Electronic position indicator for latching solenoid valves

Electronic circuit connected to solenoid valve coils visually indicates the position of the valve stem. Transient suppression is provided to prevent damaging voltage spikes

Low-energy magnetic radiation: deviations from GOE

A pronounced spike at low energy in the strength function for magnetic radiation (LEMAR) is found by means of Shell Model calculations, which explains the experimentally observed enhancement of the dipole strength. LEMAR originates from statistical low-energy M1-transitions between many excited complex states. Re-coupling of the proton and neutron high-j orbitals generates the strong magnetic radiation. LEMAR is closely related to Magnetic Rotation. LEMAR is predicted for nuclides participating in the r-process of element synthesis and is expected to change the reaction rates. An exponential decrease of the strength function and a power law for the size distribution of the $B(M1)$ values are found, which strongly deviate from the ones of the GOE of random matrices, which is commonly used to represent complex compound states.Comment: Proceedings of the conference on Nuclei and Mesoscopic Physics 2014, MSU, to be published AIP Conference Proceeding

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

Robustness of edge states in graphene quantum dots

We analyze the single particle states at the edges of disordered graphene quantum dots. We show that generic graphene quantum dots support a number of edge states proportional to circumference of the dot over the lattice constant. Our analytical theory agrees well with numerical simulations. Perturbations breaking electron-hole symmetry like next-nearest neighbor hopping or edge impurities shift the edge states away from zero energy but do not change their total amount. We discuss the possibility of detecting the edge states in an antidot array and provide an upper bound on the magnetic moment of a graphene dot.Comment: Added figure 6, extended discussion (version as accepted by Physical Review B

Weak localization in mesoscopic hole transport: Berry phases and classical correlations

We consider phase-coherent transport through ballistic and diffusive two-dimensional hole systems based on the Kohn-Luttinger Hamiltonian. We show that intrinsic heavy-hole light-hole coupling gives rise to clear-cut signatures of an associated Berry phase in the weak localization which renders the magneto-conductance profile distinctly different from electron transport. Non-universal classical correlations determine the strength of these Berry phase effects and the effective symmetry class, leading even to antilocalization-type features for circular quantum dots and Aharonov-Bohm rings in the absence of additional spin-orbit interaction. Our semiclassical predictions are quantitatively confirmed by numerical transport calculations

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