Applicability of layered sine-Gordon models to layered superconductors: II. The case of magnetic coupling

In this paper, we propose a quantum field theoretical renormalization group approach to the vortex dynamics of magnetically coupled layered superconductors, to supplement our earlier investigations on the Josephson-coupled case. We construct a two-dimensional multi-layer sine-Gordon type model which we map onto a gas of topological excitations. With a special choice of the mass matrix for our field theoretical model, vortex dominated properties of magnetically coupled layered superconductors can be described. The well known interaction potentials of fractional flux vortices are consistently obtained from our field-theoretical analysis, and the physical parameters (vortex fugacity and temperature parameter) are also identified. We analyse the phase structure of the multi-layer sine--Gordon model by a differential renormalization group method for the magnetically coupled case from first principles. The dependence of the transition temperature on the number of layers is found to be in agreement with known results based on other methods.Comment: 7 pages, 1 figure, published in J. Phys.: Condens. Matte

Larkin-Ovchinnikov-Fulde-Ferrell state in quasi-one-dimensional superconductors

The properties of a quasi-one-dimensional (quasi-1D) superconductor with {\it an open Fermi surface} are expected to be unusual in a magnetic field. On the one hand, the quasi-1D structure of the Fermi surface strongly favors the formation of a non-uniform state (Larkin-Ovchinnikov-Fulde-Ferrell (LOFF) state) in the presence of a magnetic field acting on the electron spins. On the other hand, a magnetic field acting on an open Fermi surface induces a dimensional crossover by confining the electronic wave-functions wave-functions along the chains of highest conductivity, which results in a divergence of the orbital critical field and in a stabilization at low temperature of a cascade of superconducting phases separated by first order transistions. In this paper, we study the phase diagram as a function of the anisotropy. We discuss in details the experimental situation in the quasi-1D organic conductors of the Bechgaard salts family and argue that they appear as good candidates for the observation of the LOFF state, provided that their anisotropy is large enough. Recent experiments on the organic quasi-1D superconductor (TMTSF)$_2$ClO$_4$ are in agreement with the results obtained in this paper and could be interpreted as a signature of a high-field superconducting phase. We also point out the possibility to observe a LOFF state in some quasi-2D organic superconductors.Comment: 24 pages+17 figures (upon request), RevTex, ORSAY-LPS-24109

Treatment with apolipoprotein A-1 mimetic peptide reduces lupus-like manifestations in a murine lupus model of accelerated atherosclerosis

Abstract Introduction The purpose of this study was to evaluate the effects of L-4F, an apolipoprotein A-1 mimetic peptide, alone or with pravastatin, in apoE-/-Fas-/-C57BL/6 mice that spontaneously develop immunoglobulin G (IgG) autoantibodies, glomerulonephritis, osteopenia, and atherosclerotic lesions on a normal chow diet. Methods Female mice, starting at eight to nine weeks of age, were treated for 27 weeks with 1) pravastatin, 2) L-4F, 3) L-4F plus pravastatin, or 4) vehicle control, followed by disease phenotype assessment. Results In preliminary studies, dysfunctional, proinflammatory high-density lipoproteins (piHDL) were decreased six hours after a single L-4F, but not scrambled L-4F, injection in eight- to nine-week old mice. After 35 weeks, L-4F-treated mice, in the absence/presence of pravastatin, had significantly smaller lymph nodes and glomerular tufts (PL, LP < 0.05), lower serum levels of IgG antibodies to double stranded DNA (dsDNA) (PL < 0.05) and oxidized phospholipids (oxPLs) (PL, LP < 0.005), and elevated total and vertebral bone mineral density (PL, LP < 0.01) compared to vehicle controls. Although all treatment groups presented larger aortic root lesions compared to vehicle controls, enlarged atheromas in combination treatment mice had significantly less infiltrated CD68+ macrophages (PLP < 0.01), significantly increased mean α-actin stained area (PLP < 0.05), and significantly lower levels of circulating markers for atherosclerosis progression, CCL19 (PL, LP < 0.0005) and VCAM-1 (PL < 0.0002). Conclusions L-4F treatment, alone or with pravastatin, significantly reduced IgG anti-dsDNA and IgG anti-oxPLs, proteinuria, glomerulonephritis, and osteopenia in a murine lupus model of accelerated atherosclerosis. Despite enlarged aortic lesions, increased smooth muscle content, decreased macrophage infiltration, and decreased pro-atherogenic chemokines in L-4F plus pravastatin treated mice suggest protective mechanisms not only on lupus-like disease, but also on potential plaque remodeling in a murine model of systemic lupus erythematosus (SLE) and accelerated atherosclerosis

Bulk vs. Boundary Dynamics in Anti-de Sitter Spacetime

We investigate the details of the bulk-boundary correspondence in Lorentzian signature anti-de Sitter space. Operators in the boundary theory couple to sources identified with the boundary values of non-normalizable bulk modes. Such modes do not fluctuate and provide classical backgrounds on which bulk excitations propagate. Normalizable modes in the bulk arise as a set of saddlepoints of the action for a fixed boundary condition. They fluctuate and describe the Hilbert space of physical states. We provide an explicit, complete set of both types of modes for free scalar fields in global and Poincar\'e coordinates. For \ads{3}, the normalizable and non-normalizable modes originate in the possible representations of the isometry group \SL_L\times\SL_R for a field of given mass. We discuss the group properties of mode solutions in both global and Poincar\'e coordinates and their relation to different expansions of operators on the cylinder and on the plane. Finally, we discuss the extent to which the boundary theory is a useful description of the bulk spacetime.Comment: Standard LaTeX, 28 pages, 2 postscript figures. v2: References added. Substantial revision in section 3 of treatment of global modes; non-normalizable modes have arbitrary time dependence. Revised discussion of low-mass modes and puzzle raised re: coupling of the dual boundary operators. v3: unwanted paragraph removed. v4: Sec. 5.2 correcte

Deficiency of CCAAT/Enhancer Binding Protein-Epsilon Reduces Atherosclerotic Lesions in LDLR-/- Mice

The CCAAT/enhancer binding proteins (C/EBPs) are transcription factors involved in hematopoietic cell development and induction of several inflammatory mediators. C/EBPε is expressed only in myeloid cells including monocytes/macrophages. Atherosclerosis is an inflammatory disorder of the vascular wall and circulating immune cells such as monocytes/macrophages. Mice deficient in the low density lipoprotein (LDL) receptor (Ldlr-/-) fed on a high cholesterol diet (HCD) show elevated blood cholesterol levels and are widely used as models to study human atherosclerosis. In this study, we generated Ldlr and Cebpe double-knockout (llee) mice and compared their atherogenic phenotypes to Ldlr single deficient (llEE) mice after HCD. Macrophages from llee mice have reduced lipid uptake by foam cells and impaired phagokinetic motility in vitro compared to macrophages from llEE mice. Also, compared to llEE mice, llee mice have alterations of lipid metabolism, and reduced atheroma and obesity, particularly the males. Peritoneal macrophages of llee male mice have reduced mRNA expression of FABP4, a fatty acid binding protein implicated in atherosclerosis. Overall, our study suggests that the myeloid specific factor C/EBPε is involved in systemic lipid metabolism and that silencing of C/EBPε could decrease the development of atherosclerosis

Genetic Control of Obesity and Gut Microbiota Composition in Response to High-Fat, High-Sucrose Diet in Mice

Obesity is a highly heritable disease driven by complex interactions between genetic and environmental factors. Human genome-wide association studies (GWAS) have identified a number of loci contributing to obesity; however, a major limitation of these studies is the inability to assess environmental interactions common to obesity. Using a systems genetics approach, we measured obesity traits, global gene expression, and gut microbiota composition in response to a high-fat/high-sucrose (HF/HS) diet of more than 100 inbred strains of mice. Here we show that HF/HS feeding promotes robust, strain-specific changes in obesity that is not accounted for by food intake and provide evidence for a genetically determined set-point for obesity. GWAS analysis identified 11 genome-wide significant loci associated with obesity traits, several of which overlap with loci identified in human studies. We also show strong relationships between genotype and gut microbiota plasticity during HF/HS feeding and identify gut microbial phylotypes associated with obesity