43 research outputs found

    Holographic Anyons in the ABJM Theory

    Full text link
    We consider the holographic anyons in the ABJM theory from three different aspects of AdS/CFT correspondence. First, we identify the holographic anyons by using the field equations of supergravity, including the Chern-Simons terms of the probe branes. We find that the composite of Dp-branes wrapped over CP3 with the worldvolume magnetic fields can be the anyons. Next, we discuss the possible candidates of the dual anyonic operators on the CFT side, and find the agreement of their anyonic phases with the supergravity analysis. Finally, we try to construct the brane profile for the holographic anyons by solving the equations of motion and Killing spinor equations for the embedding profile of the wrapped branes. As a by product, we find a BPS spiky brane for the dual baryons in the ABJM theory.Comment: 1+33 pages, 3 figures; v2 discussion for D4-D6 case added, references added; v3 comments adde

    On Flux Quantization in F-Theory

    Full text link
    We study the problem of four-form flux quantization in F-theory compactifications. We prove that for smooth, elliptically fibered Calabi-Yau fourfolds with a Weierstrass representation, the flux is always integrally quantized. This implies that any possible half-integral quantization effects must come from 7-branes, i.e. from singularities of the fourfold. We subsequently analyze the quantization rule on explicit fourfolds with Sp(N) singularities, and connect our findings via Sen's limit to IIB string theory. Via direct computations we find that the four-form is half-integrally quantized whenever the corresponding 7-brane stacks wrap non-spin complex surfaces, in accordance with the perturbative Freed-Witten anomaly. Our calculations on the fourfolds are done via toric techniques, whereas in IIB we rely on Sen's tachyon condensation picture to treat bound states of branes. Finally, we give general formulae for the curvature- and flux-induced D3 tadpoles for general fourfolds with Sp(N) singularities.Comment: 46 page

    Ucma/GRP inhibits phosphate-induced vascular smooth muscle cell calcification via SMAD-dependent BMP signalling

    Get PDF
    Vascular calcification (VC) is the process of deposition of calcium phosphate crystals in the blood vessel wall, with a central role for vascular smooth muscle cells (VSMCs). VC is highly prevalent in chronic kidney disease (CKD) patients and thought, in part, to be induced by phosphate imbalance. The molecular mechanisms that regulate VC are not fully known. Here we propose a novel role for the mineralisation regulator Ucma/GRP (Upper zone of growth plate and Cartilage Matrix Associated protein/Gla Rich Protein) in phosphate-induced VSMC calcification. We show that Ucma/GRP is present in calcified atherosclerotic plaques and highly expressed in calcifying VSMCs in vitro. VSMCs from Ucma/GRP(-/-) mice showed increased mineralisation and expression of osteo/chondrogenic markers (BMP-2, Runx2, beta-catenin, p-SMAD1/5/8, ALP, OCN), and decreased expression of mineralisation inhibitor MGP, suggesting that Ucma/GRP is an inhibitor of mineralisation. Using BMP signalling inhibitor noggin and SMAD1/5/8 signalling inhibitor dorsomorphin we showed that Ucma/GRP is involved in inhibiting the BMP-2-SMAD1/5/8 osteo/chondrogenic signalling pathway in VSMCs treated with elevated phosphate concentrations. Additionally, we showed for the first time evidence of a direct interaction between Ucma/GRP and BMP-2. These results demonstrate an important role of Ucma/GRP in regulating osteo/chondrogenic differentiation and phosphate-induced mineralisation of VSMCs.NWO ZonMw [MKMD 40-42600-98-13007]; FCT [SFRH/BPD/70277/2010]info:eu-repo/semantics/publishedVersio

    Theories of Class F and Anomalies

    Get PDF
    We consider the 6d (2,0) theory on a fibration by genus g curves, and dimensionally reduce along the fiber to 4d theories with duality defects. This generalizes class S theories, for which the fibration is trivial. The non-trivial fibration in the present setup implies that the gauge couplings of the 4d theory, which are encoded in the complex structures of the curve, vary and can undergo S-duality transformations. These monodromies occur around 2d loci in space-time, the duality defects, above which the fiber is singular. The key role that the fibration plays here motivates refering to this setup as theories of class F. In the simplest instance this gives rise to 4d N=4 Super-Yang-Mills with space-time dependent coupling that undergoes SL(2, Z) monodromies. We determine the anomaly polynomial for these theories by pushing forward the anomaly polynomial of the 6d (2,0) theory along the fiber. This gives rise to corrections to the anomaly polynomials of 4d N=4 SYM and theories of class S. For the torus case, this analysis is complemented with a field theoretic derivation of a U(1) anomaly in 4d N=4 SYM. The corresponding anomaly polynomial is tested against known expressions of anomalies for wrapped D3-branes with varying coupling, which are known field theoretically and from holography. Extensions of the construction to 4d N = 0 and 1, and 2d theories with varying coupling, are also discussed.Comment: 54 pages, 1 figure, v2: added discussion of non-supersymmetric extension, v3: version as appears in JHE

    Lessons from non-canonical splicing

    Get PDF
    Recent improvements in experimental and computational techniques that are used to study the transcriptome have enabled an unprecedented view of RNA processing, revealing many previously unknown non-canonical splicing events. This includes cryptic events located far from the currently annotated exons and unconventional splicing mechanisms that have important roles in regulating gene expression. These non-canonical splicing events are a major source of newly emerging transcripts during evolution, especially when they involve sequences derived from transposable elements. They are therefore under precise regulation and quality control, which minimizes their potential to disrupt gene expression. We explain how non-canonical splicing can lead to aberrant transcripts that cause many diseases, and also how it can be exploited for new therapeutic strategies
    corecore