43 research outputs found
Holographic Anyons in the ABJM Theory
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
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
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
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
Impact of vascular calcification on cardiovascular mortality in hemodialysis patients: clinical significance, mechanisms and possible strategies for treatment
Lessons from non-canonical splicing
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