Electronic Structure in Gapped Graphene with Coulomb Potential

In this paper, we numerically study the bound electron states induced by long range Coulomb impurity in gapped graphene and the quasi-bound states in supercritical region based on the lattice model. We present a detailed comparison between our numerical simulations and the prediction of the continuum model which is described by the Dirac equation in (2+1)-dimensional Quantum Electrodynamics (QED). We also use the Fano's formalism to investigate the quasi-bound state development and design an accessible experiments to test the decay of the supercritical vacuum in the gapped graphene.Comment: 5 page, 4 figure

RAB18, a protein associated with Warburg Micro syndrome, controls neuronal migration in the developing cerebral cortex

There is no apparently changed after overexpression of RAB18 in cortical neuronal migration. A Representative coronal section showing migration of transfected neurons 4 d after electroporated at E14.5 with GFP plasmid together with indicated constructs. Scale bar: 100 μm. B Quantitative analysis of GFP positive neurons in different cortical regions in A. Data represent the mean ± SEM (n = 3). (PDF 76 kb

CIR-Net: Cross-modality Interaction and Refinement for RGB-D Salient Object Detection

Focusing on the issue of how to effectively capture and utilize cross-modality information in RGB-D salient object detection (SOD) task, we present a convolutional neural network (CNN) model, named CIR-Net, based on the novel cross-modality interaction and refinement. For the cross-modality interaction, 1) a progressive attention guided integration unit is proposed to sufficiently integrate RGB-D feature representations in the encoder stage, and 2) a convergence aggregation structure is proposed, which flows the RGB and depth decoding features into the corresponding RGB-D decoding streams via an importance gated fusion unit in the decoder stage. For the cross-modality refinement, we insert a refinement middleware structure between the encoder and the decoder, in which the RGB, depth, and RGB-D encoder features are further refined by successively using a self-modality attention refinement unit and a cross-modality weighting refinement unit. At last, with the gradually refined features, we predict the saliency map in the decoder stage. Extensive experiments on six popular RGB-D SOD benchmarks demonstrate that our network outperforms the state-of-the-art saliency detectors both qualitatively and quantitatively.Comment: Accepted by IEEE Transactions on Image Processing 2022, 16 pages, 11 figure

Incremental feedforward collective pitch control method for wind turbines

In recent years, wind turbines are becoming larger, which will exacerbate the complexity of loads Complex load change affect the output power quality and wind turbine service life so that must be studied. Pitch control is usually used to reduce wind turbine load. In this paper, based on the Light Detection and Ranging (LiDAR) technology and incremental feedforward control theory, an incremental feedforward collective pitch controller is proposed. The controller can be directly superimposed on the traditional collective pitch controller so that the incremental pitch angle can fully compensate wind influence. The effectiveness of the controller is verified by multi-software platform joint simulation and hardware-in-the-loop experiment. The results show that the controller can effectively reduce the wind turbine power and load fluctuation when the variation trend of wind speed in the rotor plane estimate by LiDAR data is the same as the actual wind speed

Co-inhibition of HDAC and MLL-menin interaction targets MLL-rearranged acute myeloid leukemia cells via disruption of DNA damage checkpoint and DNA repair.

While the aberrant translocation of the mixed-lineage leukemia (MLL) gene drives pathogenesis of acute myeloid leukemia (AML), it represents an independent predictor for poor prognosis of adult AML patients. Thus, small molecule inhibitors targeting menin-MLL fusion protein interaction have been emerging for the treatment of MLL-rearranged AML. As both inhibitors of histone deacetylase (HDAC) and menin-MLL interaction target the transcription-regulatory machinery involving epigenetic regulation of chromatin remodeling that governs the expression of genes involved in tumorigenesis, we hypothesized that these two classes of agents might interact to kill MLL-rearranged (MLL-r) AML cells. Here, we report that the combination treatment with subtoxic doses of the HDAC inhibitor chidamide and the menin-MLL interaction inhibitor MI-3 displayed a highly synergistic anti-tumor activity against human MLL-r AML cells in vitro and in vivo, but not those without this genetic aberration. Mechanistically, co-exposure to chidamide and MI-3 led to robust apoptosis in MLL-r AML cells, in association with loss of mitochondrial membrane potential and a sharp increase in ROS generation. Combined treatment also disrupted DNA damage checkpoint at the level of CHK1 and CHK2 kinases, rather than their upstream kinases (ATR and ATM), as well as DNA repair likely via homologous recombination (HR), but not non-homologous end joining (NHEJ). Genome-wide RNAseq revealed gene expression alterations involving several potential signaling pathways (e.g., cell cycle, DNA repair, MAPK, NF-κB) that might account for or contribute to the mechanisms of action underlying anti-leukemia activity of chidamide and MI-3 as a single agent and particularly in combination in MLL-r AML. Collectively, these findings provide a preclinical basis for further clinical investigation of this novel targeted strategy combining HDAC and Menin-MLL interaction inhibitors to improve therapeutic outcomes in a subset of patients with poor-prognostic MLL-r leukemia