Locality of three-qubit Greenberger-Horne-Zeilinger-symmetric states

The hierarchy of nonlocality and entanglement in multipartite systems is one of the fundamental problems in quantum physics. Existing studies on this topic to date were limited to the entanglement classification according to the numbers of particles enrolled. Equivalence under stochastic local operations and classical communication provides a more detailed classification, e. g. the genuine three-qubit entanglement being divided into W and GHZ classes. We construct two families of local models for the three-qubit Greenberger-Horne-Zeilinger (GHZ)-symmetric states, whose entanglement classes have a complete description. The key technology of construction the local models in this work is the GHZ symmetrization on tripartite extensions of the optimal local-hidden-state models for Bell diagonal states. Our models show that entanglement and nonlocality are inequivalent for all the entanglement classes (biseparable, W, and GHZ) in three-qubit systems.Comment: 3 figures, 6 pages. Many spelling errors have been corrected. Submitted versio

New Understandings of Ethanol Oxidation Reaction Mechanism on Pd/C and Pd2Ru/C Catalysts in Alkaline Direct Ethanol Fuel Cells

Ethanol oxidation reaction (EOR) on Pd2Ru/C and Pd/C catalysts in alkaline media is studied comprehensively by cyclic voltammetry, chronoamperometry, in situ FTIR, single fuel cell test and electrochemical impedance spectroscopy measurements. The results show that, as compared to Pd/C, Pd2Ru/C favors acetaldehyde formation and hinders its oxidation. Based on X-ray absorption data, which evidence that Ru promotes a larger electronic vacancy of the Pd 4d band, it is expected that the formation of adsorbed ethoxy is favored on Pd2Ru/C and followed by its oxidation to acetaldehyde facilitated by oxygenated species provided by Ru. In contrast, acetaldehyde oxidation is more difficult on Pd2Ru/C than on Pd/C likely because the adsorption energy of the reactive species is increased. We also show that the performance of Pd2Ru/C anode in alkaline direct ethanol fuel cell (ADEFC) is initially better but degrades much more rapidly than that with Pd/C anode under the same test conditions. The degradation is demonstrated to result from the accumulation of large amounts of acetaldehyde, which in alkaline media forms dimers by the aldol condensation reaction. The dimers tend to be responsible for blocking the active sites for further ethanol oxidation. This comprehensive study provides new understandings of the roles of Ru in Pd2Ru/C for EOR in alkaline media, unveils the causes of the performance degradation of fuel cells with Pd2Ru/C and demonstrates that initial good performances are not necessarily a valid criterion for selecting appropriate anode catalysts for ADEFC applications

Tetra­aqua­bis­(1,10-phenanthroline-κ2 N,N′)strontium 5,5′-diazene­diyl­ditetra­zolide

The title complex, [Sr(C12H8N2)2(H2O)4](C2N10), contains an [Sr(phen)2(H2O)4]2+ cation (phen is 1,10-phenanthroline) and a 5,5′-diazenediylditetra­zolide anion (site symmetry 2). The Sr2+ cation (site symmetry 2) is coordinated by four N atoms from two chelating phen and four water mol­ecules. In the crystal structure, the water mol­ecules and the N atoms in the tetra­zolide rings form an extensive range of O—H⋯N hydrogen bonds which link the complex into a two-dimensional structure. An adjacent layer further yields a three-dimensional supramolecular network by offset face-to-face π–π stacking inter­actions of the phen ligands [with centroid–centroid distances of 3.915 (2) and 4.012 (2) Å]. The two bridging N atoms of the anion are equally disordered about the twofold rotation axis

Nurr1 regulates Top IIβ and functions in axon genesis of mesencephalic dopaminergic neurons

<p>Abstract</p> <p>Background</p> <p>NURR1 (also named as NR4A2) is a member of the steroid/thyroid hormone receptor family, which can bind to DNA and modulate expression of target genes. Previous studies have shown that NURR1 is essential for the nigral dopaminergic neuron phenotype and function maintenance, and the defects of the gene are possibly associated with Parkinson's disease (PD).</p> <p>Results</p> <p>In this study, we used new born <it>Nurr1 </it>knock-out mice combined with Affymetrix genechip technology and real time polymerase chain reaction (PCR) to identify <it>Nurr1 </it>regulated genes, which led to the discovery of several transcripts differentially expressed in the nigro-striatal pathway of <it>Nurr1 </it>knock-out mice. We found that an axon genesis gene called <it>Topoisomerase IIβ </it>(<it>Top IIβ</it>) was down-regulated in <it>Nurr1 </it>knock-out mice and we identified two functional NURR1 binding sites in the proximal <it>Top IIβ </it>promoter. While in <it>Top IIβ </it>null mice, we saw a significant loss of dopaminergic neurons in the substantial nigra and lack of neurites along the nigro-striatal pathway. Using specific TOP II antagonist ICRF-193 or <it>Top IIβ </it>siRNA in the primary cultures of ventral mesencephalic (VM) neurons, we documented that suppression of TOP IIβ expression resulted in VM neurites shortening and growth cones collapsing. Furthermore, microinjection of ICRF-193 into the mouse medial forebrain bundle (MFB) led to the loss of nigro-striatal projection.</p> <p>Conclusion</p> <p>Taken together, our findings suggest that <it>Top IIβ </it>might be a down-stream target of <it>Nurr1</it>, which might influence the processes of axon genesis in dopaminergic neurons via the regulation of TOP IIβ expression. The <it>Nurr1-Top IIβ </it>interaction may shed light on the pathologic role of <it>Nurr1 </it>defect in the nigro-striatal pathway deficiency associated with PD.</p

A Toll-Like Receptor 7, 8, and 9 Antagonist Inhibits Th1 and Th17 Responses and Inflammasome Activation in a Model of IL-23-Induced Psoriasis

Psoriasis is a chronic inflammatory skin disease that involves the induction of T-helper 1 (Th1) and T-helper 17 (Th17) cell responses and the aberrant expression of proinflammatory cytokines, including IL-1β. Copious evidence suggests that abnormal activation of Toll-like receptors (TLRs) contributes to the initiation and maintenance of psoriasis. We have evaluated an antagonist of TLR7, 8, and 9 as a therapeutic agent in an IL-23-induced psoriasis model in mice. Psoriasis-like skin lesions were induced in C57BL/6 mice by intradermal injection of IL-23 in the ear or dorsum. IL-23-induced increase in ear thickness was inhibited in a dose-dependent manner by treatment with antagonist. Histological examination of ear and dorsal skin tissues demonstrated a reduction in epidermal hyperplasia in mice treated with the antagonist. Treatment with antagonist also reduced the induction of Th1 and Th17 cytokines in skin and/or serum, as well as dermal expression of inflammasome components, NLRP3 and AIM2, and antimicrobial peptides. These results indicate that targeting TLR7, 8, and 9 may provide a way to neutralize multiple inflammatory pathways that are involved in the development of psoriasis. The antagonist has the potential for the treatment of psoriasis and other autoimmune diseases

Association between non-scarring alopecia and hypothyroidism: a bidirectional two-sample Mendelian randomization study

BackgroundNon-scarring alopecia is typically represented by two main types: alopecia areata (AA) and androgenetic alopecia (AGA). While previous observational studies have indicated a link between non-scarring alopecia and hypothyroidism, the precise causal relationship remains uncertain. To determine the potential links between non-scarring alopecia and hypothyroidism, we conducted a bidirectional two-sample Mendelian randomization (MR) analysis.MethodsWe used independent genetic instruments from the FinnGen consortium for AA (682 cases, 361,140 controls) and AGA (195 cases, 201,019 controls) to investigate the association with hypothyroidism in the UK Biobank study (22,687 cases, 440,246 controls). The primary analysis was performed using the inverse variance-weighted method. Complementary approaches were employed to evaluate the pleiotropy and heterogeneity.ResultsGenetically predicted AA exhibited a positive causal effect on hypothyroidism (odds ratio [OR], 1.0017; 95% confidence interval [CI], 1.0004-1.0029; P = 0.0101). Additionally, hypothyroidism was found to be strongly correlated with an increase in the risk of AA (OR, 45.6839; 95% CI, 1.8446-1131.4271, P = 0.0196). However, no causal relationship was demonstrated between AGA and hypothyroidism. A sensitivity analysis validated the integrity of these causal relationships.ConclusionThis MR study supports a bidirectional causal link between AA and hypothyroidism. Nevertheless, additional research is needed to gain a more thorough comprehension of the causal relationship between non-scarring alopecia and hypothyroidism