs9264942 contributing to the HLA-B*57:01 effect) and that several HLA allele associations were in fact caused by SNPs in linkage disequilibrium (LD). Upon investigating SNPs in LD with the selected 6 SNPs and 3 HLA class I alleles for their impact on protein function (either damaging or differential expression), we identified several compelling mechanisms potentially explaining EC among which: a multi-action mechanism of HLA-B*57:01 involving MICA mutations and MICB differential expression overcoming the HIV-1 blockade of NK cell response, and overexpression of ZBTB12 with a possible anti-HIV-1 effect through HERV-K interference; a deleterious mutation in PPP1R18 favoring viral budding associated with rs1233396. Conclusion: Our results show that MHC influence on EC likely extends beyond traditional HLA class I or class II allele associations, encompassing other MHC SNPs with various biological impacts. They point to the key role of NK cells in preventing HIV-1 infection. Our analysis shows that HLA-B*57:01 is indeed associated with partially functional MICA/MICB proteins which could also explain this marker's involvement in other diseases such as psoriasis. More broadly, our findings suggest that within any HLA class I and II association in diseases, there may exist distinct causal SNPs within this crucial, gene-rich, and LD-rich MHC region. [ABSTRACT FROM AUTHOR]

Optimizations are expected in the development of immunotherapy for the treatment of Triple‐negative breast cancer (TNBC). We studied the expression of galectin‐9 (Gal‐9) after irradiation and assessed the differential impacts of its targeting with or without radiotherapy. Tumor resections from TNBC patients who received neoadjuvant radiotherapy revealed higher levels of Gal‐9 in comparison to their baseline level, only in non‐responder patients. Gal‐9 expression was also found to be increased in TNBC tumor biopsies and cell lines after irradiation. We investigated the therapeutic advantage of targeting Gal‐9 after radiotherapy in mice. Irradiated 4T1 cells or control non‐irradiated 4T1 cells were injected into BALB/c mice. Anti‐Gal‐9 antibody treatment decreased tumor progression only in mice injected with irradiated 4T1 cells. This proof‐of‐concept study demonstrates that Gal‐9 could be considered as a dynamic biomarker after radiotherapy for TNBC and suggests that Gal‐9 induced‐overexpression could represent an opportunity to develop new therapeutic strategies for TNBC patients. [ABSTRACT FROM AUTHOR]