Ethical living: relinking ethics and consumption through care in Chile and Brazil

Mainstream conceptualizations of ‘ethical consumption’ equate the notion with conscious, individual, market-mediated choices motivated by ethical or political aims that transcend ordinary concerns. Drawing on recent sociology and anthropology of consumption literature on the links between ordinary ethics and ethical consumption, this article discusses some of the limitations of this conceptualization. Using data from 32 focus groups conducted in Chile and Brazil, we propose a conceptualization of ethical consumption that does not centre on individual, market-mediated choices but understands it at the level of practical outcomes, which we refer to as different forms of ‘ethical living’. To do that, we argue, we need to depart from the deontological understanding of ethics that underpins mainstream approaches to ethical consumption and adopt a more consequentialist view focusing on ethical outcomes. We develop these points through describing one particular ordinary moral regime that seemed to be predominant in participants’ accounts of ethics and consumption in both Chile and Brazil: one that links consumption and ethics through care. We show that the moral regime of care leads to ‘ethical outcomes’, such as energy saving or limiting overconsumption, yet contrary to the mainstream view of ethical consumption emphasizing politicized choice expressed through markets, these result from following ordinary ethics, often through routines of practices

Global analysis of DNA methylation in early-stage liver fibrosis

<p>Abstract</p> <p>Background</p> <p>Liver fibrosis is caused by chemicals or viral infection. The progression of liver fibrosis results in hepatocellular carcinogenesis in later stages. Recent studies have revealed the importance of DNA hypermethylation in the progression of liver fibrosis to hepatocellular carcinoma (HCC). However, the importance of DNA methylation in the early-stage liver fibrosis remains unclear.</p> <p>Methods</p> <p>To address this issue, we used a pathological mouse model of early-stage liver fibrosis that was induced by treatment with carbon tetrachloride (CCl₄) for 2 weeks and performed a genome-wide analysis of DNA methylation status. This global analysis of DNA methylation was performed using a combination of methyl-binding protein (MBP)-based high throughput sequencing (MBP-seq) and bioinformatic tools, IPA and Oncomine. To confirm functional aspect of MBP-seq data, we complementary used biochemical methods, such as bisulfite modification and <it>in-vitro</it>-methylation assays.</p> <p>Results</p> <p>The genome-wide analysis revealed that DNA methylation status was reduced throughout the genome because of CCl₄treatment in the early-stage liver fibrosis. Bioinformatic and biochemical analyses revealed that a gene associated with fibrosis, <it>secreted phosphoprotein 1 </it>(<it>Spp1</it>), which induces inflammation, was hypomethylated and its expression was up-regulated. These results suggest that DNA hypomethylation of the genes responsible for fibrosis may precede the onset of liver fibrosis. Moreover, <it>Spp1 </it>is also known to enhance tumor development. Using the web-based database, we revealed that <it>Spp1 </it>expression is increased in HCC.</p> <p>Conclusions</p> <p>Our study suggests that hypomethylation is crucial for the onset of and in the progression of liver fibrosis to HCC. The elucidation of this change in methylation status from the onset of fibrosis and subsequent progression to HCC may lead to a new clinical diagnosis.</p