17 research outputs found

    Additional file 5: of Detection of genomic signatures of recent selection in commercial broiler chickens

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    Table S5. Major haplotypes and their frequencies detected in the purebred lines at the high-confidence selection regions that span at least 5 SNPs in our genotype data (XLSX 12 kb

    Neural conduction and excitability following a simple warm up

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    Objective This study examined the effect of a generic, active warm up on neural and muscular conduction time. Design Single group, pre-post design. Methods Central and peripheral neuromuscular conduction time was quantified in the abductor pollicis brevis (APB) and gastrocnemius muscles of 18 healthy participants (mean age 25.9 ± 5.8 years, 12 males) using transcranial magnetic stimulation (TMS) and M-wave techniques, prior to and immediately following an active warm up consisting of 5 min running at 65% of maximum heart rate. Neural conduction time, for both TMS and M-wave, was quantified as the time between stimulus artefact and deflection of the wave form, whilst muscle conduction time for TMS and M-wave, was quantified from the stimulus artefact to the absolute peak twitch response. Results Following the warm up protocol, a significant reduction in muscle conduction time was found in both TMS and M-wave of 0.43 ms (P = 0.02) and 0.30 ms (P = 0.001) for the APB; and 0.29 ms (P < 0.001) and 0.87 ms (P = 0.003) for the gastrocnemius, respectively. No change was found in neural conduction using either TMS or M-wave techniques. Conclusions These findings support previous data which demonstrate an improvement in muscular conduction time and subsequent improvement in athletic performance post warm up. The data also make evident that changes in muscular conduction time are a global response to warm up and are not directly related to muscular activity. In contrast, neural conduction time did not change and should not be confused with changes in muscular conduction time in the literature

    Organic Photovoltaics with Stacked Graphene Anodes

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    Graphene has recently been used to achieve power conversion efficiencies (PCEs) equal to those of ITO-based devices, although they remain a challenging and costly replacement for ITO. Herein, we employed chemical vapor deposition to grow graphene islands and transferred them onto a transparent substrate. The resulting stacked graphene films were characterized by Raman and UV–vis spectroscopies and conductivity measurements. Solar cells fabricated with stacked graphene (one to four layers)/PEDOT:PSS/P3HT:PCBM/Ca/Al architecture showed an enhancement of PCE as a function of the number of stacked layers. The highest efficiency was measured for the double-layered graphene anode because of its optimal conductance and transmittance. This work establishes that readily prepared layered graphene islands are a viable and economical substitute for ITO

    Additional file 4: Table S4. of Melanoma genome evolution across species

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    ZMELR1 vs. ZMEL1 mRNA differential expression. This file contains the differentially expressed genes from RNA-seq of the ZMEL1 line vs. the ZMELR1 line. (XLSX 3569 kb

    Defect Structure Guided Room Temperature Ferromagnetism of Y‑Doped CeO<sub>2</sub> Nanoparticles

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    In this study, the defect structure of Y doped CeO<sub>2</sub> nanoparticles (NPs) was investigated systematically by using spectroscopy and microscopy. The doping level of Y ranges from 0% to 15%. It is demonstrated that Y<sup>3+</sup> substitutes Ce and governs the formation of oxygen vacancy. At low doping level, Y<sup>3+</sup> randomly distributed throughout the particle. However, as doping level increased above 9%, Y<sup>3+</sup> aggregates at the surface and forms Y-rich clusters. Room temperature ferromagnetism (FM) was observed in these Y-doped CeO<sub>2</sub> NPs. It is found that the value of saturation magnetization (M<sub>s</sub>) increases until Y reaches 9%, then it decreases. Raman, X-ray absorption near edge spectroscopy and X-ray magnetic circular dichroism (XMCD) analysis has provided several aspects on the electronic properties of theses nanoparticles. A charge delocalization occurs upon Y doping on the Ce­(Y)-O­(V<sub>O</sub>)-Ce­(Y) orbitals. The magnetism is evidenced by XMCD spectroscopy only on Ce orbitals, and the magnetism intensity is mainly related to the amount of Ce<sup>3+</sup> at the surface. These features plead for the presence of a defect band at the surface, related to the Ce<sup>3+</sup>–Y interaction, as the origin of the ferromagnetism

    V, D, and J segment use in mouse is also highly uneven.

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    <p>Lines indicate cumulative distributions (measured on right-hand side y-axis) (a)–(c). Out of space considerations only V segments present at ≥1% are shown. Insets show cumulative distributions. VDJ combinations also appear unevenly, with the ∼200 most frequent VDJ combinations responsible for 50 percent of all recombination events (d).</p

    Additional file 1: Table S1. of Melanoma genome evolution across species

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    ZMEL1 whole-genome sequencing. This file contains all of the mutations called by MuTect and Shimmer, along with their associated quality scores and overlapping mutations. (XLSX 6276 kb

    V, D, and J segment use in human is highly uneven.

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    <p>Lines indicate cumulative distributions (measured on right-hand side y-axis) (a)–(c). Not all V segments are labeled on the x-axis. V, D, and J segments appear at similar frequencies in two different human subjects (d)–(f). Each point corresponds to a single segment. Insets show cumulative distributions. VDJ combinations also appear unevenly, with the 100 most frequent VDJ combinations responsible for 50 percent of all recombination events (g).</p

    Hierarchical Clustering of Genome-Wide Profiles Identifies Mechanistic Relationships Between Drugs and Functional Relationships Between Genes

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    <div><p>(A) Clustergram containing all strains significant in two or more array experiments. Raw fitness-defect values were hierarchically clustered using Spearman's rank correlation. Colored bars represent gene clusters of note, including NER (<i>RAD2, RAD4, RAD10, RAD14,</i> and <i>RAD1—</i>blue); error-prone TLS (<i>REV1</i> and <i>REV3—</i>red); PRR (<i>RAD6, RAD18,</i> and <i>RAD5—</i>yellow); homologous recombination (<i>RAD57, RAD51,</i> and <i>RAD54—</i>green); cell-cycle checkpoint control (<i>RAD9, RAD24, RAD17, DDC1,</i> and <i>MEC3—</i>orange); and a cluster shown in (B) (<i>SHU2, SHU1, CSM2, MPH1,</i> and <i>PSY3—</i>magenta).</p><p>(B) Zoom view showing one cluster containing the class I NER genes and a second cluster containing several uncharacterized DNA-repair genes. Four of these five genes <i>(SHU1, SHU2, CSM2,</i> and <i>PSY3)</i> are known to encode proteins that physically interact [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0010024#pgen-0010024-b65" target="_blank">65</a>,<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0010024#pgen-0010024-b77" target="_blank">77</a>,<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0010024#pgen-0010024-b78" target="_blank">78</a>].</p><p>(C) Individual growth curves of single and double deletion strains with <i>MPH1</i> in 0.002% MMS. In all panels, the growth of wild-type (BY4741) is represented by the black curve and the growth of <i>mph1Δ</i> by the red curve. The growth of eight different deletion strains <i>(shu1Δ, shu2Δ, csm2Δ, psy3Δ, mag1Δ, mus81Δ, rad51Δ,</i> and <i>rad54Δ)</i> are shown in green, and double mutants, in which the <i>MPH1</i> deletion is added to each of the above, are shown in blue. Double mutants of <i>MPH1, MAG1,</i> and <i>MUS81</i> show additive or synergistic sensitivity to MMS, whereas double mutants of <i>MPH1,</i> with the four other genes in its cluster, show no additional sensitivity to MMS, suggesting that <i>MPH1</i> is epistatic with <i>SHU1, SHU2, CSM2,</i> and <i>PSY3</i>.</p></div

    Additional file 2: Table S2. of Melanoma genome evolution across species

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    ZMEL1 validation primers for MiSeq run. This file contains all of the PCR primer sequences used to validate the subset of 384 called mutations that were validated in the ZMEL1 line via MiSeq. (XLSX 58 kb
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