Modeling of columnar-to-equiaxed transition in solidified Al-Si alloys

A Cellular-Automaton Finite-Volume-Method (CAFVM) algorithm has been developed, coupling with macroscopic model for heat transfer calculation and microscopic models for nucleation and growth. The solution equations have been solved to determine the time-dependent constitutional undercooling and interface retardation during solidification. The constitutional undercooling is then coupled into the CAFVM algorithm to investigate both the effects of thermal and constitutional undercooling on columnar growth and crystal selection in the columnar zone, and formation of equiaxed crystals in the bulk liquid. The model cannot only simulate microstructures of alloys but also investigates nucleation mechanisms and growth kinetics of alloys solidified with various solute concentrations and solidification morphologies.

Signature of mott-insulator transition with ultracold fermions in a one-dimensional optical lattice

Using the exact Bethe ansatz solution of the Hubbard model and Luttinger liquid theory, we investigate the density profiles and collective modes of one-dimensional ultracold fermions confined in an optical lattice with a harmonic trapping potential. We determine a generic phase diagram in terms of a characteristic filling factor and a dimensionless coupling constant. The collective oscillations of the atomic mass density, a technique that is commonly used in experiments, provide a signature of the quantum phase transition from the metallic phase to the Mott-insulator phase. A detailed experimental implementation is proposed.

Complete assignments of (1)H and (13)C NMR spectral data for 7,7 `-dihydroarylnaphthalene lignan lactones

In this article we present a complete (1)H and (13)C NMR spectral analysis of three 7,7`-dihydroarylnaphthalene lignan lactones using modern NMR techniques such as COSY, HSQC, HMBC and NOE experiments. Complete assignment and homonuclear hydrogen coupling constant measurements were performed. Copyright (C) 2009 John Wiley & Sons, Ltd.

Finite-temperature correlations and density profiles of an inhomogeneous interacting one-dimensional Bose gas

We calculate the density profiles and density correlation functions of the one-dimensional Bose gas in a harmonic trap, using the exact finite-temperature solutions for the uniform case, and applying a local density approximation. The results are valid for a trapping potential that is slowly varying relative to a correlation length. They allow a direct experimental test of the transition from the weak-coupling Gross-Pitaevskii regime to the strong-coupling, fermionic Tonks-Girardeau regime. We also calculate the average two-particle correlation which characterizes the bulk properties of the sample, and find that it can be well approximated by the value of the local pair correlation in the trap center.

Ground-State Entanglement of the BCS Model

The concept of local concurrence is used to quantify the entanglement between a single qubit and the remainder of a multiqubit system. For the ground state of the BCS model in the thermodynamic limit the set of local concurrences completely describes the entanglement. As a measure for the entanglement of the full system we investigate the average local concurrence (ALC). We find that the ALC satisfies a simple relation with the order parameter. We then show that for finite systems with a fixed particle number, a relation between the ALC and the condensation energy exposes a threshold coupling. Below the threshold, entanglement measures besides the ALC are significant.

Mechanical loading modulates glutamate receptor subunit expression in bone

The cellular mechanisms coupling mechanical loading with bone remodeling remain unclear. In the CNS, the excitatory amino acid glutamate (Glu) serves as a potent neurotransmitter exerting its effects via various membrane Glu receptors (GluR). Nerves containing Glu exist close to bone cells expressing functional GluRs. Demonstration of a mechanically sensitive glutamate/aspartate transporter protein and the ability of glutamate to stimulate bone resorption in vitro suggest a role for glutamate linking mechanical load and bone remodeling. We used immunohistochemical techniques to identify the expression of N-methyl-D-aspartate acid (NMDA) and non-NMDA (AMPA or kainate) ionotropic GluR subunits on bone cells in vivo. In bone sections from young adult rats, osteoclasts expressed numerous GluR subunits including AMPA (GluR2/3 and GluR4), kainic acid (GluR567) and NMDA (NMDAR2A, NMDAR2B and NMDAR2C) receptor subtypes. Bone lining cells demonstrated immunoexpression for NMDAR2A, NMDAR2B, NMDAR2C, GluR567, GluR23, GuR2 and GluR4 subunits. Immunoexpression was not evident on osteocytes, chondrocytes or vascular channels. To investigate the effects of mechanical loading on GluR expression, we used a Materials Testing System (MTS) to apply 10 N sinusoidal axial compressive loads percutaneously to the right limbs (radius/ulna, tibia/fibula) of rats. Each limb underwent 300-load cycles/day (cycle rate, 1 Hz) for 4 consecutive days. Contralateral, non-loaded limbs served as controls. Mechanically loaded limbs revealed a load-induced loss of immunoexpression for GluR2/3, GluR4, GluR567 and NMDAR2A on osteoclasts and NMDAR2A, NMDAR2B, GluR2/3 and GluR4 on bone lining cells. Both neonatal rabbit and rat osteoclasts were cultured on bone slices to investigate the effect of the NMDA receptor antagonist, MK801, and the AMPA/kainic acid receptor antagonist, NBQX, on osteoclast resorptive activity in vitro. The inhibition of resorptive function seen suggested that both NMDAR and kainic acid receptor function are required for normal osteoclast function. While the exact role of ionotropic GluRs in skeletal tissue remains unclear, the modulation of GluR subunit expression by mechanical loading lends further support for participation of Glu as a mechanical loading effector. These ionotropic receptors appear to be functionally relevant to normal osteoclast resorptive activity. (C) 2005 Elsevier Inc. All rights reserved.

Characterization of inflammatory responses to eccentric exercise in humans

Eccentric exercise commonly results in muscle damage. The primary sequence of events leading to exercise-induced muscle damage is believed to involve initial mechanical disruption of sarcomeres, followed by impaired excitation-contraction coupling and calcium signaling, and finally, activation of calcium-sensitive degradation pathways. Muscle damage is characterized by ultrastructural changes to muscle architecture, increased muscle proteins and enzymes in the bloodstream, loss of muscular strength and range of motion and muscle soreness. The inflammatory response to exercise-induced muscle damage is characterized by leukocyte infiltration and production of pro-inflammatory cytokines within damaged muscle tissue, systemic release of leukocytes and cytokines, in addition to alterations in leukocyte receptor expression and functional activity. Current evidence suggests that inflammatory responses to muscle damage are dependent on the type of eccentric exercise, previous eccentric loading (repeated bouts), age and gender. Circulating neutrophil counts and systemic cytokine responses are greater after eccentric exercise using a large muscle mass (e.g. downhill running, eccentric cycling) than after other types of eccentric exercise involving a smaller muscle mass. After an initial bout of eccentric exercise, circulating leukocyte counts and cell surface receptor expression are attenuated. Leukocyte and cytokine responses to eccentric exercise are impaired in elderly individuals, while cellular infiltration into skeletal muscle is greater in human females than males after eccentric exercise. Whether alterations in intracellular calcium homeostasis influence inflammatory responses to muscle damage is uncertain. Furthermore, the effects of antioxidant supplements are variable, and the limited data available indicates that anti-inflammatory drugs largely have no influence on inflammatory responses to eccentric exercise. In this review, we compare local versus systemic inflammatory responses, and discuss some of the possible mechanisms regulating the inflammatory responses to exercise-induced muscle damage in humans.

Molecular orbital calculations of two-electron states for P-donor solid-state spin qubits

We theoretically study the Hilbert space structure of two neighboring P-donor electrons in silicon-based quantum computer architectures. To use electron spins as qubits, a crucial condition is the isolation of the electron spins from their environment, including the electronic orbital degrees of freedom. We provide detailed electronic structure calculations of both the single donor electron wave function and the two-electron pair wave function. We adopted a molecular orbital method for the two-electron problem, forming a basis with the calculated single donor electron orbitals. Our two-electron basis contains many singlet and triplet orbital excited states, in addition to the two simple ground state singlet and triplet orbitals usually used in the Heitler-London approximation to describe the two-electron donor pair wave function. We determined the excitation spectrum of the two-donor system, and study its dependence on strain, lattice position, and interdonor separation. This allows us to determine how isolated the ground state singlet and triplet orbitals are from the rest of the excited state Hilbert space. In addition to calculating the energy spectrum, we are also able to evaluate the exchange coupling between the two donor electrons, and the double occupancy probability that both electrons will reside on the same P donor. These two quantities are very important for logical operations in solid-state quantum computing devices, as a large exchange coupling achieves faster gating times, while the magnitude of the double occupancy probability can affect the error rate.

Determination of the solution structures of conantokin-G and conantokin-T by CD and NMR spectroscopy

Conantokin-G and conantokin-T are two paralytic polypeptide toxins originally isolated from the venom of the fish-hunting cone snails of the genus Conus. Conantokin-G and conantokin-T are the only naturally occurring peptidic compounds which possess N-methyl-D-aspartate receptor antagonist activity, produced by a selective non-competitive antagonism of polyamine responses, They are also structurally unusual in that they contain a disproportionately large number of acid labile post-translational gamma-carboxyglutamic acid (Gla) residues, Although no precise structural information has previously been published for these peptides, early spectroscopic measurements have indicated that both conantokin-G and conantokin-T form alpha-helical structures, although there is some debate whether the presence of calcium ions is required for these peptides to adopt this fold, We now report a detailed structural study of synthetic conantokin-G and conantokin-T in a range of solution conditions using CD and H-1 NMR spec troscopy. The three-dimensional structures of conantokin-T and conantokin-G were calculated from H-1 NMR-derived distance and dihedral restraints. Both conantokins were found to contain a mixture of alpha- and 3(10) helix, that give rise to curved and straight helical conformers. Conantokin-G requires the presence of divalent cations (Zn2+, Ca2+, Cu2+, Or Mg2+) to form a stable iv-helix, while conantokin-T adopts a stable alpha-helical structure in aqueous conditions, in the presence or absence of divalent cations (Zn2+, Ca2+, Cu2+, Or Mg2+).

Paramagnetism of caesium titanium alum

Caesium titanium alum, CsTi(SO4)(2) . 12H(2)O, is a beta alum and exhibits a large trigonal field and a dynamic Jahn-Teller effect. Exact calculations of the linear (2)T(2)xe Jahn-Teller coupling show that in the strict S-6 Site symmetry the ground multiplet consists of a Kramers doublet 2 Gamma(6) with magnetic splitting factors g(parallel to)=1.1 and g perpendicular to=0, a Gamma(4) Gamma(5) doublet at similar to 60 cm(-1) with g(parallel to)=2.51 and g(perpendicular to)=0.06 and another Gamma(4) Gamma(5) doublet at similar to 270 cm(-1) with g(parallel to)=1.67 and g(perpendicular to)=1.83. The controversial g values observed below 4.2 K, g(parallel to)=1.25 and g(perpendicular to)=1.14, are shown to arise from low symmetry distortions. These distortions couple the vibronic levels and induce into the ground state the off-diagonal axial Zeeman interaction that exists between the first excited and the ground vibronic levels. (C) 1997 American Institute of Physics.

Zipping up transcription factors: Rational design of anti-Jun and anti-Fos peptides

Various members of the bZip and bHLH-Zip families of eukaryotic transcription factors, including Jun, Fos, and Myc, have been identified as oncoproteins; mutation or deregulated expression of these proteins leads to certain types of cancer. These proteins can only bind to their cognate DNA enhancer sites following homodimerization, or heterodimerization with another family member, via their leucine zipper domain. Thus, a novel anticancer strategy would be to inhibit dimerization of these proteins, thereby blocking their DNA binding and transactivation functions. In this paper we show that it is possible to rationally design leucine zipper peptides that bind with high affinity to the leucine zipper dimerization domains of c-Jun and c-Fos, thus preventing the formation of functional c-Jun homodimers and c-Jun:c-Fos heterodimers; we refer to such peptides as superzippers (SZs). In vivo, c-Jun:SZ and c-Fos:SZ heterodimers should be nonfunctional as they lack one of the two basic domains that are essential for DNA binding. While the transport of a peptidic agent into cells often poses a severe obstacle to its therapeutic use, we show that a 46-residue leucine zipper peptide can be transported into HeLa cells by coupling it to a 17-residue carrier peptide from the Antennapedia homeodomain, thus paving the way for detailed studies of the therapeutic potential of superzipper peptides.

Anisotropic correlated electron model associated with the Temperley-Lieb algebra

We present an anisotropic correlated electron model on a periodic lattice, constructed from an R-matrix associated with the Temperley-Lieb algebra. By modification of the coupling of the first and last sites we obtain a model with quantum algebra invariance.

Modulation of human cardiac function through 4 beta-adrenoceptor populations

In human heart there is now evidence for the involvement of four beta-adrenoceptor populations, three identical to the recombinant beta(1)-, beta(2)- and beta(3)-adrenoceptors, and a fourth as yet uncloned putative beta-adrenoceptor population, which we designate provisionally as the cardiac putative beta(4)-adrenoceptor. This review described novel features of beta-adrenoceptors as modulators of cardiac systolic and diastolic function. We also discuss evidence for modulation by unoccupied beta(1)- and beta(2)-adrenoceptors. Human cardiac and recombinant beta(1)- and beta(2)-adrenoceptors are both mainly coupled to adenylyl cyclase through Gs protein, the latter more tightly than the former. Activation of both human beta(1)- and beta(2)-adrenoceptors not only increases cardiac force during systole but also hastens relaxation through cyclic AMP-dependent phosphorylation of phospholamban and troponin I, thereby facilitating diastolic function. Furthermore, both beta(1) and beta(2)-adrenoceptors can mediate experimental arrhythmias in human cardiac preparations elicited by noradrenaline and adrenaline. Human ventricular beta(3)-adrenoceptors appear to be coupled to a pertussis toxin-sensitive protein (Gi?). beta(3)-Adrenoceptor-selective agonists shorten the action potential and cause cardiodepression, suggesting direct coupling of a Gi protein to a K+ channel. In a variety of species, including man, cardiac putative beta(4)-adrenoceptors mediate cardiostimulant effects of non-conventional partial agonists, i.e. high affinity beta(1)- and beta(2)-adrenoceptor blockers that cause agonist effects at concentrations considerably higher than those that block these receptors. Putative beta(4)-adrenoceptors appear to be coupled positively to a cyclic AMP-dependent cascade and can undergo some desensitisation.

Isotopically resolved (B)over-tilde<-(X)over-tilde electronic spectrum of Ag-3 and calculation of its Jahn-Teller effects

Ag-3 was produced by pulsed-nozzle laser vaporisation and jet-cooled in a Ne supersonic expansion. One-color resonant two-photon ionisation (R2PI) spectra of the (B) over tilde(2) E '' <-- (X) over tilde(2) E' transition of Ag-3 were separately measured for all four isotopic combinations. Long vibrational progressions are observed, involving clearly resolved bands at low energy, merging into a dense but resolvable spectrum up to 1000 cm(-1) above the origin. Both the ground (X) over tilde(2) E' and excited (B) over tilde(2) E '' states of Ag-3 are susceptible to Jahn-Teller distortion along the degenerate e' bending coordinate. The Jahn-Teller analysis includes both linear and quadratic terms, simultaneously with the spin-orbit coupling. Following extensive parameter fitting, the absorption spectrum is calculated, and bands assigned. The spin-orbit splitting is quenched below the localization energy, but becomes observable approximate to 300 cm(-1) above the origin.

The structure of a novel insecticidal neurotoxin, omega-atracotoxin-HV1, from the venom of an Australian funnel web spider

A family of potent insecticidal toxins has recently been isolated from the venom of Australian funnel web spiders. Among these is the 37-residue peptide omega-atracotoxin-HV1 (omega-ACTX-HV1) from Hadronyche versuta. We have chemically synthesized and folded omega-ACTX-HV1, shown that it is neurotoxic, ascertained its disulphide bonding pattern, and determined its three-dimensional solution structure using NMR spectroscopy. The structure consists of a solvent-accessible beta-hairpin protruding from a disulphide-bonded globular core comprising four beta-turns. The three intramolecular disulphide bonds form a cystine knot motif similar to that seen in several other neurotoxic peptides. Despite limited sequence identity, omega-ACTX-HV1 displays significant structural homology with the omega-agatoxins and omega-conotoxins, both of which are vertebrate calcium channel antagonists; however, in contrast with these toxins, we show that omega-ACTX-HV1 inhibits insect, but not mammalian, voltage-gated calcium channel currents.