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Objectives Tests the idea that the frequency distribution typically observed in cross-sectional crime victimization data sampled from surveys of general populations is a heterogeneously distributed result of the mixing of two latent processes associated, respectively, with each of the tails of the distribution. Methods Datasets are assembled from a number of samples taken from the British Crime Survey and the Scottish Crime Victimization Survey. Latent class analysis is used to explore the probable, latent distributions of individual property crime and personal crime victimization matrices that express the frequency and type of victimization that are self-reported by respondents over the survey recall period. Results The analysis obtains broadly similar solutions for both types of victimization across the respective datasets. It is demonstrated that a hypothesized mixing process will produce a heterogeneous set of local sub-distributions: a large sub-population that is predominantly not victimized, a very small 'chronic' sub-population that is frequently and consistently victimized across crime-type, and an 'intermediate' sub-population (whose granularity varies with sample size) to whom the bulk of victimization occurs. Additionally, attention is paid to the position of very high frequency victimization within these sub-populations. Conclusions The analysis supports the idea that crime victimization may be a function of two propensities: for immunity, and exposure. It demonstrates that zero-inflation is also a defìning feature of the distribution that needs to be set alongside the significance that has been attached to the thickness of its right tail. The results suggest a new baseline model for investigating population distributions of crime victimization.

The earth's biodiversity currently faces an extinction crisis that is unprecedented. Conservationists attempt to intervene in the extinction process either locally by protecting or restoring important species and habitats, or at national and international levels by influencing key policies and promoting debate. Reliable information is the foundation upon which these efforts are based, which places research at the heart of biodiversity conservation. The role of research in such conservation is diverse. It includes understanding why biodiversity is important, defining 'units' of biodiversity, priority-setting for species and sites, managing endangered and declining populations, understanding large-scale processes, making predictions about the future and interfacing with training, education, public awareness and policy initiatives. Using examples from a wide range of bird conservation work worldwide, researchers consider the principles underlying these issues, and illustrate how these principles have been applied to address actual conservation problems for students, practitioners and researchers in conservation biology.

They did, 53-38. It was St. Stephen's/St. Agnes's second Sleepy Thompson title in three years and its ninth overall. It was the 10th straight win for the Saints (18-8) since a loss to Paul VI Catholic left them with a .500 record. Now St. Stephen's/St. Agnes will enter next week's Virginia Independent Schools state tournament with plenty of momentum. Episcopal fell to 9-14. Loudoun County senior guard Octavia Trammell scored 14 second- half points, emblematic of her team's play after halftime, lifting the Raiders to a 53-43 victory over previously unbeaten Charlottesville in the Virginia AA Region II final at James Madison University in Harrisonburg. Riverbend girls' basketball coach Claude Tyler doesn't want to put any pressure on his good friend, Jamestown Coach Jason Asbell, but he has seen all eight teams that will be playing in the upcoming Virginia AA tournament, and he believes Asbell's Eagles are the best of them.

The home floor at Centreville again was a comfortable place for the Westfield volleyball team last night. There, the Bulldogs met Centreville in what is easily the most storied rivalry in the eight- year history of the Virginia AAA Northern Region tournament. In yesterday afternoon's Virginia AAA title game at Oakton, [Claye Rhea] watched what she might have only dreamed about as a sophomore in high school -- her daughter Taylor, a freshman at Cox, scored one of the Falcons' two goals as Cox topped Maury, 2-1, for the 13th state title in school history. Cox finished the season 23-0, and Norfolk's Maury -- playing in its first state championship game - - finished 19-5-1. Rhea scored the game's first goal with 11 minutes 45 second remaining in the first half. Senior Kaitlyn Hiltz scored the second goal for Cox with 4:32 remaining in the first half. Both goals came via assists from senior Danielle Scissom. Lindsey Vellines scored Maury's goal with 2:35 left in the first half.

Key Points Infection and injury cause controlled immune and inflammatory responses involving complex molecular signalling networks that lead to the production of bioactive lipid mediators. Eicosanoids are bioactive lipid mediators derived from oxygenated polyunsaturated fatty acids. Similar to cytokine signalling and inflammasome formation, eicosanoid signalling has been viewed primarily as a pro-inflammatory component of innate immunity. Recent advances in lipidomics technologies have helped to elucidate unique eicosanoids and related docosanoids with anti-inflammatory and pro-resolution functions that are a key component of the inflammatory response. Receptor activation initiated by Toll-like receptors (TLRs), purinergic receptors and other signalling pathways induced by infectious agents generates both pro-inflammatory and anti-inflammatory metabolites resulting in an eicosanoid storm. Lipidomics has advanced our overall understanding of the inflammatory response and its therapeutic implications, and has suggested new pharmacological approaches. Eicosanoids are bioactive signalling lipids that regulate numerous homeostatic and inflammatory processes. Here, the authors review our current understanding of cellular eicosanoid metabolism and the physiological functions of pro-inflammatory and pro-resolving eicosanoids in infection and inflammation. Controlled immune responses to infection and injury involve complex molecular signalling networks with coordinated and often opposing actions. Eicosanoids and related bioactive lipid mediators derived from polyunsaturated fatty acids constitute a major bioactive lipid network that is among the most complex and challenging pathways to map in a physiological context. Eicosanoid signalling, similar to cytokine signalling and inflammasome formation, has primarily been viewed as a pro-inflammatory component of the innate immune response; however, recent advances in lipidomics have helped to elucidate unique eicosanoids and related docosanoids with anti-inflammatory and pro-resolution functions. This has advanced our overall understanding of the inflammatory response and its therapeutic implications. The induction of a pro-inflammatory and anti-inflammatory eicosanoid storm through the activation of inflammatory receptors by infectious agents is reviewed here.

The dust shells of three intermediate-mass stars are observed to lie remarkably close to the photosphere and to be composed of unexpectedly large grains, consistent with mass loss from such stars occurring by means of ejection of this dust by photon scattering rather than as a result of radiation pressure. Last gasp of a red giant Towards the ends of their lives, intermediate-mass stars lose much of their mass in the form of gas and dust ejected in a slow, dense wind. The underlying processes driving these outflows are poorly understood, owing in part to difficulties in observing such ejected material. Norris et al . use an innovative technique that combines interferometric imaging with high-precision differential polarimetry to observe three red giants. Their images reveal circumstellar dust shells with remarkably small radii (less than two times the radius of the star), made up of unexpectedly large dust grains approximately 300 nanometres in radius. The authors suggest that these observations support a wind-driving model based on acceleration of dust grains by the scattering, rather than absorption, of starlight. An intermediate-mass star ends its life by ejecting the bulk of its envelope in a slow, dense wind 1 , 2 , 3 . Stellar pulsations are thought to elevate gas to an altitude cool enough for the condensation of dust 1 , which is then accelerated by radiation pressure, entraining the gas and driving the wind 2 , 4 , 5 . Explaining the amount of mass loss, however, has been a problem because of the difficulty of observing tenuous gas and dust only tens of milliarcseconds from the star. For this reason, there is no consensus on the way sufficient momentum is transferred from the light from the star to the outflow. Here we report spatially resolved, multiwavelength observations of circumstellar dust shells of three stars on the asymptotic giant branch of the Hertzsprung–Russell diagram. When imaged in scattered light, dust shells were found at remarkably small radii (less than about two stellar radii) and with unexpectedly large grains (about 300 nanometres in radius). This proximity to the photosphere argues for dust species that are transparent to the light from the star and, therefore, resistant to sublimation by the intense radiation field. Although transparency usually implies insufficient radiative pressure to drive a wind 6 , 7 , the radiation field can accelerate these large grains through photon scattering rather than absorption 8 —a plausible mass loss mechanism for lower-amplitude pulsating stars.

Resolution of acute inflammation is an active process orchestrated by endogenous mediators and mechanisms pivotal in host defense and homeostasis. The macrophage mediator in resolving inflammation, maresin 1 (MaR1), is a potent immunoresolvent, stimulating resolution of acute inflammation and organ protection. Using an unbiased screening of greater than 200 GPCRs, we identified MaR1 as a stereoselective activator for human leucine-rich repeat containing G protein-coupled receptor 6 (LGR6), expressed in phagocytes. MaR1 specificity for recombinant human LGR6 activation was established using reporter cells expressing LGR6 and functional impedance sensing. MaR1-specific binding to LGR6 was confirmed using 3H-labeled MaR1. With human and mouse phagocytes, MaR1 (0.01-10 nM) enhanced phagocytosis, efferocytosis, and phosphorylation of a panel of proteins including the ERK and cAMP response element-binding protein. These MaR1 actions were significantly amplified with LGR6 overexpression and diminished by gene silencing in phagocytes. Thus, we provide evidence for MaR1 as an endogenous activator of human LGR6 and a novel role of LGR6 in stimulating MaR1's key proresolving functions of phagocytes.

Boron and carbon isotope data, used in an Earth system model, show that the Palaeocene–Eocene Thermal Maximum was associated with a much greater release of carbon than thought, most probably triggered by volcanism in the North Atlantic. Volcanic carbon warmed the ancient climate The Palaeocene–Eocene Thermal Maximum was a surface warming event associated with ecological disruption that occurred about 56 million years ago. A large amount of carbon is thought to have been released during this event, but the total amount and the sources of carbon remain uncertain. This paper combines boron and carbon isotope data in an Earth system model and finds that the source of carbon was much larger than previously thought and that most of the carbon was probably released by volcanism associated with the North Atlantic Igneous Province. The study also suggests that the amplifying organic carbon–climate feedbacks did not have a prominent role in driving the event, but that enhanced burial of organic matter was important for sequestering the released carbon and accelerating the recovery of the climate system. The Palaeocene–Eocene Thermal Maximum 1 , 2 (PETM) was a global warming event that occurred about 56 million years ago, and is commonly thought to have been driven primarily by the destabilization of carbon from surface sedimentary reservoirs such as methane hydrates 3 . However, it remains controversial whether such reservoirs were indeed the source of the carbon that drove the warming 1 , 3 , 4 , 5 . Resolving this issue is key to understanding the proximal cause of the warming, and to quantifying the roles of triggers versus feedbacks. Here we present boron isotope data—a proxy for seawater pH—that show that the ocean surface pH was persistently low during the PETM. We combine our pH data with a paired carbon isotope record in an Earth system model in order to reconstruct the unfolding carbon-cycle dynamics during the event 6 , 7 . We find strong evidence for a much larger (more than 10,000 petagrams)—and, on average, isotopically heavier—carbon source than considered previously 8 , 9 . This leads us to identify volcanism associated with the North Atlantic Igneous Province 10 , 11 , rather than carbon from a surface reservoir, as the main driver of the PETM. This finding implies that climate-driven amplification of organic carbon feedbacks probably played only a minor part in driving the event. However, we find that enhanced burial of organic matter seems to have been important in eventually sequestering the released carbon and accelerating the recovery of the Earth system 12 .

Proinflammatory eicosanoids (prostaglandins and leukotrienes) and specialized pro-resolving mediators (SPM) are temporally regulated during infections. Here we show that human macrophage phenotypes biosynthesize unique lipid mediator signatures when exposed to pathogenic bacteria. E. coli and S. aureus each stimulate predominantly proinflammatory 5-lipoxygenase (LOX) and cyclooxygenase pathways (i.e., leukotriene B 4 and prostaglandin E 2 ) in M1 macrophages. These pathogens stimulate M2 macrophages to produce SPMs including resolvin D2 (RvD2), RvD5, and maresin-1. E. coli activates M2 macrophages to translocate 5-LOX and 15-LOX-1 to different subcellular locales in a Ca 2+ -dependent manner. Neither attenuated nor non-pathogenic E. coli mobilize Ca 2+ or activate LOXs, rather these bacteria stimulate prostaglandin production. RvD5 is more potent than leukotriene B 4 at enhancing macrophage phagocytosis. These results indicate that M1 and M2 macrophages respond to pathogenic bacteria differently, producing either leukotrienes or resolvins that further distinguish inflammatory or pro-resolving phenotypes. M1 and M2 cells are representative of proinflammatory versus resolving macrophages, respectively. Here the authors characterize the lipid mediator response to bacterial infection by these cells and show that differing panels of leukotrienes and specialized pro-resolving mediators contribute to control of the dichotomy.