187 research outputs found

    X-ray fluorescence mapping of mercury on suspended mineral particles and diatoms in a contaminated freshwater system

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    Mercury (Hg) bioavailability and geochemical cycling is affected by its partitioning between the aqueous and particulate phases. We applied a synchrotron-based X-ray fluorescence (XRF) microprobe to visualize and quantify directly the spatial localization of Hg and its correlations with other elements of interest on suspended particles from a Hg-contaminated freshwater system. Up to 175 Οg g⁝š Hg is found on suspended particles, but less than 0.01% is in the form of methylmercury. Mercury is heterogeneously distributed among phytoplankton (e.g., diatoms) and mineral particles that are rich in iron oxides and natural organic matter (NOM). The diatom-bound Hg is mostly found on outer surfaces of the cells, suggesting passive sorption of Hg on diatoms. Our results indicate that localized sorption of Hg onto suspended particles, including diatoms and NOM-coated oxide minerals, may play an important role in affecting the partitioning, reactivity, and biogeochemical cycling of Hg in natural aquatic environments

    Quantification of Lung Abnormalities in Cystic Fibrosis using Deep Networks

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    Cystic fibrosis is a genetic disease which may appear in early life with structural abnormalities in lung tissues. We propose to detect these abnormalities using a texture classification approach. Our method is a cascade of two convolutional neural networks. The first network detects the presence of abnormal tissues. The second network identifies the type of the structural abnormalities: bronchiectasis, atelectasis or mucus plugging.We also propose a network computing pixel-wise heatmaps of abnormality presence learning only from the patch-wise annotations. Our database consists of CT scans of 194 subjects. We use 154 subjects to train our algorithms and the 40 remaining ones as a test set. We compare our method with random forest and a single neural network approach. The first network reaches an accuracy of 0,94 for disease detection, 0,18 higher than the random forest classifier and 0,37 higher than the single neural network. Our cascade approach yields a final class-averaged F1-score of 0,33, outperforming the baseline method and the single network by 0,10 and 0,12.Comment: SPIE - Medical Imaging 2018: Image Processin

    Protein Oxidation Implicated as the Primary Determinant of Bacterial Radioresistance

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    In the hierarchy of cellular targets damaged by ionizing radiation (IR), classical models of radiation toxicity place DNA at the top. Yet, many prokaryotes are killed by doses of IR that cause little DNA damage. Here we have probed the nature of Mn-facilitated IR resistance in Deinococcus radiodurans, which together with other extremely IR-resistant bacteria have high intracellular Mn/Fe concentration ratios compared to IR-sensitive bacteria. For in vitro and in vivo irradiation, we demonstrate a mechanistic link between Mn(II) ions and protection of proteins from oxidative modifications that introduce carbonyl groups. Conditions that inhibited Mn accumulation or Mn redox cycling rendered D. radiodurans radiation sensitive and highly susceptible to protein oxidation. X-ray fluorescence microprobe analysis showed that Mn is globally distributed in D. radiodurans, but Fe is sequestered in a region between dividing cells. For a group of phylogenetically diverse IR-resistant and IR-sensitive wild-type bacteria, our findings support the idea that the degree of resistance is determined by the level of oxidative protein damage caused during irradiation. We present the case that protein, rather than DNA, is the principal target of the biological action of IR in sensitive bacteria, and extreme resistance in Mn-accumulating bacteria is based on protein protection

    The Parasitoid, Verticia fasciventris Causes Morphological and Behavioral Changes in Infected Soldiers of the Fungus-Growing Termite, Macrotermes carbonarius

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    The larval parasitoid Verticia fasciventris Malloch (Diptera: Calliphoridae) develops in the head of soldiers of the fungus-growing termite Macrotermes carbonarius (Hagen) (Isoptera: Termitidae). Morphological and behavioral changes in the host were evaluated and the termite castes and stages that were parasitized were identified. The larval emergence process is also described and possible mechanisms for the parasitoid fly's entry into the host body are discussed based on qualitative observations. Only a single larva per host was found. The mature larva pupated outside the host's body by exiting between the abdominal cerci. Parasitized soldiers possess a short and square-shaped head capsule, a pair of notably short mandibles, and a pair of 18-segmented antennae. Although parasitized soldiers were statistically less aggressive than healthy soldiers (P < 0.05), they expressed varying levels of aggression. Both minor and major soldiers can be parasitized and based on evidence from presoldiers, parasitization may begin during the precursor stages of soldiers. However, the stage at which parasitism first occurs has not been determined

    Atypical disengagement from faces and its modulation by the control of eye fixation in children with Autism Spectrum Disorder

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    By using the gap overlap task, we investigated disengagement from faces and objects in children (9–17 years old) with and without autism spectrum disorder (ASD) and its neurophysiological correlates. In typically developing (TD) children, faces elicited larger gap effect, an index of attentional engagement, and larger saccade-related event-related potentials (ERPs), compared to objects. In children with ASD, by contrast, neither gap effect nor ERPs differ between faces and objects. Follow-up experiments demonstrated that instructed fixation on the eyes induces larger gap effect for faces in children with ASD, whereas instructed fixation on the mouth can disrupt larger gap effect in TD children. These results suggest a critical role of eye fixation on attentional engagement to faces in both groups

    c-Type Cytochrome-Dependent Formation of U(IV) Nanoparticles by Shewanella oneidensis

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    Modern approaches for bioremediation of radionuclide contaminated environments are based on the ability of microorganisms to effectively catalyze changes in the oxidation states of metals that in turn influence their solubility. Although microbial metal reduction has been identified as an effective means for immobilizing highly-soluble uranium(VI) complexes in situ, the biomolecular mechanisms of U(VI) reduction are not well understood. Here, we show that c-type cytochromes of a dissimilatory metal-reducing bacterium, Shewanella oneidensis MR-1, are essential for the reduction of U(VI) and formation of extracelluar UO (2) nanoparticles. In particular, the outer membrane (OM) decaheme cytochrome MtrC (metal reduction), previously implicated in Mn(IV) and Fe(III) reduction, directly transferred electrons to U(VI). Additionally, deletions of mtrC and/or omcA significantly affected the in vivo U(VI) reduction rate relative to wild-type MR-1. Similar to the wild-type, the mutants accumulated UO (2) nanoparticles extracellularly to high densities in association with an extracellular polymeric substance (EPS). In wild-type cells, this UO (2)-EPS matrix exhibited glycocalyx-like properties and contained multiple elements of the OM, polysaccharide, and heme-containing proteins. Using a novel combination of methods including synchrotron-based X-ray fluorescence microscopy and high-resolution immune-electron microscopy, we demonstrate a close association of the extracellular UO (2) nanoparticles with MtrC and OmcA (outer membrane cytochrome). This is the first study to our knowledge to directly localize the OM-associated cytochromes with EPS, which contains biogenic UO (2) nanoparticles. In the environment, such association of UO (2) nanoparticles with biopolymers may exert a strong influence on subsequent behavior including susceptibility to oxidation by O (2) or transport in soils and sediments

    Autism as a disorder of neural information processing: directions for research and targets for therapy

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    The broad variation in phenotypes and severities within autism spectrum disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients. Identification of these factors, and the common developmental path into which theyfeed, is hampered bythe large degrees of convergence from causal factors to altered brain development, and divergence from abnormal brain development into altered cognition and behaviour. Genetic, neurochemical, neuroimaging and behavioural findings on autism, as well as studies of normal development and of genetic syndromes that share symptoms with autism, offer hypotheses as to the nature of causal factors and their possible effects on the structure and dynamics of neural systems. Such alterations in neural properties may in turn perturb activity-dependent development, giving rise to a complex behavioural syndrome many steps removed from the root causes. Animal models based on genetic, neurochemical, neurophysiological, and behavioural manipulations offer the possibility of exploring these developmental processes in detail, as do human studies addressing endophenotypes beyond the diagnosis itself

    Time courses of improvement and symptom remission in children treated with atomoxetine for attention-deficit/hyperactivity disorder: analysis of Canadian open-label studies

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    <p>Abstract</p> <p>Background</p> <p>The relatively short durations of the initial pivotal randomized placebo-controlled trials involving atomoxetine HCl for the treatment of attention-deficit/hyperactivity disorder (ADHD) provided limited insight into the time courses of ADHD core symptom responses to this nonstimulant, selective norepinephrine reuptake inhibitor. The aim of this analysis was to evaluate time courses of treatment responses or remission, as assessed by attainment of prespecified scores on the ADHD Rating Scale-IV-Parent Version: Investigator Administered and Scored (ADHDRS-IV-PI) and the Clinical Global Impressions-ADHD-Severity (CGI-ADHD-S) scales, during up to 1 year of atomoxetine treatment in children with ADHD.</p> <p>Methods</p> <p>Using pooled data from three Canadian open-label studies involving 338 children ages 6-11 years with ADHD who were treated with atomoxetine for 3, 6 and 12 months, and survival analysis methods for interval-censored data, we estimated the time to: 1) improvement and robust improvement defined by ≥25% and ≥40% reductions from baseline ADHDRS-IV-PI total scores, respectively; and 2) remission using two definitions: a final score of ADHDRS-IV-PI ≤18 or a final score of CGI-ADHD-S ≤2.</p> <p>Results</p> <p>The median time to improvement was 3.7 weeks (~1 month), but remission of symptoms did not occur until a median of 14.3 weeks (~3.5 months) using the most stringent CGI-ADHD-S threshold. Probabilities of robust improvement were 47% at or before 4 weeks of treatment; 76% at 12 weeks; 85% at 26 weeks; and 96% at 52 weeks. Probabilities of remission at these corresponding time points were 30%, 59%, 77%, and 85% (using the ADHDRS-IV scale) and 8%, 47%, 67%, and 75% (using the CGI-ADHD-S scale). The change from atomoxetine treatment month 5 to month 12 of -1.01 (1.03) was not statistically significant (<it>p </it>= .33).</p> <p>Conclusions</p> <p>Reductions in core ADHD symptoms during atomoxetine treatment are gradual. Although approximately one-half of study participants showed improvement at 1 month of atomoxetine treatment, remission criteria were not met until about 3 months. Understanding the time course of children's responses to atomoxetine treatment may inform clinical decision making and also influence the durations of trials comparing the effects of this medication with other ADHD treatments.</p> <p>Trial Registrations</p> <p>clinicaltrials.gov: <a href="http://www.clinicaltrials.gov/ct2/show/NCT00191633">NCT00191633</a>, <a href="http://www.clinicaltrials.gov/ct2/show/NCT00216918">NCT00216918</a>, <a href="http://www.clinicaltrials.gov/ct2/show/NCT00191880">NCT00191880</a>.</p
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