In this article we examine the marketing representations of the Toyota Prius, the first 'green' massproduced automobile. Drawing on an interpretive analysis of Prius print advertisements in Canadian publications between 2006-2011 and a matched sample of other automobile advertisements, we observe how the Prius advertisements invoke imagination and how this process is channelled, via the integration of text and images offered in the advertising space, to particular themes and ideas. Through the use of an ambiguous system of signs, audiences are invited to imagine and thereby co-create the significance of hybrid electric vehicles. Three areas of imagining are emphasized by the advertisement structure-nature, harmony and agency-and we analyze these imaginings as potential moments of knowledge creation about climate change. We examine how the activity of imagining in relation to these three areas influences viewers' knowledge and perception of climate change as well as their sense of responsibility for anthropogenic climate change. We discuss the consequences of using ambiguous messages to promote socially and politically charged products for consumers' understanding and imagination.To say that we are a consumer culture means that our central shared values have to do with consumption. Accordingly, a consumer culture has effects far beyond actual consumption and its associated advertising.

Background GNE myopathy is a rare genetic disease characterized by progressive muscle atrophy and weakness. It is caused by biallelic mutations in the GNE gene that encodes for the bifunctional enzyme, uridine diphosphate (UDP)‐N‐acetylglucosamine (GlcNAc) 2‐epimerase/N‐acetylmannosamine (ManNAc) kinase. Typical characteristics of GNE myopathy include progressive myopathy, first involving anterior tibialis muscle and sparing the quadriceps, and rimmed vacuoles on muscle biopsy. Identifying biallelic mutations by sequencing of the GNE gene confirms the diagnosis of GNE myopathy. In a subset of patients, diagnostic confirmation is challenged by the identification of mutations in only one allele, suggesting mutations in deep intronic regions or regulatory regions.MethodsWe performed targeted sequencing and copy number variant (CNV) analysis of GNE in two siblings who clinically presented with GNE myopathy. Further molecular and biochemical studies were done to characterize the effect of a previously uncharacterized GNE mutation.ResultsWe report two siblings of Indian descent with characteristic features of GNE myopathy, including progressive skeletal muscle weakness initially involving the anterior tibialis, and rimmed vacuoles on muscle biopsy, in which a heterozygous mutation, p.Val727Met, was identified in both affected siblings, but no other deleterious variants in either coding region or exon–intron boundaries of the gene. Subsequent insertion/deletion analysis identified a novel 11.3‐kb deletion (Chr9 [GRCh37]: g.36257583_36268910del) encompassing the GNE promoter region, with breakpoints residing in Alu repeats. Gene expression analysis revealed reduced GNE mRNA and protein levels, confirming decreased expression of the deleted allele harboring the deletion.ConclusionsWe have identified GNE as one of the genes susceptible to Alu‐mediated recombination. Our findings suggest that the deletion may encompass the promoter or another region necessary for GNE expression. In patients with typical manifestations of GNE myopathy and a single GNE variant identified, copy number variant (CNV) analysis may be useful in arriving at the diagnosis.

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