Anisotropy in the helicity modulus of a 3D XY-model: application to YBCO

We present a Monte Carlo study of the helicity moduli of an anisotropic classical three-dimensional (3D) XY-model of YBCO in superconducting state. It is found that both the ab-plane and the c-axis helicity moduli, which are proportional to the inverse square of the corresponding magnetic field penetration depth, vary linearly with temperature at low temperatures. The result for the c-axis helicity modulus is in disagreement with the experiments on high quality samples of YBCO. Thus we conclude that purely classical phase fluctuations of the superconducting order parameter cannot account for the observed c-axis electrodynamics of YBCO.Comment: 7 pages, 1 figur

Magnetization Jump in a Model for Flux Lattice Melting at Low Magnetic Fields

Using a frustrated XY model on a lattice with open boundary conditions, we numerically study the magnetization change near a flux lattice melting transition at low fields. In both two and three dimensions, we find that the melting transition is followed at a higher temperature by the onset of large dissipation associated with the zero-field XY transition. It is characterized by the proliferation of vortex-antivortex pairs (in 2D) or vortex loops (in 3D). At the upper transition, there is a sharp increase in magnetization, in qualitative agreement with recent local Hall probe experiments.Comment: updated figures and texts. new movies available at http://www.physics.ohio-state.edu:80/~ryu/jj.html. Accepted for publication in Physical Review Letter

Body weight changes and incidence of cachexia after stroke

Background: Body weight loss is a frequent complication after stroke, and its adverse effect on clinical outcome has been shown in several clinical trials. The purpose of this prospective longitudinal single-centre observational study was to investigate dynamical changes of body composition and body weight after ischemic stroke and an association with functional outcome. Methods: Sixty-seven consecutive patients (age 69 ± 11 years, body mass index 27.0 ± 4.1 kg/m2, 42% female patient, mean ± SD) with acute ischemic stroke with mild to moderate neurological deficit (National Institute of Health Stroke Scale median 4, ranged 0–12) were analysed in the acute phase (4 ± 2 days) and at 12 months (389 ± 26 days) follow-up. Body composition was examined by dual energy X-ray absorptiometry. Cachexia was defined according to the consensus definition by body weight loss ≥5% within 1 year and additional clinical signs. Lean tissue wasting was considered if a ratio of upper and lower limbs lean mass sum to squared height (kg/m2) was ≤5.45 kg/m2 for female patient and ≤7.25 kg/m2 for male patient. Results: According to the body weight changes after 12 months, 42 (63%) patients had weight gain or stable weight, 11 (16%) patients had moderate weight loss, and 14 (21%) patients became cachectic. A relative decline of 19% of fat tissue and 6.5% of lean tissue was observed in cachectic patients, while no changes of lean tissue were observed in non-cachectic patients after 12 months. The modified Rankin Scale was 48% higher (2.1 ± 1.6, P < 0.05), Barthel Index was 22% lower (71 ± 39, P < 0.01), and handgrip strength was 34% lower (21.9 ± 13.0, P < 0.05) in cachectic compared to non-cachectic patients after 12 months. The low physical performance if defined by Barthel Index <60 points was linked to the lean tissue wasting (OR 44.8, P < 0.01), presence of cachexia (OR 20.8, P < 0.01), and low body mass index <25 kg/m2 (OR 11.5, P < 0.05). After adjustment for cofounders, lean tissue wasting remained independently associated with the low physical performance at 12 months follow-up (OR 137.9, P < 0.05). Conclusions: In this cohort study, every fifth patient with ischemic stroke fulfilled the criteria of cachexia within 12 months after index event. The incidence of cachexia was 21%. Cachectic patients showed the lowest functional and physical capacity

Molecular Dynamics Simulation of Compressible Fluid Flow in Two-Dimensional Channels

We study compressible fluid flow in narrow two-dimensional channels using a novel molecular dynamics simulation method. In the simulation area, an upstream source is maintained at constant density and temperature while a downstream reservoir is kept at vacuum. The channel is sufficiently long in the direction of the flow that the finite length has little effect on the properties of the fluid in the central region. The simulated system is represented by an efficient data structure, whose internal elements are created and manipulated dynamically in a layered fashion. Consequently the code is highly efficient and manifests completely linear performance in simulations of large systems. We obtain the steady-state velocity, temperature, and density distributions in the system. The velocity distribution across the channel is very nearly a quadratic function of the distance from the center of the channel and reveals velocity slip at the boundaries; the temperature distribution is only approximately a quartic function of this distance from the center to the channel. The density distribution across the channel is non-uniform. We attribute this non-uniformity to the relatively high Mach number, approximately 0.5, in the fluid flow. An equation for the density distribution based on simple compressibility arguments is proposed; its predictions agree well with the simulation results. Validity of the concept of local dynamic temperature and the variation of the temperature along the channel are discussed.Comment: 16 pages (in latex) + 8 figures (in a single ps file). Submitted to the Physical Review

On the theory of diamagnetism in granular superconductors

We study a highly disordered network of superconducting granules linked by weak Josephson junctions in magnetic field and develop a mean field theory for this problem. The diamagnetic response to a slow {\it variations} of magnetic field is found to be analogous to the response of a type-II superconductor with extremely strong pinning. We calculate an effective penetration depth $\lambda_g$ and critical current $j_c$ and find that both $\lambda_g^{-1}$ and $j_c$ are non-zero but are strongly suppressed by frustration.Comment: REVTEX, 12 pages, two Postscript figure

Nonlinear Seebeck Effect in a Model Granular Superconductor

The change of the Josephson supercurrent density of a weakly-connected granular superconductor in response to externally applied arbitrary thermal gradient dT/dx (nonlinear Seebeck effect) is considered within a model of 3D Josephson junction arrays. For dT/dx>(dT/dx)_c, where (dT/dx)_c is estimated to be of the order of 10^4 K/m for YBCO ceramics with an average grain's size of 10 microns, the weak-links-dominated thermopower S (Seebeck coefficient) is predicted to become strongly dT/dx-dependent.Comment: REVTEX, no figure

Systemic Inflammation Mediates Age-Related Cognitive Deficits

The association between systemic inflammation and cognitive deficits is well-documented. Further, previous studies have shown that systemic inflammation levels increase with age. The present study took a novel approach by examining the extent to which systemic inflammation levels mediated age-related cognitive decline. Forty-seven young and 46 older generally healthy adults completed two cognitive tasks measuring processing speed and short-term memory, respectively. Serum concentrations of three inflammatory biomarkers (including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP)) were measured in each participant. Both cognitive measures showed age-related deficits. In addition, levels of IL-6 and TNF-α were elevated with age. IL-6 partially mediated the difference in processing speed between the young and the older participant age group; there was no mediation effect for TNF-α and CRP. Considering chronological age, IL-6 partially accounted for age-related impairment in processing speed within older but not young participants. No effects were found for short-term memory. Evidence from this research supports the role of inflammatory processes in age-related cognitive decline. Processes involved in this mediation and differences in inflammatory influence on specific cognitive functions are discussed