Spin and chiral orderings of frustrated quantum spin chains

Ordering of frustrated S=1/2 and 1 XY and Heisenberg spin chains with the competing nearest- and next-nearest-neighbor antiferromagnetic couplings is studied by exact diagonalization and density-matrix renormalization-group methods. It is found that the S=1 XY chain exhibits both gapless and gapped `chiral' phases characterized by the spontaneous breaking of parity, in which the long-range order parameter is a chirality, $\kappa_i = S_i^xS_{i+1}^y-S_i^yS_{i+1}^x$, whereas the spin correlation decays either algebraically or exponentially. Such chiral phases are not realized in the S=1/2 XY chain nor in the Heisenberg chains.Comment: 4 pages, 5 EPS-figures, LaTeX(RevTeX),to appear in J.Phys.Soc.Japa

Microscopic model for the magnetization plateaus in NH4CuCl3

A simple model consisting of three distinct dimer sublattices is proposed to describe the magnetism of NH4CuCl3. It explains the occurrence of magnetization plateaus only at 1/4 and 3/4 of the saturation magnetization. The field dependence of the excitation modes observed by ESR measurements is also explained by the model. The model predicts that the magnetization plateaus should disappear under high pressure.Comment: 4 pages, 5 figures, REVTeX

Semi-classical description of the frustrated antiferromagnetic chain

The antiferromagnetic Heisenberg model on a chain with nearest and next nearest neighbor couplings is mapped onto the $SO(3)$ nonlinear sigma model in the continuum limit. In one spatial dimension this model is always in its disordered phase and a gap opens to excited states. The latter form a doubly degenerate spin-1 branch at all orders in $1/N$. We argue that this feature should be present in the spin-1 Heisenberg model itself. Exact diagonalizations are used to support this claim. The inapplicability of this model to half-integer spin chains is discussed.Comment: 19 pages (RevTeX 3.0), 6 PostScript figures appended (printing instructions included), preprint CRPS-94-1

ApoE−/− PGC-1α−/− Mice Display Reduced IL-18 Levels and Do Not Develop Enhanced Atherosclerosis

BACKGROUND: Atherosclerosis is a chronic inflammatory disease that evolves from the interaction of activated endothelial cells, macrophages, lymphocytes and modified lipoproteins (LDLs). In the last years many molecules with crucial metabolic functions have been shown to prevent important steps in the progression of atherogenesis, including peroxisome proliferator activated receptors (PPARs) and the class III histone deacetylase (HDAC) SIRT1. The PPARγ coactivator 1 alpha (Ppargc1a or PGC-1α) was identified as an important transcriptional cofactor of PPARγ and is activated by SIRT1. The aim of this study was to analyze total PGC-1α deficiency in an atherosclerotic mouse model. METHODOLOGY/PRINCIPAL FINDINGS: To investigate if total PGC-1α deficiency affects atherosclerosis, we compared ApoE(-/-) PGC-1α(-/-) and ApoE(-/-) PGC-1α(+/+) mice kept on a high cholesterol diet. Despite having more macrophages and a higher ICAM-1 expression in plaques, ApoE(-/-) PGC-1α(-/-) did not display more or larger atherosclerotic plaques than their ApoE(-/-) PGC-1α(+/+) littermates. In line with the previously published phenotype of PGC-1α(-/-) mice, ApoE(-/-) PGC-1α(-/-) mice had marked reduced body, liver and epididymal white adipose tissue (WAT) weight. VLDL/LDL-cholesterol and triglyceride contents were also reduced. Aortic expression of PPARα and PPARγ, two crucial regulators for adipocyte differentiation and glucose and lipid metabolism, as well as the expression of some PPAR target genes was significantly reduced in ApoE(-/-) PGC-1α(-/-) mice. Importantly, the epididymal WAT and aortic expression of IL-18 and IL-18 plasma levels, a pro-atherosclerotic cytokine, was markedly reduced in ApoE(-/-) PGC-1α(-/-) mice. CONCLUSIONS/SIGNIFICANCE: ApoE(-/-) PGC-1α(-/-) mice, similar as PGC-1α(-/-) mice exhibit markedly reduced total body and visceral fat weight. Since inflammation of visceral fat is a crucial trigger of atherogenesis, decreased visceral fat in PGC-1α-deficient mice may explain why these mice do not develop enhanced atherosclerosis

Azi-isoflurane, a Photolabel Analog of the Commonly Used Inhaled General Anesthetic Isoflurane

Volatility and low-affinity hamper an ability to define molecular targets of the inhaled anesthetics. Photolabels have proven to be a useful approach in this regard, although none have closely mimicked contemporary drugs. We report here the synthesis and validation of azi-isoflurane, a compound constructed by adding a diazirinyl moiety to the methyl carbon of the commonly used general anesthetic isoflurane. Azi-isoflurane is slightly more hydrophobic than isoflurane, and more potent in tadpoles. This novel compound inhibits Shaw2 K(+) channel currents similarly to isoflurane and binds to apoferritin with enhanced affinity. Finally, when irradiated at 300 nm, azi-isoflurane adducts to residues known to line isoflurane-binding sites in apoferritin and integrin LFA-1, the only proteins with isoflurane binding sites defined by crystallography. This reagent should allow rapid discovery of isoflurane molecular targets and binding sites within those targets

FRET Detection of Lymphocyte Function-Associated Antigen-1 Conformational Extension

Lymphocyte function-associated antigen 1 (LFA-1, CD11a/CD18, αLβ2-integrin) and its ligands are essential for adhesion between T-cells and antigen-presenting cells, formation of the immunological synapse, and other immune cell interactions. LFA-1 function is regulated through conformational changes that include the modulation of ligand binding affinity and molecular extension. However, the relationship between molecular conformation and function is unclear. Here fluorescence resonance energy transfer (FRET) with new LFA-1-specific fluorescent probes showed that triggering of the pathway used for T-cell activation induced rapid unquenching of the FRET signal consistent with extension of the molecule. Analysis of the FRET quenching at rest revealed an unexpected result that can be interpreted as a previously unknown LFA-1 conformation

Metastatic colorectal cancer to a primary thyroid cancer

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