Exact Thermodynamics of Disordered Impurities in Quantum Spin Chains

Exact results for the thermodynamic properties of ensembles of magnetic impurities with randomly distributed host-impurity couplings in the quantum antiferromagnetic Heisenberg model are presented. Exact calculations are done for arbitrary values of temperature and external magnetic field. We have shown that for strong disorder the quenching of the impurity moments is absent. For weak disorder the screening persists, but with the critical non-Fermi-liquid behaviors of the magnetic susceptibility and specific heat. A comparison with the disordered Kondo effect experiments in dirty metallic alloys is performed.Comment: 4 pages Late

Expanding the 3- O -Sulfate Proteome—Enhanced Binding of Neuropilin-1 to 3- O -Sulfated Heparan Sulfate Modulates Its Activity

Binding of proteins to heparan sulfate is driven predominantly by electrostatic interactions between positively charged amino acid residues in the protein and negatively charged sulfate groups located at various positions along the polysaccharide chain. Although many heparin/heparan-sulfate-binding proteins have been described, few exhibit preferential binding for heparan sulfates containing relatively rare 3-O-sulfated glucosamine residues. To expand the "3-O-sulfate proteome," affinity matrices were created from Chinese hamster ovary (CHO) cell heparan sulfate engineered in vitro with and without 3-O-sulfate groups. Fractionation of different animal sera yielded several proteins that bound specifically to columns containing 3-O-sulfated heparan sulfate modified by two members of the heparan sulfate 3-O-sulfotransferase superfamily, Hs3st1 and Hs3st2. Neuropilin-1 was analyzed in detail because it has been implicated in angiogenesis and axon guidance. We show that 3-O-sulfation enhanced the binding of neuropilin-1 to heparan sulfate immobilized on plastic plates and to heparan sulfate present on cultured cells. Chemoenzymatically synthesized 3-O-sulfated heparan sulfate dodecamers protected neuropilin-1 from thermal denaturation and inhibited neuropilin-1-dependent, semaphorin-3a-induced growth cone collapse of neurons derived from murine dorsal root ganglia. The effect of 3-O-sulfation was cell autonomous and specific to Hs3st2 based on collapse assays of neurons derived from Hs3st1- and Hs3st2-deficient mice. Finally, 3-O-sulfated heparan sulfate enhanced the inhibition of endothelial cell sprouting by exogenous heparan sulfate. These findings demonstrate a reliable method to identify members of the 3-O-sulfate proteome and that 3-O-sulfation of heparan sulfate can modulate axonal growth cone collapse and endothelial cell sprouting

Mitochondrial Oxidative Stress Alters a Pathway in Caenorhabditis elegans Strongly Resembling That of Bile Acid Biosynthesis and Secretion in Vertebrates

Mammalian bile acids (BAs) are oxidized metabolites of cholesterol whose amphiphilic properties serve in lipid and cholesterol uptake. BAs also act as hormone-like substances that regulate metabolism. The Caenorhabditis elegans clk-1 mutants sustain elevated mitochondrial oxidative stress and display a slow defecation phenotype that is sensitive to the level of dietary cholesterol. We found that: 1) The defecation phenotype of clk-1 mutants is suppressed by mutations in tat-2 identified in a previous unbiased screen for suppressors of clk-1. TAT-2 is homologous to ATP8B1, a flippase required for normal BA secretion in mammals. 2) The phenotype is suppressed by cholestyramine, a resin that binds BAs. 3) The phenotype is suppressed by the knock-down of C. elegans homologues of BA–biosynthetic enzymes. 4) The phenotype is enhanced by treatment with BAs. 5) Lipid extracts from C. elegans contain an activity that mimics the effect of BAs on clk-1, and the activity is more abundant in clk-1 extracts. 6) clk-1 and clk-1;tat-2 double mutants show altered cholesterol content. 7) The clk-1 phenotype is enhanced by high dietary cholesterol and this requires TAT-2. 8) Suppression of clk-1 by tat-2 is rescued by BAs, and this requires dietary cholesterol. 9) The clk-1 phenotype, including the level of activity in lipid extracts, is suppressed by antioxidants and enhanced by depletion of mitochondrial superoxide dismutases. These observations suggest that C. elegans synthesizes and secretes molecules with properties and functions resembling those of BAs. These molecules act in cholesterol uptake, and their level of synthesis is up-regulated by mitochondrial oxidative stress. Future investigations should reveal whether these molecules are in fact BAs, which would suggest the unexplored possibility that the elevated oxidative stress that characterizes the metabolic syndrome might participate in disease processes by affecting the regulation of metabolism by BAs

SCARFACE Encodes an ARF-GAP That Is Required for Normal Auxin Efflux and Vein Patterning in Arabidopsis

To identify molecular mechanisms controlling vein patterns, we analyzed scarface (sfc) mutants. sfc cotyledon and leaf veins are largely fragmented, unlike the interconnected networks in wild-type plants. SFC encodes an ADP ribosylation factor GTPase activating protein (ARF-GAP), a class with well-established roles in vesicle trafficking regulation. Quadruple mutants of SCF and three homologs (ARF-GAP DOMAIN1, 2, and 4) showed a modestly enhanced vascular phenotype. Genetic interactions between sfc and pinoid and between sfc and gnom suggest a possible function for SFC in trafficking of auxin efflux regulators. Genetic analyses also revealed interaction with cotyledon vascular pattern2, suggesting that lipid-based signals may underlie some SFC ARF-GAP functions. To assess possible roles for SFC in auxin transport, we analyzed sfc roots, which showed exaggerated responses to exogenous auxin and higher auxin transport capacity. To determine whether PIN1 intracellular trafficking was affected, we analyzed PIN1:green fluorescent protein (GFP) dynamics using confocal microscopy in sfc roots. We found normal PIN1:GFP localization at the apical membrane of root cells, but treatment with brefeldin A resulted in PIN1 accumulating in smaller and more numerous compartments than in the wild type. These data suggest that SFC is required for normal intracellular transport of PIN1 from the plasma membrane to the endosome

Expanding the 3‑<i>O</i>‑Sulfate ProteomeEnhanced Binding of Neuropilin‑1 to 3‑<i>O</i>‑Sulfated Heparan Sulfate Modulates Its Activity

Binding of proteins to heparan sulfate is driven predominantly by electrostatic interactions between positively charged amino acid residues in the protein and negatively charged sulfate groups located at various positions along the polysaccharide chain. Although many heparin/heparan-sulfate-binding proteins have been described, few exhibit preferential binding for heparan sulfates containing relatively rare 3-<i>O</i>-sulfated glucosamine residues. To expand the “3-<i>O</i>-sulfate proteome,” affinity matrices were created from Chinese hamster ovary (CHO) cell heparan sulfate engineered <i>in vitro</i> with and without 3-<i>O</i>-sulfate groups. Fractionation of different animal sera yielded several proteins that bound specifically to columns containing 3-<i>O</i>-sulfated heparan sulfate modified by two members of the heparan sulfate 3-<i>O</i>-sulfotransferase superfamily, Hs3st1 and Hs3st2. Neuropilin-1 was analyzed in detail because it has been implicated in angiogenesis and axon guidance. We show that 3-<i>O</i>-sulfation enhanced the binding of neuropilin-1 to heparan sulfate immobilized on plastic plates and to heparan sulfate present on cultured cells. Chemoenzymatically synthesized 3-<i>O</i>-sulfated heparan sulfate dodecamers protected neuropilin-1 from thermal denaturation and inhibited neuropilin-1-dependent, semaphorin-3a-induced growth cone collapse of neurons derived from murine dorsal root ganglia. The effect of 3-<i>O</i>-sulfation was cell autonomous and specific to Hs3st2 based on collapse assays of neurons derived from Hs3st1- and Hs3st2-deficient mice. Finally, 3-<i>O</i>-sulfated heparan sulfate enhanced the inhibition of endothelial cell sprouting by exogenous heparan sulfate. These findings demonstrate a reliable method to identify members of the 3-<i>O</i>-sulfate proteome and that 3-<i>O</i>-sulfation of heparan sulfate can modulate axonal growth cone collapse and endothelial cell sprouting

Analytic model of a magnetically insulated transmission line with collisional flow electrons

We have developed a relativistic-fluid model of the flow-electron plasma in a steady-state one-dimensional magnetically insulated transmission line (MITL). The model assumes that the electrons are collisional and, as a result, drift toward the anode. The model predicts that in the limit of fully developed collisional flow, the relation between the voltage V_{a}, anode current I_{a}, cathode current I_{k}, and geometric impedance Z_{0} of a 1D planar MITL can be expressed as V_{a}=I_{a}Z_{0}h(χ), where h(χ)≡[(χ+1)/4(χ-1)]^{1/2}-ln⁡⌊χ+(χ^{2}-1)^{1/2}⌋/2χ(χ-1) and χ≡I_{a}/I_{k}. The relation is valid when V_{a}≳1   MV. In the minimally insulated limit, the anode current I_{a,min⁡}=1.78V_{a}/Z_{0}, the electron-flow current I_{f,min⁡}=1.25V_{a}/Z_{0}, and the flow impedance Z_{f,min⁡}=0.588Z_{0}. {The electron-flow current I_{f}≡I_{a}-I_{k}. Following Mendel and Rosenthal [Phys. Plasmas 2, 1332 (1995)PHPAEN1070-664X10.1063/1.871345], we define the flow impedance Z_{f} as V_{a}/(I_{a}^{2}-I_{k}^{2})^{1/2}.} In the well-insulated limit (i.e., when I_{a}≫I_{a,min⁡}), the electron-flow current I_{f}=9V_{a}^{2}/8I_{a}Z_{0}^{2} and the flow impedance Z_{f}=2Z_{0}/3. Similar results are obtained for a 1D collisional MITL with coaxial cylindrical electrodes, when the inner conductor is at a negative potential with respect to the outer, and Z_{0}≲40   Ω. We compare the predictions of the collisional model to those of several MITL models that assume the flow electrons are collisionless. We find that at given values of V_{a} and Z_{0}, collisions can significantly increase both I_{a,min⁡} and I_{f,min⁡} above the values predicted by the collisionless models, and decrease Z_{f,min⁡}. When I_{a}≫I_{a,min⁡}, we find that, at given values of V_{a}, Z_{0}, and I_{a}, collisions can significantly increase I_{f} and decrease Z_{f}. Since the steady-state collisional model is valid only when the drift of electrons toward the anode has had sufficient time to establish fully developed collisional flow, and collisionless models assume there is no net electron drift toward the anode, we expect these two types of models to provide theoretical bounds on I_{a}, I_{f}, and Z_{f}

Foot-Pulse Radiation Drive Necessary for ICF Ignition Capsule Demonstrated on Z Generator

Summary form only given. Implosion and ignition of an indirectly-driven ICF capsule operating near a Fermi-degenerate isentrope requires initial Planckian-radiation-drive temperatures of 70-to-90 eV to be present for a duration of 10-to-15 ns prior to the main drive pulse. Such capsules are being designed for high pulsed-power generators such as X1. This foot-pulse drive capability has been recently demonstrated in a NIF-sized (6-mm 1=7-mm), gold hohlraum, using a one-sided static-wall hohlraum geometry on the Z generator. The general arrangement utilized nested tungsten-wire arrays of radii (mass) 20 mm (2 mg) and 10 mm (1 mg) that had an axial length of -10 mm. The arrays were driven by a peak current of -21 MA and were made to implode on a 2-μm-thick Cu annulus (mass=4.5 mg), which had a radius of 4 mm and was filled with a low-density CH foam, all centered about the z-axis. The gold hohlraum was mounted on axis and above the Cu/foam target. A 2.9-mm-radius axial hole between the top of the target and hohlraum permitted the X-rays generated from the implosion to enter the hohlraum. The radiation within the hohlraum was monitored by viewing the hohlraum through a 3-mm diameter hole on the lateral side of the hohlraum with a suite of diagnostics. The radiation entering the hohlraum was estimated by an additional suite of on-axis diagnostics, in a limited number of separate shots, when the hohlraum was not present. Additionally, the radiation generated outside the Cu annulus was monitored, for all shots, through a 3-mm diameter aperture located on the outside of the current return ca