How Does One "Open" Science? Questions of Value in Biological Research.

Open Science policies encourage researchers to disclose a wide range of outputs from their work, thus codifying openness as a specific set of research practices and guidelines that can be interpreted and applied consistently across disciplines and geographical settings. In this paper, we argue that this "one-size-fits-all" view of openness sidesteps key questions about the forms, implications, and goals of openness for research practice. We propose instead to interpret openness as a dynamic and highly situated mode of valuing the research process and its outputs, which encompasses economic as well as scientific, cultural, political, ethical, and social considerations. This interpretation creates a critical space for moving beyond the economic definitions of value embedded in the contemporary biosciences landscape and Open Science policies, and examining the diversity of interests and commitments that affect research practices in the life sciences. To illustrate these claims, we use three case studies that highlight the challenges surrounding decisions about how--and how best--to make things open. These cases, drawn from ethnographic engagement with Open Science debates and semistructured interviews carried out with UK-based biologists and bioinformaticians between 2013 and 2014, show how the enactment of openness reveals judgments about what constitutes a legitimate intellectual contribution, for whom, and with what implications.

Metabolizing Data in the Cloud.

Cloud-based bioinformatic platforms address the fundamental demands of creating a flexible scientific environment, facilitating data processing and general accessibility independent of a countries' affluence. These platforms have a multitude of advantages as demonstrated by omics technologies, helping to support both government and scientific mandates of a more open environment.

How Do Scientists Define Openness? Exploring the Relationship Between Open Science Policies and Research Practice.

This article documents how biomedical researchers in the United Kingdom understand and enact the idea of "openness." This is of particular interest to researchers and science policy worldwide in view of the recent adoption of pioneering policies on Open Science and Open Access by the U.K. government-policies whose impact on and implications for research practice are in need of urgent evaluation, so as to decide on their eventual implementation elsewhere. This study is based on 22 in-depth interviews with U.K. researchers in systems biology, synthetic biology, and bioinformatics, which were conducted between September 2013 and February 2014. Through an analysis of the interview transcripts, we identify seven core themes that characterize researchers' understanding of openness in science and nine factors that shape the practice of openness in research. Our findings highlight the implications that Open Science policies can have for research processes and outcomes and provide recommendations for enhancing their content, effectiveness, and implementation.

Neonatal environment exerts a sustained influence on the development of the intestinal microbiota and metabolic phenotype.

The postnatal environment, including factors such as weaning and acquisition of the gut microbiota, has been causally linked to the development of later immunological diseases such as allergy and autoimmunity, and has also been associated with a predisposition to metabolic disorders. We show that the very early-life environment influences the development of both the gut microbiota and host metabolic phenotype in a porcine model of human infants. Farm piglets were nursed by their mothers for 1 day, before removal to highly controlled, individual isolators where they received formula milk until weaning at 21 days. The experiment was repeated, to create two batches, which differed only in minor environmental fluctuations during the first day. At day 1 after birth, metabolic profiling of serum by (1)H nuclear magnetic resonance spectroscopy demonstrated significant, systemic, inter-batch variation which persisted until weaning. However, the urinary metabolic profiles demonstrated that significant inter-batch effects on 3-hydroxyisovalerate, trimethylamine-N-oxide and mannitol persisted beyond weaning to at least 35 days. Batch effects were linked to significant differences in the composition of colonic microbiota at 35 days, determined by 16 S pyrosequencing. Different weaning diets modulated both the microbiota and metabolic phenotype independently of the persistent batch effects. We demonstrate that the environment during the first day of life influences development of the microbiota and metabolic phenotype and thus should be taken into account when interrogating experimental outcomes. In addition, we suggest that intervention at this early time could provide 'metabolic rescue' for at-risk infants who have undergone aberrant patterns of initial intestinal colonisation.

Multivariate statistics and the enactment of metabolic complexity.

This ethnographic study, based on fieldwork at the Computational and Systems Medicine laboratory at Imperial College London, shows how researchers in the field of metabolomics--the post-genomic study of the molecules and processes that make up metabolism--enact and coproduce complex views of biology with multivariate statistics. From this data-driven science, metabolism emerges as a multiple, informational and statistical object, which is both produced by and also necessitates particular forms of data production and analysis. Multivariate statistics emerge as 'natural' and 'correct' ways of engaging with a metabolism that is made up of many variables. In this sense, multivariate statistics allow researchers to engage with and conceptualize metabolism, and also disease and processes of life, as complex entities. Consequently, this article builds on studies of scientific practice and visualization to examine data as material objects rather than black-boxed representations. Data practices are not merely the technological components of experimentation, but are simultaneously technologies and methods and are intertwined with ways of seeing and enacting the biological world. Ultimately, this article questions the increasing invocation and role of complexity within biology, suggesting that discourses of complexity are often imbued with reductionist and determinist ways of thinking about biology, as scientists engage with complexity in calculated and controlled, but also limited, ways.

Toll-like receptor 6 drives differentiation of tolerogenic dendritic cells and contributes to LcrV-mediated plague pathogenesis.

Educating dendritic cells (DC) to become tolerogenic DC, which promote regulatory IL-10 immune responses, represents an effective immune evasion strategy for pathogens. Yersinia pestis virulence factor LcrV is reported to induce IL-10 production via interaction with Toll-like receptor (TLR) 2. However, TLR2-/- mice are not protected against subcutaneous plague infection. Using complementary in vitro and in vivo approaches and LcrV as a model, we show that TLR6 associates with TLR2 to induce tolerogenic DC and regulatory type-1 T cells selectively secreting IL-10. In contrast, TLR1 heterodimerizes with TLR2 to promote proinflammatory IL-12p40 cytokine, producing DC and inflammatory T cell differentiation. LcrV specifically hijacks the TLR2/6 pathway to stimulate IL-10 production, which blocks host protective inflammatory responses. These results explain why TLR2 can mediate both pro- and anti-inflammatory responses and identify TLR6 as a distinct receptor driving regulatory IL-10 responses.