Chiral charge density wave and backscattering-immune orbital texture in monolayer 1T-TiTe2

Non-trivial electronic states are attracting intense attention in low-dimensional physics. Though chirality has been identified in charge states with a scalar order parameter, its intertwining with charge density waves (CDW), film thickness and the impact on the electronic behaviors remain less well understood. Here, using scanning tunneling microscopy, we report a 2 x 2 chiral CDW as well as a strong suppression of the Te-5p hole-band backscattering in monolayer 1T-TiTe2. These exotic characters vanish in bilayer TiTe2 with a non-CDW state. Theoretical calculations approve that chirality comes from a helical stacking of the triple-q CDW components and therefore can persist at the two-dimensional limit. Furthermore, the chirality renders the Te-5p bands an unconventional orbital texture that prohibits electron backscattering. Our study establishes TiTe2 as a promising playground for manipulating the chiral ground states at the monolayer limit and provides a novel path to engineer electronic properties from an orbital degree.Comment: 21 pages, 5 figure

Detection of the deep-sea plankton community in marine ecosystem with underwater robotic platform.

Variations in the quantity of plankton impact the entire marine ecosystem. It is of great significance to accurately assess the dynamic evolution of the plankton for monitoring the marine environment and global climate change. In this paper, a novel method is introduced for deep-sea plankton community detection in marine ecosystem using an underwater robotic platform. The videos were sampled at a distance of 1.5 m from the ocean floor, with a focal length of 1.5–2.5 m. The optical flow field is used to detect plankton community. We showed that for each of the moving plankton that do not overlap in space in two consecutive video frames, the time gradient of the spatial position of the plankton are opposite to each other in two consecutive optical flow fields. Further, the lateral and vertical gradients have the same value and orientation in two consecutive optical flow fields. Accordingly, moving plankton can be accurately detected under the complex dynamic background in the deep-sea environment. Experimental comparison with manual ground-truth fully validated the efficacy of the proposed methodology, which outperforms six state-of-the-art approaches

GeoSegNet: Point Cloud Semantic Segmentation via Geometric Encoder-Decoder Modeling

Semantic segmentation of point clouds, aiming to assign each point a semantic category, is critical to 3D scene understanding.Despite of significant advances in recent years, most of existing methods still suffer from either the object-level misclassification or the boundary-level ambiguity. In this paper, we present a robust semantic segmentation network by deeply exploring the geometry of point clouds, dubbed GeoSegNet. Our GeoSegNet consists of a multi-geometry based encoder and a boundary-guided decoder. In the encoder, we develop a new residual geometry module from multi-geometry perspectives to extract object-level features. In the decoder, we introduce a contrastive boundary learning module to enhance the geometric representation of boundary points. Benefiting from the geometric encoder-decoder modeling, our GeoSegNet can infer the segmentation of objects effectively while making the intersections (boundaries) of two or more objects clear. Experiments show obvious improvements of our method over its competitors in terms of the overall segmentation accuracy and object boundary clearness. Code is available at https://github.com/Chen-yuiyui/GeoSegNet

Evidence of nematic order and nodal superconducting gap along [110] direction in RbFe₂As₂

Unconventional superconductivity often intertwines with various forms of order, such as the nematic order which breaks the rotational symmetry of the lattice. Here we report a scanning tunneling microscopy study on RbFe2As2, a heavily hole-doped Fe-based superconductor (FeSC). We observe significant symmetry breaking in its electronic structure and magnetic vortex which differentiates the (π, π) and (π, -π) directions of the unfolded Brillouin zone. It is thus a novel nematic state, distinct from the nematicity of undoped/lightly-doped FeSCs which breaks the (π, 0)/(0, π) equivalence. Moreover, we observe a clear V-shaped superconducting gap. The gap is suppressed on surface Rb vacancies and step edges, and the suppression is particularly strong at the [110]-oriented edges. This is possibly due to a dx2−y2 like pairing component with nodes along the [110] directions. Our results thus highlight the intimate connection between nematicity and superconducting pairing in iron-based superconductors

Acute Progression of BCR-FGFR1 Induced Murine B-Lympho/Myeloproliferative Disorder Suggests Involvement of Lineages at the Pro-B Cell Stage

Constitutive activation of FGFR1, through rearrangement with various dimerization domains, leads to atypical myeloproliferative disorders where, although T cell lymphoma are common, the BCR-FGFR1 chimeric kinase results in CML-like leukemia. As with the human disease, mouse bone marrow transduction/transplantation with BCR-FGFR1 leads to CML-like myeloproliferation as well as B-cell leukemia/lymphoma. The murine disease described in this report is virtually identical to the human disease in that both showed bi-lineage involvement of myeloid and B-cells, splenomegaly, leukocytosis and bone marrow hypercellularity. A CD19+ IgM− CD43+ immunophenotype was seen both in primary tumors and two cell lines derived from these tumors. In all primary tumors, subpopulations of these CD19+ IgM− CD43+ were also either B220+ or B220−, suggesting a block in differentiation at the pro-B cell stage. The B220− phenotype was retained in one of the cell lines while the other was B220+. When the two cell lines were transplanted into syngeneic mice, all animals developed the same B-lymphoblastic leukemia within 2-weeks. Thus, the murine model described here closely mimics the human disease with bilineage myeloid and B-cell leukemia/lymphoma which provides a representative model to investigate therapeutic intervention and a better understanding of the etiology of the disease

Derangement of a Factor Upstream of RARα Triggers the Repression of a Pleiotropic Epigenetic Network

Chromatin adapts and responds to extrinsic and intrinsic cues. We hypothesize that inheritable aberrant chromatin states in cancer and aging are caused by genetic/environmental factors. In previous studies we demonstrated that either genetic mutations, or loss, of retinoic acid receptor alpha (RARalpha), can impair the integration of the retinoic acid (RA) signal at the chromatin of RA-responsive genes downstream of RARalpha, and can lead to aberrant repressive chromatin states marked by epigenetic modifications. In this study we tested whether the mere interference with the availability of RA signal at RARalpha, in cells with an otherwise functional RARalpha, can also induce epigenetic repression at RA-responsive genes downstream of RARalpha.To hamper the availability of RA at RARalpha in untransformed human mammary epithelial cells, we targeted the cellular RA-binding protein 2 (CRABP2), which transports RA from the cytoplasm onto the nuclear RARs. Stable ectopic expression of a CRABP2 mutant unable to enter the nucleus, as well as stable knock down of endogenous CRABP2, led to the coordinated transcriptional repression of a few RA-responsive genes downstream of RARalpha. The chromatin at these genes acquired an exacerbated repressed state, or state "of no return". This aberrant state is unresponsive to RA, and therefore differs from the physiologically repressed, yet "poised" state, which is responsive to RA. Consistent with development of homozygosis for epigenetically repressed loci, a significant proportion of cells with a defective CRABP2-mediated RA transport developed heritable phenotypes indicative of loss of function.Derangement/lack of a critical factor necessary for RARalpha function induces epigenetic repression of a RA-regulated gene network downstream of RARalpha, with major pleiotropic biological outcomes

Disruption of Retinoic Acid Receptor Alpha Reveals the Growth Promoter Face of Retinoic Acid

Retinoic acid (RA), the bioactive derivative of Vitamin A, by epigenetically controlling transcription through the RA-receptors (RARs), exerts a potent antiproliferative effect on human cells. However, a number of studies show that RA can also promote cell survival and growth. In the course of one of our studies we observed that disruption of RA-receptor alpha, RARalpha, abrogates the RA-mediated growth-inhibitory effects and unmasks the growth-promoting face of RA (Ren et al., Mol. Cell. Biol., 2005, 25:10591). The objective of this study was to investigate whether RA can differentially govern cell growth, in the presence and absence of RARalpha, through differential regulation of the "rheostat" comprising ceramide (CER), the sphingolipid with growth-inhibitory activity, and sphingosine-1-phosphate (S1P), the sphingolipid with prosurvival activity.We found that functional inhibition of endogenous RARalpha in breast cancer cells by using either RARalpha specific antagonists or a dominant negative RARalpha mutant hampers on one hand the RA-induced upregulation of neutral sphingomyelinase (nSMase)-mediated CER synthesis, and on the other hand the RA-induced downregulation of sphingosine kinase 1, SK1, pivotal for S1P synthesis. In association with RA inability to regulate the sphingolipid rheostat, cells not only survive, but also grow more in response to RA both in vitro and in vivo. By combining genetic, pharmacological and biochemical approaches, we mechanistically demonstrated that RA-induced growth is, at least in part, due to non-RAR-mediated activation of the SK1-S1P signaling.In the presence of functional RARalpha, RA inhibits cell growth by concertedly, and inversely, modulating the CER and S1P synthetic pathways. In the absence of a functional RARalpha, RA-in a non-RAR-mediated fashion-promotes cell growth by activating the prosurvival S1P signaling. These two distinct, yet integrated processes apparently concur to the growth-promoter effects of RA