Critical Current of the Spin-Triplet Superconducting Phase in Sr2_2RuO4_4

There have been two different proposals for the spin-triplet order parameter of the superconducting phase in Sr$_2$RuO$_4$; an $f$-wave order parameter and the multigap model where some of the bands have the line node. In an effort to propose an experiment that can distinguish two cases, we study the behavior of the supercurrent and compute the critical current for these order parameters when the sample is a thin film with the thickness $d \ll \xi$ where $\xi$ is the coherence length. It is found that the supercurrent behaves very differently in two models. This will serve as a sharp test for the identification of the correct order parameter.Comment: 4 pages, 1 figur

Elevated intracellular cAMP exacerbates vulnerability to oxidative stress in optic nerve head astrocytes.

Glaucoma is characterized by a progressive loss of retinal ganglion cells and their axons, but the underlying biological basis for the accompanying neurodegeneration is not known. Accumulating evidence indicates that structural and functional abnormalities of astrocytes within the optic nerve head (ONH) have a role. However, whether the activation of cyclic adenosine 3',5'-monophosphate (cAMP) signaling pathway is associated with astrocyte dysfunction in the ONH remains unknown. We report here that the cAMP/protein kinase A (PKA) pathway is critical to ONH astrocyte dysfunction, leading to caspase-3 activation and cell death via the AKT/Bim/Bax signaling pathway. Furthermore, elevated intracellular cAMP exacerbates vulnerability to oxidative stress in ONH astrocytes, and this may contribute to axonal damage in glaucomatous neurodegeneration. Inhibition of intracellular cAMP/PKA signaling activation protects ONH astrocytes by increasing AKT phosphorylation against oxidative stress. These results strongly indicate that activation of cAMP/PKA pathway has an important role in astrocyte dysfunction, and suggest that modulating cAMP/PKA pathway has therapeutic potential for glaucomatous ONH degeneration

Silibinin induces apoptosis via calpain-dependent AIF nuclear translocation in U87MG human glioma cell death

<p>Abstract</p> <p>Background</p> <p>Silibinin, a natural polyphenolic flavonoid, has been reported to induce cell death in various cancer cell types. However, the molecular mechanism is not clearly defined. Our previous study showed that silibinin induces glioma cell death and its effect was effectively prevented by calpain inhibitor. The present study was therefore undertaken to examine the role of calpain in the silibinin-induced glioma cell death.</p> <p>Methods</p> <p>U87MG cells were grown on well tissue culture plates and cell viability was measured by MTT assay. ROS generation and △ψ_mwere estimated using the fluorescence dyes. PKC activation and Bax expression were measured by Western blot analysis. AIF nuclear translocation was determined by Western blot and immunocytochemistry.</p> <p>Results</p> <p>Silibinin induced activation of calpain, which was blocked by EGTA and the calpain inhibitor Z-Leu-Leu-CHO. Silibinin caused ROS generation and its effect was inhibited by calpain inhibitor, the general PKC inhibitor GF 109203X, the specific PKC_δinhibitor rottlerin, and catalase. Silibinin-induce cell death was blocked by calpain inhibitor and PKC inhibitors. Silibinin-induced PKC_δactivation and disruption of △ψ_mwere prevented by the calpain inhibitor. Silibinin induced AIF nuclear translocation and its effect was prevented by calpain inhibitor. Transfection of vector expressing microRNA of AIF prevented the silibinin-induced cell death.</p> <p>Conclusions</p> <p>Silibinin induces apoptotic cell death through a calpain-dependent mechanism involving PKC, ROS, and AIF nuclear translocation in U87MG human glioma cells.</p

Orbital-selective confinement effect of Ru 4d4d orbitals in SrRuO3_3 ultrathin film

The electronic structure of SrRuO$_3$ thin film with thickness from 50 to 1 unit cell (u.c.) is investigated via the resonant inelastic x-ray scattering (RIXS) technique at the O K-edge to unravel the intriguing interplay of orbital and charge degrees of freedom. We found that orbital-selective quantum confinement effect (QCE) induces the splitting of Ru $4d$ orbitals. At the same time, we observed a clear suppression of the electron-hole continuum across the metal-to-insulator transition (MIT) occurring at the 4 u.c. sample. From these two clear observations we conclude that QCE gives rise to a Mott insulating phase in ultrathin SrRuO$_3$ films. Our interpretation of the RIXS spectra is supported by the configuration interaction calculations of RuO$_6$ clusters.Comment: 7 pages, 7 figure

Mesoporous TiO\u3csub\u3e2\u3c/sub\u3e Bragg Stack Templated by Graft Copolymer for Dye-Sensitized Solar Cells

Organized mesoporous TiO2 Bragg stacks (om-TiO2 BS) consisting of alternating high and low refractive index organized mesoporous TiO2(om-TiO2) films were prepared to enhance dye loading, light harvesting, electron transport, and electrolyte pore-infiltration in dye-sensitized solar cells (DSSCs). The om-TiO2 films were synthesized via a sol-gel reaction using amphiphilic graft copolymers consisting of poly(vinyl chloride) backbones and poly(oxyethylene methacrylate) side chains, i.e., PVC-g-POEM as templates. To generate high and low index films, the refractive index of om-TiO2 film was tuned by controlling the grafting ratio of PVC-g-POEM via atomic transfer radical polymerization (ATRP). A polymerized ionic liquid (PIL)-based DSSC fabricated with a 1.2-μm-thick om-TiO2 BS-based photoanode exhibited an efficiency of 4.3%, which is much higher than that of conventional DSSCs with a nanocrystalline TiO2 layer (nc-TiO2 layer) (1.7%). A PIL-based DSSC with a heterostructured photoanode consisting of 400-nm-thick organized mesoporous TiO2 interfacial (om-TiO2 IF) layer, 7-μm-thick nc-TiO2, and 1.2-μm-thick om-TiO2 BS as the bottom, middle and top layers, respectively, exhibited an excellent efficiency of 7.5%, which is much higher than that of nanocrystaline TiO2 photoanode (3.5%

Decreased health-related quality of life in disease-free survivors of differentiated thyroid cancer in Korea

<p>Abstract</p> <p>Background</p> <p>Concern regarding the health-related quality of life (HRQOL) of long-term survivors of thyroid cancer has risen due to the rapid increase in the incidence of thyroid cancer, which generally has an excellent prognosis. The aim of this study was to evaluate the status of HRQOL in disease-free survivors of differentiated thyroid carcinoma (DTC) and to evaluate the important determinants of HRQOL.</p> <p>Methods</p> <p>This was a cross-sectional study in which we interviewed consecutive disease-free survivors of DTC. Three different validated questionnaires ("EORTC QLQ-C30" for various functional domains, the "brief fatigue inventory (BFI)" and the "hospital anxiety and depression scale" (HADS)) were used. Data from a large, population based survey of 1,000 people were used as a control.</p> <p>Results</p> <p>The response rate for the questionnaires was 78.9% (316/401). Disease-free survivors of DTC showed a decreased HRQOL in all five functional domains (physical, role, cognitive, emotional, and social) on the EORTC QLQ-C30 compared with controls (<it>P </it>< 0.01). BFI and HADS-anxiety scores also showed greater distress in disease-free survivors of DTC than in controls (<it>P </it>< 0.05). A multiple regression analysis for the determinants of HRQOL showed that the HADS-anxiety, HADS-depression, and BFI scores were the most significant components of decreased HRQOL.</p> <p>Conclusions</p> <p>Although disease-free survivors of DTC are expected to have disease-specific survival comparable to the general population, they experience a significantly decreased HRQOL. Anxiety, depression, and fatigue were the major determinants of the decreased HRQOL. Supportive psychological care should be integrated into the management of long-term survivors of DTC.</p