13 research outputs found

    A Second Look at String-Inspired Models for Proton-Proton Scattering via Pomeron Exchange

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    We re-examine a string dual model for elastic proton-proton scattering via Pomeron exchange. We argue that the method of "Reggeizing" a propagator to take into account an entire trajectory of exchanged particles can be generalized, in particular by modifying the value of the mass-shell parameter in the model. We then fit the generalized model to scattering data at large s and small t. The fitting results are inconclusive, but suggest that a better fit might be obtained by allowing the mass-shell to vary. The model fits the data equally well (roughly) for a wide range of values of the mass-shell parameter, but the other fitting parameters (the slope and intercept of the Regge trajectory, and the coupling constant and dipole mass from the proton-proton-glueball coupling) are then inconsistent with what we expect. On the other hand, using the traditional method of Reggeization generates a weaker fit, but the other parameters obtain more physically reasonable values. In analyzing the fitting results, we also found that our model is more consistent with the sqrt(s) = 1800 GeV coming from the E710 experiment than that coming from the CDF experiment, and that our model has the greatest discrepancy with the data in the range 0.5 GeV^2 < |t| < 0.6 GeV^2, suggesting that the transition from soft Pomeron to hard Pomeron may occur closer to t = -0.5 GeV^2 rather than t = -0.6 GeV^2 as previously thought.Comment: 16 pages, 7 figures, 2 table

    QTL mapping of <i>let-60 ras</i> modifiers.

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    <p><b>(A)</b> RAS/MAPK signaling induces three VPCs. P6.p receives most of the inductive EGF signal from the anchor cell and activates the EGFR/RAS/MAPK pathway inducing the 1° cell fate (green arrows). Lateral signaling via the Notch pathway induces the 2° cell fate in the neighboring VPCs P5.p and P7.p (red arrows). The remaining VPCs (blue) adopt the non-vulval 3° cell fate. <b>(B)</b> Crossing scheme to generate the <i>let-60(n1046gf)</i> miRILs. Hawaii males (red) were crossed with Bristol <i>let-60(n1046gf)</i> mutants (blue). For each example animal, the two chromosomes IV carrying the <i>n1046</i> mutation and another arbitrary chromosome pair are shown. Random segregation of the two parental genomes was allowed except for the <i>let-60(gf)</i> mutation that was kept homozygous from F2 generation onwards. After ten generations of self-fertilization to drive all regions to homozygosity, 228 independent miRILs were obtained. <b>(C)</b> Genotypes and phenotypes of the <i>let-60(gf)</i> miRILs sorted by increasing VI. Genotypes determined by FLP mapping [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005236#pgen.1005236.ref015" target="_blank">15</a>] are plotted on the y-axis versus the miRIL numbers on the x-axis. Hawaii genotypes are indicated with red, Bristol genotypes with blue and missing genotypes with gray colors. The VIs for each miRIL are shown below the genotypes. Error bars indicate the standard error of the mean. <b>(D)</b> QTL mapping identified three regions (QTL1 through QTL3) above the threshold LOD score of 3 (dotted red line). In each of the panels showing chromosomes I through X, the locations of the FLP markers used for genotyping are indicated on the x-axis with vertical lines. For the exact locations of the FLPs used, see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005236#sec011" target="_blank">Materials and Methods</a> and [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005236#pgen.1005236.ref015" target="_blank">15</a>].</p

    Systemic inhibition of RAS/MAPK signaling by Serotonin and its metabolites.

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    <p><b>(A)</b> Function of MAOA in DA and 5-HT degradation. <b>(B)</b> 5-HT levels in total extracts of wild-type and <i>amx-2(ok1235)</i> animals. <b>(C)</b> Effect of DA, 5-HT and its metabolites on the VI of <i>let-60(n1046gf)</i> single and <i>amx-2(ok1235); let-60(n1046gf)</i> double mutants. <b>(D)</b> Examples of (top) a 5-HIAA treated and (bottom) an untreated <i>let-60(n1046gf)</i> L4 larva. The normal vulva and the ectopically induced cells are underlined. <b>(E)</b> Dose-dependent reduction of the VI by 5-HT and <b>(F)</b> 5-HIAA treatments. Note in <b>(E)</b> the different sensitivities of the two strains to 1μM 5-HT. <b>(G)</b> Effect of 5-HIAA on mutations activating the EGFR/RAS/MAPK pathway at different levels. <b>(H)</b> Resistance of some 5-HT pathway mutants to 5-HIAA treatment. Error bars indicate the standard error of the mean. The numbers of animals scored are indicated in brackets or inside the columns. *** indicates p<0.001, ** p<0.01, and n.s. p>0.1 in a Student’s t-test.</p

    5-HIAA inhibits RAS/MAPK signaling and MPK-1 phosphorylation in multiple organs of <i>C</i>. <i>elegans</i>.

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    <p><b>(A)</b> Partial suppression of the germline defect in <i>let-60(ga89ts)</i> mutants treated with 5-HIAA and grown at 25°C. The images show the gonads of 5-HIAA treated (top) and untreated (bottom) young adults. Note the regularly stacked oocytes in 5-HIAA treated and the irregularly stacked and smaller oocytes in untreated animals. <b>(B)</b> Partial suppression of the duct cell duplication phenotype in <i>let-60(n1046gf)</i> mutants by 5-HIAA. The images show the single duct cell in a 5-HIAA treated <i>let-60(n1046gf)</i> L4 larva (top) and the two duct cells in an untreated larva (bottom). The arrows point at the nuclei of the duct cells expressing the <i>lin-48</i>::<i>gfp</i> marker. <b>(C)</b> MPK-1 phosphorylation in total extracts of <i>let-60(n1046gf)</i> single and <i>amx-2(ok1235); let-60(n1046gf)</i> double mutant larvae treated with 4mM 5-HT or 5-HIAA. The ratios of phosphoMPK-1 to total MPK-1 levels were determined in three independent experiments as described in [<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005236#pgen.1005236.ref011" target="_blank">11</a>] and Materials and Methods. Values were normalized to the ratios in untreated animals. The numbers of animals scored are indicated in brackets or inside the columns. *** indicates p<0.001 and ** p<0.01 in a Student’s t-test</p

    AMX-2 negatively regulates RAS/MAPK signaling.

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    <p><b>(A)</b> Fine-mapping of QTL1 with ILs. For each IL, the regions containing the Hawaii (black) genome in the Bristol (grey) background are indicated, and the corresponding VIs are plotted below. Black columns indicate the average VI of three independent lines carrying an introgression and gray columns the average VI of three sibling lines without introgression. Dashed boxes indicate the QTL1a and QTL1b sub-regions. <b>(B)</b> Allele-specific effects of <i>amx-2</i> RNAi compared to empty vector controls. <b>(C)</b> Two copies of Bristol but not Hawaii <i>amx-2</i> rescue the increased VI of <i>amx-2(ok1235); let-60(n1046gf)</i> double mutants. <b>(D)</b> Epistasis analysis of <i>amx-2(ok1235)</i>. The dashed line indicates the wild-type VI of 3. <b>(E-H)</b> Expression pattern of a transcriptional <i>P</i><sub>amx-2</sub>::<i>gfp</i> reporter in the pharynx and head neurons <b>(E)</b>, the adult vulva <b>(F)</b>, the intestine <b>(G)</b> and some rectal cells <b>(H)</b> of L4 larvae. The scale bar is 10μm. <b>(I)</b> Tissue-specific <i>amx-2</i> RNAi. Knock-down in the intestine but not the vulval cells increases the VI of <i>let-60(n1046gf)</i> mutants <b>(J)</b> Quantitative PCR of <i>amx-2</i> and <i>amx-1</i>. Expression levels were normalized to the N2 wild-type Bristol strain. Error bars in <b>(A)</b> to <b>(I)</b> indicate the standard error of the mean and in <b>(J)</b> the standard deviation measured in three independent experiments. The numbers of animals scored are shown inside the columns. *** indicates p<0.001, ** p<0.01, *<0.05 and n.s. p>0.1 in a Student’s t-test.</p

    Constitutional complaint and civil proceedings

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    Raw data for the analysis of N2, CB4856, and the npr-1 mutants. Sheet 1, Lawn leaving behavior of N2 and CB4856 from Bacillus thuringiensis - Raw data for Fig. 1; sheet 2, Lawn leaving behavior of mutants from Bacillus thuringiensis - Raw data for Fig. 4; sheet 3, Surival of N2 and CB4856 on Bacillus thuringiensis - Raw data for Additional file 9; sheet 4, Surival of mutants on Bacillus thuringiensis - Raw data for Fig. 5; sheet 5, Lawn leaving behavior of N2 and CB4856 from Pseudomonas aeruginosa PA14 - Raw data for Additional file 10; sheet 6, Lawn leaving behavior of mutants from Pseudomonas aeruginosa PA14 - Raw data for Fig. 6; sheet 7, Surival of mutants on Pseudomonas PA14 - Raw data for Fig. 5. (XLS 482 kb

    Disparate gain and loss of parasitic abilities among nematode lineages - Fig 1

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    <p><b>Pictures of the head (A, C) and the middle regions (B, D) of two relatively basal representatives of the Tylenchida</b>. This speciose nematode order harbours most of the economically high impact plant-parasitic nematode species. Morphometrics of the stylet, an injection-needle like device used to puncture the plant cell wall (A, C), and the lateral field, indentations in the cuticle present in both sides of the nematode (B, D), are used for species identification. For these pictures, standard light microscopy was combined with differential interference contrast (DIC) optics (magnification: 1,000x).</p

    A generalized overview of the phylogenetic relationships within the phylum Nematoda based on (nearly) full-length small subunit ribosomal DNA (SSU rDNA) sequences.

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    <p>For clade designation, we adhered to Holterman et al. [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0185445#pone.0185445.ref007" target="_blank">7</a>]. Plant parasites are found in Clades 1, 2, 10 and 12, and icons are used to distinguish four types of plant-parasitic nematodes: ectoparasites, semi-endoparasites, migratory endoparasites, and sedentary endoparasites.</p
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