Peak effect at the weak- to strong pinning crossover

In type-II superconductors, the magnetic field enters in the form of vortices; their flow under application of a current introduces dissipation and thus destroys the defining property of a superconductor. Vortices get immobilized by pinning through material defects, thus resurrecting the supercurrent. In weak collective pinning, defects compete and only fluctuations in the defect density produce pinning. On the contrary, strong pins deform the lattice and induce metastabilities. Here, we focus on the crossover from weak- to strong bulk pinning, which is triggered either by increasing the strength $f_\mathrm{p}$ of the defect potential or by decreasing the effective elasticity of the lattice (which is parametrized by the Labusch force $f_\mathrm{Lab}$). With an appropriate Landau expansion of the free energy we obtain a peak effect with a sharp rise in the critical current density $j_\mathrm{c} \sim j_0 (a_0\xi^2 n_p) (\xi^2/a_0^2) (f_\mathrm{p}/f_\mathrm{Lab} -1)^2$.Comment: 6 pages, 5 figures (Proceedings of the Third European Conference on Vortex Matter in Superconductors, to be published in Physica C

Weak- to strong pinning crossover

Material defects in hard type II superconductors pin the flux lines and thus establish the dissipation-free current transport in the presence of a finite magnetic field. Depending on the density and pinning force of the defects and the vortex density, pinning is either weak-collective or strong. We analyze the weak- to strong pinning crossover of vortex matter in disordered superconductors and discuss the peak effect appearing naturally in this context.Comment: 4 pages, 2 figure

Transcription of TIR1-Controlled Genes Can be Regulated within 10 Min by an Auxin-Induced Process. Can TIR1 be the Receptor?

ABP1 and TIR1/AFBs are known as auxin receptors. ABP1 is linked to auxin responses several of which are faster than 10 min. TIR1 regulates auxin-induced transcription of early auxin genes also within minutes. We use transcription of such TIR1-dependent genes as indicator of TIR1 activity to show the rapid regulation of TIR1 by exogenous auxin. To this end, we used quantification of transcription of a set of fifteen early auxin-induced reporter genes at t = 10 and t = 30 min to measure this as a TIR1-dependent auxin response. We conducted this study in 22 mutants of auxin transporters (pin5, abcb1, abcb19, and aux1/lax3), protein kinases and phosphatases (ibr5, npr1, cpk3, CPK3-OX, d6pk1, d6pkl1-1, d6pkl3-2, d6pkl1-1/d6pkl2-2, and d6pkl1-1/d6pkl3-2), of fatty acid metabolism (fad2-1, fad6-1, ssi2, lacs4, lacs9, and lacs4/lacs9) and receptors (tir1, tir1/afb2, and tir1/afb3) and compared them to the wild type. After 10 min auxin application, in 18 out of 22 mutants mis-regulated expression of at least one reporter was found, and in 15 mutants transcription of two-to-three out of five selected auxin reporter genes was mis-regulated. After 30 min of auxin application to mutant plants, mis-regulation of reporter genes ranged from one to 13 out of 15 tested reporter genes. Those genes chosen as mutants were themselves not regulated in their expression by auxin for at least 1 h, excluding an influence of TIR1/AFBs on their transcription. The expression of TIR1/AFB genes was also not modulated by auxin for up to 3 h. Together, this excludes a feedback or feedforward of these mutant genes/proteins on TIR1/AFBs output of transcription in this auxin-induced response. However, an auxin-induced response needed an as yet unknown auxin receptor. We suggest that the auxin receptor necessary for the fast auxin-induced transcription modulation could be, instead, ABP1. The alternative hypothesis would be that auxin-induced expression of a protein, initiated by TIR1/AFBs receptors, could initiate these responses and that this unknown protein regulated TIR1/AFB activities within 10 min.DLR/50WB133DFG/Sche207/24-

Complementation of the embryo-lethal T-DNA insertion mutant of AUXIN-BINDING-PROTEIN 1 (ABP1) with abp1 point mutated versions reveals crosstalk of ABP1 and phytochromes

AUXIN BINDING PROTEIN1 (ABP1) mutants have properties of auxin- and red light-signalling mutants. A novel concept for growth control by ABP1 and phytochromes is indicated by this functional lin

Complementation of the embryo-lethal T-DNA insertion mutant of AUXIN-BINDING-PROTEIN 1 (ABP1) with abp1 point mutated versions reveals crosstalk of ABP1 and phytochromes

The function of the extracytoplasmic AUXIN-BINDING-PROTEIN1 (ABP1) is largely enigmatic. We complemented a homozygous T-DNA insertion null mutant of ABP1 in Arabidopsis thaliana Wassilewskia with three mutated and one wild-type (wt) ABP1 cDNA, all tagged C-terminally with a strepII–FLAG tag upstream the KDEL signal. Based on in silico modelling, the abp1 mutants were predicted to have altered geometries of the auxin binding pocket and calculated auxin binding energies lower than the wt. Phenotypes linked to auxin transport were compromised in these three complemented abp1 mutants. Red light effects, such as elongation of hypocotyls in constant red (R) and far-red (FR) light, in white light supplemented by FR light simulating shade, and inhibition of gravitropism by R or FR, were all compromised in the complemented lines. Using auxin- or light-induced expression of marker genes, we showed that auxin-induced expression was delayed already after 10min, and light-induced expression within 60min, even though TIR1/AFB or phyB are thought to act as receptors relevant for gene expression regulation. The expression of marker genes in seedlings responding to both auxin and shade showed that for both stimuli regulation of marker gene expression was altered after 10–20min in the wild type and phyB mutant. The rapidity of expression responses provides a framework for the mechanics of functional interaction of ABP1 and phyB to trigger interwoven signalling pathways

A Family of Maximum Margin Criterion for Adaptive Learning

In recent years, pattern analysis plays an important role in data mining and recognition, and many variants have been proposed to handle complicated scenarios. In the literature, it has been quite familiar with high dimensionality of data samples, but either such characteristics or large data have become usual sense in real-world applications. In this work, an improved maximum margin criterion (MMC) method is introduced firstly. With the new definition of MMC, several variants of MMC, including random MMC, layered MMC, 2D^2 MMC, are designed to make adaptive learning applicable. Particularly, the MMC network is developed to learn deep features of images in light of simple deep networks. Experimental results on a diversity of data sets demonstrate the discriminant ability of proposed MMC methods are compenent to be adopted in complicated application scenarios.Comment: 14 page

Depinning transition of dislocation assemblies: pileup and low-angle grain boundary

We investigate the depinning transition occurring in dislocation assemblies. In particular, we consider the cases of regularly spaced pileups and low angle grain boundaries interacting with a disordered stress landscape provided by solute atoms, or by other immobile dislocations present in non-active slip systems. Using linear elasticity, we compute the stress originated by small deformations of these assemblies and the corresponding energy cost in two and three dimensions. Contrary to the case of isolated dislocation lines, which are usually approximated as elastic strings with an effective line tension, the deformations of a dislocation assembly cannot be described by local elastic interactions with a constant tension or stiffness. A nonlocal elastic kernel results as a consequence of long range interactions between dislocations. In light of this result, we revise statistical depinning theories and find novel results for Zener pinning in grain growth. Finally, we discuss the scaling properties of the dynamics of dislocation assemblies and compare theoretical results with numerical simulations.Comment: 13 pages, 8 figure

Vortex Entanglement and Broken Symmetry

Based on the London approximation, we investigate numerically the stability of the elementary configurations of entanglement, the twisted-pair and the twisted-triplet, in the vortex-lattice and -liquid phases. We find that, except for the dilute limit, the twisted-pair is unstable and hence irrelevant in the discussion of entanglement. In the lattice phase the twisted-triplet constitutes a metastable, confined configuration of high energy. Loss of lattice symmetry upon melting leads to deconfinement and the twisted-triplet turns into a low-energy helical configuration.Comment: 4 pages, RevTex, 2 figures on reques

Local mapping of dissipative vortex motion

We explore, with unprecedented single vortex resolution, the dissipation and motion of vortices in a superconducting ribbon under the influence of an external alternating magnetic field. This is achieved by combing the phase sensitive character of ac-susceptibility, allowing to distinguish between the inductive-and dissipative response, with the local power of scanning Hall probe microscopy. Whereas the induced reversible screening currents contribute only inductively, the vortices do leave a fingerprint in the out-of-phase component. The observed large phase-lag demonstrates the dissipation of vortices at timescales comparable to the period of the driving force (i.e. 13 ms). These results indicate the presence of slow microscopic loss mechanisms mediated by thermally activated hopping transport of vortices between metastable states.Comment: 5 pages, 2 figure