Operator entanglement of two-qubit joint unitary operations revisited: Schmidt number approach

Operator entanglement of two-qubit joint unitary operations is revisited. Schmidt number is an important attribute of a two-qubit unitary operation, and may have connection with the entanglement measure of the unitary operator. We found the entanglement measure of two-qubit unitary operators is classified by the Schmidt number of the unitary operators. The exact relation between the operator entanglement and the parameters of the unitary operator is clarified too.Comment: To appear in the Brazilian Journal of Physic

Nociception-induced spatial and temporal plasticity of synaptic connection and function in the hippocampal formation of rats: a multi-electrode array recording

<p>Abstract</p> <p>Background</p> <p>Pain is known to be processed by a complex neural network (neuromatrix) in the brain. It is hypothesized that under pathological state, persistent or chronic pain can affect various higher brain functions through ascending pathways, leading to co-morbidities or mental disability of pain. However, so far the influences of pathological pain on the higher brain functions are less clear and this may hinder the advances in pain therapy. In the current study, we studied spatiotemporal plasticity of synaptic connection and function in the hippocampal formation (HF) in response to persistent nociception.</p> <p>Results</p> <p>On the hippocampal slices of rats which had suffered from persistent nociception for 2 h by receiving subcutaneous bee venom (BV) or formalin injection into one hand paw, multisite recordings were performed by an 8 × 8 multi-electrode array probe. The waveform of the field excitatory postsynaptic potential (fEPSP), induced by perforant path electrical stimulation and pharmacologically identified as being activity-dependent and mediated by ionotropic glutamate receptors, was consistently positive-going in the dentate gyrus (DG), while that in the CA1 was negative-going in shape in naïve and saline control groups. For the spatial characteristics of synaptic plasticity, BV- or formalin-induced persistent pain significantly increased the number of detectable fEPSP in both DG and CA1 area, implicating enlargement of the synaptic connection size by the injury or acute inflammation. Moreover, the input-output function of synaptic efficacy was shown to be distinctly enhanced by the injury with the stimulus-response curve being moved leftward compared to the control. For the temporal plasticity, long-term potentiation produced by theta burst stimulation (TBS) conditioning was also remarkably enhanced by pain. Moreover, it is strikingly noted that the shape of fEPSP waveform was drastically deformed or split by a TBS conditioning under the condition of persistent nociception, while that in naïve or saline control state was not affected. All these changes in synaptic connection and function, confirmed by the 2-dimentional current source density imaging, were found to be highly correlated with peripheral persistent nociception since pre-blockade of nociceptive impulses could eliminate all of them. Finally, the initial pharmacological investigation showed that AMPA/KA glutamate receptors might play more important roles in mediation of pain-associated spatiotemporal plasticity than NMDA receptors.</p> <p>Conclusion</p> <p>Peripheral persistent nociception produces great impact upon the higher brain structures that lead to not only temporal plasticity, but also spatial plasticity of synaptic connection and function in the HF. The spatial plasticity of synaptic activities is more complex than the temporal plasticity, comprising of enlargement of synaptic connection size at network level, deformed fEPSP at local circuit level and, increased synaptic efficacy at cellular level. In addition, the multi-synaptic model established in the present investigation may open a new avenue for future studies of pain-related brain dysfunctions at the higher level of the neuromatrix.</p

Gold nanocrystals with variable index facets as highly effective cathode catalysts for lithium-oxygen batteries

© 2015 Nature Publishing Group All rights reserved. Cathode catalysts are the key factor in improving the electrochemical performance of lithium-oxygen (Li-O2) batteries via their promotion of the oxygen reduction and oxygen evolution reactions (ORR and OER). Generally, the catalytic performance of nanocrystals (NCs) toward ORR and OER depends on both composition and shape. Herein, we report the synthesis of polyhedral Au NCs enclosed by a variety of index facets: cubic gold (Au) NCs enclosed by {100} facets; truncated octahedral Au NCs enclosed by {100} and {110} facets; and trisoctahedral (TOH) Au NCs enclosed by 24 high-index {441} facets, as effective cathode catalysts for Li-O2 batteries. All Au NCs can significantly reduce the charge potential and have high reversible capacities. In particular, TOH Au NC catalysts demonstrated the lowest charge-discharge overpotential and the highest capacity of ∼ 20 298 mA h g-1. The correlation between the different Au NC crystal planes and their electrochemical catalytic performances was revealed: high-index facets exhibit much higher catalytic activity than the low-index planes, as the high-index planes have a high surface energy because of their large density of atomic steps, ledges and kinks, which can provide a high density of reactive sites for catalytic reactions

Multi-objective optimization for optimum tolerance synthesis with process and machine selection using a genetic algorithm

This paper presents a new approach to the tolerance synthesis of the component parts of assemblies by simultaneously optimizing three manufacturing parameters: manufacturing cost, including tolerance cost and quality loss cost; machining time; and machine overhead/idle time cost. A methodology has been developed using the Genetic Algorithm (GA) technique to solve this multi-objective optimization problem. The effectiveness of the proposed methodology has been demonstrated by solving a wheel mounting assembly problem consisting of five components, two subassemblies, two critical dimensions, two functional tolerances, and eight operations. Significant cost saving can be achieved by employing this methodology

EBV-Encoded LMP1 Upregulates Igκ 3′Enhancer Activity and Igκ Expression in Nasopharyngeal Cancer Cells by Activating the Ets-1 through ERKs Signaling

Accumulating evidence indicates that epithelial cancer cells, including nasopharyngeal carcinoma (NPC) cells, express immunoglobulins (Igs). We previously found that the expression of the kappa light chain protein in NPC cells can be upregulated by the EBV-encoded latent membrane protein 1 (LMP1). In the present study, we used NPC cell lines as models and found that LMP1-augmented kappa production corresponds with elevations in ERKs phosphorylation. PD98059 attenuates LMP1-induced ERKs phosphorylation resulting in decreased expression of the kappa light chain. ERK-specific small interfering RNA blunts LMP1-induced kappa light chain gene expression. Luciferase reporter assays demonstrate that immunoglobulin κ 3′ enhancer (3′Eκ) is active in Igκ-expressing NPC cells and LMP1 upregulates the activity of 3′Eκ in NPC cells. Moreover, mutation analysis of the PU binding site in 3′Eκ and inhibition of the MEK/ERKs pathway by PD98059 indicate that the PU site is functional and LMP1-enhanced 3′Eκ activity is partly regulated by this site. PD98059 treatment also leads to a concentration-dependent inhibition of LMP1-induced Ets-1 expression and phosphorylation, which corresponds with a dose-dependent attenuation of LMP1-induced ERK phosphorylation and kappa light chain expression. Suppression of endogenous Ets-1 by small interfering RNA is accompanied by a decrease of Ig kappa light chain expression. Gel shift assays using nuclear extracts of NPC cells indicate that the transcription factor Ets-1 is recruited by LMP1 to the PU motif within 3′Eκ in vitro. ChIP assays further demonstrate Ets-1 binding to the PU motif of 3′Eκ in cells. These results suggest that LMP1 upregulates 3′Eκ activity and kappa gene expression by activating the Ets-1 transcription factor through the ERKs signaling pathway. Our studies provide evidence for a novel regulatory mechanism of kappa expression, by which virus-encoded proteins activate the kappa 3′ enhancer through activating transcription factors in non-B epithelial cancer cells