190 research outputs found

    Studying model suspensions using high resolution synchrotron X-ray microtomography

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    The addition of minor quantities of secondary liquids to suspensions may lead to a transition from a fluid-like structure to paste-like structure for the system. Previous studies have shown how rheological properties such as viscosity and yield stress are affected, however, qualitative visual observation on the micro-scale during both short and long term storage has yet to be achieved or reported. This research focuses on the movement of a secondary immiscible liquid (water or saturated sucrose solution) when added to a model food system. The model food system used in this study is a suspension of sucrose particles in a continuous oil phase to better understand the interactions between the particles and the liquid phases present. This was accomplished using dynamic X-ray computer tomography to study the behaviour of the sample. This non-destructive approach allowed the movement of the secondary liquid as well as the solid particles from the bulk suspension to be monitored through a time lapse of scans. This was achieved by observing the changes in the grey scale range of the droplet with time, which was then correlated to the uptake and movement of sucrose into the secondary liquid using an innovative method. This movement was due to the hydrophilicity and solubility of sucrose with gravity/sedimentation playing a minimal role

    A Non-parametric Approach to Measuring the \kpi{} Amplitudes in \dpkkpi{} Decay

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    Using a large sample of \dpkkpi{} decays collected by the FOCUS photoproduction experiment at Fermilab, we present the first non-parametric analysis of the \kpi{} amplitudes in \dpkkpi{} decay. The technique is similar to the technique used for our non-parametric measurements of the \krzmndk{} form factors. Although these results are in rough agreement with those of E687, we observe a wider S-wave contribution for the \ksw{} contribution than the standard, PDG \cite{pdg} Breit-Wigner parameterization. We have some weaker evidence for the existence of a new, D-wave component at low values of the Kπ+K^- \pi^+ mass.Comment: 13 pages 3 figure

    A Study of D0 --> K0(S) K0(S) X Decay Channels

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    Using data from the FOCUS experiment (FNAL-E831), we report on the decay of D0D^0 mesons into final states containing more than one KS0K^0_S. We present evidence for two Cabibbo favored decay modes, D0KS0KS0Kπ+D^0\to K^0_SK^0_S K^- \pi^+ and D0KS0KS0K+πD^0\to K^0_SK^0_S K^+ \pi^-, and measure their combined branching fraction relative to D0Kˉ0π+πD^0\to \bar{K} ^0\pi^+\pi^- to be Γ(D0KS0KS0K±π)Γ(D0Kˉ0π+π)\frac{\Gamma(D^0\to K^0_SK^0_SK^{\pm}\pi^{\mp})}{\Gamma(D^0\to \bar{K} ^0\pi^+\pi^-)} = 0.0106 ±\pm 0.0019 ±\pm 0.0010. Further, we report new measurements of Γ(D0KS0KS0KS0)Γ(D0Kˉ0π+π)\frac{\Gamma(D^0\to K^0_SK^0_SK^0_S)}{\Gamma(D^0\to \bar{K} ^0\pi^+\pi^-)} = 0.0179 ±\pm 0.0027 ±\pm 0.0026, Γ(D0K0Kˉ0)Γ(D0Kˉ0π+π)\frac{\Gamma(D^0\to K^0\bar{K} ^0)}{\Gamma(D^0\to \bar{K} ^0\pi^+\pi^-)} = 0.0144 ±\pm 0.0032 ±\pm 0.0016, and Γ(D0KS0KS0π+π)Γ(D0Kˉ0π+π)\frac{\Gamma(D^0\to K^0_SK^0_S\pi^+\pi^-)}{\Gamma(D^0\to \bar{K} ^0\pi^+\pi^-)} = 0.0208 ±\pm 0.0035 ±\pm 0.0021 where the first error is statistical and the second is systematic.Comment: 11 pages, 3 figures, typos correcte

    Study of Cabibbo Suppressed Decays of the Ds Charmed-Strange Meson involving a KS

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    We study the decay of Ds meson into final states involving a Ks and report the discovery of Cabibbo suppressed decay modes Ds -> Kspi-pi+pi+ (179 +/- 36 events) and Ds -> Kspi+ (113 +/-26 events). The branching ratios for the new modes are Gamma(Ds -> Kspi-pi+pi+)/Gamma(Ds -> KsK-pi+pi+) = 0.18 +/- 0.04 +/- 0.05 and Gamma(Ds -> Kspi+)/Gamma(Ds -> KsK+) = 0.104 +/- 0.024 +/- 0.013.Comment: 11 pages, 6 figure

    The Kπ+K^-\pi^+ S-wave from the D+Kπ+π+D^+ \to K^-\pi^+\pi^+ decay

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    Using data from FOCUS (E831) experiment at Fermilab, we present a model independent partial-wave analysis of the Kπ+K^-\pi^+ S-wave amplitude from the decay D+Kπ+π+D^+ \to K^-\pi^+\pi^+. The S-wave is a generic complex function to be determined directly from the data fit. The P- and D-waves are parameterized by a sum of Breit-Wigner amplitudes. The measurement of the S-wave amplitude covers the whole elastic range of the Kπ+K^-\pi^+ system.Comment: 13 pages, 9 figures, submitted to Physics Letters

    RTL551 Treatment of EAE Reduces CD226 and T-bet+ CD4 T Cells in Periphery and Prevents Infiltration of T-bet+ IL-17, IFN-γ Producing T Cells into CNS

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    Recombinant T cell receptor ligands (RTLs) that target encephalitogenic T-cells can reverse clinical and histological signs of EAE, and are currently in clinical trials for treatment of multiple sclerosis. To evaluate possible regulatory mechanisms, we tested effects of RTL therapy on expression of pathogenic and effector T-cell maturation markers, CD226, T-bet and CD44, by CD4+ Th1 cells early after treatment of MOG-35-55 peptide-induced EAE in C57BL/6 mice. We showed that 1–5 daily injections of RTL551 (two-domain I-Ab covalently linked to MOG-35-55 peptide), but not the control RTL550 (“empty” two-domain I-Ab without a bound peptide) or Vehicle, reduced clinical signs of EAE, prevented trafficking of cells outside the spleen, significantly reduced the frequency of CD226 and T-bet expressing CD4+ T-cells in blood and inhibited expansion of CD44 expressing CD4+ T-cells in blood and spleen. Concomitantly, RTL551 selectively reduced CNS inflammatory lesions, absolute numbers of CNS infiltrating T-bet expressing CD4+ T-cells and IL-17 and IFN-γ secretion by CNS derived MOG-35-55 reactive cells cultured ex vivo. These novel results demonstrate that a major effect of RTL therapy is to attenuate Th1 specific changes in CD4+ T-cells during EAE and prevent expansion of effector T-cells that mediate clinical signs and CNS inflammation in EAE

    Pleosporales

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    One hundred and five generic types of Pleosporales are described and illustrated. A brief introduction and detailed history with short notes on morphology, molecular phylogeny as well as a general conclusion of each genus are provided. For those genera where the type or a representative specimen is unavailable, a brief note is given. Altogether 174 genera of Pleosporales are treated. Phaeotrichaceae as well as Kriegeriella, Zeuctomorpha and Muroia are excluded from Pleosporales. Based on the multigene phylogenetic analysis, the suborder Massarineae is emended to accommodate five families, viz. Lentitheciaceae, Massarinaceae, Montagnulaceae, Morosphaeriaceae and Trematosphaeriaceae

    Asymmetric Bidirectional Transcription from the FSHD-Causing D4Z4 Array Modulates DUX4 Production

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    Facioscapulohumeral Disease (FSHD) is a dominantly inherited progressive myopathy associated with aberrant production of the transcription factor, Double Homeobox Protein 4 (DUX4). The expression of DUX4 depends on an open chromatin conformation of the D4Z4 macrosatellite array and a specific haplotype on chromosome 4. Even when these requirements are met, DUX4 transcripts and protein are only detectable in a subset of cells indicating that additional constraints govern DUX4 production. Since the direction of transcription, along with the production of non-coding antisense transcripts is an important regulatory feature of other macrosatellite repeats, we developed constructs that contain the non-coding region of a single D4Z4 unit flanked by genes that report transcriptional activity in the sense and antisense directions. We found that D4Z4 contains two promoters that initiate sense and antisense transcription within the array, and that antisense transcription predominates. Transcriptional start sites for the antisense transcripts, as well as D4Z4 regions that regulate the balance of sense and antisense transcripts were identified. We show that the choice of transcriptional direction is reversible but not mutually exclusive, since sense and antisense reporter activity was often present in the same cell and simultaneously upregulated during myotube formation. Similarly, levels of endogenous sense and antisense D4Z4 transcripts were upregulated in FSHD myotubes. These studies offer insight into the autonomous distribution of muscle weakness that is characteristic of FSHD

    A cre-inducible DUX4 transgenic mouse model for investigating facioscapulohumeral muscular dystrophy

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    The Double homeobox 4 (DUX4) gene is an important regulator of early human development and its aberrant expression is causal for facioscapulohumeral muscular dystrophy (FSHD). The DUX4-full length (DUX4-fl) mRNA splice isoform encodes a transcriptional activator; however, DUX4 and its unique DNA binding preferences are specific to old-world primates. Regardless, the somatic cytotoxicity caused by DUX4 expression is conserved when expressed in cells and animals ranging from fly to mouse. Thus, viable animal models based on DUX4-fl expression have been difficult to generate due in large part to overt developmental toxicity of low DUX4-fl expression from leaky transgenes. We have overcome this obstacle and here we report the generation and initial characterization of a line of conditional floxed DUX4-fl transgenic mice, FLExDUX4, that is viable and fertile. In the absence of cre, these mice express a very low level of DUX4-fl mRNA from the transgene, resulting in mild phenotypes. However, when crossed with appropriate cre-driver lines of mice, the double transgenic offspring readily express DUX4-fl mRNA, protein, and target genes with the spatiotemporal pattern of nuclear cre expression dictated by the chosen system. When cre is expressed from the ACTA1 skeletal muscle-specific promoter, the double transgenic animals exhibit a developmental myopathy. When crossed with tamoxifen-inducible cre lines, DUX4-mediated pathology can be induced in adult animals. Thus, the appearance and progression of pathology can be controlled to provide readily screenable phenotypes useful for assessing therapeutic approaches targeting DUX4-fl mRNA and protein. Overall, the FLExDUX4 line of mice is quite versatile and will allow new investigations into mechanisms of DUX4-mediated pathophysiology as well as much-needed pre-clinical testing of DUX4-targeted FSHD interventions in vivo
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