34 research outputs found

    COMPARISON OF HOP DOWNY MILDEW EPIDEMICS USING SPATIAL ANALYSIS

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    Methods of spatial analysis including distribution fitting, variance-to-mean ratios, Morisita\u27s index, doublet and runs analyses, Greig-Smith analysis and variography were used to investigate the spatial pattern of hop downy mildew. Use of these methods allowed examination of the spatial structure of hop downy mildew at three spatial scales: within hop hills, between nearby hop hills, and for hop hills more separated in space. The results obtained were in general agreement for methods of analysis which assessed spatial structure at the same spatial scale with the exception of Morisita\u27s index of clumping which did not identify clumps of diseased hills of the same size as Greig-Smith analysis and semi-variograms

    Spatial distributions of perchloroethylene reactive transport parameters in the Borden Aquifer

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    We determined the descriptive statistical and spatial geostatistical properties of the perchloroethene ln Kd and the ln k of a 1.5 m thick by 10 m horizontal transect of the Borden aquifer near the location of the Stanford-Waterloo (SW) tracer experiment. The ln Kd distribution is not normal and is right skewed because of a few high values that occur localized in two regions of the transect. In contrast, the ln k data can be characterized by a normal distribution. A linear regression of ln Kd on ln k yields a statistically significant positive correlation, also shown at small lags in the cross correlogram. No significant vertical or horizontal trend in the ln Kd data was detected. The semivariogram ranges of ln k and ln Kd differ from one another in the vertical direction (0.33 ± 0.06 m and 0.20 ± 0.04 m, respectively) and are much less than the horizontal ranges (a few meters). Despite significant effort the horizontal range of ln Kd remains poorly characterized because of limitations of the sample locations. Many of the characteristics described above do not match those assumed in prior theoretical studies that examined the importance of various aquifer characteristics on SW tracer transport. We suggest that there is knowledge to be gained by revisiting the conclusions of these prior studies in light of the new information presented here

    The Origin and Evolution of Mutations in Acute Myeloid Leukemia

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    SummaryMost mutations in cancer genomes are thought to be acquired after the initiating event, which may cause genomic instability and drive clonal evolution. However, for acute myeloid leukemia (AML), normal karyotypes are common, and genomic instability is unusual. To better understand clonal evolution in AML, we sequenced the genomes of M3-AML samples with a known initiating event (PML-RARA) versus the genomes of normal karyotype M1-AML samples and the exomes of hematopoietic stem/progenitor cells (HSPCs) from healthy people. Collectively, the data suggest that most of the mutations found in AML genomes are actually random events that occurred in HSPCs before they acquired the initiating mutation; the mutational history of that cell is “captured” as the clone expands. In many cases, only one or two additional, cooperating mutations are needed to generate the malignant founding clone. Cells from the founding clone can acquire additional cooperating mutations, yielding subclones that can contribute to disease progression and/or relapse

    Ultra-rare genetic variation in common epilepsies: a case-control sequencing study

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    BACKGROUND:Despite progress in understanding the genetics of rare epilepsies, the more common epilepsies have proven less amenable to traditional gene-discovery analyses. We aimed to assess the contribution of ultra-rare genetic variation to common epilepsies. METHODS:We did a case-control sequencing study with exome sequence data from unrelated individuals clinically evaluated for one of the two most common epilepsy syndromes: familial genetic generalised epilepsy, or familial or sporadic non-acquired focal epilepsy. Individuals of any age were recruited between Nov 26, 2007, and Aug 2, 2013, through the multicentre Epilepsy Phenome/Genome Project and Epi4K collaborations, and samples were sequenced at the Institute for Genomic Medicine (New York, USA) between Feb 6, 2013, and Aug 18, 2015. To identify epilepsy risk signals, we tested all protein-coding genes for an excess of ultra-rare genetic variation among the cases, compared with control samples with no known epilepsy or epilepsy comorbidity sequenced through unrelated studies. FINDINGS:We separately compared the sequence data from 640 individuals with familial genetic generalised epilepsy and 525 individuals with familial non-acquired focal epilepsy to the same group of 3877 controls, and found significantly higher rates of ultra-rare deleterious variation in genes established as causative for dominant epilepsy disorders (familial genetic generalised epilepsy: odd ratio [OR] 2·3, 95% CI 1·7-3·2, p=9·1 × 10-8; familial non-acquired focal epilepsy 3·6, 2·7-4·9, p=1·1 × 10-17). Comparison of an additional cohort of 662 individuals with sporadic non-acquired focal epilepsy to controls did not identify study-wide significant signals. For the individuals with familial non-acquired focal epilepsy, we found that five known epilepsy genes ranked as the top five genes enriched for ultra-rare deleterious variation. After accounting for the control carrier rate, we estimate that these five genes contribute to the risk of epilepsy in approximately 8% of individuals with familial non-acquired focal epilepsy. Our analyses showed that no individual gene was significantly associated with familial genetic generalised epilepsy; however, known epilepsy genes had lower p values relative to the rest of the protein-coding genes (p=5·8 × 10-8) that were lower than expected from a random sampling of genes. INTERPRETATION:We identified excess ultra-rare variation in known epilepsy genes, which establishes a clear connection between the genetics of common and rare, severe epilepsies, and shows that the variants responsible for epilepsy risk are exceptionally rare in the general population. Our results suggest that the emerging paradigm of targeting of treatments to the genetic cause in rare devastating epilepsies might also extend to a proportion of common epilepsies. These findings might allow clinicians to broadly explain the cause of these syndromes to patients, and lay the foundation for possible precision treatments in the future. FUNDING:National Institute of Neurological Disorders and Stroke (NINDS), and Epilepsy Research UK

    EUROPEAN RESEARCH IN MATHEMATICS EDUCATION III ASSOCIATION OF COURSE PERFORMANCE WITH STUDENT BELIEFS: AN ANALYSIS BY GENDER AND INSTRUCTIONAL SOFTWARE ENVIRONMENT

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    Claims and counter claims characterize the debate about the impact on learning related to educational technologies. We hypothesize that some of the impact may reflect the influence of the technology on student subject-related beliefs and that those beliefs may differ by gender. We desired to assess how course performance may be associated with student beliefs, and how the association may differ depending on instructional software environment and gender

    Association of course performance with student beliefs: An analysis by gender and instructional software environment

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    The effect of educational technologies on learning is an area of active interest. We conducted an experiment to compare the impact of instructional software on student performance. We hypothesize that some of the impact on student performance may reflect the influence of the technology on student subject-related beliefs and that those beliefs may differ by gender. We desired to assess how course performance may be associated with student beliefs, and how the association may differ depending on instructional software environment and gender

    MANIOC MOTHERS: SUBSISTENCE STABILITY AND THE INFLUENCE OF TOURISM AMONG THE NAPO KICHWAS IN THE ECUADORIAN AMAZON By

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    AUTUMN AND WINTER FOOD HABITS OF BOBCATS IN WASHINGTON STATE

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    Volume: 44Start Page: 70End Page: 7
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