Single nonmagnetic impurity resonance in FeSe-based 122-type superconductors as a probe for pairing symmetry

We study the effect of a single non-magnetic impurity in A$_{y}$Fe$_{2-x}$Se$_{2}$ (A=K, Rb, or Cs) superconductors by considering various pairing states based on a three-orbital model consistent with the photoemission experiments. The local density of states on and near the impurity site has been calculated by solving the Bogoliubov-de Gennes equations self-consistently. The impurity-induced in-gap bound states are found only for attractive impurity scattering potential, as in the cases of doping of Co or Ni, which is characterized by the strong particle-hole asymmetry, in the nodeless $d_{x^2-y^2}$ wave pairing state. This property may be used to probe the pairing symmetry of FeSe-based 122-type superconductors.Comment: 7 pages, 7 figure

The effect of multiple thermal cycles on Ti-6Al-4V deposits fabricated by wire-arc directed energy deposition:Microstructure evolution, mechanical properties, and corrosion resistance

Thermal cycles have an important effect on the microstructure and properties of the components fabricated by wire-arc directed energy deposition (wire-arc DED). In this study, a Gleeble thermal-mechanical simulator was adopted to create closer-to-reality thermal cycles with the assistance of a numerical simulation model and experimental Ti-6Al-4V deposition. Step-by-step microstructure evolution, including αm, retained β, and GB α, microhardness gradual variation, and the corrosion resistance change before and after the entire thermal cycle were investigated. Therefore, combining phase orientation and high-magnification morphology, transformed and untransformed α that occurred in low- and medium-temperature thermal cycles can be distinguished. After the entire thermal cycle, αm laths coarsened from ∼1 µm to ∼1.2 µm, and the content of retained β phase became more and more. The αm formed around grain boundaries partially disappeared and was occupied by α laths from the inner grain. GB α was more continuously distributed along prior β grain boundaries due to its lower formation temperature during the subsequent thermal cycles that were occurring incomplete α→β transformation. The severe preferential orientation of α phases formed after the deposition and high-temperature thermal cycle was also alleviated through the twice low-temperature thermal cycles. Besides, the microhardness decreased from 318.78 ± 7.5 HV to 285.17 ± 5.3 HV after the high-temperature thermal cycle but eventually increased significantly to 330.5 ± 6.4 HV after experiencing the final low-temperature thermal cycle. The corrosion resistance decreased after the entire thermal cycle, indicating a performance difference between the top and bottom regions of the Ti-6Al-4 V component fabricated by wire-arc DED.</p

Characterization of intrinsic properties of cingulate pyramidal neurons in adult mice after nerve injury

The anterior cingulate cortex (ACC) is important for cognitive and sensory functions including memory and chronic pain. Glutamatergic excitatory synaptic transmission undergo long-term potentiation in ACC pyramidal cells after peripheral injury. Less information is available for the possible long-term changes in neuronal action potentials or intrinsic properties. In the present study, we characterized cingulate pyramidal cells in the layer II/III of the ACC in adult mice. We then examined possible long-term changes in intrinsic properties of the ACC pyramidal cells after peripheral nerve injury. In the control mice, we found that there are three major types of pyramidal cells according to their action potential firing pattern: (i) regular spiking (RS) cells (24.7%), intrinsic bursting (IB) cells (30.9%), and intermediate (IM) cells (44.4%). In a state of neuropathic pain, the population distribution (RS: 21.3%; IB: 31.2%; IM: 47.5%) and the single action potential properties of these three groups were indistinguishable from those in control mice. However, for repetitive action potentials, IM cells from neuropathic pain animals showed higher initial firing frequency with no change for the properties of RS and IB neurons from neuropathic pain mice. The present results provide the first evidence that, in addition to synaptic potentiation reported previously, peripheral nerve injury produces long-term plastic changes in the action potentials of cingulate pyramidal neurons in a cell type-specific manner

HCCS1-armed, quadruple-regulated oncolytic adenovirus specific for liver cancer as a cancer targeting gene-viro-therapy strategy

<p>Abstract</p> <p>Background</p> <p>In previously published studies, oncolytic adenovirus-mediated gene therapy has produced good results in targeting cancer cells. However, safety and efficacy, the two most important aspects in cancer therapy, remain serious challenges. The specific expression or deletion of replication related genes in an adenovirus has been frequently utilized to regulate the cancer cell specificity of a virus. Accordingly, in this study, we deleted 24 bp in E1A (bp924-bp947) and the entirety of E1B, including those genes encoding E1B 55kDa and E1B19kDa. We used the survivin promoter (SP) to control E1A in order to construct a new adenovirus vector named Ad.SP.E1A(Δ24).ΔE1B (briefly Ad.SPDD). HCCS1 (hepatocellular carcinoma suppressor 1) is a novel tumor suppressor gene that is able to specifically induce apoptosis in cancer cells. The expression cassette AFP-HCCS1-WPRE-SV40 was inserted into Ad.SPDD to form Ad.SPDD-HCCS1, enabling us to improve the safety and efficacy of oncolytic-mediated gene therapy for liver cancer.</p> <p>Results</p> <p>Ad.SPDD showed a decreased viral yield and less toxicity in normal cells but enhanced toxicity in liver cancer cells, compared with the cancer-specific adenovirus ZD55 (E1B55K deletion). Ad.SPDD-HCCS1 exhibited a potent anti-liver-cancer ability and decreased toxicity in vitro. Ad.SPDD-HCCS1 also showed a measurable capacity to inhibit Huh-7 xenograft tumor growth on nude mice. The underlying mechanism of Ad.SPDD-HCCS1-induced liver cancer cell death was found to be via the mitochondrial apoptosis pathway.</p> <p>Conclusions</p> <p>These results demonstrate that Ad.SPDD-HCCS1 was able to elicit reduced toxicity and enhanced efficacy both in vitro and in vivo compared to a previously constructed oncolytic adenovirus. Ad.SPDD-HCCS1 could be a promising candidate for liver cancer therapy.</p

A minimum single-band model for low-energy excitations in superconducting Kx_xFe2_2Se2_2

We propose a minimum single-band model for the newly discovered iron-based superconducting K$_x$Fe$_2$Se$_2$. Our model is found to be numerically consistent with the five-orbital model at low energies. Based on our model and the random phase approximation, we study the spin fluctuation and the pairing symmetry of superconducting gap function. The $(\pi/2,\pi/2)$ spin excitation and the $d_{x^2-y^2}$ pairing symmetry are revealed. All of the results can well be understood in terms of the interplay between the Fermi surface topology and the local spin interaction, providing a sound picture to explain why the superconducting transition temperature is as high as to be comparable to those in pnictides and some cuprates. A common origin of superconductivity is elucidated for this compound and other high-T$_c$ materials.Comment: 5 pages, 4 figure

Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.

Caveolin-1 (Cav1) is a scaffold protein and pathogen receptor in the mucosa of the gastrointestinal tract. Chronic infection of gastric epithelial cells by Helicobacter pylori (H. pylori) is a major risk factor for human gastric cancer (GC) where Cav1 is frequently down-regulated. However, the function of Cav1 in H. pylori infection and pathogenesis of GC remained unknown. We show here that Cav1-deficient mice, infected for 11 months with the CagA-delivery deficient H. pylori strain SS1, developed more severe gastritis and tissue damage, including loss of parietal cells and foveolar hyperplasia, and displayed lower colonisation of the gastric mucosa than wild-type B6129 littermates. Cav1-null mice showed enhanced infiltration of macrophages and B-cells and secretion of chemokines (RANTES) but had reduced levels of CD25+ regulatory T-cells. Cav1-deficient human GC cells (AGS), infected with the CagA-delivery proficient H. pylori strain G27, were more sensitive to CagA-related cytoskeletal stress morphologies ("humming bird") compared to AGS cells stably transfected with Cav1 (AGS/Cav1). Infection of AGS/Cav1 cells triggered the recruitment of p120 RhoGTPase-activating protein/deleted in liver cancer-1 (p120RhoGAP/DLC1) to Cav1 and counteracted CagA-induced cytoskeletal rearrangements. In human GC cell lines (MKN45, N87) and mouse stomach tissue, H. pylori down-regulated endogenous expression of Cav1 independently of CagA. Mechanistically, H. pylori activated sterol-responsive element-binding protein-1 (SREBP1) to repress transcription of the human Cav1 gene from sterol-responsive elements (SREs) in the proximal Cav1 promoter. These data suggested a protective role of Cav1 against H. pylori-induced inflammation and tissue damage. We propose that H. pylori exploits down-regulation of Cav1 to subvert the host's immune response and to promote signalling of its virulence factors in host cells

Synergistic Activation of Cardiac Genes by Myocardin and Tbx5

Myocardial differentiation is associated with the activation and expression of an array of cardiac specific genes. However, the transcriptional networks that control cardiac gene expression are not completely understood. Myocardin is a cardiac and smooth muscle-specific expressed transcriptional coactivator of Serum Response Factor (SRF) and is able to potently activate cardiac and smooth muscle gene expression during development. We hypothesize that myocardin discriminates between cardiac and smooth muscle specific genes by associating with distinct co-factors. Here, we show that myocardin directly interacts with Tbx5, a member of the T-box family of transcription factors involved in the Holt-Oram syndrome. Tbx5 synergizes with myocardin to activate expression of the cardiac specific genes atrial natriuretic factor (ANF) and alpha myosin heavy chain (α-MHC), but not that of smooth muscle specific genes SM22 or smooth muscle myosin heavy chain (SM-MHC). We found that this synergistic activation of shared target genes is dependent on the binding sites for Tbx5, T-box factor-Binding Elements (TBEs). Myocardin and Tbx5 physically interact and their interaction domains were mapped to the basic domain and the coil domain of myocardin and Tbx5, respectively. Our analysis demonstrates that the Tbx5G80R mutation, which leads to the Holt-Oram syndrome in humans, failed to synergize with myocardin to activate cardiac gene expression. These data uncover a key role for Tbx5 and myocardin in establishing the transcriptional foundation for cardiac gene activation and suggest that the interaction of myocardin and Tbx5 maybe involved in cardiac development and diseases

A simulation study on the measurement of D0-D0bar mixing parameter y at BES-III

We established a method on measuring the \dzdzb mixing parameter $y$ for BESIII experiment at the BEPCII $e^+e^-$ collider. In this method, the doubly tagged $\psi(3770) \to D^0 \overline{D^0}$ events, with one $D$ decays to CP-eigenstates and the other $D$ decays semileptonically, are used to reconstruct the signals. Since this analysis requires good $e/\pi$ separation, a likelihood approach, which combines the $dE/dx$, time of flight and the electromagnetic shower detectors information, is used for particle identification. We estimate the sensitivity of the measurement of $y$ to be 0.007 based on a $20fb^{-1}$ fully simulated MC sample.Comment: 6 pages, 7 figure

Determinant representations of scalar products for the open XXZ chain with non-diagonal boundary terms

With the help of the F-basis provided by the Drinfeld twist or factorizing F-matrix for the open XXZ spin chain with non-diagonal boundary terms, we obtain the determinant representations of the scalar products of Bethe states of the model.Comment: Latex file, 28 pages, based on the talk given by W. -L. Yang at Statphys 24, Cairns, Australia, 19-23 July, 201