Adaptive Computation of the Swap-Insert Correction Distance

The Swap-Insert Correction distance from a string $S$ of length $n$ to another string $L$ of length $m\geq n$ on the alphabet $[1..d]$ is the minimum number of insertions, and swaps of pairs of adjacent symbols, converting $S$ into $L$. Contrarily to other correction distances, computing it is NP-Hard in the size $d$ of the alphabet. We describe an algorithm computing this distance in time within $O(d^2 nm g^{d-1})$, where there are $n_\alpha$ occurrences of $\alpha$ in $S$, $m_\alpha$ occurrences of $\alpha$ in $L$, and where $g=\max_{\alpha\in[1..d]} \min\{n_\alpha,m_\alpha-n_\alpha\}$ measures the difficulty of the instance. The difficulty $g$ is bounded by above by various terms, such as the length of the shortest string $S$, and by the maximum number of occurrences of a single character in $S$. Those results illustrate how, in many cases, the correction distance between two strings can be easier to compute than in the worst case scenario.Comment: 16 pages, no figures, long version of the extended abstract accepted to SPIRE 201

Locality-Sensitive Hashing of Curves

We study data structures for storing a set of polygonal curves in ${\rm R}^d$ such that, given a query curve, we can efficiently retrieve similar curves from the set, where similarity is measured using the discrete Fr\'echet distance or the dynamic time warping distance. To this end we devise the first locality-sensitive hashing schemes for these distance measures. A major challenge is posed by the fact that these distance measures internally optimize the alignment between the curves. We give solutions for different types of alignments including constrained and unconstrained versions. For unconstrained alignments, we improve over a result by Indyk from 2002 for short curves. Let $n$ be the number of input curves and let $m$ be the maximum complexity of a curve in the input. In the particular case where $m \leq \frac{\alpha}{4d} \log n$, for some fixed $\alpha>0$, our solutions imply an approximate near-neighbor data structure for the discrete Fr\'echet distance that uses space in $O(n^{1+\alpha}\log n)$ and achieves query time in $O(n^{\alpha}\log^2 n)$ and constant approximation factor. Furthermore, our solutions provide a trade-off between approximation quality and computational performance: for any parameter $k \in [m]$, we can give a data structure that uses space in $O(2^{2k}m^{k-1} n \log n + nm)$, answers queries in $O( 2^{2k} m^{k}\log n)$ time and achieves approximation factor in $O(m/k)$.Comment: Proc. of 33rd International Symposium on Computational Geometry (SoCG), 201

Highly efficient organic light-emitting diodes with hole injection layer of transition metal oxides

We report on the advantage of interlayers using transition-metal oxides, such as iridium oxide (IrOx) and ruthenium oxide (RuOx), between indium tin oxide (ITO) anodes and 4'-bis[N-(1-naphtyl)-N-phenyl-amino]biphenyl (alpha-NPD) hole transport layers on the electrical and optical properties of organic light-emitting diodes (OLEDs). The operation voltage at a current density of 100 mA/cm(2) decreased from 17 to 11 V for OLEDs with 3-nm-thick IrOx interlayers and from 17 to 14 V for OLEDs with 2-nm-thick RuOx ones. The maximum luminance value increased about 50% in OLED using IrOx and 108% in OLED using RuOx. Synchrotron radiation photoelectron spectroscopy results revealed that core levels of Ru 3d and Ir 4f shifted to high binding energies and that the valence band was splitting from metallic Fermi level as the surface of the transition metal was treated with O-2 plasma. This provides evidence that the transition-metal surface transformed to a transition-metal oxide. The surface of the transition metal became smoother with the O-2 plasma treatment. The thickness was calculated to be 0.4 nm for IrOx and 0.6 nm for RuOx using x-ray reflectivity measurements. Secondary electron emission spectra showed that the work function increased by 0.6 eV for IrOx and by 0.4 eV for RuOx. Thus, the transition-metal oxides lowered the potential barrier for hole injection from ITO to alpha-NPD, reducing the turn-on voltage of OLEDs and increasing the quantum efficiency. (c) 2005 American Institute of Physicsclose403

Isolation, structure, and activity of GID, a novel alpha 4/7-conotoxin with an extended N-terminal sequence

Using assay-directed fractionation of Conus geographus crude venom, we isolated a-conotoxin GID, which acts selectively at neuronal nicotinic acetylcholine receptors (nAChRs). Unlike other neuronally selective alpha-conotoxins, alpha-GID has a four amino acid N-terminal tail, gamma-carboxyglutamate (Gla), and hydroxyproline (0) residues, and lacks an amidated C terminus. GID inhibits alpha7 and alpha3beta2 nAChRs with IC50 values of 5 and 3 nm, respectively and is at least 1000-fold less potent at the alpha1beta1gammadelta, alpha3beta4, and alpha4beta4 combinations. GID also potently inhibits the alpha4beta2 subtype (IC50 of 150 nm). Deletion of the N-terminal sequence (GIDDelta1-4) significantly decreased activity at the alpha4beta2 nAChR but hardly affected potency at alpha3beta2 and alpha7 nAChRs, despite enhancing the off-rates at these receptors. In contrast, Arg(12) contributed to alpha4beta2 and alpha7 activity but not to alpha3beta2 activity. The three-dimensional structure of GID is well defined over residues 4-19 with a similar motif to other a-conotoxins. However, despite its influence on activity, the tail appears to be disordered in solution. Comparison of GID with other alpha4/7-conotoxins which possess an NN(P/O) motif in loop II, revealed a correlation between increasing length of the aliphatic side-chain in position 10 (equivalent to 13 in GID) and greater alpha7 versus alpha3beta2 selectivity

Lipid peroxidation is essential for α-synuclein-induced cell death.

Parkinson's disease is the second most common neurodegenerative disease and its pathogenesis is closely associated with oxidative stress. Deposition of aggregated α-synuclein (α-Syn) occurs in familial and sporadic forms of Parkinson's disease. Here, we studied the effect of oligomeric α-Syn on one of the major markers of oxidative stress, lipid peroxidation, in primary co-cultures of neurons and astrocytes. We found that oligomeric but not monomeric α-Syn significantly increases the rate of production of reactive oxygen species, subsequently inducing lipid peroxidation in both neurons and astrocytes. Pre-incubation of cells with isotope-reinforced polyunsaturated fatty acids (D-PUFAs) completely prevented the effect of oligomeric α-Syn on lipid peroxidation. Inhibition of lipid peroxidation with D-PUFAs further protected cells from cell death induced by oligomeric α-Syn. Thus, lipid peroxidation induced by misfolding of α-Syn may play an important role in the cellular mechanism of neuronal cell loss in Parkinson's disease. We have found that aggregated α-synuclein-induced production of reactive oxygen species (ROS) that subsequently stimulates lipid peroxidation and cell death in neurons and astrocytes. Specific inhibition of lipid peroxidation by incubation with reinforced polyunsaturated fatty acids (D-PUFAs) completely prevented the effect of α-synuclein on lipid peroxidation and cell death

Decay-assisted collinear resonance ionization spectroscopy: Application to neutron-deficient francium

This paper reports on the hyperfine-structure and radioactive-decay studies of the neutron-deficient francium isotopes $^{202-206}$Fr performed with the Collinear Resonance Ionization Spectroscopy (CRIS) experiment at the ISOLDE facility, CERN. The high resolution innate to collinear laser spectroscopy is combined with the high efficiency of ion detection to provide a highly-sensitive technique to probe the hyperfine structure of exotic isotopes. The technique of decay-assisted laser spectroscopy is presented, whereby the isomeric ion beam is deflected to a decay spectroscopy station for alpha-decay tagging of the hyperfine components. Here, we present the first hyperfine-structure measurements of the neutron-deficient francium isotopes $^{202-206}$Fr, in addition to the identification of the low-lying states of $^{202,204}$Fr performed at the CRIS experiment.Comment: Accepted for publication with Physical Review

α_1L-adrenoceptors mediate contraction of human erectile tissue

α1-adrenoceptor antagonists can impact upon sexual function and have potential in the treatment of erectile dysfunction. Human erectile tissue contains predominantly α1A-adrenoceptors, and here we examined whether contractions of this tissue are mediated by the functional phenotype, the α1L-adrenoceptor. Functional experiments using subtype selective agonists and antagonists, along with radioligand ([3H]tamsulosin) binding assays, were used to determine the α1-adrenoceptor population. A61603, a α1A-adrenoceptor agonist, was a full agonist with a potency 21-fold greater than that of noradrenaline. The α1A- and α1D-adrenoceptor antagonist tamsulosin antagonized noradrenaline responses with high affinity (pKD = 9.7 ± 0.3), whilst BMY7378 (100 nM) (α1D-adrenoceptor antagonist) failed to antagonize responses. In contrast, relatively low affinity estimates were obtained for both prazosin (pKD = 8.2 ± 0.1) and RS17053 (pKD = 6.9 ± 0.2), antagonists which discriminate between the α1A- and α1L-adrenoceptors. [3H]Tamsulosin bound with high affinity to the receptors of human erectile tissue (pKD = 10.3 ± 0.1) with a receptor density of 28.1 ± 1.4 fmol mg−1 protein. Prazosin displacement of [3H]tamsulosin binding revealed a single homogenous population of binding sites with a relatively low affinity for prazosin (pKi = 8.9). Taken together these data confirm that the receptor mediating contraction in human erectile tissue has the pharmacological properties of the α1L-adrenoceptor. Keywords: Erectile tissue, α1-adrenoceptor subtypes, α1L-adrenoceptor, Tamsulosin, Prazosi