Current patterns and magnetic impurities in time-reversal breaking superconductor

We study the impurity effect in the time reversal symmetry (${\cal T}$) breaking superconductor based on the Bogoliubov-de Gennes (BdG) equations. In ${\cal T}$-violating superconductors, spontaneous currents are induced around the impurity. The current patterns around the impurity reflect the structures of the Cooper pairs. We investigate impurity problem numerically for two kinds of ${\cal T}$ violating superconductors $(p_{x}\pm {\rm i}p_{y}$ and $d+{\rm i}s)$ and investigate the currents around the impurity. We also study the effects of the magnetic impurity in p-wave ($p_{x}\pm {\rm i}p_{y}$) superconductor, especially in view of the zero-energy crossing of energy levels related to the phase transition of the ground state.Comment: 18 page

Influence of electrolyte co-additives on the performance of dye-sensitized solar cells

The presence of specific chemical additives in the redox electrolyte results in an efficient increase of the photovoltaic performance of dye-sensitized solar cells (DSCs). The most effective additives are 4-tert-butylpyridine (TBP), N-methylbenzimidazole (NMBI) and guanidinium thiocyanate (GuNCS) that are adsorbed onto the photoelectrode/electrolyte interface, thus shifting the semiconductor's conduction band edge and preventing recombination with triiodides. In a comparative work, we investigated in detail the action of TBP and NMBI additives in ionic liquid-based redox electrolytes with varying iodine concentrations, in order to extract the optimum additive/I2 ratio for each system. Different optimum additive/I2 ratios were determined for TBP and NMBI, despite the fact that both generally work in a similar way. Further addition of GuNCS in the optimized electrolytic media causes significant synergistic effects, the action of GuNCS being strongly influenced by the nature of the corresponding co-additive. Under the best operation conditions, power conversion efficiencies as high as 8% were obtained

Analysis of Alfven eigenmodes destabilization by energetic particles in TJ-II using a Landau-closure model

Alfven Eigenmodes (AE) can be destabilized by energetic particles in neutral beam injection (NBI) heated plasmas through inverse Landau damping and couplings with gap modes in the shear Alfven continua. We describe the linear evolution of the poloidal flux and the toroidal component of the vorticity in a full 3D system using the reduced MHD equations, density and parallel velocity moments for the energetic particles as well as the geodesic acoustic wave dynamics. A closure relation adds the Landau damping and resonant destabilization effects in the model. We apply the model to study the Alfven modes stability in TJ-II, performing a parametric analysis in a range of realistic values of energetic particle beta (beta(f)), ratios of thermal/Alfven velocities (V-th/V-A0), energetic particle density profiles and toroidal modes (n) including toroidal and helical couplings. The study predicts a large helical coupling between different toroidal modes and the destabilization of helical Alfven eigenmodes (HAE) with frequencies similar to the AE activity measured in TJ-II, between 50-400 kHz. The analysis has also revealed the destabilization of GAE (global Alfven eigenmodes), TAE (toroidal Alfven eigenmodes) and EPM (energetic particle modes). For the modes considered here, optimized TJ-II operations require a t profile in the range of [0.845, 0.979] to stabilize AEs in the inner and middle plasma. AEs in the plasma periphery cannot be fully stabilized, although for a configuration with t = [0.945, 1.079], only n = 7, 11, 15 AE are unstable with a growth rate 4 times smaller compared to the standard t = [1.54, 1.68] case and a frequency of 100 kHz. We reproduce the frequency sweeping evolution of the AE frequency observed in TJ-II as the t profile is varied. The AE frequency sweeping is caused by consecutive changes of the instability dominant modes between different helical families.This material based on work is supported both by the U.S. Department of Energy, Office of Science, under Contract DE-AC05-00OR22725 with UT-Battelle, LLC. This research was sponsored in part by the Ministerio of Economia y Competitividad of Spain under project no. ENE2015-68265-P. We also want to acknowledge Alexander Melnikov and the TJ-II group at CIEMAT for providing us the initial VMEC equilibria and useful discussions regarding the experimental phenomena

Cimetidine inhibits salivary gland tumor cell adhesion to neural cells and induces apoptosis by blocking NCAM expression

<p>Abstract</p> <p>Background</p> <p>Cimetidine, a histamine type-2 receptor antagonist, has been reported to inhibit the growth of glandular tumors such as colorectal cancer, however the mechanism of action underlying this effect is unknown. Adenoid cystic carcinoma is well known as a malignant salivary gland tumor which preferentially invades neural tissues. We demonstrated previously that human salivary gland tumor (HSG) cells spontaneously express neural cell adhesion molecule (NCAM), that HSG cell proliferation may be controlled via a homophilic (NCAM-NCAM) binding mechanism and that NCAM may be associated with perineural invasion by malignant salivary gland tumors. We further demonstrated that cimetidine inhibited NCAM expression and induced apoptosis in HSG cells. Here, we investigated the effects of cimetidine on growth and perineural/neural invasion of salivary gland tumor cells.</p> <p>Methods</p> <p>In this study, we have examined the effect of cimetidine on cancer cell adhesion to neural cells <it>in vitro</it>, one of the critical steps of cancer invasion and metastasis. We have also used an <it>in vivo </it>carcinogenesis model to confirm the effect of cimetidine.</p> <p>Results</p> <p>We have demonstrated for the first time that cimetidine can block the adhesion of HSG cells to neural cell monolayers and that it can also induce significant apoptosis in the tumor mass in a nude mouse model. We also demonstrated that these apoptotic effects of cimetidine might occur through down-regulation of the cell surface expression of NCAM on HSG cells. Cimetidine-mediated down-regulation of NCAM involved suppression of the nuclear translocation of NF-κB, a transcriptional activator of NCAM gene expression.</p> <p>Conclusion</p> <p>These findings suggest that growth and perineural/neural invasion of salivary gland tumors can be blocked by administration of cimetidine via induction of apoptosis and in which NCAM plays a role.</p

Short-Term Synaptic Plasticity in the Dentate Gyrus of Monkeys

The hippocampus plays an important role in learning and memory. Synaptic plasticity in the hippocampus, short-term and long-term, is postulated to be a neural substrate of memory trace. Paired-pulse stimulation is a standard technique for evaluating a form of short-term synaptic plasticity in rodents. However, evidence is lacking for paired-pulse responses in the primate hippocampus. In the present study, we recorded paired-pulse responses in the dentate gyrus of monkeys while stimulating to the medial part of the perforant path at several inter-pulse intervals (IPIs) using low and high stimulus intensities. When the stimulus intensity was low, the first pulse produced early strong depression (at IPIs of 10–30 ms) and late slight depression (at IPIs of 100–1000 ms) of field excitatory postsynaptic potentials (fEPSPs) generated by the second pulse, interposing no depression IPIs (50–70 ms). When the stimulus intensity was high, fEPSPs generated by the second pulse were depressed by the first pulse at all IPIs except for the longest one (2000 ms). Population spikes (PSs) generated by the second pulse were completely blocked or strongly depressed at shorter IPIs (10–100 or 200 ms, respectively), while no depression or slight facilitation occurred at longer IPIs (500–2000 ms). Administration of diazepam slightly increased fEPSPs, while it decreased PSs produced by the first pulse. It also enhanced the facilitation of PSs produced by the second stimulation at longer IPIs. The present results, in comparison with previous studies using rodents, indicate that paired-pulse responses of fEPSPs in the monkey are basically similar to those of rodents, although paired-pulse responses of PSs in the monkey are more delayed than those in rodents and have a different sensitivity to diazepam

Fluvastatin synergistically enhances the antiproliferative effect of gemcitabine in human pancreatic cancer MIAPaCa-2 cells

The new combination between the nucleoside analogue gemcitabine and the cholesterol-lowering drug fluvastatin was investigated in vitro and in vivo on the human pancreatic tumour cell line MIAPaCa-2. The present study demonstrates that fluvastatin inhibits proliferation, induces apoptosis in pancreatic cancer cells harbouring a p21ras mutation at codon 12 and synergistically potentiates the cytotoxic effect of gemcitabine. The pharmacologic activities of fluvastatin are prevented by administration of mevalonic acid, suggesting that the shown inhibition of geranyl-geranylation and farnesylation of cellular proteins, including p21rhoA and p21ras, plays a major role in its anticancer effect. Fluvastatin treatment also indirectly inhibits the phosphorylation of p42ERK2/mitogen-activated protein kinase, the cellular effector of ras and other signal transduction peptides. Moreover, fluvastatin administration significantly increases the expression of the deoxycytidine kinase, the enzyme required for the activation of gemcitabine, and simultaneously reduces the 5′-nucleotidase, responsible for deactivation of gemcitabine, suggesting a possible additional role of these enzymes in the enhanced cytotoxic activity of gemcitabine. Finally, a significant in vivo antitumour effect on MIAPaCa-2 xenografts was observed with the simultaneous combination of fluvastatin and gemcitabine, resulting in an almost complete suppression and a marked delay in relapse of tumour growth. In conclusion, the combination of fluvastatin and gemcitabine is an effective cytotoxic, proapoptotic treatment in vitro and in vivo against MIAPaCa-2 cells by a mechanism of action mediated, at least in part, by the inhibition of p21ras and rhoA prenylation. The obtained experimental findings might constitute the basis for a novel translational research in humans

Validation of pharmacodynamic assays to evaluate the clinical efficacy of an antisense compound (AEG 35156) targeted to the X-linked inhibitor of apoptosis protein XIAP

The inhibitor of apoptosis protein, XIAP, is frequently overexpressed in chemoresistant human tumours. An antisense oligonucleotide (AEG 35156/GEM 640) that targets XIAP has recently entered phase I trials in the UK. Method validation data are presented on three pharmacodynamic assays that will be utilised during this trial. Quantitative RT-PCR was based on a Taqman assay and was confirmed to be specific for XIAP. Assay linearity extended over four orders of magnitude. MDA-MB-231/U6-E1 cells and clone X-G4 stably expressing an RNAi vector against XIAP were chosen as high and low XIAP expression quality controls (QCs). Within-day and between-day coefficients of variation (CVs) in precision for cycle threshold (CT) and delta CT values (employing GAPDH and beta 2 microglobulin as housekeepers) were always less than 10%. A Western blotting technique was validated using a GST–XIAP fusion protein as a standard and HeLa cells and SF268 (human glioblastoma) cells as high and low XIAP expression QCs. Specificity of the final choice of antibody for XIAP was evaluated by analysing a panel of cell lines including clone X-G4. The assay was linear over a 29-fold range of protein concentration and between-day precision was 29% for the low QC and 23% for the high QC when normalised to GAPDH. XIAP protein was also shown to be stable at −80°C for at least 60 days. M30-Apoptosense™ plasma Elisa detects a caspase-cleaved fragment of cytokeratin 18 (CK18), believed to be a surrogate marker for tumour cell apoptosis. Generation of an independent QC was achieved through the treatment of X-G4 cells with staurosporine and collection of media. Measurements on assay precision and kit-to-kit QC were always less than 10%. The M30 antigen (CK18-Asp396) was stable for 3 months at −80°C, while at 37°C it had a half-life of 80–100 h in healthy volunteer plasma. Results from the phase I trial are eagerly awaited

Functional Modifications of Acid-Sensing Ion Channels by Ligand-Gated Chloride Channels

Together, acid-sensing ion channels (ASICs) and epithelial sodium channels (ENaC) constitute the majority of voltage-independent sodium channels in mammals. ENaC is regulated by a chloride channel, the cystic fibrosis transmembrane conductance regulator (CFTR). Here we show that ASICs were reversibly inhibited by activation of GABAA receptors in murine hippocampal neurons. This inhibition of ASICs required opening of the chloride channels but occurred with both outward and inward GABAA receptor-mediated currents. Moreover, activation of the GABAA receptors modified the pharmacological features and kinetic properties of the ASIC currents, including the time course of activation, desensitization and deactivation. Modification of ASICs by open GABAA receptors was also observed in both nucleated patches and outside-out patches excised from hippocampal neurons. Interestingly, ASICs and GABAA receptors interacted to regulate synaptic plasticity in CA1 hippocampal slices. The activation of glycine receptors, which are similar to GABAA receptors, also modified ASICs in spinal neurons. We conclude that GABAA receptors and glycine receptors modify ASICs in neurons through mechanisms that require the opening of chloride channels

Lifestyle and diet in relation to risk of type 2 diabetes in Vietnam: a hospital-based case-control study.

BACKGROUND: Lifestyle and diet are important determinants of type 2 diabetes (T2D). Their impact on T2D can be evaluated using clinical and epidemiological approaches. Randomised controlled trials are the most rigorous design but expensive to conduct, whereas prospective cohort studies are time-consuming and less powerful for populations with a low incidence of the disease. Case-control studies are considered appropriate in resource-limited settings. A hospital-based case-control study protocol has been developed to investigate the role of lifestyle and dietary factors in T2D aetiology for adults in Vietnam. METHODS: A total of 1100 patients aged 40-65 years (550 T2D cases and 550 controls) will be recruited from a tertiary hospital in Hanoi, the capital city of Vietnam. Cases and controls will be frequency-matched on age (±3 years), gender, and residential location. T2D will be diagnosed according to the 2006 World Health Organisation criteria. Habitual physical activity will be assessed by the Vietnamese version of the International Physical Activity Questionnaire-Short Form. Food and beverage consumption will be ascertained using a Validated Food Frequency Questionnaire, specifically developed for the Vietnamese population. Information on demographic and other personal characteristics will be collected, together with anthropometric and blood pressure measurements. Descriptive statistics and unconditional logistic regression analyses will be performed to examine factors associated with the T2D prevalence. DISCUSSION: The proposed study will elucidate the role of lifestyle and diet in T2D prevalence among Vietnamese adults. Findings concerning pertinent factors will provide epidemiological evidence for the development of focused interventions, and contribute to the formulation of national policies to prevent and control T2D in Vietnam