Tensor coupling effects on spin symmetry in anti-Lambda spectrum of hypernuclei

The effects of $\bar\Lambda\bar\Lambda\omega$-tensor coupling on the spin symmetry of $\bar{\Lambda}$ spectra in $\bar{\Lambda}$-nucleus systems have been studied with the relativistic mean-field theory. Taking $^{12}$C+$\bar{\Lambda}$ as an example, it is found that the tensor coupling enlarges the spin-orbit splittings of $\bar\Lambda$ by an order of magnitude although its effects on the wave functions of $\bar{\Lambda}$ are negligible. Similar conclusions has been observed in $\bar{\Lambda}$-nucleus of different mass regions, including $^{16}$O+$\bar{\Lambda}$, $^{40}$Ca+$\bar{\Lambda}$ and $^{208}$Pb+$\bar{\Lambda}$. It indicates that the spin symmetry in anti-lambda-nucleus systems is still good irrespective of the tensor coupling.Comment: 12 pages, 3 figures

The average mixing matrix signature

Laplacian-based descriptors, such as the Heat Kernel Signature and the Wave Kernel Signature, allow one to embed the vertices of a graph onto a vectorial space, and have been successfully used to find the optimal matching between a pair of input graphs. While the HKS uses a heat di↵usion process to probe the local structure of a graph, the WKS attempts to do the same through wave propagation. In this paper, we propose an alternative structural descriptor that is based on continuoustime quantum walks. More specifically, we characterise the structure of a graph using its average mixing matrix. The average mixing matrix is a doubly-stochastic matrix that encodes the time-averaged behaviour of a continuous-time quantum walk on the graph. We propose to use the rows of the average mixing matrix for increasing stopping times to develop a novel signature, the Average Mixing Matrix Signature (AMMS). We perform an extensive range of experiments and we show that the proposed signature is robust under structural perturbations of the original graphs and it outperforms both the HKS and WKS when used as a node descriptor in a graph matching task

Quantum theory of electronic double-slit diffraction

The phenomena of electron, neutron, atomic and molecular diffraction have been studied by many experiments, and these experiments are explained by some theoretical works. In this paper, we study electronic double-slit diffraction with quantum mechanical approach. We can obtain the results: (1) When the slit width $a$ is in the range of $3\lambda\sim 50\lambda$ we can obtain the obvious diffraction patterns. (2) when the ratio of $\frac{d+a}{a}=n (n=1, 2, 3,\cdot\cdot\cdot)$, order $2n, 3n, 4n,\cdot\cdot\cdot$ are missing in diffraction pattern. (3)When the ratio of $\frac{d+a}{a}\neq n (n=1, 2, 3,\cdot\cdot\cdot)$, there isn't missing order in diffraction pattern. (4) We also find a new quantum mechanics effect that the slit thickness $c$ has a large affect to the electronic diffraction patterns. We think all the predictions in our work can be tested by the electronic double-slit diffraction experiment.Comment: 9pages, 14figure

P311 induces the transdifferentiation of epidermal stem cells to myofibroblast-like cells by stimulating transforming growth factor β1 expression

Background: Epithelial to mesenchymal transition, especially to myofibroblasts, plays an important role in wound healing, fibrosis, and carcinogenesis. Epidermal stem cells (EpSCs) are responsible for epidermal renewal and wound re-epithelialization. However, it remains unclear whether and how EpSCs transdifferentiate into myofibroblasts or myofibroblast-like cells (MFLCs). Here, we provide the first evidence showing that P311 induces EpSC to MFLC transdifferentiation (EpMyT) via TGF β 1/Smad signaling. Methods: Wound healing and mesenchymal features were observed in the P311 KO and P311 WT mouse model of superficial second-degree burns. After the primary human or mouse EpSCs were forced to highly express P311 using an adenoviral vector, EpMyT was observed by immunofluorescence, real-time PCR, and western blot. The activity of TGF β 1 and Smad2/3 in EpSCs with different P311 levels was observed by western blot. The T β RI/II inhibitor LY2109761 and Smad3 siRNA were applied to block the EpMyT in P311-overexpressing EpSCs and exogenous TGF β 1 was to restore the EpMyT in P311 KO EpSCs. Furthermore, the mechanism of P311 regulating TGF β 1 was investigated by bisulfite sequencing PCR, luciferase activity assay, and real-time PCR. Results: P311 KO mouse wounds showed delayed re-epithelialization and reduced mesenchymal features. ThehumanormouseEpSCswithoverexpressedP311exhib ited fusiform morphological changes, upregulated expression of myofibroblast markers ( α -SMA and vimentin), and downregu lated expression of EpSC markers ( β 1-integrin and E-cadherin). P311-expressing EpSCs showed decreased TGF β 1mRNAandincreasedTGF β 1 protein, T β RI/II mRNA, and activated Smad2/3. Moreover, LY2109761 and Smad3 siRNA reversed P311-induced EpMyT. Under the stimulation of exogenous TGF β 1, the phosphorylation of Smad2 and Smad3 in P311 KO EpSCs was significantly lower than that in P311 WT EpSCs and the EpMyT in P311 KO EpSCs was restored. Furthermore, P311 enhanced the methylation of TGF β 1 promoter and increased activities of TGF β 15 ′ /3 ′ untranslated regions (UTRs) to stimulate TGF β 1 expression. P311 + α -SMA + cells and P311 + vimentin + cells were observed in the epidermis of human burn wounds. Also, P311 was upregulated by IL-1 β , IL-6, TNF α ,andhypoxia. Conclusions: P311 is a novel TGF β 1/Smad signaling-mediated regulator o f transdifferentiation in EpSCs during cutaneous wound healing. Furthermore, P311 might stimulate TGF β 1 expression by promoting TGF β 1 promoter methylation and by activating the TGF β 15 ′ /3 ′ UTR

Discovery of Novel Tacrine-Pyrimidone Hybrids as Potent Dual AChE/GSK-3 Inhibitors for the Treatment of Alzheimer's Disease

Based on a multitarget strategy, a series of novel tacrine-pyrimidone hybrids were identified for the potential treatment of Alzheimer's disease (AD). Biological evaluation results demonstrated that these hybrids exhibited significant inhibitory activities toward acetylcholinesterase (AChE) and glycogen synthase kinase 3 (GSK-3). The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3β: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells. Furthermore, compound 27g exhibited eligible pharmacokinetic properties, good kinase selectivity, and moderate neuroprotection against GA-induced reduction in cell viability and neurite damage in SH-SY5Y-derived neurons. The multifunctional profiles of compound 27g suggest that it deserves further investigation as a promising lead for the prospective treatment of AD