Quantum simulation of exotic PT-invariant topological nodal loop bands with ultracold atoms in an optical lattice

Since the well-known PT symmetry has its fundamental significance and implication in physics, where PT denotes the combined operation of space-inversion P and time-reversal T, it is extremely important and intriguing to completely classify exotic PT-invariant topological metals and to physically realize them. Here we, for the first time, establish a rigorous classification of topological metals that are protected by the PT symmetry using KO-theory. As a physically realistic example, a PT-invariant nodal loop (NL) model in a 3D Brillouin zone is constructed, whose topological stability is revealed through its PT-symmetry-protected nontrivial Z2 topological charge. Based on these exact results, we propose an experimental scheme to realize and to detect tunable PT-invariant topological NL states with ultracold atoms in an optical lattice, in which atoms with two hyperfine spin states are loaded in a spin-dependent 3D OL and two pairs of Raman lasers are used to create out-of-plane spin-flip hopping with site-dependent phase. Such a realistic cold-atom setup can yield topological NL states, having a tunable ring-shaped band-touching line with the two-fold degeneracy in the bulk spectrum and non-trivial surface states. The states are actually protected by the combined PT symmetry even in the absence of both P and T symmetries, and are characterized by a Z2-type invariant (a quantized Berry phase). Remarkably, we demonstrate with numerical simulations that (i) the characteristic NL can be detected by measuring the atomic transfer fractions in a Bloch-Zener oscillation; (ii) the topological invariant may be measured based on the time-of-flight imaging; and (iii) the surface states may be probed through Bragg spectroscopy. The present proposal for realizing topological NL states in cold atom systems may provide a unique experimental platform for exploring exotic PT-invariant topological physics.Comment: 11 pages, 6 figures; accepted for publication in Phys. Rev.

Graphical Nonbinary Quantum Error-Correcting Codes

In this paper, based on the nonbinary graph state, we present a systematic way of constructing good non-binary quantum codes, both additive and nonadditive, for systems with integer dimensions. With the help of computer search, which results in many interesting codes including some nonadditive codes meeting the Singleton bounds, we are able to construct explicitly four families of optimal codes, namely, $[[6,2,3]]_p$, $[[7,3,3]]_p$, $[[8,2,4]]_p$ and $[[8,4,3]]_p$ for any odd dimension $p$ and a family of nonadditive code $((5,p,3))_p$ for arbitrary $p>3$. In the case of composite numbers as dimensions, we also construct a family of stabilizer codes $((6,2\cdot p^2,3))_{2p}$ for odd $p$, whose coding subspace is {\em not} of a dimension that is a power of the dimension of the physical subsystem.Comment: 12 pages, 5 figures (pdf

Small molecules from natural products targeting the Wnt/β-catenin pathway as a therapeutic strategy.

The Wnt/β-catenin signaling pathway is an evolutionarily conserved developmental signaling event that plays a critical role in regulating tissue development and maintaining homeostasis, the dysregulation of which contributes to various diseases. Natural products have been widely recognized as a treasure trove of novel drug discovery for millennia, and many clinical drugs are derived from natural small molecules. Mounting evidence has demonstrated that many natural small molecules could inhibit the Wnt/β-catenin pathway, while the efficacy of natural products remains to be determined. Therefore, this paper primarily reviews the targeting mechanism of natural small molecules for aberrant Wnt/β-catenin pathway that is intimately implicated in the pathogenesis of myriad diseases, such as cancers, renal diseases, neurodegenerative diseases and bone disorders. In addition, this review also highlights some natural products that have the potential to halt Wnt/β-catenin pathway, especially for porcupine, the receptors of Wnt ligands, β-catenin and β-catenin-dependent proteins. Additionally, a series of natural small molecules have shown good therapeutic effects against mutations of the Wnt/β-catenin pathway, which may dramatically facilitate the development of natural products in Wnt/β-catenin pathway intervention

AXAF VETA-I mirror encircled energy measurements and data reduction

The AXAF VETA-I mirror encircled energy was measured with a series of apertures and two flow gas proportional counters at five X-ray energies ranging from 0.28 to 2.3 keV. The proportional counter has a thin plastic window with an opaque wire mesh supporting grid. Depending on the counter position, this mesh can cause the X-ray transmission to vary as much as +/-9 percent, which directly translates into an error in the encircled energy. In order to correct this wire mesh effect, window scan measurements were made, in which the counter was scanned in both horizontal (Y) and vertical (Z) directions with the aperture fixed. Post VETA measurement of the VXDS setup were made to determine the exact geometry and position of the mesh grid. Computer models of the window mesh were developed to simulate the X-ray transmission based on this measurement. The window scan data were fitted to such mesh models and corrections were made. After this study, the mesh effect was well understood and the final results of the encircled energy were obtained with an uncertainty of less than 0.8 percent

Combined melatonin and poricoic acid A inhibits renal fibrosis through modulating the interaction of Smad3 and β-catenin pathway in AKI-to-CKD continuum.

BackgroundAcute kidney injury (AKI) is one of the major risk factors for progression to chronic kidney disease (CKD) and renal fibrosis. However, effective therapies remain poorly understood. Here, we examined the renoprotective effects of melatonin and poricoic acid A (PAA) isolated from the surface layer of Poria cocos, and investigated the effects of combined therapy on the interaction of TGF-β/Smad and Wnt/β-catenin in a rat model of renal ischemia-reperfusion injury (IRI) and hypoxia/reoxygenation (H/R) or TGF-β1-induced HK-2 cells.MethodsWestern blot and immunohistochemical staining were used to examine protein expression, while qRT-PCR was used to examine mRNA expression. Coimmunoprecipitation, chromatin immunoprecipitation, RNA interference, and luciferase reporter gene analysis were employed to explore the mechanisms of PAA and melatonin's renoprotective effects.ResultsPAA and combined therapy exhibited renoprotective and antifibrotic effects, but the underlying mechanisms were different during AKI-to-CKD continuum. Melatonin suppressed Smad-dependent and Smad-independent pathways, while PAA selectively inhibited Smad3 phosphorylation through distrupting the interactions of Smad3 with TGFβRI and SARA. Further studies demonstrated that the inhibitory effects of melatonin and PAA were partially depended on Smad3, especially PAA. Melatonin and PAA also inhibited the Wnt/β-catenin pathway and its profibrotic downstream targets, and PAA performed better. We further determined that IRI induced a nuclear Smad3/β-catenin complex, while melatonin and PAA disturbed the interaction of Smad3 and β-catenin, and supplementing with PAA could enhance the inhibitory effects of melatonin on the TGF-β/Smad and Wnt/β-catenin pathways.ConclusionsCombined melatonin and PAA provides a promising therapeutic strategy to treat renal fibrosis during the AKI-to-CKD continuum

Novel MnS/(Inx_{x}Cu1−x_{1-x})2_{2}S3_{3} composite for robust solar hydrogen sulphide splitting via the synergy of solid solution and heterojunction

Large photocatalytic hydrogen (H$_{2}$) production from copious waste hydrogen sulphide (H$_{2}$S) can meet the increasing demand for H$_{2}$ in a sustainable manor which is beneficial from both environmental and energy standpoints. In this work, we reported a robust MnS/(In$_{x}$Cu$_{1-x}$)$_{2}$S$_{3}$ composite photocatalyst. Both experimental results and density functional theory (DFT) calculations proved that Cu does not act as a cocatalyst but forms a solid solution ((In$_{x}$Cu$_{1-x}$)$_{2}$S$_{3}$) in the composites, which plays dual roles in improving the photocatalytic performance of H2S splitting: (i) enhancing solar light absorption, and (ii) promoting the desorption of sulfur (S) adsorbed on the catalyst surface. Moreover, the formation of a heterojunction between γ-MnS and (In$_{x}$Cu$_{1-x}$)$_{2}$S$_{3}$ can significantly improve charge separation and migration in the composites. As a result, the MnS/(In$_{x}$Cu$_{1-x}$)$_{2}$S$_{3}$ exhibits greatly extended visible light absorption up to 599 nm and extraordinarily high photocatalytic H$_{2}$ production under visible light from H$_{2}$S with a maximum rate of 29,252 μmol h$^{-1}$ g$^{-1}$. The corresponding apparent quantum efficiencies (AQE) at 420 and 450 nm are as high as 65.2% and 62.6%, respectively. They are the highest so far for the visible light photocatalytic splitting of H$_{2}$S in the absence of noble-metal co-catalysts

Comparative genomic analysis of the Tribolium immune system

The annotation, and comparison with homologous genes in other species, of immunity-related genes in the Tribolium castaneum genome allowed the identification of around 300 candidate defense proteins, and revealed a framework of information on Tribolium immunity

Scara1 deficiency impairs clearance of soluble Amyloid-β by mononuclear phagocytes and accelerates Alzheimer’s-like disease progression

In Alzheimer’s disease soluble amyloid beta (sAβ) causes synaptic dysfunction and neuronal loss. Receptors involved in clearance of sAβ are not known. Here we use shRNA screening and identify the scavenger receptor Scara1 as a receptor for sAβ expressed on myeloid cells. To determine the role of Scara1 in clearance of sAβ in vivo, we cross Scara1 null mice with PS1-APP mice, a mouse model of Alzheimer’s disease and generate PS1-APP- Scara1-deficient mice. Scara1 deficiency markedly accelerates Aβ accumulation leading to increased mortality. In contrast, pharmacological upregulation of Scara1 expression on mononuclear phagocytes increases Aβ clearance. This approach is a potential treatment strategy for Alzheimer’s disease

Scara1 deficiency impairs clearance of soluble Amyloid-β by mononuclear phagocytes and accelerates Alzheimer’s-like disease progression

In Alzheimer’s disease soluble amyloid beta (sAβ) causes synaptic dysfunction and neuronal loss. Receptors involved in clearance of sAβ are not known. Here we use shRNA screening and identify the scavenger receptor Scara1 as a receptor for sAβ expressed on myeloid cells. To determine the role of Scara1 in clearance of sAβ in vivo, we cross Scara1 null mice with PS1-APP mice, a mouse model of Alzheimer’s disease and generate PS1-APP- Scara1-deficient mice. Scara1 deficiency markedly accelerates Aβ accumulation leading to increased mortality. In contrast, pharmacological upregulation of Scara1 expression on mononuclear phagocytes increases Aβ clearance. This approach is a potential treatment strategy for Alzheimer’s disease

Long-Wavelength AIE-Based Fluorescent Probes for Mitochondria-Targeted Imaging and Photodynamic Therapy of Hepatoma Cells

With this research, we have developed two long-wavelength theranostic probes (DCMT and DCMC) with aggregation-induced emission (AIE)-based properties for image-guided photodynamic therapy (PDT) of hepatoma cells. Introduction of a triphenylamine or carbazole group to a dicyanomethylene-4H-pyran dye with long-wavelength fluorescence emission produces the AIE-based probes, which were subsequently modified with triphenyl-phosphonium cation for actively targeting the mitochondria of hepatoma cells. Solution-based experiments show that the probes exhibit a mixed photophysical mechanism of twisted-intramolecular charge transfer and AIE at different aggregation states. The molecular aggregation of the probes also leads to an enhanced ability for oxygen photosensitization, suggesting their potential for PDT of cancer cells. Our subsequent cell-based assays show that the probes localize in the mitochondria of hepatoma cells and the use of light leads to cell death through the intracellular production of reactive oxygen species. </p