740 research outputs found

    ZFOURGE: Extreme 5007A˚\AA emission may be a common early-lifetime phase for star-forming galaxies at z>2.5z > 2.5

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    Using the \prospector\ spectral energy distribution (SED) fitting code, we analyze the properties of 19 Extreme Emission Line Galaxies (EELGs) identified in the bluest composite SED in the \zfourge\ survey at 2.5z42.5 \leq z \leq 4. \prospector\ includes a physical model for nebular emission and returns probability distributions for stellar mass, stellar metallicity, dust attenuation, and nonparametric star formation history (SFH). The EELGs show evidence for a starburst in the most recent 50 Myr, with the median EELG having a specific star formation rate (sSFR) of 4.6 Gyr1^{-1} and forming 15\% of its mass in this short time. For a sample of more typical star-forming galaxies (SFGs) at the same redshifts, the median SFG has a sSFR of 1.1 Gyr1^{-1} and forms only 4%4\% of its mass in the last 50 Myr. We find that virtually all of our EELGs have rising SFHs, while most of our SFGs do not. From our analysis, we hypothesize that many, if not most, star-forming galaxies at z2.5z \geq 2.5 undergo an extreme Hβ\beta+[\hbox{{\rm O}\kern 0.1em{\sc iii}}] emission line phase early in their lifetimes. In a companion paper, we obtain spectroscopic confirmation of the EELGs as part of our {\sc MOSEL} survey. In the future, explorations of uncertainties in modeling the UV slope for galaxies at z>2z>2 are needed to better constrain their properties, e.g. stellar metallicities.Comment: 11 pages, 5 figures (main figure is fig 5), accepted for publication in Ap

    The Outstanding Decisions of the United States Supreme Court in 1954

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    We perform a kinematic and morphological analysis of 44 star-forming galaxies at z ̃ 2 in the COSMOS legacy field using near-infrared spectroscopy from Keck/MOSFIRE and F160W imaging from CANDELS/3D-HST as part of the ZFIRE survey. Our sample consists of cluster and field galaxies from 2.0 < z < 2.5 with K-band multi-object slit spectroscopic measurements of their Hα emission lines. Hα rotational velocities and gas velocity dispersions are measured using the Heidelberg Emission Line Algorithm (HELA), which compares directly to simulated 3D data cubes. Using a suite of simulated emission lines, we determine that HELA reliably recovers input S 0.5 and angular momentum at small offsets, but V 2.2/σ g values are offset and highly scattered. We examine the role of regular and irregular morphology in the stellar mass kinematic scaling relations, deriving the kinematic measurement S 0.5, and finding {log}({S}0.5)=(0.38+/- 0.07){log}(M/{M}☉ -10)+(2.04+/- 0.03) with no significant offset between morphological populations and similar levels of scatter (̃0.16 dex). Additionally, we identify a correlation between M ⋆ and V 2.2/σ g for the total sample, showing an increasing level of rotation dominance with increasing M ⋆, and a high level of scatter for both regular and irregular galaxies. We estimate the specific angular momenta (j disk) of these galaxies and find a slope of 0.36 ± 0.12, shallower than predicted without mass-dependent disk growth, but this result is possibly due to measurement uncertainty at M ⋆ < 9.5 However, through a Kolmogorov-Smirnov test we find irregular galaxies to have marginally higher j disk values than regular galaxies, and high scatter at low masses in both populations

    The Endogenous Th17 Response in NO<inf>2</inf>-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer

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    Severe, glucocorticoid-resistant asthma comprises 5-7% of patients with asthma. IL-17 is a biomarker of severe asthma, and the adoptive transfer of Th17 cells in mice is sufficient to induce glucocorticoid-resistant allergic airway disease. Nitrogen dioxide (NO2) is an environmental toxin that correlates with asthma severity, exacerbation, and risk of adverse outcomes. Mice that are allergically sensitized to the antigen ovalbumin by exposure to NO2 exhibit a mixed Th2/Th17 adaptive immune response and eosinophil and neutrophil recruitment to the airway following antigen challenge, a phenotype reminiscent of severe clinical asthma. Because IL-1 receptor (IL-1R) signaling is critical in the generation of the Th17 response in vivo, we hypothesized that the IL-1R/Th17 axis contributes to pulmonary inflammation and airway hyperresponsiveness (AHR) in NO2-promoted allergic airway disease and manifests in glucocorticoid-resistant cytokine production. IL-17A neutralization at the time of antigen challenge or genetic deficiency in IL-1R resulted in decreased neutrophil recruitment to the airway following antigen challenge but did not protect against the development of AHR. Instead, IL-1R-/- mice developed exacerbated AHR compared to WT mice. Lung cells from NO2-allergically inflamed mice that were treated in vitro with dexamethasone (Dex) during antigen restimulation exhibited reduced Th17 cytokine production, whereas Th17 cytokine production by lung cells from recipient mice of in vitro Th17-polarized OTII T-cells was resistant to Dex. These results demonstrate that the IL-1R/Th17 axis does not contribute to AHR development in NO2-promoted allergic airway disease, that Th17 adoptive transfer does not necessarily reflect an endogenously-generated Th17 response, and that functions of Th17 responses are contingent on the experimental conditions in which they are generated. © 2013 Martin et al

    Biodiversity Loss and the Taxonomic Bottleneck: Emerging Biodiversity Science

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    Human domination of the Earth has resulted in dramatic changes to global and local patterns of biodiversity. Biodiversity is critical to human sustainability because it drives the ecosystem services that provide the core of our life-support system. As we, the human species, are the primary factor leading to the decline in biodiversity, we need detailed information about the biodiversity and species composition of specific locations in order to understand how different species contribute to ecosystem services and how humans can sustainably conserve and manage biodiversity. Taxonomy and ecology, two fundamental sciences that generate the knowledge about biodiversity, are associated with a number of limitations that prevent them from providing the information needed to fully understand the relevance of biodiversity in its entirety for human sustainability: (1) biodiversity conservation strategies that tend to be overly focused on research and policy on a global scale with little impact on local biodiversity; (2) the small knowledge base of extant global biodiversity; (3) a lack of much-needed site-specific data on the species composition of communities in human-dominated landscapes, which hinders ecosystem management and biodiversity conservation; (4) biodiversity studies with a lack of taxonomic precision; (5) a lack of taxonomic expertise and trained taxonomists; (6) a taxonomic bottleneck in biodiversity inventory and assessment; and (7) neglect of taxonomic resources and a lack of taxonomic service infrastructure for biodiversity science. These limitations are directly related to contemporary trends in research, conservation strategies, environmental stewardship, environmental education, sustainable development, and local site-specific conservation. Today’s biological knowledge is built on the known global biodiversity, which represents barely 20% of what is currently extant (commonly accepted estimate of 10 million species) on planet Earth. Much remains unexplored and unknown, particularly in hotspots regions of Africa, South Eastern Asia, and South and Central America, including many developing or underdeveloped countries, where localized biodiversity is scarcely studied or described. ‘‘Backyard biodiversity’’, defined as local biodiversity near human habitation, refers to the natural resources and capital for ecosystem services at the grassroots level, which urgently needs to be explored, documented, and conserved as it is the backbone of sustainable economic development in these countries. Beginning with early identification and documentation of local flora and fauna, taxonomy has documented global biodiversity and natural history based on the collection of ‘‘backyard biodiversity’’ specimens worldwide. However, this branch of science suffered a continuous decline in the latter half of the twentieth century, and has now reached a point of potential demise. At present there are very few professional taxonomists and trained local parataxonomists worldwide, while the need for, and demands on, taxonomic services by conservation and resource management communities are rapidly increasing. Systematic collections, the material basis of biodiversity information, have been neglected and abandoned, particularly at institutions of higher learning. Considering the rapid increase in the human population and urbanization, human sustainability requires new conceptual and practical approaches to refocusing and energizing the study of the biodiversity that is the core of natural resources for sustainable development and biotic capital for sustaining our life-support system. In this paper we aim to document and extrapolate the essence of biodiversity, discuss the state and nature of taxonomic demise, the trends of recent biodiversity studies, and suggest reasonable approaches to a biodiversity science to facilitate the expansion of global biodiversity knowledge and to create useful data on backyard biodiversity worldwide towards human sustainability

    Electromagnetic Meson Production in the Nucleon Resonance Region

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    Recent experimental and theoretical advances in investigating electromagnetic meson production reactions in the nucleon resonance region are reviewed.Comment: 75 pages, 42 figure

    The role of population PK-PD modelling in paediatric clinical research

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    Children differ from adults in their response to drugs. While this may be the result of changes in dose exposure (pharmacokinetics [PK]) and/or exposure response (pharmacodynamics [PD]) relationships, the magnitude of these changes may not be solely reflected by differences in body weight. As a consequence, dosing recommendations empirically derived from adults dosing regimens using linear extrapolations based on body weight, can result in therapeutic failure, occurrence of adverse effect or even fatalities. In order to define rational, patient-tailored dosing schemes, population PK-PD studies in children are needed. For the analysis of the data, population modelling using non-linear mixed effect modelling is the preferred tool since this approach allows for the analysis of sparse and unbalanced datasets. Additionally, it permits the exploration of the influence of different covariates such as body weight and age to explain the variability in drug response. Finally, using this approach, these PK-PD studies can be designed in the most efficient manner in order to obtain the maximum information on the PK-PD parameters with the highest precision. Once a population PK-PD model is developed, internal and external validations should be performed. If the model performs well in these validation procedures, model simulations can be used to define a dosing regimen, which in turn needs to be tested and challenged in a prospective clinical trial. This methodology will improve the efficacy/safety balance of dosing guidelines, which will be of benefit to the individual child

    Surfactant Protein a Attenuates Generalized and Localized Neuroinflammation in Neonatal Mice

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    Surfactant protein A (SP-A) has important roles in innate immunity and modulation of pulmonary and extrapulmonary inflammation. Given SP-A has been detected in rat and human brain, we sought to determine if SP-A has a role in modulating inflammation in the neonatal mouse brain. Neonatal wildtype (WT) and SP-A-deficient (SP-

    Surfactant Protein a Attenuates Generalized and Localized Neuroinflammation in Neonatal Mice

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    Surfactant protein A (SP-A) has important roles in innate immunity and modulation of pulmonary and extrapulmonary inflammation. Given SP-A has been detected in rat and human brain, we sought to determine if SP-A has a role in modulating inflammation in the neonatal mouse brain. Neonatal wildtype (WT) and SP-A-deficient (SP-A−/−) mice were subjected to three models of brain inflammation: systemic sepsis, intraventricular hemorrhage (IVH) and hypoxic-ischemic encephalopathy (HIE). Following treatment, RNA was isolated from brain tissue and expression of cytokine and SP-A mRNA was determined by real-time quantitative RT-PCR analysis. In the sepsis model, expression of most cytokine mRNAs was significantly increased in brains of WT and SP-A−/− neonates with significantly greater expression of all cytokine mRNA levels in SP-A−/− mice compared to WT. In the IVH model, expression of all cytokine mRNAs was significantly increased in WT and SP-A−/− mice and levels of cytokine mRNAs were significantly increased in SP-A−/− mice compared to WT. In the HIE model, only TNF-α mRNA levels were significantly increased in WT brain tissue while most cytokine mRNAs were significantly increased in SP-A−/− mice, and all cytokine mRNA levels were significantly higher in SP-A−/− mice compared to WT. SP-A mRNA was not detectable in brain tissue of adult WT mice nor of WT neonates subjected to the models. These results suggest that SP-A−/− neonatal mice subjected to models of neuroinflammation are more susceptible to generalized and localized neuroinflammation compared to WT mice, thus supporting the hypothesis that SP-A attenuates inflammation in neonatal mouse brain

    Erratum to: 36th International Symposium on Intensive Care and Emergency Medicine

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    [This corrects the article DOI: 10.1186/s13054-016-1208-6.]
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