8,150 research outputs found

    Nonmonotonic temperature dependence of critical current in diffusive d-wave junctions

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    We study the Josephson effect in D/I/DN/I/D junctions, where I, DN and D denote an insulator, a diffusive normal metal and a d-wave superconductor, respectively.The Josephson current is calculated based on the quasiclassical Green's function theory with a general boundary condition for unconventional superconducting junctions. In contrast to s-wave junctions, the product of the Josephson current and the normal state resistance is enhanced by making the interface barriers stronger. The Josephson current has a nonmonotonic temperature dependence due to the competition between the proximity effect and the midgap Andreev resonant states.Comment: 5 pages, 4 figure

    Angular dependence of Josephson currents in unconventional superconducting junctions

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    Josephson effect in junctions between unconventional superconductors is studied theoretically within the model describing the effects of interface roughness. The particularly important issue of applicability of the frequently used Sigrist-Rice formula for Josephson current in d-wave superconductor / insulator / d-wave superconductor junctions is addressed. We show that although the SR formula is not applicable in the ballistic case, it works well for rough interfaces when the diffusive normal metal regions exist between the d-wave superconductor and the insulator. It is shown that the SR approach only takes into account the component of the d-wave pair potential symmetric with respect to an inversion around the plane perpendicular to the interface. Similar formula can be derived for general unconventional superconductors with arbitrary angular momentum l.Comment: 4 pages, 4 figure

    Isoflurane Inhibits Synaptic Vesicle Exocytosis through Reduced Ca2+ Influx, not Ca2+-Exocytosis Coupling

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    Identifying presynaptic mechanisms of general anesthetics is critical to understanding their effects on synaptic transmission. We show that the volatile anesthetic isoflurane inhibits synaptic vesicle (SV) exocytosis at nerve terminals in dissociated rat hippocampal neurons through inhibition of presynaptic Ca2+ influx without significantly altering the Ca2+ sensitivity of SV exocytosis. A clinically relevant concentration of isoflurane (0.7 mM) inhibited changes in [Ca2+]i driven by single action potentials (APs) by 25 ± 3%, which in turn led to 62 ± 3% inhibition of single AP-triggered exocytosis at 4 mM extracellular Ca2+ ([Ca2+]e). Lowering external Ca2+ to match the isoflurane-induced reduction in Ca2+ entry led to an equivalent reduction in exocytosis. These data thus indicate that anesthetic inhibition of neurotransmitter release from small SVs occurs primarily through reduced axon terminal Ca2+ entry without significant direct effects on Ca2+-exocytosis coupling or on the SV fusion machinery. Isoflurane inhibition of exocytosis and Ca2+ influx was greater in glutamatergic compared with GABAergic nerve terminals, consistent with selective inhibition of excitatory synaptic transmission. Such alteration in the balance of excitatory to inhibitory transmission could mediate reduced neuronal interactions and network-selective effects observed in the anesthetized central nervous system

    Assessing patterns of T2/T1rho change in grade 1 cartilage lesions of the distal femur using an angle/layer dependent approach.

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    PURPOSE:To assess changes in the patterns of T2 and T1rho values within grade 1 cartilage lesions of osteoarthritis (OA) patients compared to healthy controls. MATERIALS AND METHODS:Twenty healthy knees and 25 OA knees were examined on a 3 T scanner. Areas of signal heterogeneity within the cartilage of the distal femur were identified using fat suppressed proton density-weighted imagines. T2 and T1rho values in each OA patient with grade 1 lesions were compared to average T2 and T1rho values of the corresponding areas in healthy subjects. RESULTS:A total of 28 areas including grade 1 lesion were identified. Compared to normal cartilage, the majority of grade 1 cartilage lesions demonstrated either no significant change or a statistically significant increase in both T2 values (18/28, 64%) and T1rho values (23/28, 82%). Compared to T2, T1rho demonstrated a greater proportion of statistically significantly higher values in OA patients than those from the normal controls. However, T2 and T1rho values in grade 1 lesions can be decreased, or demonstrate mixed patterns compared to those in healthy cartilage. CONCLUSION:Our results suggest that early degenerative cartilage lesions can demonstrate various patterns of T2 and T1rho changes

    Ecdysone-dependent and ecdysone-independent programmed cell death in the developing optic lobe of Drosophila

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    AbstractThe adult optic lobe of Drosophila develops from the primordium during metamorphosis from mid-3rd larval stage to adult. Many cells die during development of the optic lobe with a peak of the number of dying cells at 24h after puparium formation (h APF). Dying cells were observed in spatio-temporal specific clusters. Here, we analyzed the function of a component of the insect steroid hormone receptor, EcR, in this cell death. We examined expression patterns of two EcR isoforms, EcR-A and EcR-B1, in the optic lobe. Expression of each isoform altered during development in isoform-specific manner. EcR-B1 was not expressed in optic lobe neurons from 0 to 6h APF, but was expressed between 9 and 48h APF and then disappeared by 60h APF. In each cortex, its expression was stronger in older glia-ensheathed neurons than in younger ones. EcR-B1 was also expressed in some types of glia. EcR-A was expressed in optic lobe neurons and many types of glia from 0 to 60h APF in a different pattern from EcR-B1. Then, we genetically analyzed EcR function in the optic lobe cell death. At 0h APF, the optic lobe cell death was independent of any EcR isoforms. In contrast, EcR-B1 was required for most optic lobe cell death after 24h APF. It was suggested that cell death cell-autonomously required EcR-B1 expressed after puparium formation. βFTZ-F1 was also involved in cell death in many dying-cell clusters, but not in some of them at 24h APF. Altogether, the optic lobe cell death occurred in ecdysone-independent manner at prepupal stage and ecdysone-dependent manner after 24h APF. The acquisition of ecdysone-dependence was not directly correlated with the initiation or increase of EcR-B1 expression
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