Self-Trapping of Bose-Einstein Condensates in an Optical Lattice: the Effect of the System Dimension

In the present paper, we investigate the dynamics of a Bose-Einstein condensates (BEC) loaded into an deep optical lattice of 1D, 2D and 3D, both analytically and numerically. We focus on the self-trapping state and the effect of the system dimension. Under the tight-binding approximation we obtain an analytical criterion for the self-trapping state of BEC using time-dependent variational method. The phase diagram for self-trapping, soliton, breather, or diffusion of the BEC cloud is obtained accordingly and verified by directly solving the discrete Gross-Pitaevskii equation (GPE) numerically. In particular, we find that the criterion and the phase diagrams are modified dramatically by the dimension of the lattices.Comment: 8pages, 9 figure

Creep behaviors and microstructural stabilities of Co-Al-W-Ta-Ti-based Superalloys

In last decade, the discovery of high-temperature stable γ\u27-Co3(Al, W) phase in Co-Al-W-base alloys motivated plentiful interests in designing the next generation γ\u27-strengthened Co-based superalloys. Continued efforts have been focused on increasing the γ\u27 solvus temperature and enhancing the γ/γ\u27 microstructural stability as well as improving the creep resistance at elevated temperatures in this class of superalloys. In the present work, the effects of Ti and Ta additions on the creep properties and the microstructural stabilities of Co-Al-W-Ta-Ti-based superalloys are investigated by means of integrated the experimental and computational approaches. The chemistry design of Co-Al-W-Ta-Ti alloys was supported by the thermodynamic calculations of phase stability using the Co-base alloys database in PandatTMdeveloped by the CALPHAD method. The atomic and the electronic structures for solute-strengthened (001) anti-phase boundaries (APB) of Co3(Al, TM) are investigated by first-principles calculations based on the density functional theory (DFT), where TM denotes transition metals. It is observed that at 1000oC, the creep property of a Co-based single-crystal superalloy containing Ti and Ta is superior in comparison with the other reported Co-Al-W-base single crystal alloys and the 1st generation commercial Ni-base single-crystal superalloys. The different creep behaviors between Co-based and Ni-based superalloys indicate that the creep deformation mechanism of Co-based superalloys is mainly associated with the stacking faults and anti-phase boundaries. Moreover, Co-Al-W-Ta-Ti model alloys have been developed with the variation of alloying additions, recently. Our designed alloys show better microstructural stability at higher temperature as well as high γ\u27 solvus temperature. DFT-based first principles calculations further reveal the complex electron structures induced by the variation of the lattice distortion around the fault layers in the solute-containing (001) APB. It is observed that the formation of the (001) APB in Co3Al changes the Co-centered deformation electron density isosurface from the typical tetrahedral shape in the FCC lattice into the “S” shape. With the segregation of solute atoms at (001) APB, the bond strength around the fault layers are increased by the electron redistribution by forming chemical bonds with Co, providing fundamental insights on interactions among alloying elements and their effects on APB and creep properties. The current study is helpful for continuous efforts on alloy design and development to improve temperature capability of γ\u27-strengthened Co-base superalloys

5,5′-Bis(diethyl­amino)-2,2′-[butane-1,4-diyldioxy­bis(nitrilo­methyl­idyne)]­diphenol

The title complex, C26H38N4O4, was synthesized by the reaction of 4-diethyl­amino-2-hydroxy­benzaldehyde with 1,4-bis­(amino­oxy)butane in ethanol. It crystallizes as discrete centrosymmetric molecules adopting an extended conformation where the two salicylaldoxime groups are separated from each other. Intra­molecular O—H⋯N hydrogen bonding is observed between the hydr­oxy groups and oxime N atoms. Inter­molecular π–π stacking inter­actions [3.979 (2) Å] between aromatic rings are apparent in the crystal structure. Each ethyl group is disordered over two positions; in one the site occupancy factors are 0.55 and 0.45, in the other 0.53 and 0.47

EGFR deficiency leads to impaired self-renewal and pluripotency of mouse embryonic stem cells

Background Self-renewal and pluripotency are considered as unwavering features of embryonic stem cells (ESCs). How ESCs regulate the self-renewal and differentiation is a central question in development and regenerative medicine research. Epidermal growth factor receptor (EGFR) was identified as a critical regulator in embryonic development, but its role in the maintenance of ESCs is poorly understood. Methods Here, EGFR was disrupted by its specific inhibitor AG1478 in mouse ESCs (mESCs), and its self-renewal and pluripotency were characterized according to their proliferation, expression of pluripotency markers, embryoid body (EB) formation, and mRNA expression patterns. We also used another EGFR inhibitor (gefitinib) and RNA interference assay to rule out the possibility of non-specific effects of AG1478. Results EGFR inhibition by AG1478 treatment in mESCs markedly reduced cell proliferation, caused cell cycle arrest at G0/G1 phase, and altered protein expressions of the cell cycle regulatory genes (CDK2 (decreased 11.3%) and proliferating cell nuclear antigen (decreased 25.2%)). The immunoreactivities and protein expression of pluripotency factors (OCT4 (decreased 26.9%)) also dramatically decreased, while the differentiation related genes (GATA4 (increased 1.6-fold)) were up-regulated in mESCs after EGFR inhibition. Meanwhile, EGFR inhibition in mESCs disrupted EB formation, indicating its impaired pluripotency. Additionally, the effects observed by EGFR inhibition with another inhibitor gefitinib and siRNA were consistent with those observed by AG1478 treatment in mESCs. These effects were manifested in the decreased expression of proliferative and pluripotency-related genes and the increased expression of genes involved in differentiation. Moreover, RNA-seq analysis displayed that transcript profiling was changed significantly after EGFR inhibition by AG1478. A large number of differentially expressed genes were involved in cell cycle, apoptotic process, epigenetic modification, and metabolic process, which were related to self-renewal and pluripotency, confirming that EGFR deficiency impaired self-renewal and pluripotency in mESCs. Conclusions Taken together, our results demonstrated the importance of EGFR in guarding the stemness of mESCs

Effect of Corilagin on the Proliferation and NF- κ

Background. This study is to explore the effect of corilagin on the proliferation and NF-κB signaling pathway in U251 glioblastoma cells and U251 glioblastoma stem-like cells. Methods. CD133 positive U251 glioblastoma cells were separated by immunomagnetic beads to isolate glioblastoma stem-like cells. U251 cells and stem-like cells were intervened by different corilagin concentrations (0, 25, 50, and 100 μg/mL) for 48 h, respectively. Cell morphology, cell counting kit-8 assay, flow cytometry, dual luciferase reporter assay, and a western blot were used to detect and analyze the cell proliferation and cell cycle and investigate the expression of IKBα protein in cytoplasm and NF-κB/p65 in nucleus. Results. Corilagin inhibited the cell proliferation of U251 cells and their stem-like cells and the inhibition role was stronger in U251 stem-like cells (P<0.05). The cell cycle was arrested at G2/M phase in the U251 cells following corilagin intervention; the proportion of cells in G2/M phase increased as the concentration of corilagin increased (P<0.05). The U251 stem-like cells were arrested at the S phase following treatment with corilagin; the proportion of cells in the S phase increased as the concentration of corilagin increased (P<0.05). The ratio of dual luciferase activities of U251 stem-like cells was lower than that of U251 cells in the same corilagin concentration. With increasing concentrations of corilagin, the IKBα expression in cytoplasm of U251 cells and U251 stem-like cells was increased, but the p65 expression in nucleus of U251 cells and U251 stem-like cells was decreased (P<0.05). Conclusion. Corilagin can inhibit the proliferation of glioblastoma cells and glioblastoma stem-like cells; the inhibition on glioblastoma stem-like cell proliferation is stronger than glioblastoma cells. This different result indicates that the effect of corilagin on U251 cells and U251 stem-like cells may have close relationships with mechanism of cell cycle and NF-κB signaling pathway; however, the real antitumor mechanism of corilagin is not yet clear and requires further study

Induction and Suppression of Innate Antiviral Responses by Hepatitis A Virus

Hepatitis A virus (HAV) belongs to the family Picornaviridae. It is the pathogen of acute viral hepatitis caused by fecal-oral transmission. RNA viruses are sensed by pathogen-associated pattern recognition receptors (PRRs) such as Toll-like receptor 3 (TLR3), retinoic acid-inducible gene I (RIG-I), and melanoma differentiation-associated gene 5 (MDA5). PRR activation leads to production of type 1 interferon (IFN-α/β), serving as the first line of defense against viruses. However, HAV has developed various strategies to compromise the innate immune system and promote viral propagation within the host cells. The long coevolution of HAV in hosts has prompted the development of effective immune antagonism strategies that actively fight against host antiviral responses. Proteases encoded by HAV can cleave the mitochondrial antiviral signaling protein (MAVS, also known as IPS-1, VISA, or Cardif), TIR domain- containing adaptor inducing IFN-β (TRIF, also known as TICAM-1) and nuclear factor-κB (NF-κB) essential modulator (NEMO), which are key adaptor proteins in RIG-I-like receptor (RLR), TLR3 and NF-κB signaling, respectively. In this mini-review, we summarize all the recent progress on the interaction between HAV and the host, especially focusing on how HAV abrogates the antiviral effects of the innate immune system