Emergence of massless Dirac fermions in graphene's Hofstadter butterfly at switches of the quantum Hall phase connectivity

The fractal spectrum of magnetic minibands (Hofstadter butterfly), induced by the moir\'e super- lattice of graphene on an hexagonal crystal substrate, is known to exhibit gapped Dirac cones. We show that the gap can be closed by slightly misaligning the substrate, producing a hierarchy of conical singularities (Dirac points) in the band structure at rational values Phi = (p/q)(h/e) of the magnetic flux per supercell. Each Dirac point signals a switch of the topological quantum number in the connected component of the quantum Hall phase diagram. Model calculations reveal the scale invariant conductivity sigma = 2qe^2 / pi h and Klein tunneling associated with massless Dirac fermions at these connectivity switches.Comment: 4 pages, 6 figures + appendix (3 pages, 1 figure

Theory of the topological Anderson insulator

We present an effective medium theory that explains the disorder-induced transition into a phase of quantized conductance, discovered in computer simulations of HgTe quantum wells. It is the combination of a random potential and quadratic corrections proportional to p^2 sigma_z to the Dirac Hamiltonian that can drive an ordinary band insulator into a topological insulator (having an inverted band gap). We calculate the location of the phase boundary at weak disorder and show that it corresponds to the crossing of a band edge rather than a mobility edge. Our mechanism for the formation of a topological Anderson insulator is generic, and would apply as well to three-dimensional semiconductors with strong spin-orbit coupling.Comment: 4 pages, 3 figures (updated figures, calculated DOS

Tauroursodeoxycholic acid exerts anticholestatic effects by a cooperative cPKC alpha-/PKA-dependent mechanism in rat liver.

Objective: Ursodeoxycholic acid (UDCA) exerts anticholestatic effects in part by protein kinase C (PKC)-dependent mechanisms. Its taurine conjugate, TUDCA, is a cPKCa agonist. We tested whether protein kinase A (PKA) might contribute to the anticholestatic action of TUDCA via cooperative cPKCa-/PKA-dependent mechanisms in taurolithocholic acid (TLCA)-induced cholestasis. Methods: In perfused rat liver, bile flow was determined gravimetrically, organic anion secretion spectrophotometrically, lactate dehydrogenase (LDH) release enzymatically, cAMP response-element binding protein (CREB) phosphorylation by immunoblotting, and cAMP by immunoassay. PKC/PKA inhibitors were tested radiochemically. In vitro phosphorylation of the conjugate export pump, Mrp2/Abcc2, was studied in rat hepatocytes and human Hep-G2 hepatoma cells. Results: In livers treated with TLCA (10 mmol/l)+TUDCA (25 mmol/l), combined inhibition of cPKC by the cPKCselective inhibitor Go¨6976 (100 nmol/l) or the nonselective PKC inhibitor staurosporine (10 nmol/l) and of PKA by H89 (100 nmol/l) reduced bile flow by 36% (p,0.05) and 48% (p,0.01), and secretion of the Mrp2/ Abcc2 substrate, 2,4-dinitrophenyl-S-glutathione, by 31% (p,0.05) and 41% (p,0.01), respectively; bile flow was unaffected in control livers or livers treated with TUDCA only or TLCA+taurocholic acid. Inhibition of cPKC or PKA alone did not affect the anticholestatic action of TUDCA. Hepatic cAMP levels and CREB phosphorylation as readout of PKA activity were unaffected by the bile acids tested, suggesting a permissive effect of PKA for the anticholestatic action of TUDCA. Rat and human hepatocellular Mrp2 were phosphorylated by phorbol ester pretreatment and recombinant cPKCa, nPKCe, and PKA, respectively, in a staurosporine-sensitive manner. Conclusion: UDCA conjugates exert their anticholestatic action in bile acid-induced cholestasis in part via cooperative post-translational cPKCa-/PKA-dependent mechanisms. Hepatocellular Mrp2 may be one target of bile acid-induced kinase activation

Fibroblast growth factor receptor 4 single nucleotide polymorphism Gly388Arg in head and neck carcinomas

BACKGROUND Head and neck squamous cell carcinoma (HNSCC) is considered to be a progressive disease resulting from alterations in multiple genes regulating cell proliferation and differentiation like receptor tyrosine kinases (RTKs) and members of the fibroblast growth factor receptors (FGFR)-family. Single-nucleotide polymorphism (SNP) Arg388 of the FGFR4 is associated with a reduced overall survival in patients with cancers of various types. We speculate that FGFR4 expression and SNP is associated with worse survival in patients with HSNCC. AIM To investigate the potential clinical significance of FGFR4 Arg388 in the context of tumors arising in HNSCC, a comprehensive analysis of FGFR4 receptor expression and genotype in tumor tissues and correlated results with patients' clinical data in a large cohort of patients with HNSCC was conducted. METHODS Surgical specimens from 284 patients with HNSCC were retrieved from the Institute of Pathology at the Ludwig-Maximilian-University in Germany. Specimens were analyzed using immunohistochemistry and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The expression of FGFR4 was analyzed in 284 surgical specimens of HNSCC using immunohistochemstry. FGFR4 polymorphism was detected by PCR-RFLP. Patients' clinical data with a minimum follow-up of 5 syears were statistically evaluated with a special emphasis on survival analysis employing Kaplan-Meier estimator and Cox regression analysis. RESULTS Concerning the invasive tumor areas the intensity of the FGFR4 expression was evaluated in a four-grade system: no expression, low expression, intermediate and high expression. FGFR4 expression was scored as "high" (+++) in 74 (26%), "intermediate" (++) in 103 (36.3%), and "low" (+) in 107 (36.7%) cases. Analyzing the FGFR4 mutation it was found in 96 tumors (33.8%), 84 of them (29.6%) having a heterozygous and 12 (4.2%) homozygous mutated Arg388 allele. The overall frequency concerning the mutant alleles demonstrated 65% vs 34% mutated alleles in general. FGFR4 Arg388 was significantly associated with advanced tumor stage (P < 0.004), local metastasis (P < 0.0001) and reduced disease-free survival (P < 0.01). Furthermore, increased expression of FGFR4 correlated significantly with worse overall survival (P < 0.003). CONCLUSION In conclusion, the FGFR4 Arg388 genotype and protein expression of FGFR4 impacts tumor progression in patients with HNSCC and may present a useful target within a multimodal therapeutic intervention

Andreev reflection from a topological superconductor with chiral symmetry

It was pointed out by Tewari and Sau that chiral symmetry (H -> -H if e h) of the Hamiltonian of electron-hole (e-h) excitations in an N-mode superconducting wire is associated with a topological quantum number Q\in\mathbb{Z} (symmetry class BDI). Here we show that Q=Tr(r_{he}) equals the trace of the matrix of Andreev reflection amplitudes, providing a link with the electrical conductance G. We derive G=(2e^2/h)|Q| for |Q|=N,N-1, and more generally provide a Q-dependent upper and lower bound on G. We calculate the probability distribution P(G) for chaotic scattering, in the circular ensemble of random-matrix theory, to obtain the Q-dependence of weak localization and mesoscopic conductance fluctuations. We investigate the effects of chiral symmetry breaking by spin-orbit coupling of the transverse momentum (causing a class BDI-to-D crossover), in a model of a disordered semiconductor nanowire with induced superconductivity. For wire widths less than the spin-orbit coupling length, the conductance as a function of chemical potential can show a sequence of 2e^2/h steps - insensitive to disorder.Comment: 10 pages, 5 figures. Corrected typo (missing square root) in equations A13 and A1

The SNARE machinery is involved in apical plasma membrane trafficking in MDCK cells.

We have investigated the controversial involvement of components of the SNARE (soluble N-ethyl maleimide-sensitive factor [NSF] attachment protein [SNAP] receptor) machinery in membrane traffic to the apical plasma membrane of polarized epithelial (MDCK) cells. Overexpression of syntaxin 3, but not of syntaxins 2 or 4, caused an inhibition of TGN to apical transport and apical recycling, and leads to an accumulation of small vesicles underneath the apical plasma membrane. All other tested transport steps were unaffected by syntaxin 3 overexpression. Botulinum neurotoxin E, which cleaves SNAP-23, and antibodies against alpha-SNAP inhibit both TGN to apical and basolateral transport in a reconstituted in vitro system. In contrast, we find no evidence for an involvement of N-ethyl maleimide-sensitive factor in TGN to apical transport, whereas basolateral transport is NSF-dependent. We conclude that syntaxin 3, SNAP-23, and alpha-SNAP are involved in apical membrane fusion. These results demonstrate that vesicle fusion with the apical plasma membrane does not use a mechanism that is entirely unrelated to other cellular membrane fusion events, but uses isoforms of components of the SNARE machinery, which suggests that they play a role in providing specificity to polarized membrane traffic

Quantized conductance at the Majorana phase transition in a disordered superconducting wire

Superconducting wires without time-reversal and spin-rotation symmetries can be driven into a topological phase that supports Majorana bound states. Direct detection of these zero-energy states is complicated by the proliferation of low-lying excitations in a disordered multi-mode wire. We show that the phase transition itself is signaled by a quantized thermal conductance and electrical shot noise power, irrespective of the degree of disorder. In a ring geometry, the phase transition is signaled by a period doubling of the magnetoconductance oscillations. These signatures directly follow from the identification of the sign of the determinant of the reflection matrix as a topological quantum number.Comment: 7 pages, 4 figures; v3: added appendix with numerics for long-range disorde

One-loop surface tensions of (supersymmetric) kink domain walls from dimensional regularization

We consider domain walls obtained by embedding the 1+1-dimensional $\phi^4$-kink in higher dimensions. We show that a suitably adapted dimensional regularization method avoids the intricacies found in other regularization schemes in both supersymmetric and non-supersymmetric theories. This method allows us to calculate the one-loop quantum mass of kinks and surface tensions of kink domain walls in a very simple manner, yielding a compact d-dimensional formula which reproduces many of the previous results in the literature. Among the new results is the nontrivial one-loop correction to the surface tension of a 2+1 dimensional N=1 supersymmetric kink domain wall with chiral domain-wall fermions.Comment: 23 pages, LATeX; v2: 25 pages, 2 references added, extended discussion of renormalization schemes which dispels apparent contradiction with previous result