415 research outputs found
\u3ci\u3ePeople v. Bradshaw:\u3c/i\u3e Has the Appearance of Impropriety Standard Supplanted the Requirement of Demonstrating Prejudice in \u3ci\u3eEx Parte\u3c/i\u3e Communications?
Are all threats equal? Associations of childhood exposure to physical attack versus threatened violence with preadolescent brain structure
Background: Neurodevelopmental studies of childhood adversity often define threatening experiences as those involving harm or the threat of harm. Whether effects differ between experiences involving harm (“physical attack”) versus the threat of harm alone (“threatened violence”) remains underexplored. We hypothesized that while both types of experiences would be associated with smaller preadolescent global and corticolimbic brain volumes, associations with physical attack would be greater. Methods: Generation R Study researchers (the Netherlands) acquired T1-weighted scans from 2905 preadolescent children, computed brain volumes using FreeSurfer, and asked mothers whether their children ever experienced physical attack (n = 202) or threatened violence (n = 335). Using standardized global (cortical, subcortical, white matter) and corticolimbic (amygdala, hippocampus, anterior cingulate cortex, orbitofrontal cortex) volumes, we fit confounder-adjusted models. Results: Physical attack was associated with smaller global volumes (βcortical=−0.14; 95% CI: −0.26, −0.02); βwhite matter= −0.16; 95% CI: − 0.28, − 0.03) and possibly some corticolimbic volumes, e.g., βamygdala/ICV-adjusted= −0.10 (95% CI: −0.21, 0.01). We found no evidence of associations between threatened violence and smaller volumes in any outcome; instead, such estimates were small, highly uncertain, and positive in direction. Conclusions: Experiences of physical attack and threatened violence may have quantitively different neurodevelopmental effects. Thus, differences between types of threatening experiences may be neurodevelopmentally salient.</p
Behavioral and neurostructural correlates of childhood physical violence victimization:Interaction with family functioning
Violence victimization may cause child behavior problems and neurostructural differences associated with them. Healthy family environments may buffer these effects, but neural pathways explaining these associations remain inadequately understood. We used data from 3154 children (x̅age = 10.1) to test whether healthy family functioning moderated possible associations between violence victimization, behavior problems, and amygdala volume (a threat-responsive brain region). Researchers collected data on childhood violence victimization, family functioning (McMaster Family Assessment Device, range 0-3, higher scores indicate healthier functioning), and behavior problems (Achenbach Child Behavior Checklist [CBCL] total problem score, range 0-117), and they scanned children with magnetic resonance imaging. We standardized amygdala volumes and fit confounder-adjusted models with "victimization × family functioning" interaction terms. Family functioning moderated associations between victimization, behavior problems, and amygdala volume. Among lower functioning families (functioning score = 1.0), victimization was associated with a 26.1 (95% confidence interval [CI]: 9.9, 42.4) unit higher CBCL behavior problem score, yet victimized children from higher functioning families (score = 3.0) exhibited no such association. Unexpectedly, victimization was associated with higher standardized amygdala volume among lower functioning families (ŷ = 0.5; 95% CI: 0.1, 1.0) but lower volume among higher functioning families (ŷ = -0.4; 95% CI: -0.7, -0.2). Thus, healthy family environments may mitigate some neurobehavioral effects of childhood victimization.</p
Filling the void: an optimized polymicrobial interkingdom biofilm model for assessing novel antimicrobial agents in endodontic infection
There is a growing realization that endodontic infections are often polymicrobial, and may contain Candida spp. Despite this understanding, the development of new endodontic irrigants and models of pathogenesis remains limited to mono-species biofilm models and is bacterially focused. The purpose of this study was to develop and optimize an interkingdom biofilm model of endodontic infection and use this to test suitable anti-biofilm actives. Biofilms containing Streptococcus gordonii, Fusobacterium nucleatum, Porphyromonas gingivalis, and Candida albicans were established from ontological analysis. Biofilms were optimized in different media and atmospheric conditions, prior to quantification and imaging, and subsequently treated with chlorhexidine, EDTA, and chitosan. These studies demonstrated that either media supplemented with serum were equally optimal for biofilm growth, which were dominated by S. gordonii, followed by C. albicans. Assessment of antimicrobial activity showed significant effectiveness of each antimicrobial, irrespective of serum. Chitosan was most effective (3 log reduction), and preferentially targeted C. albicans in both biofilm treatment and inhibition models. Chitosan was similarly effective at preventing biofilm growth on a dentine substrate. This study has shown that a reproducible and robust complex interkingdom model, which when tested with the antifungal chitosan, supports the notion of C. albicans as a key structural component
Hypoxia shapes the immune landscape in lung injury and promotes the persistence of inflammation
Hypoxemia is a defining feature of acute respiratory distress syndrome (ARDS), an often-fatal complication of pulmonary or systemic inflammation, yet the resulting tissue hypoxia, and its impact on immune responses, is often neglected. In the present study, we have shown that ARDS patients were hypoxemic and monocytopenic within the first 48 h of ventilation. Monocytopenia was also observed in mouse models of hypoxic acute lung injury, in which hypoxemia drove the suppression of type I interferon signaling in the bone marrow. This impaired monopoiesis resulted in reduced accumulation of monocyte-derived macrophages and enhanced neutrophil-mediated inflammation in the lung. Administration of colony-stimulating factor 1 in mice with hypoxic lung injury rescued the monocytopenia, altered the phenotype of circulating monocytes, increased monocyte-derived macrophages in the lung and limited injury. Thus, tissue hypoxia altered the dynamics of the immune response to the detriment of the host and interventions to address the aberrant response offer new therapeutic strategies for ARDS
Meteorites on Mars observed with the Mars Exploration Rovers
Reduced weathering rates due to the lack of liquid water and significantly greater typical surface ages should result in a higher density of meteorites on the surface of Mars compared to Earth. Several meteorites were identified among the rocks investigated during Opportunity’s traverse across the sandy Meridiani plains. Heat Shield Rock is a IAB iron meteorite and has been officially recognized as ‘‘Meridiani Planum.’’ Barberton is olivine-rich and contains metallic Fe in the form of kamacite, suggesting a meteoritic origin. It is chemically most consistent with a mesosiderite silicate clast. Santa Catarina is a brecciated rock with a chemical and mineralogical composition similar to Barberton. Barberton, Santa Catarina, and cobbles adjacent to Santa Catarina may be part of a strewn field. Spirit observed two probable iron meteorites from its Winter Haven location in the Columbia Hills in Gusev Crater. Chondrites have not been identified to date, which may be a result of their lower strengths and probability to survive impact at current atmospheric pressures. Impact craters directly associated with Heat Shield Rock, Barberton, or Santa Catarina have not been observed, but such craters could have been erased by eolian-driven erosion.Additional co-authors: DW Ming, RV Morris, PA de Souza Jr, SW Squyres, C Weitz, AS Yen, J Zipfel, T Economo
Submarine volcanic morphology of the western Galapagos based on EM300 bathymetry and MR1 side-scan sonar
Author Posting. © American Geophysical Union, 2007. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geochemistry Geophysics Geosystems 8 (2007): Q03010, doi:10.1029/2006GC001464.A compilation of high-resolution EM300 multibeam bathymetric and existing MR1 side-scan sonar data was used to investigate the volcanic morphology of the flanks of the western Galápagos Islands. The data portray an assortment of constructional volcanic features on the shallow to deep submarine flanks of Fernandina, Isabela, and Santiago Islands, including rift zones and groups of cones that are considered to be the primary elements in constructing the archipelagic apron. Ten submarine rift zones were mapped, ranging in length from 5 to 20 km, comparable in length to western Canary Island rift zones but significantly shorter than Hawaiian submarine rift zones. A detailed analysis of the northwestern Fernandina submarine rift, including calculated magnetization from a surface-towed magnetic study, suggests that the most recent volcanism has focused at the shallow end of the rift. Small submarine volcanic cones with various morphologies (e.g., pointed, cratered, and occasionally breached) are common in the submarine western Galápagos both on rift zones and on the island flanks where no rifts are present. At depths greater than ∼3000 m, large lava flow fields in regions of low bathymetric relief have been previously identified as a common seafloor feature in the western Galápagos by Geist et al. (2006); however, their source(s) remained enigmatic. The new EM300 data show that a number of the deep lava flows originate from small cones along the mid-lower portion of the NW submarine rift of Fernandina, suggesting that the deep flows owe their origin, at least in part, to submarine rift zone volcanism.Data collected on TN188
was funded by NSF grant OCE0326148 and NOAA grant
NA04OAR460009 to S.M.W. Support for data collected on
previous multibeam and MR1 cruises was provided by NSF
grants OCE9811504 and OCE0002461 (D.J.F.)
Hypoxia shapes the immune landscape in lung injury and promotes the persistence of inflammation
Hypoxemia is a defining feature of acute respiratory distress syndrome (ARDS), an often-fatal complication of pulmonary or systemic inflammation, yet the resulting tissue hypoxia, and its impact on immune responses, is often neglected. In the present study, we have shown that ARDS patients were hypoxemic and monocytopenic within the first 48 h of ventilation. Monocytopenia was also observed in mouse models of hypoxic acute lung injury, in which hypoxemia drove the suppression of type I interferon signaling in the bone marrow. This impaired monopoiesis resulted in reduced accumulation of monocyte-derived macrophages and enhanced neutrophil-mediated inflammation in the lung. Administration of colony-stimulating factor 1 in mice with hypoxic lung injury rescued the monocytopenia, altered the phenotype of circulating monocytes, increased monocyte-derived macrophages in the lung and limited injury. Thus, tissue hypoxia altered the dynamics of the immune response to the detriment of the host and interventions to address the aberrant response offer new therapeutic strategies for ARDS
- …