‘Happy Families?’: Single Mothers, the Press and the Politicians

FOR THOSE OF US who have been following how lone parents are represented in media and political debates over the last few years, the shift was all too apparent. By Spring 1997, the political scapegoating of single mothers as being responsible for tearing apart the moral fabric of society had become less frequent; tabloid headlines which screamed ‘family breakdown’, ‘scroungers' and ‘welfare benefit crisis' appeared less often; and many politicians had started to project themselves as, at the least, concerned about the welfare of lone parents and their children. Surprising really, that is, until we remember the backdrop—the UK General Election and 1.3 million UK lone parent voters. By April 1997, a growing backlash against the more extreme and pathologising accusations against single mothers had rendered explicit vilification unacceptable. To pull votes a different sort of language had to come into play—one which didn't risk turning off the electorate but would still allow a freezing or cutting of welfare spending on lone parent families. Since it was now politically inexpedient to engage in vitriolic attack, there emerged a new discourse—one which reappropriated and redefined lone parents as chief targets of government aid. Close scrutiny of the texts circulating from 1992 to the time of the General Election offers insights of how policy agendas, political rhetoric and news interweave to construct a definition of lone parents which bears little resemblance to how they may see themselves

A comprehensive 1,000 Genomes-based genome-wide association meta-analysis of coronary artery disease

Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largely based on genome-wide association study (GWAS) analysis of common SNPs. Leveraging phased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of similar to 185,000 CAD cases and controls, interrogating 6.7 million common (minor allele frequency (MAF) > 0.05) and 2.7 million low-frequency (0.005 < MAF < 0.05) variants. In addition to confirming most known CAD-associated loci, we identified ten new loci (eight additive and two recessive) that contain candidate causal genes newly implicating biological processes in vessel walls. We observed intralocus allelic heterogeneity but little evidence of low-frequency variants with larger effects and no evidence of synthetic association. Our analysis provides a comprehensive survey of the fine genetic architecture of CAD, showing that genetic susceptibility to this common disease is largely determined by common SNPs of small effect size