In PLOS Genetics, researchers from Sweden, the UK, Estonia, and the US describe four lipid-related metabolites with shifts in blood levels linked to coronary heart disease. The team used mass spectrometry to profile metabolomics patterns in samples from more than 1,000 individuals enrolled in the Uppsala Longitudinal Study of Adult Men. When they compared metabolomics patterns in samples from the 131 individuals who developed heart disease over around 10 years of follow-up with those who didn't, the investigators narrowed in a few dozen metabolites with apparent ties to coronary heart disease risk. They subsequently verified associations for four markers using data for almost 1,700 individuals with or without heart disease. GenomeWeb has more on the study here.
Despite some batch-to-batch expression differences related to experimental conditions, a new meta-analysis suggests two fish model organisms tend to show relatively high levels of transcriptomic conservation. As it reported in PLOS One, a team from the US Environmental Protection Agency and elsewhere considered array-based expression data on ovarian tissues samples from more than 500 fathead minnows and 80 zebrafish that were untreated and had reached sexual maturity. "The high degree of conservation offers promising opportunities in not only studying fish molecular responses to environmental stressors by a comparative biology approach," the study authors say, "but also effective sharing of a large amount of existing public transcriptomics data for developing toxicogenomics applications."
For another PLOS One study, researchers from the Translational Genomics Research Institute present findings from an integrated whole-exome and transcriptomic sequencing study of X inactivation, an epigenetic process by which either the maternal or paternal copy of the X chromosome is randomly inactivated. The team applied this approach to samples from a 12-year-old girl with an undiagnosed neurobehavioral condition and her unaffected family members. The search uncovered a disease-related deletion in the X chromosome inherited from the girl's father that appeared to contribute to unusual X chromosome inactivation characteristics favoring expression of the unaffected, maternal version of the chromosome.