A 10-year ecosystem restoration community of practice tracks large-scale restoration trends

In 2004, a group of large-scale ecosystem restoration practitioners across the United States convened to start the process of sharing restoration science, management, and best practices under the auspices of a traditional conference umbrella. This forum allowed scientists and decision makers to interact in a new type of setting, with science being presented from a perspective that informed ecosystem restoration decisions, and decision makers articulating their decision needs in a manner that informed the types of science questions that needed to be addressed. From that beginning, a core ecosystem restoration practitioner group has formed a community of practice that continues to build and maintain momentum for this type of ecosystem restoration engagement. In the fall of 2013, this community of practice became permanently organized as the Large-scale Ecosystem Restoration Section within the Society for Ecological Restoration. Over the past decade, this community has evaluated and expanded upon ecosystem restoration themes ranging from defining and measuring success, adaptive management, adaptive governance, and linking science with management decision-making. Current and future themes include novel ecosystems, ecosystem goods and services, urban ecosystem restoration, and climate change and ecosystem resilience

Peptide Bbeta(15-42) preserves endothelial barrier function in shock

Loss of vascular barrier function causes leak of fluid and proteins into tissues, extensive leak leads to shock and death. Barriers are largely formed by endothelial cell-cell contacts built up by VE-cadherin and are under the control of RhoGTPases. Here we show that a natural plasmin digest product of fibrin, peptide Bß15-42 (also called FX06), significantly reduces vascular leak and mortality in animal models for Dengue shock syndrome. The ability of Bß15-42 to preserve endothelial barriers is confirmed in rats i.v.-injected with LPS. In endothelial cells, Bß15-42 prevents thrombin-induced stress fiber formation, myosin light chain phosphorylation and RhoA activation. The molecular key for the protective effect of Bß15-42 is the src kinase Fyn, which associates with VE-cadherin-containing junctions. Following exposure to Bß15-42 Fyn dissociates from VE-cadherin and associates with p190RhoGAP, a known antagonists of RhoA activation. The role of Fyn in transducing effects of Bß15-42 is confirmed in Fyn -/- mice, where the peptide is unable to reduce LPS-induced lung edema, whereas in wild type littermates the peptide significantly reduces leak. Our results demonstrate a novel function for Bß15-42. Formerly mainly considered as a degradation product occurring after fibrin inactivation, it has now to be considered as a signaling molecule. It stabilizes endothelial barriers and thus could be an attractive adjuvant in the treatment of shock

Time-Weighted Average SPME Analysis for in Planta Determination of CVOCs

The Potential of Phytoscreening for Plume Delineation at Contaminated Sites Has Promoted Interest in Innovative, Sensitive Contaminant Sampling Techniques. Solid-Phase Microextraction (SPME) Methods Have Been Developed, Offering Quick, Undemanding, Noninvasive Sampling Without the Use of Solvents. in This Study, Time-Weighted Average SPME (TWA-SPME) Sampling Was Evaluated for in Planta Quantification of Chlorinated Solvents. TWA-SPME Was Found to Have Increased Sensitivity over Headspace and Equilibrium SPME Sampling. using a Variety of Chlorinated Solvents and a Polydimethylsiloxane/carboxen (PDMS/CAR) SPME Fiber, Most Compounds Exhibited Near Linear or Linear Uptake over the Sampling Period. Smaller, Less Hydrophobic Compounds Exhibited More Nonlinearity Than Larger, More Hydrophobic Molecules. using a Specifically Designed in Planta Sampler, Field Sampling Was Conducted at a Site Contaminated with Chlorinated Solvents. Sampling with TWA-SPME Produced Instrument Responses Ranging from 5 to over 200 Times Higher Than Headspace Tree Core Sampling. This Work Demonstrates that TWA-SPME Can Be Used for in Planta Detection of a Broad Range of Chlorinated Solvents and Methods Can Likely Be Applied to Other Volatile and Semivolatile Organic Compounds. © 2012 American Chemical Society

Post-Transcriptional Dysregulation by miRNAs Is Implicated in the Pathogenesis of Gastrointestinal Stromal Tumor [GIST]

peer-reviewedIn contrast to adult mutant gastrointestinal stromal tumors [GISTs], pediatric/wild-type GISTs remain poorly understood overall, given their lack of oncogenic activating tyrosine kinase mutations. These GISTs, with a predilection for gastric origin in female patients, show limited response to therapy with tyrosine kinase inhibitors and generally pursue a more indolent course, but still may prove fatal. Defective cellular respiration appears to underpin tumor development in these wild-type cases, which as a group lack expression of succinate dehydrogenase [SDH] B, a surrogate marker for respiratory chain metabolism. Yet, only a small subset of the wild-type tumors show mutations in the genes coding for the SDH subunits [SDHx]. To explore additional pathogenetic mechanisms in these wild-type GISTs, we elected to investigate posttranscriptional regulation of these tumors by conducting microRNA (miRNA) profiling of a mixed cohort of 73 cases including 18 gastric pediatric wild-type, 25 (20 gastric, 4 small bowel and 1 retroperitoneal) adult wild-type GISTs and 30 gastric adult mutant GISTs. By this approach we have identified distinct signatures for GIST subtypes which correlate tightly with clinico-pathological parameters. A cluster of miRNAs on 14q32 show strikingly different expression patterns amongst GISTs, a finding which appears to be explained at least in part by differential allelic methylation of this imprinted region. Small bowel and retroperitoneal wild-type GISTs segregate with adult mutant GISTs and express SDHB, while adult wildtype gastric GISTs are dispersed amongst adult mutant and pediatric wild-type cases, clustering in this situation on the basis of SDHB expression. Interestingly, global methylation analysis has recently similarly demonstrated that these wild-type, SDHB-immunonegative tumors show a distinct pattern compared with KIT and PDGFRA mutant tumors, which as a rule do express SDHB. All cases with Carney triad within our cohort cluster together tightly.Funding was obtained from the Medical Research Charities Group (http://www.mrcg.ie/) and Health Research Board of Ireland (http://www.hrb.ie) (MO’S), The Children’s Medical and Research Foundation (http://www.cmrf.org) (MO’S), the GIST Cancer Awareness Foundation [GCAF] (http://www. gistawareness.org/)(MO’S), and research grants from the Life Raft Group (http://www.liferaftgroup.org/)(MD-R) and from the Fonds voor Wetenschappelijk Onderzoek Vlaanderen (http://www.fwo.be/)(grant # G.0286.05 MD-R)

Coiled-coil irregularities of the M1 protein structure promote M1-fibrinogen interaction and influence group A Streptococcus host cell interactions and virulence

Group A Streptococcus (GAS) is a human pathogen causing a wide range of mild to severe and life-threatening diseases. The GAS M1 protein is a major virulence factor promoting GAS invasiveness and resistance to host innate immune clearance. M1 displays an irregular coiled-coil structure, including the B-repeats that bind fibrinogen. Previously, we found that B-repeat stabilisation generates an idealised version of M1 (M1*) characterised by decreased fibrinogen binding in vitro. To extend these findings based on a soluble truncated version of M1, we now studied the importance of the B-repeat coiled-coil irregularities in full length M1 and M1* expressed in live GAS and tested whether the modulation of M1-fibrinogen interactions would open up novel therapeutic approaches. We found that altering either the M1 structure on the GAS cell surface or removing its target host protein fibrinogen blunted GAS virulence. GAS expressing M1* showed an impaired ability to adhere to and to invade human endothelial cells, was more readily killed by whole blood or neutrophils and most importantly was less virulent in a murine necrotising fasciitis model. M1-mediated virulence of wild-type GAS was strictly dependent on the presence and concentration of fibrinogen complementing our finding that M1-fibrinogen interactions are crucial for GAS virulence. Consistently blocking M1-fibrinogen interactions by fragment D reduced GAS virulence in vitro and in vivo. This supports our conclusion that M1-fibrinogen interactions are crucial for GAS virulence and that interference may open up novel complementary treatment options for GAS infections caused by the leading invasive GAS strain M

Securitization and the construction of security

Those interested in the construction of security in contemporary international politics have increasingly turned to the conceptual framework of `securitization'. This article argues that while an important and innovative contribution, the securitization framework is problematically narrow in three senses. First, the form of act constructing security is defined narrowly, with the focus on the speech of dominant actors. Second, the context of the act is defined narrowly, with the focus only on the moment of intervention. Finally, the framework of securitization is narrow in the sense that the nature of the act is defined solely in terms of the designation of threats. In outlining this critique, the article points to possibilities for developing the framework further as well as for the need for those applying it to recognize both limits of their claims and the normative implications of their analysis. I conclude by pointing to how the framework might fit within a research agenda concerned with the broader construction of security

Type I Interferon Production Induced by Streptococcus pyogenes-Derived Nucleic Acids Is Required for Host Protection

Streptococcus pyogenes is a Gram-positive human pathogen that is recognized by yet unknown pattern recognition receptors (PRRs). Engagement of these receptor molecules during infection with S. pyogenes, a largely extracellular bacterium with limited capacity for intracellular survival, causes innate immune cells to produce inflammatory mediators such as TNF, but also type I interferon (IFN). Here we show that signaling elicited by type I IFNs is required for successful defense of mice against lethal subcutaneous cellulitis caused by S. pyogenes. Type I IFN signaling was accompanied with reduced neutrophil recruitment to the site of infection. Mechanistic analysis revealed that macrophages and conventional dendritic cells (cDCs) employ different signaling pathways leading to IFN-beta production. Macrophages required IRF3, STING, TBK1 and partially MyD88, whereas in cDCs the IFN-beta production was fully dependent on IRF5 and MyD88. Furthermore, IFN-beta production by macrophages was dependent on the endosomal delivery of streptococcal DNA, while in cDCs streptococcal RNA was identified as the IFN-beta inducer. Despite a role of MyD88 in both cell types, the known IFN-inducing TLRs were individually not required for generation of the IFN-beta response. These results demonstrate that the innate immune system employs several strategies to efficiently recognize S. pyogenes, a pathogenic bacterium that succeeded in avoiding recognition by the standard arsenal of TLRs

Red Sea SAR11 and Prochlorococcus Single-cell Genomes Reflect Globally Distributed Pangenomes

Evidence suggests many marine bacteria are cosmopolitan, with widespread but sparse strains poised to seed abundant populations under conducive growth conditions. However, studies supporting this "microbial seed bank" hypothesis have analyzed taxonomic marker genes rather than whole genomes/metagenomes, leaving open the possibility that disparate ocean regions harbor endemic gene content. The Red Sea is isolated geographically from the rest of the ocean and has a combination of high irradiance, high temperature, and high salinity that is unique among the oceans; we therefore asked whether it harbors endemic gene content. We sequenced and assembled single-cell genomes of 21 SAR11 (subclades Ia, Ib, Id, and II) and 5 Prochlorococcus (ecotype HLII) samples from the Red Sea and combined them with globally sourced reference genomes to cluster genes into ortholog groups (OGs). Ordination of OG composition could distinguish clades, including phylogenetically cryptic Prochlorococcus ecotypes LLII and LLIII. Compared with reference genomes, 1% of Prochlorococcus and 17% of SAR11 OGs were unique to the Red Sea genomes (RS-OGs). Most (83%) RS-OGs had no annotated function, but 65% of RS-OGs were expressed in diel Red Sea metatranscriptomes, suggesting they are functional. Searching Tara Oceans metagenomes, RS-OGs were as likely to be found as non-RS-OGs; nevertheless, Red Sea and other warm samples could be distinguished from cooler samples using the relative abundances of OGs. The results suggest that the prevalence of OGs in these surface ocean bacteria is largely cosmopolitan, with differences in population metagenomes manifested by differences in relative abundance rather than complete presence/absence of OGs.IMPORTANCE Studies have shown that as we sequence seawater from a selected environment deeper and deeper, we approach finding every bacterial taxon known for the ocean as a whole. However, such studies have focused on taxonomic marker genes rather than on whole genomes, raising the possibility that the lack of endemism results from the method of investigation. We took a geographically isolated water body, the Red Sea, and sequenced single cells from it. We compared those single-cell genomes to available genomes from around the ocean and to ocean-spanning metagenomes. We showed that gene ortholog groups found in Red Sea genomes but not in other genomes are nevertheless common across global ocean metagenomes. These results suggest that Baas Becking's hypothesis "everything is everywhere, but the environment selects" also applies to gene ortholog groups. This widely dispersed functional diversity may give oceanic microbial communities the functional capacity to respond rapidly to changing conditions

Rotation Speed of the First Stars

We estimate the rotation speed of Population III (Pop III) stars within a minihalo at z ~ 20 using a smoothed particle hydrodynamics (SPH) simulation, beginning from cosmological initial conditions. We follow the evolution of the primordial gas up to densities of 10^12 cm^-3. Representing the growing hydrostatic cores with accreting sink particles, we measure the velocities and angular momenta of all particles that fall onto these protostellar regions. This allows us to record the angular momentum of the sinks and estimate the rotational velocity of the Pop III stars expected to form within them. The rotation rate has important implications for the evolution of the star, the fate encountered at the end of its life, and the potential for triggering a gamma-ray burst (GRB). We find that there is sufficient angular momentum to yield rapidly rotating stars (> 1000 km s^-1, or near break-up speeds). This indicates that Pop III stars likely experienced strong rotational mixing, impacting their structure and nucleosynthetic yields. A subset of them was also likely to result in hypernova explosions, and possibly GRBs.Comment: 14 pages, 7 figures, accepted for publication in MNRA