996 research outputs found

    Vortex Solid-Liquid Transition in Bi2_{2}Sr2_{2}CaCu2_{2}O8+δ_{8+\delta} with a High Density of Strong Pins

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    The introduction of a large density of columnar defects in %underdoped Bi2_{2}Sr2_{2}CaCu2_{2}O8+δ_{8+\delta} crystals does not, at sufficiently low vortex densities, increase the irreversibility line beyond the first order transition (FOT) field of pristine crystals. At such low fields, the flux line wandering length rwr_{w} behaves as in pristine %Bi2_{2}Sr2_{2}CaCu2_{2}O8+δ_{8+\delta} crystals. Next, vortex positional correlations along the cc--axis in the vortex Bose glass at fields above the FOT are smaller than in the low--field vortex solid. Third, the Bose-glass-to-vortex liquid transition is signaled by a rapid decrease in c-axis phase correlations. These observations are understood in terms of the ``discrete superconductor'' model.Comment: 4 pages, 4 figures Submitted to Phys. Rev. B Rapid Comm. 16-1-2004 Revised version 18-3-200

    The magnetization of PrFeAsO0.60_{0.60}F$_{0.12} sueprconductor

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    The magnetization of the PrFeAsO0.60_{0.60}F0.12_{0.12} polycrystalline sample has been measured as functions of temperature and magnetic field (H)(H). The observed total magnetization is the sum of a superconducting irreversible magnetization (MsM_s) and a paramagnetic magnetization (MpM_p). Analysis of dc susceptibility χ(T)\chi(T) in the normal state shows that the paramagnetic component of magnetization comes from the Pr+3^{+3} magnetic moments. The intragrain critical current density (JL)(J_L) derived from the magnetization measurement is large. The JL(H)J_L(H) curve displays a second peak which shifts towards the high-field region with decreasing temperature. In the low-field region, a plateau up to a field H∗H^* followed by a power law H−5/8H^{-5/8} behavior of JL(H)J_L(H) is the characteristic of the strong pinning. A vortex phase diagram for the present superconductor has been obtained from the magnetization and resistivity data.Comment: A revised version with modified title,8 pages, 7 figure

    Timing and mechanism of the rise of the Shillong Plateau in the Himalayan foreland

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    The Shillong Plateau (northeastern India) constitutes the only significant topography in the Himalayan foreland. Knowledge of its surface uplift history is key to understanding topographic development and unraveling tectonic–climate–topographic coupling in the eastern Himalaya. We use the sedimentary record of the Himalayan foreland basin north of the Shillong Plateau to show that the paleo-Brahmaputra river was redirected north and west by the rising plateau at 5.2–4.9 Ma. We suggest that onset of plateau uplift is a result of increased fault-slip rates in response to stresses caused by the Indian lithosphere bending beneath the Himalaya

    New High Field State of Flux Line Lattice in Unconventional Superconductor CeCoIn_5

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    Ultrasound velocity measurements of the unconventional superconductor CeCoIn_5 with extremely large Pauli paramagnetic susceptibility reveal an unusual structural transformation of the flux line lattice (FLL) in the vicinity of the upper critical field. The transition field coincides with that at which heat capacity measurements reveal a second order phase transition. The lowering of the sound velocity at the transition is consistent with the collapse of the FLL tilt modulus and a crossover to quasi two-dimensional FLL pinning. These results provide a strong evidence that the high field state is the Fulde-Ferrel-Larkin-Ovchinikov phase, in which the order parameter is spatially modulated and has planar nodes aligned perpendicular to the vortices.Comment: 5 pages, 4 figure

    Intracoronary infusion of mononuclear cells after PCI-treated myocardial infarction and arrhythmogenesis: is it safe?

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    To reduce long-term morbidity after revascularised acute myocardial infarction, different therapeutic strategies have been investigated. Cell therapy with mononuclear cells from bone marrow (BMMC) or peripheral blood (PBMC) has been proposed to attenuate the adverse processes of remodelling and subsequent heart failure. Previous trials have suggested that cell therapy may facilitate arrhythmogenesis. In the present substudy of the HEBE cell therapy trial, we investigated whether intracoronary cell therapy alters the prevalence of ventricular arrhythmias after 1 month or the rate of severe arrhythmogenic events (SAE) in the first year. In 164 patients of the trial we measured function and infarct size with cardiovascular magnetic resonance (CMR) imaging. Holter registration was performed after 1 month from which the number of triplets (3 successive PVCs) and ventricular tachycardias (VT, ≥4 successive PVCs) was assessed. Thirty-three patients (20%) showed triplets and/or VTs, with similar distribution amongst the groups (triplets: control n = 8 vs. BMMC n = 9, p = 1.00; vs. PBMC n = 10, p = 0.67. VT: control n = 9 vs. BMMC n = 9, p = 0.80; vs. PBMC n = 11, p = 0.69). SAE occurred in 2 patients in the PBMC group and 1 patient in the control group. In conclusion, intracoronary cell therapy is not associated with an increase in ventricular arrhythmias or SAE

    Depinning transition in type-II superconductors

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    The surface impedance Z(f) of conventional isotropic materials has been carefully measured for frequencies f ranging from 1 kHz to 3 MHz, allowing a detailed investigation of the depinning transition. Our results exhibit the irrelevance of classical ideas to the dynamics of vortex pinning. We propose a new picture, where the linear ac response is entirely governed by disordered boundary conditions of a rough surface, whereas in the bulk vortices respond freely. The universal law for Z(f) thus predicted is in remarkable agreement with experiment, and tentatively applies to microwave data in YBaCuO films.Comment: 4 pages, 4 figures, 14 reference

    Naturally Occurring Lipid A Mutants in Neisseria meningitidis from Patients with Invasive Meningococcal Disease Are Associated with Reduced Coagulopathy

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    Neisseria meningitidis is a major cause of bacterial meningitis and sepsis worldwide. Lipopolysaccharide (LPS), a major component of the Gram-negative bacterial outer membrane, is sensed by mammalian cells through Toll-like receptor 4 (TLR4), resulting in activation of proinflammatory cytokine pathways. TLR4 recognizes the lipid A moiety of the LPS molecule, and the chemical composition of the lipid A determines how well it is recognized by TLR4. N. meningitidis has been reported to produce lipid A with six acyl chains, the optimal number for TLR4 recognition. Indeed, meningococcal sepsis is generally seen as the prototypical endotoxin-mediated disease. In the present study, we screened meningococcal disease isolates from 464 patients for their ability to induce cytokine production in vitro. We found that around 9% of them were dramatically less potent than wild-type strains. Analysis of the lipid A of several of the low-activity strains by mass spectrometry revealed they were penta-acylated, suggesting a mutation in the lpxL1 or lpxL2 genes required for addition of secondary acyl chains. Sequencing of these genes showed that all the low activity strains had mutations that inactivated the lpxL1 gene. In order to see whether lpxL1 mutants might give a different clinical picture, we investigated the clinical correlate of these mutations in a prospective nationwide observational cohort study of adults with meningococcal meningitis. Patients infected with an lpxL1 mutant presented significantly less frequently with rash and had higher thrombocyte counts, consistent with reduced cytokine induction and less activation of tissue-factor mediated coagulopathy. In conclusion, here we report for the first time that a surprisingly large fraction of meningococcal clinical isolates have LPS with underacylated lipid A due to mutations in the lpxL1 gene. The resulting low-activity LPS may have an important role in virulence by aiding the bacteria to evade the innate immune system. Our results provide the first example of a specific mutation in N. meningitidis that can be correlated with the clinical course of meningococcal disease
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