21 research outputs found

    D* Production in Deep Inelastic Scattering at HERA

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    This paper presents measurements of D^{*\pm} production in deep inelastic scattering from collisions between 27.5 GeV positrons and 820 GeV protons. The data have been taken with the ZEUS detector at HERA. The decay channel D+(D0Kπ+)π+D^{*+}\to (D^0 \to K^- \pi^+) \pi^+ (+ c.c.) has been used in the study. The e+pe^+p cross section for inclusive D^{*\pm} production with 5<Q2<100GeV25<Q^2<100 GeV^2 and y<0.7y<0.7 is 5.3 \pms 1.0 \pms 0.8 nb in the kinematic region {1.3<pT(D±)<9.01.3<p_T(D^{*\pm})<9.0 GeV and η(D±)<1.5| \eta(D^{*\pm}) |<1.5}. Differential cross sections as functions of p_T(D^{*\pm}), η(D±),W\eta(D^{*\pm}), W and Q2Q^2 are compared with next-to-leading order QCD calculations based on the photon-gluon fusion production mechanism. After an extrapolation of the cross section to the full kinematic region in p_T(D^{*\pm}) and η\eta(D^{*\pm}), the charm contribution F2ccˉ(x,Q2)F_2^{c\bar{c}}(x,Q^2) to the proton structure function is determined for Bjorken xx between 2 \cdot 104^{-4} and 5 \cdot 103^{-3}.Comment: 17 pages including 4 figure

    Mortality and preoperative cardiac function in vascular amputees: an N-terminal pro-brain natriuretic peptide (NT-proBNP) pilot study

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    Objective: To determine preoperative ventricular function in vascular amputees by measuring N-terminal pro-brain natriuretic peptide (NT-proBNP) and to analyse the relationship between NT-proBNP levels and 30-day postoperative mortality. Design: Prospective pilot study.Subjects and methods: In 19 patients planned for a lower limb amputation for non-reconstructable peripheral arterial disease NT-proBNP was measured the day before amputation.Results: Four amputees died within 30 days after the amputation. In 17 of 19 patients NT-proBNP values were found more than 2 standard deviations above the age corrected reference value. Pre-amputation NT-proBNP levels did not differ significantly between non-survivors and survivors (P = 0.162).Conclusion: Preoperative NT-proBNP levels are not significantly related to 30-day mortality after lower limb amputation procedure. Preoperative NT-proBNP levels are very high, indicating that serious ventricular dysfunction may be present in vascular amputees

    Sponsoring sportif : le choix des activités

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    Les choix sportifs des sponsors : critères de choix économiques, communicationnels (audience des pratiques, couverture médiatique, image et mise en scène de l'évènement) intérêt porté au sport, valeurs attribuées aux sports

    Sialic Acid Glycoengineering Using an Unnatural Sialic Acid for the Detection of Sialoglycan Biosynthesis Defects and On-Cell Synthesis of Siglec Ligands

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    Item does not contain fulltextSialoglycans play a vital role in physiology, and aberrant sialoglycan expression is associated with a broad spectrum of diseases. Since biosynthesis of sialoglycans is only partially regulated at the genetic level, chemical tools are crucial to study their function. Here, we report the development of propargyloxycarbonyl sialic acid (Ac5NeuNPoc) as a powerful tool for sialic acid glycoengineering. Ac5NeuNPoc showed strongly increased labeling efficiency and exhibited less toxicity compared to those of widely used mannosamine analogues in vitro and was also more efficiently incorporated into sialoglycans in vivo. Unlike mannosamine analogues, Ac5NeuNPoc was exclusively utilized in the sialoglycan biosynthesis pathway, allowing a genetic defect in sialic acid biosynthesis to be specifically detected. Furthermore, Ac5NeuNPoc-based sialic acid glycoengineering enabled the on-cell synthesis of high-affinity Siglec-7 ligands and the identification of a novel Siglec-2 ligand. Thus, Ac5NeuNPoc glycoengineering is a highly efficient, nontoxic, and selective approach to study and modulate sialoglycan interactions on living cells.11 p

    A longitudinal study of fitness and activity in girls predisposed to obesity

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    OBJECTIVE: To identify the underlying genetic defect in 5 patients from a consanguineous family with a Walker-Warburg phenotype, together with intracranial calcifications. METHODS: Homozygosity mapping and exome sequencing, followed by Sanger sequencing of the obtained candidate gene, was performed. Expression of the candidate gene was tested by reverse transcription PCR. Patient fibroblasts were converted to myotubes, and the expression and function of dystroglycan was tested by Western blotting. RESULTS: We detected a homozygous loss-of-function frameshift mutation in the DAG1 gene and showed that this mutation results in a complete absence of both alpha- and beta-dystroglycan. CONCLUSIONS: A loss-of-function mutation in DAG1 can result in Walker-Warburg syndrome and is not embryonic lethal

    Cytidine Diphosphate-Ribitol Analysis for Diagnostics and Treatment Monitoring of Cytidine Diphosphate-l-Ribitol Pyrophosphorylase A Muscular Dystrophy

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    BACKGROUND: Many muscular dystrophies currently remain untreatable. Recently, dietary ribitol has been suggested as a treatment for cytidine diphosphate (CDP)-l-ribitol pyrophosphorylase A (CRPPA, ISPD), fukutin (FKTN), and fukutin-related protein (FKRP) myopathy, by raising CDP-ribitol concentrations. Thus, to facilitate fast diagnosis, treatment development, and treatment monitoring, sensitive detection of CDP-ribitol is required. METHODS: An LC-MS method was optimized for CDP-ribitol in human and mice cells and tissues. RESULTS: CDP-ribitol, the product of CRPPA, was detected in all major human and mouse tissues. Moreover, CDP-ribitol concentrations were reduced in fibroblasts and skeletal muscle biopsies from patients with CRPPA myopathy, showing that CDP-ribitol could serve as a diagnostic marker to identify patients with CRPPA with severe Walker-Warburg syndrome and mild limb-girdle muscular dystrophy (LGMD) phenotypes. A screen for potentially therapeutic monosaccharides revealed that ribose, in addition to ribitol, restored CDP-ribitol concentrations and the associated O-glycosylation defect of alpha-dystroglycan. As the effect occurred in a mutation-dependent manner, we established a CDP-ribitol blood test to facilitate diagnosis and predict individualized treatment response. Ex vivo incubation of blood cells with ribose or ribitol restored CDP-ribitol concentrations in a patient with CRPPA LGMD. CONCLUSIONS: Sensitive detection of CDP-ribitol with LC-MS allows fast diagnosis of patients with severe and mild CRPPA myopathy. Ribose offers a readily testable dietary therapy for CRPPA myopathy, with possible applicability for patients with FKRP and FKTN myopathy. Evaluation of CDP-ribitol in blood is a promising tool for the evaluation and monitoring of dietary therapies for CRPPA myopathy in a patient-specific manner
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