23 research outputs found

    The new Magnetic Measurement System at the Advanced Photon Source

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    A new system for precise measurements of the field integrals and multipole components of the APS magnetic insertion devices is described. A stretched coil is used to measure magnetic field characteristics. The hardware includes a number of servomotors to move (translate or rotate) the coil and a fast data acquisition board to measure the coil signal. A PC under Linux is used as a control workstation. The user interface is written as a Tcl/tk script. The hardware is accessed from the script through a shared C-library. A description of the hardware system and the control program is given.Comment: 3 pages, 5 figures, paper 3271 submitted to ICALEPCS 2001 Conferenc

    Phagocytosis depends on TRPV2-mediated calcium influx and requires TRPV2 in lipids rafts: alteration in macrophages from patients with cystic fibrosis.

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    Whereas many phagocytosis steps involve ionic fluxes, the underlying ion channels remain poorly defined. As reported in mice, the calcium conducting TRPV2 channel impacts the phagocytic process. Macrophage phagocytosis is critical for defense against pathogens. In cystic fibrosis (CF), macrophages have lost their capacity to act as suppressor cells and thus play a significant role in the initiating stages leading to chronic inflammation/infection. In a previous study, we demonstrated that impaired function of CF macrophages is due to a deficient phagocytosis. The aim of the present study was to investigate TRPV2 role in the phagocytosis capacity of healthy primary human macrophage by studying its activity, its membrane localization and its recruitment in lipid rafts. In primary human macrophages, we showed that P. aeruginosa recruits TRPV2 channels at the cell surface and induced a calcium influx required for bacterial phagocytosis. We presently demonstrate that to be functional and play a role in phagocytosis, TRPV2 might require a preferential localization in lipid rafts. Furthermore, CF macrophage displays a perturbed calcium homeostasis due to a defect in TRPV2. In this context, deregulated TRPV2-signaling in CF macrophages could explain their defective phagocytosis capacity that contribute to the maintenance of chronic infection

    Self-amplified spontaneous emission saturation at the Advanced Photon Source free-electron laser (abstract) (invited)

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    A Hepatic Protein, Fetuin-A, Occupies a Protective Role in Lethal Systemic Inflammation

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    A liver-derived protein, fetuin-A, was first purified from calf fetal serum in 1944, but its potential role in lethal systemic inflammation was previously unknown. This study aims to delineate the molecular mechanisms underlying the regulation of hepatic fetuin-A expression during lethal systemic inflammation (LSI), and investigated whether alterations of fetuin-A levels affect animal survival, and influence systemic accumulation of a late mediator, HMGB1.LSI was induced by endotoxemia or cecal ligation and puncture (CLP) in fetuin-A knock-out or wild-type mice, and animal survival rates were compared. Murine peritoneal macrophages were challenged with exogenous (endotoxin) or endogenous (IFN-Îł) stimuli in the absence or presence of fetuin-A, and HMGB1 expression and release was assessed. Circulating fetuin-A levels were decreased in a time-dependent manner, starting between 26 h, reaching a nadir around 24-48 h, and returning towards base-line approximately 72 h post onset of endotoxemia or sepsis. These dynamic changes were mirrored by an early cytokine IFN-Îł-mediated inhibition (up to 50-70%) of hepatic fetuin-A expression. Disruption of fetuin-A expression rendered animals more susceptible to LSI, whereas supplementation of fetuin-A (20-100 mg/kg) dose-dependently increased animal survival rates. The protection was associated with a significant reduction in systemic HMGB1 accumulation in vivo, and parallel inhibition of IFN-Îł- or LPS-induced HMGB1 release in vitro.These experimental data suggest that fetuin-A is protective against lethal systemic inflammation partly by inhibiting active HMGB1 release

    Voltage-dependent translocation of R18 and DiI across lipid bilayers leads to fluorescence changes.

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    We show that the lipophilic, cationic fluorescent dyes R18 and Dil translocate from one monolayer of a phospholipid bilayer membrane to the other in a concentration and voltage-dependent manner. When the probes were incorporated into voltage-clamped planar membranes and potentials were applied, displacement currents resulted. The charged probes sensed a large fraction of the applied field. When these probes were added to only one monolayer, displacement currents were symmetrical around 0 mV, indicating that the probes distributed equally between the two monolayers. Charge translocation required that the bilayer be fluid. When membranes were in a condensed gel phase, displacement currents were not observed; raising the temperature to above the gel-liquid crystalline transition restored the currents. Translocation of R18 was also shown by fluorescence measurements. When R18 was in the bilayer at high, self-quenching concentrations, voltage pulses led to voltage-dependent fluorescence changes. The kinetics of the fluorescence changes and charge translocations correlated. Adding the quencher I- to one aqueous phase caused fluorescence to decrease or increase when voltage moved R18 toward or away from the quencher at low, nonquenching concentrations of R18. In contrast to R18, Dil incorporated into bilayers was a carrier fo I-, and hence I- altered Dil currents. Voltage-driven translocations allow R18 and Dil to be used to probe membrane potential changes

    Characterization of Cracks and their Effects on the Effective Transport Pathways in Ni-YSZ Anodes after Reoxidation Using X-Ray Nanotomography

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    Reduction-oxidation cycling of Ni-based electrodes for solid oxide fuel/electrolysis cells irreversibly alters their microstructure and can cause the fracture of the electrolyte. Non-destructive 3-D imaging enables tracking of microstructural changes that occur during cycling. Despite recent advances, the understanding of how local 3-D geometrical features in the heterogeneous electrode material contribute to the material degradation remains incomplete. Absorption contrast X-ray nanotomography (XNT) of a same Ni(O)-yttria-stabilized zirconia (YSZ) sample was performed at the Ni K-edge white-line peak (8348 eV), before and after exposure to air at 800°C during 45 minutes. A complimentary XNT at 8376 eV confirmed a degree of oxidation in the range of 98%. The morphology of the Ni(O) phase was as expected completely different after re-oxidation. The spatial resolution better than 20 nm enabled the detection of cracks in the brittle YSZ phase above this dimension. The detrimental effects of the cracks on the effective 3-D transport pathways in the Ni-YSZ anode under polarization was investigated using a skeleton-based discrete representation of the imaged volume and an analytical electrochemical fin model. Topological properties, effective ionic conductivity and polarization resistance were calculated before and after oxidation. For the latter estimate, the effect of the cracked YSZ network was considered alone so far; that of the spatial redistribution of triple-phase boundaries induced by re-oxidation will be included in the future. Cracks in the brittle YSZ phase induced an increase in the effective ionic resistivity and in the polarization resistance in the range of 25 ± 9% and 12 ± 5%, respectively
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