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Responses by peripheral blood leukocytes may contribute to the pathogenesis of dengue hemorrhagic fever (DHF). We used DNA microarrays to reveal transcriptional patterns in the blood of 14 adults with DHF. Acute DHF was defined by an abundance of transcripts from cell cycle- and endoplasmic reticulum (ER)-related genes, suggesting a proliferative response accompanied by ER stress. Transcript-abundance levels for immunoresponse-associated genes, including cell surface markers, immunoglobulin, and innate response elements, were also elevated. Twenty-four genes were identified for which transcript abundance distinguished patients with dengue shock syndrome (DSS) from those without DSS. All the gene transcripts associated with DSS, many of which are induced by type I interferons, were less abundant in patients with DSS than in those without DSS. To our knowledge, these data provide the first snapshot of gene-expression patterns in peripheral blood during acute dengue and suggest that DSS is associated with attenuation of selected aspects of the innate host response.

For too many Scots, the existing economic model is failing. Far from improving their lives, it traps them in a cycle of economic hardship. Yet it is possible to overcome poverty, both in Scotland and across the UK - many of the solutions already exist, hidden within the very communities hit hardest by an economic model that worships at the altar of ‘economic growth’. The extraordinary work of our partners in Scotland has helped frame this report, where we hope to show how allocating resources in a more effective and sustainable way can deliver lasting change. In this paper we argue that the Scottish economy must pursue policies which deliver for the people, and policy-makers must play a central and driving role as underwriters of community solutions. Some of our recommendations include: - Build on the National Performance Framework and the Oxfam Humankind Index to create a better way of measuring our collective prosperity. - Create a Poverty Commissioner to ensure spending decisions are poverty proofed and to support communities to challenge Government policies and private sector actions that do not contribute to socio-economic equality. - Employers in the public and private sectors should pay a living wage. - Tax havens, offshore earnings and loopholes which allow avoidance, should be pursued and closed. Business support, corporate social responsibility awards and government plaudits should be contingent on companies meeting their tax obligations. - A Sustainable Livelihoods Approach (SLA) to social protection should be pursued. This would recognise complex barriers to work, gender differences and caring responsibilities as well as rewarding individuals’ range of skills and contributions (including activities that deliver social benefit but are currently insufficiently valued by the market). - Funding is required to make it easier for deprived communities to own assets for local benefit. As part of a socio-economic duty, council staff should support deprived communities prepare for ownership, with upfront grants enabling communities to assess the merits of an opportunity.

Whether codon usage fine-tunes mRNA translation in mammals remains controversial, with recent papers suggesting that production of proteins in specific Gene Ontological (GO) pathways can be regulated by actively modifying the codon and anticodon pools in different cellular conditions. In this work, we compared the sequence content of genes in specific GO categories with the exonic genome background. Although a substantial fraction of variability in codon usage could be explained by random sampling, almost half of GO sets showed more variability in codon usage than expected by chance. Nevertheless, by quantifying translational efficiency in healthy and cancerous tissues in human and mouse, we demonstrated that a given tRNA pool can equally well translate many different sets of mRNAs, irrespective of their cell-type specificity. This disconnect between variations in codon usage and the stability of translational efficiency is best explained by differences in GC content between gene sets. GC variation across the mammalian genome is most likely a result of the interplay between genome repair and gene duplication mechanisms, rather than selective pressures caused by codon-driven translational rates. Consequently, codon usage differences in mammalian transcriptomes are most easily explained by well-understood mutational biases acting on the underlying genome.