The citizen's voice : Albert Hirschman's Exit, Voice and Loyalty and its contribution to media citizenship debates

This paper analyses Albert Hirschman's Exit, Voice and Loyalty (Hirschman 1970) as a basis for understanding the relationship between media and citizenship. It considers the significance of Hirschman's concept of voice in relation to media policy, media participation through user-created content, and the rise of 'citizen media' and 'citizen journalism'. It associates these developments with a 'de-centering' of both media practice and media studies, as considered by Couldry (2006a, 2006b). It concludes by suggesting that voice and participation, rather than citizenship, may constitute a more suitable foundation for understanding new digital media initiatives.

Albert Namatjira: copyright estates and traditional knowledge

Albert Namatjira was Australia's first Indigenous professional artist. He adapted Western-style painting to express his cultural knowledge of the Arrernte country, for which he was a traditional custodian. In his lifetime, Albert Namatjira achieved great acclaim for his exceptional ability as an artist. However, after his untimely death, he was ignored by the mainstream Australian art world, because of the aesthetic prejudices and social policies of the time. A recent exhibition entitled Seeing the Centre: The art of Albert Namatjira (1902-1959) curated by Alison French has sought to redress this neglect, and provide a retrospective of his work. The exhibition has brought to light that the copyright in the artistic works of Albert Namatjira has not been passed onto his family descendants. In June 1957, Namatjira entered into a copyright agreement with John Brackenreg, the owner of a publishing company by the name of Legend Press, and the associated Artarmon Galleries in Sydney. It was agreed that Legend Press would pay royalties to Namatjira for the sole right to reproduce all of his paintings. Following Namatjira's death in 1959, the administration of his estate passed to the Public Trustee for the Northern Territory Government. The Public Trustee of the Northern Territory Government authorised the sale of Namatjira's copyright to Legend Press in 1983, thereby ending the ability of the descendents of Namatjira to benefit from on-going income from the reproduction of his works. Senator Aden Ridgeway of the Democrats has called on the Federal Government to enter into discussions with the Northern Territory Government to buy back the copyright in Albert Namatjira's works. He argued that exclusive control of the use and reproduction of his works should be restored to his descendants, as well as the receipt of all financial benefits that result from the use and reproduction of his works under copyright protection. The Senator said: 'By doing this, we will all be rewarded, because finally, belatedly, we will be showing Albert Namatjira the reverence that he has always deserved. We will be protecting his legacy for future generations'.

Corrections: Association of variants in MMEL1 and CTLA4 with rheumatoid arthritis in the Han Chinese population (Annals of the Rheumatic Diseases (2011) 70, (1793-1797))

Patrick Danoy, Meng Wei, Hadler Johanna, et al. Association of variants in MMEL1 and CTLA4 with rheumatoid arthritis in the Han Chinese population. Ann Rheum Dis 2011;70:1793–97. The following authors were listed as contributing equally to the study...

Genetic studies of body mass index yield new insights for obesity biology

Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10−8), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ~2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.

FTO genotype is associated with phenotypic variability of body mass index

There is evidence across several species for genetic control of phenotypic variation of complex traits1, 2, 3, 4, such that the variance among phenotypes is genotype dependent. Understanding genetic control of variability is important in evolutionary biology, agricultural selection programmes and human medicine, yet for complex traits, no individual genetic variants associated with variance, as opposed to the mean, have been identified. Here we perform a meta-analysis of genome-wide association studies of phenotypic variation using ~170,000 samples on height and body mass index (BMI) in human populations. We report evidence that the single nucleotide polymorphism (SNP) rs7202116 at the FTO gene locus, which is known to be associated with obesity (as measured by mean BMI for each rs7202116 genotype)5, 6, 7, is also associated with phenotypic variability. We show that the results are not due to scale effects or other artefacts, and find no other experiment-wise significant evidence for effects on variability, either at loci other than FTO for BMI or at any locus for height. The difference in variance for BMI among individuals with opposite homozygous genotypes at the FTO locus is approximately 7%, corresponding to a difference of ~0.5 kilograms in the standard deviation of weight. Our results indicate that genetic variants can be discovered that are associated with variability, and that between-person variability in obesity can partly be explained by the genotype at the FTO locus. The results are consistent with reported FTO by environment interactions for BMI8, possibly mediated by DNA methylation9, 10. Our BMI results for other SNPs and our height results for all SNPs suggest that most genetic variants, including those that influence mean height or mean BMI, are not associated with phenotypic variance, or that their effects on variability are too small to detect even with samples sizes greater than 100,000.