Properties of mesoscopic superconducting thin-film rings. London approach

Superconducting thin-film rings smaller than the film penetration depth (the Pearl length) are considered. The current distribution, magnetic moment, and thermodynamic potential ${\cal F}(H,N,v)$ for a flat, washer-shaped annular ring in a uniform applied field $H$ perpendicular to the film are solved analytically within the London approach for a state with winding number $N$ and a vortex at radius $v$ between the inner and outer radii.Comment: Submitted to Phys. Rev.

Reducing vortex density in superconductors using the ratchet effect

A serious obstacle that impedes the application of low and high temperature superconductor (SC) devices is the presence of trapped flux. Flux lines or vortices are induced by fields as small as the Earth's magnetic field. Once present, vortices dissipate energy and generate internal noise, limiting the operation of numerous superconducting devices. Methods used to overcome this difficulty include the pinning of vortices by the incorporation of impurities and defects, the construction of flux dams, slots and holes and magnetic shields which block the penetration of new flux lines in the bulk of the SC or reduce the magnetic field in the immediate vicinity of the superconducting device. Naturally, the most desirable would be to remove the vortices from the bulk of the SC. There is no known phenomenon, however, that could form the basis for such a process. Here we show that the application of an ac current to a SC that is patterned with an asymmetric pinning potential can induce vortex motion whose direction is determined only by the asymmetry of the pattern. The mechanism responsible for this phenomenon is the so called ratchet effect, and its working principle applies to both low and high temperature SCs. As a first step here we demonstrate that with an appropriate choice of the pinning potential the ratchet effect can be used to remove vortices from low temperature SCs in the parameter range required for various applications.Comment: 7 pages, 4 figures, Nature (in press

Magnetic-field and current-density distributions in thin-film superconducting rings and disks

We show how to calculate the magnetic-field and sheet-current distributions for a thin-film superconducting annular ring (inner radius a, outer radius b, and thickness d<<a) when either the penetration depth obeys lambda < d/2 or, if lambda > d/2, the two-dimensional screening length obeys Lambda = 2 lambda^2/d << a for the following cases: (a) magnetic flux trapped in the hole in the absence of an applied magnetic field, (b) zero magnetic flux in the hole when the ring is subjected to an applied magnetic field, and (c) focusing of magnetic flux into the hole when a magnetic field is applied but no net current flows around the ring. We use a similar method to calculate the magnetic-field and sheet-current distributions and magnetization loops for a thin, bulk-pinning-free superconducting disk (radius b) containing a dome of magnetic flux of radius a when flux entry is impeded by a geometrical barrier.Comment: 10 pages, 13 figure

The revival-collapse phenomenon in the quadrature field components of the two-mode multiphoton Jaynes-Cummings model

In this paper we consider a system consisting of a two-level atom in an excited state interacting with two modes of a radiation field prepared initially in $l$-photon coherent states. This system is described by two-mode multiphoton (, i.e., $k_1, k_2$) Jaynes-Cummings model (JCM). For this system we investigate the occurrence of the revival-collapse phenomenon (RCP) in the evolution of the single-mode, two-mode, sum and difference quadrature squeezing. We show that there is a class of states for which all these types of squeezing exhibit RCP similar to that involved in the corresponding atomic inversion. Also we show numerically that the single-mode squeezing of the first mode for $(k_1,k_2)=(3,1)$ provides RCP similar to that of the atomic inversion of the case $(k_1,k_2)=(1,1)$, however, sum and difference squeezing give partial information on that case. Moreover, we show that single-mode, two-mode and sum squeezing for the case $(k_1,k_2)=(2,2)$ provide information on the atomic inversion of the single-mode two-photon JCM. We derive the rescaled squeezing factors giving accurate information on the atomic inversion for all cases. The consequences of these results are that the homodyne and heterodyne detectors can be used to detect the RCP for the two-mode JCM.Comment: 18 pages, 6 figure

Q/R site interactions with the M3 helix in GluK2 kainate receptor channels revealed by thermodynamic mutant cycles

RNA editing at the Q/R site near the apex of the pore loop of AMPA and kainate receptors controls a diverse array of channel properties, including ion selectivity and unitary conductance and susceptibility to inhibition by polyamines and cis-unsaturated fatty acids, as well as subunit assembly into tetramers and regulation by auxiliary subunits. How these different aspects of channel function are all determined by a single amino acid substitution remains poorly understood; however, several lines of evidence suggest that interaction between the pore helix (M2) and adjacent segments of the transmembrane inner (M3) and outer (M1) helices may be involved. In the present study, we have used double mutant cycle analysis to test for energetic coupling between the Q/R site residue and amino acid side chains along the M3 helix. Our results demonstrate interaction with several M3 locations and particularly strong coupling to substitution for L614 at the level of the central cavity. In this location, replacement with smaller side chains completely and selectively reverses the effect of fatty acids on gating of edited channels, converting strong inhibition of wild-type GluK2(R) to nearly 10-fold potentiation of GluK2(R) L614A

Non-equivalent role of TM2 gating hinges in heteromeric Kir4.1/Kir5.1 potassium channels

Comparison of the crystal structures of the KcsA and MthK potassium channels suggests that the process of opening a K+ channel involves pivoted bending of the inner pore-lining helices at a highly conserved glycine residue. This bending motion is proposed to splay the transmembrane domains outwards to widen the gate at the “helix-bundle crossing”. However, in the inwardly rectifying (Kir) potassium channel family, the role of this “hinge” residue in the second transmembrane domain (TM2) and that of another putative glycine gating hinge at the base of TM2 remain controversial. We investigated the role of these two positions in heteromeric Kir4.1/Kir5.1 channels, which are unique amongst Kir channels in that both subunits lack a conserved glycine at the upper hinge position. Contrary to the effect seen in other channels, increasing the potential flexibility of TM2 by glycine substitutions at the upper hinge position decreases channel opening. Furthermore, the contribution of the Kir4.1 subunit to this process is dominant compared to Kir5.1, demonstrating a non-equivalent contribution of these two subunits to the gating process. A homology model of heteromeric Kir4.1/Kir5.1 shows that these upper “hinge” residues are in close contact with the base of the pore α-helix that supports the selectivity filter. Our results also indicate that the highly conserved glycine at the “lower” gating hinge position is required for tight packing of the TM2 helices at the helix-bundle crossing, rather than acting as a hinge residue

Selective Phosphorylation Modulates the PIP2 Sensitivity of the CaM-SK Channel Complex

Phosphatidylinositol bisphosphate (PIP2) regulates the activities of many membrane proteins including ion channels through direct interactions. However, the affinity of PIP2 is so high for some channel proteins that its physiological role as a modulator has been questioned. Here we show that PIP2 is an important cofactor for activation of small conductance Ca2+-activated potassium channels (SK) by Ca2+-bound calmodulin (CaM). Removal of the endogenous PIP2 inhibits SK channels. The PIP2-binding site resides at the interface of CaM and the SK C-terminus. We further demonstrate that the affinity of PIP2 for its target proteins can be regulated by cellular signaling. Phosphorylation of CaM T79, located adjacent to the PIP2-binding site, by Casein Kinase 2 reduces the affinity of PIP2 for the CaM-SK channel complex by altering the dynamic interactions among amino acid residues surrounding the PIP2-binding site. This effect of CaM phosphorylation promotes greater channel inhibition by G-protein-mediated hydrolysis of PIP2

Relationship between the atomic inversion and Wigner function for multiphoton multimode Jaynes-Cummings model

In this paper we consider multimode multiphoton Jaynes-Cummings model, which consists of a two-level atom, initially prepared in an excited atomic state, interacting with $N$ modes of electromagnetic field prepared in general pure quantum states. For this system we show that under certain conditions the evolution of the Wigner function at the phase space origin provides direct information on the corresponding atomic inversion. This relation is also valid even if the system includes Kerr-like nonlinearity, Stark shift effect, different types of the initial atomic state as well as moving atom. Furthermore, based on this fact we discuss for the single-mode case the possibility of detecting the atomic inversion by means of techniques similar to those used for Wigner function.Comment: 19 pages, 4 figure

Chondroprotection by urocortin involves blockade of the mechanosensitive ion channel Piezo1

Osteoarthritis (OA) is characterised by progressive destruction of articular cartilage and chondrocyte cell death. Here, we show the expression of the endogenous peptide urocortin1 (Ucn1) and two receptor subtypes, CRF-R1 and CRF-R2, in primary human articular chondrocytes (AC) and demonstrate its role as an autocrine/paracrine pro-survival factor. This effect could only be removed using the CRF-R1 selective antagonist CP-154526, suggesting Ucn1 acts through CRF-R1 when promoting chondrocyte survival. This cell death was characterised by an increase in p53 expression, and cleavage of caspase 9 and 3. Antagonism of CRF-R1 with CP-154526 caused an accumulation of intracellular calcium (Ca2+) over time and cell death. These effects could be prevented with the non-selective cation channel blocker Gadolinium (Gd3+). Therefore, opening of a non-selective cation channel causes cell death and Ucn1 maintains this channel in a closed conformation. This channel was identified to be the mechanosensitive channel Piezo1. We go on to determine that this channel inhibition by Ucn1 is mediated initially by an increase in cyclic adenosine monophosphate (cAMP) and a subsequent inactivation of phospholipase A2 (PLA2), whose metabolites are known to modulate ion channels. Knowledge of these novel pathways may present opportunities for interventions that could abrogate the progression of OA