Downhole Measurements of Shear- and Compression-Wave Velocities in Boreholes C4993, C4996, C4997 and C4998 at the Waste Treatment Plant DOE Hanford Site.

This report describes the procedures and the results of a series of downhole measurements of shear- and compression-wave velocities performed as part of the Seismic Boreholes Project at the site of the Waste Treatment Plant (WTP). The measurements were made in several stages from October 2006 through early February 2007. Although some fieldwork was carried out in conjunction with the University of Texas at Austin (UT), all data acquired by UT personnel are reported separately by that organization

The functional response of a generalist predator

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The role of parasite-driven selection in shaping landscape genomic structure in red grouse (Lagopus lagopus scotica)

Acknowledgements This study was funded by a BBSRC studentship (MAW) and NERC grants NE/H00775X/1 and NE/D000602/1 (SBP). The authors are grateful to Mario Röder and Keliya Bai for fieldwork assistance, and all estate owners, factors and keepers for access to field sites, most particularly MJ Taylor and Mike Nisbet (Airlie), Neil Brown (Allargue), RR Gledson and David Scrimgeour (Delnadamph), Andrew Salvesen and John Hay (Dinnet), Stuart Young and Derek Calder (Edinglassie), Kirsty Donald and David Busfield (Glen Dye), Neil Hogbin and Ab Taylor (Glen Muick), Alistair Mitchell (Glenlivet), Simon Blackett, Jim Davidson and Liam Donald (Invercauld), Richard Cooke and Fred Taylor† (Invermark), Shaila Rao and Christopher Murphy (Mar Lodge), and Ralph Peters and Philip Astor (Tillypronie). S.B.P. and S.M.R. conceived and designed the study. M.A.W. performed field and laboratory work. A.D. and M.C.J. developed SNP markers. M.A.W. analysed the data. M.A.W. and S.B.P. wrote the manuscript.Peer reviewedPostprin

Enteric helminths promote Salmonella co-infection by altering the intestinal metabolome

Intestinal helminth infections occur pre dominantly in regions where exposure to enteric bacterial pathogens is also common. Helminth infections inhibit host immunity against microbial pathogens, which has largely been attributed to the induction of regulatory or type 2 (Th2) immune responses. Here we demonstrate an additional three-way interaction in which helminth infection alters the metabolic environment of the host intestine to enhance bacterial pathogenicity. We show that an ongoing helminth infection increased colonization by Salmonella independently of T regulatory or Th2 cells. Instead, helminth infection altered the metabolic profile of the intestine, which directly enhanced bacterial expression of Salmonella pathogenicity island 1 (SPI-1) genes and increased intracellular invasion. These data reveal a novel mechanism by which a helminth-modified metabolome promotes susceptibility to bacterial co-infection

The conundrum of agenda-driven science in conservation

Conservation biology is a value-laden discipline predicated on conserving biodiversity (Soulé 1985), a mission that does not always sit easily with objective science (Lackey 2007; Pielke 2007; Scott et al. 2007). While some encourage scientists to be responsible advocates for conservation (Garrard et al. 2016), others worry that objectivity in conservation research may suffer (Lackey 2007). At this time, we believe advocacy by scientists is essential for environmental conservation and, indeed, humanity. It is difficult to envision the state of our environment had scientists failed to encourage policy makers and the public to address emerging conservation problems. Nevertheless, conservation scientists must avoid misusing the scientific process to promote specific conservation outcomes (Wilholt 2009); doing so erodes the credibility of science and can produce undesirable consequences (Thomas 1992; Mills 2000; Rohr and McCoy 2010). We consider intentionally engaging in activities outside of professional norms to promote desired outcomes, as part of either the production or dissemination of science, to constitute “agenda-driven science”. The issue of advocacy-related bias in conservation science merits renewed discussion because conservation conflicts in an increasingly polarized world might tempt some to engage in agenda-driven science to “win” a conflict

The extracellular heparan sulfatase SULF2 limits myeloid IFNβ signaling and Th17 responses in inflammatory arthritis

Heparan sulfate (HS) proteoglycans are important regulators of cellular responses to soluble mediators such as chemokines, cytokines and growth factors. We profiled changes in expression of genes encoding HS core proteins, biosynthesis enzymes and modifiers during macrophage polarisation, and found that the most highly regulated gene was Sulf2, an extracellular HS 6-O-sulfatase that was markedly downregulated in response to pro-inflammatory stimuli. We then generated Sulf2+/− bone marrow chimeric mice and examined inflammatory responses in antigen-induced arthritis, as a model of rheumatoid arthritis. Resolution of inflammation was impaired in myeloid Sulf2+/− chimeras, with elevated joint swelling and increased abundance of pro-arthritic Th17 cells in synovial tissue. Transcriptomic and in vitro analyses indicated that Sulf2 deficiency increased type I interferon signaling in bone marrow-derived macrophages, leading to elevated expression of the Th17-inducing cytokine IL6. This establishes that dynamic remodeling of HS by Sulf2 limits type I interferon signaling in macrophages, and so protects against Th17-driven pathology