Preservation of fatty acid signatures in three vertebrate species after six months of storage at various temperatures

Fatty acid (FA) signatures (FAS) are important tools to assess the foraging ecology of wild animals. The present study was conducted to assess how well the general FAS and the proportions of individual FA are preserved in fat samples stored at different temperatures (196, -80, -20, +4 and +20 degrees C). Using three species (laboratory rat, American mink and rainbow trout), FAS were determined immediately upon sampling. Thereafter, eight subsamples per storage temperature from the inner part of the sample unaffected by oxygen and light were re-analyzed after 1, 2, 3, 7, 28, 84 and 168 days. Each time the remaining sample was sealed in its vial after replacing air with nitrogen gas. The results were tested with the mixed model and discriminant analyses. Generally, the FAS were well preserved regardless of storage temperature, and only a few major FA showed significant changes even after the 6-month period at room temperature. After an initial first-day change in proportions, presumably due to post-mortem enzymatic activities, the remaining minor changes could not be clearly attributed to either further autolysis, decomposition or autoxidation. In the discriminant analysis, the species-specific differences dominated and remained distinct even after 6 months. Furthermore, the analysis mostly classified the samples preserved at sub- and above-freezing temperatures separate from each other, and the general deviation from the initial analysis results was present as early as after 1 day. If FAS are to be analyzed in a very precise manner, the analysis should be performed immediately upon sampling. However, FAS remain adequately reliable for long periods of time even without preservation in deep freeze, widening the availability of potential samples for studies on foraging ecology and related disciplines.Peer reviewe

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Integrative Genomics Reveals Novel Molecular Pathways and Gene Networks for Coronary Artery Disease

The majority of the heritability of coronary artery disease (CAD) remains unexplained, despite recent successes of genome-wide association studies (GWAS) in identifying novel susceptibility loci. Integrating functional genomic data from a variety of sources with a large-scale meta-analysis of CAD GWAS may facilitate the identification of novel biological processes and genes involved in CAD, as well as clarify the causal relationships of established processes. Towards this end, we integrated 14 GWAS from the CARDIoGRAM Consortium and two additional GWAS from the Ottawa Heart Institute (25,491 cases and 66,819 controls) with 1) genetics of gene expression studies of CAD-relevant tissues in humans, 2) metabolic and signaling pathways from public databases, and 3) data-driven, tissue-specific gene networks from a multitude of human and mouse experiments. We not only detected CAD-associated gene networks of lipid metabolism, coagulation, immunity, and additional networks with no clear functional annotation, but also revealed key driver genes for each CAD network based on the topology of the gene regulatory networks. In particular, we found a gene network involved in antigen processing to be strongly associated with CAD. The key driver genes of this network included glyoxalase I (GLO1) and peptidylprolyl isomerase I (PPIL1), which we verified as regulatory by siRNA experiments in human aortic endothelial cells. Our results suggest genetic influences on a diverse set of both known and novel biological processes that contribute to CAD risk. The key driver genes for these networks highlight potential novel targets for further mechanistic studies and therapeutic interventions