Spin interfaces in the Ashkin-Teller model and SLE

We investigate the scaling properties of the spin interfaces in the Ashkin-Teller model. These interfaces are a very simple instance of lattice curves coexisting with a fluctuating degree of freedom, which renders the analytical determination of their exponents very difficult. One of our main findings is the construction of boundary conditions which ensure that the interface still satisfies the Markov property in this case. Then, using a novel technique based on the transfer matrix, we compute numerically the left-passage probability, and our results confirm that the spin interface is described by an SLE in the scaling limit. Moreover, at a particular point of the critical line, we describe a mapping of Ashkin-Teller model onto an integrable 19-vertex model, which, in turn, relates to an integrable dilute Brauer model.Comment: 12 pages, 6 figure

On three-point connectivity in two-dimensional percolation

We argue the exact universal result for the three-point connectivity of critical percolation in two dimensions. Predictions for Potts clusters and for the scaling limit below p_c are also given.Comment: 10 pages, 1 figur

Boundary conformal field theories and loop models

We propose a systematic method to extract conformal loop models for rational conformal field theories (CFT). Method is based on defining an ADE model for boundary primary operators by using the fusion matrices of these operators as adjacency matrices. These loop models respect the conformal boundary conditions. We discuss the loop models that can be extracted by this method for minimal CFTs and then we will give dilute O(n) loop models on the square lattice as examples for these loop models. We give also some proposals for WZW SU(2) models.Comment: 23 Pages, major changes! title change

Hierarchical structure in the orbital entanglement spectrum in Fractional Quantum Hall systems

We investigate the non-universal part of the orbital entanglement spectrum (OES) of the nu = 1/3 fractional quantum Hall effect (FQH) ground-state with Coulomb interactions. The non-universal part of the spectrum is the part that is missing in the Laughlin model state OES whose level counting is completely determined by its topological order. We find that the OES levels of the Coulomb interaction ground-state are organized in a hierarchical structure that mimic the excitation-energy structure of the model pseudopotential Hamiltonian which has a Laughlin ground state. These structures can be accurately modeled using Jain's "composite fermion" quasihole-quasiparticle excitation wavefunctions. To emphasize the connection between the entanglement spectrum and the energy spectrum, we also consider the thermodynamical OES of the model pseudopotential Hamiltonian at finite temperature. The observed good match between the thermodynamical OES and the Coulomb OES suggests a relation between the entanglement gap and the true energy gap.Comment: 16 pages, 19 figure

Controlled nucleation of thin microcrystalline layers for the recombination junction in a-Si stacked cells

In high-efficiency a-Si : H based stacked cells, at least one of the two layers that form the internal n/p junction has preferentially to be microcrystalline so as to obtain sufficient recombination at the junction [1–6]. The crucial point is the nucleation of a very thin μc-Si : H layer on an amorphous (i-layer) substrate [2, 4]. In this study, fast nucleation is induced through the treatment of the amorphous substrate by a CO2 plasma. The resulting n-layers with a high crystalline fraction were, however, found to reduce the Voc when incorporated in tandem cells. The reduction of the Voc could be restored only by a precise control of the crystalline fraction of the n-layer. As a technologically more feasible alternative, we propose a new, combined n-layer, consisting of a first amorphous layer for a high Voc, and a second microcrystalline layer, induced by CO2 treatment, for a sufficient recombination at the n/p junction. Resulting tandem cells show no Voc losses compared to two standard single cells, and an efficient recombination of the carriers at the internal junction as proved by the low series resistance (15 Ωcm2) and the high FF ( 75%) of the stacked cells

The ADAMTS (A Disintegrin and Metalloproteinase with Thrombospondin motifs) family

The ADAMTS (A Disintegrin and Metalloproteinase with Thrombospondin motifs) enzymes are secreted, multi-domain matrix-associated zinc metalloendopeptidases that have diverse roles in tissue morphogenesis and patho-physiological remodeling, in inflammation and in vascular biology. The human family includes 19 members that can be sub-grouped on the basis of their known substrates, namely the aggrecanases or proteoglycanases (ADAMTS1, 4, 5, 8, 9, 15 and 20), the procollagen N-propeptidases (ADAMTS2, 3 and 14), the cartilage oligomeric matrix protein-cleaving enzymes (ADAMTS7 and 12), the von-Willebrand Factor proteinase (ADAMTS13) and a group of orphan enzymes (ADAMTS6, 10, 16, 17, 18 and 19). Control of the structure and function of the extracellular matrix (ECM) is a central theme of the biology of the ADAMTS, as exemplified by the actions of the procollagen-N-propeptidases in collagen fibril assembly and of the aggrecanases in the cleavage or modification of ECM proteoglycans. Defects in certain family members give rise to inherited genetic disorders, while the aberrant expression or function of others is associated with arthritis, cancer and cardiovascular disease. In particular, ADAMTS4 and 5 have emerged as therapeutic targets in arthritis. Multiple ADAMTSs from different sub-groupings exert either positive or negative effects on tumorigenesis and metastasis, with both metalloproteinase-dependent and -independent actions known to occur. The basic ADAMTS structure comprises a metalloproteinase catalytic domain and a carboxy-terminal ancillary domain, the latter determining substrate specificity and the localization of the protease and its interaction partners; ancillary domains probably also have independent biological functions. Focusing primarily on the aggrecanases and proteoglycanases, this review provides a perspective on the evolution of the ADAMTS family, their links with developmental and disease mechanisms, and key questions for the future