Bosonic Weyl excitations induced by pp-orbital interactions in a cubic optical lattice

Weyl points exist in a fascinating topological state of matter with linear band crossings analogous to magnetic monopoles. Tremendous efforts have been devoted to investigate fermionic topological matters with Weyl points in the single-particle band dispersion. It remains elusive for realizing interaction-induced Weyl points, especially for bosons. Motivated by recent experimental progress in ultracold atoms, we propose a scheme to create Weyl points for Bogoliubov excitations of a bosonic superfluid in a three-dimensional cubic optical lattice. The unique design of the lattice leads to interaction-induced time-reversal symmetry breaking for a $p$-orbital superfluid, which in turn induces Weyl Bogoliubov excitations. Analogous to Weyl semimetals of electronic systems, the superfluid also support topologically protected edge modes due to the bulk-boundary correspondence

DDM-NET: End-to-end learning of keypoint feature Detection, Description and Matching for 3D localization

In this paper, we propose an end-to-end framework that jointly learns keypoint detection, descriptor representation and cross-frame matching for the task of image-based 3D localization. Prior art has tackled each of these components individually, purportedly aiming to alleviate difficulties in effectively train a holistic network. We design a self-supervised image warping correspondence loss for both feature detection and matching, a weakly-supervised epipolar constraints loss on relative camera pose learning, and a directional matching scheme that detects key-point features in a source image and performs coarse-to-fine correspondence search on the target image. We leverage this framework to enforce cycle consistency in our matching module. In addition, we propose a new loss to robustly handle both definite inlier/outlier matches and less-certain matches. The integration of these learning mechanisms enables end-to-end training of a single network performing all three localization components. Bench-marking our approach on public data-sets, exemplifies how such an end-to-end framework is able to yield more accurate localization that out-performs both traditional methods as well as state-of-the-art weakly supervised methods

3-[4-(Trifluoro­meth­yl)phen­yl]propanoic acid

In crystal of the the title compound, C10H9F3O2, inversion dimers linked by pairs of O—H⋯O hydrogen bonds occur

Endoglin Is Essential for the Maintenance of Self-Renewal and Chemoresistance in Renal Cancer Stem Cells.

Renal cell carcinoma (RCC) is a deadly malignancy due to its tendency to metastasize and resistance to chemotherapy. Stem-like tumor cells often confer these aggressive behaviors. We discovered an endoglin (CD105)-expressing subpopulation in human RCC xenografts and patient samples with a greater capability to form spheres in vitro and tumors in mice at low dilutions than parental cells. Knockdown of CD105 by short hairpin RNA and CRISPR/cas9 reduced stemness markers and sphere-formation ability while accelerating senescence in vitro. Importantly, downregulation of CD105 significantly decreased the tumorigenicity and gemcitabine resistance. This loss of stem-like properties can be rescued by CDA, MYC, or NANOG, and CDA might act as a demethylase maintaining MYC and NANOG. In this study, we showed that Endoglin (CD105) expression not only demarcates a cancer stem cell subpopulation but also confers self-renewal ability and contributes to chemoresistance in RCC

Application of the robust estimate in SLR data preprocessing

An M-estimator, one kind of a robust estimator, has been used in satellite laser ranging (SLR) data preprocessing. It has been shown that the M-estimator has a 50 percent or more breakdown point

CRISPR-Mediated VHL Knockout Generates an Improved Model for Metastatic Renal Cell Carcinoma.

Metastatic renal cell carcinoma (mRCC) is nearly incurable and accounts for most of the mortality associated with RCC. Von Hippel Lindau (VHL) is a tumour suppressor that is lost in the majority of clear cell RCC (ccRCC) cases. Its role in regulating hypoxia-inducible factors-1α (HIF-1α) and -2α (HIF-2α) is well-studied. Recent work has demonstrated that VHL knock down induces an epithelial-mesenchymal transition (EMT) phenotype. In this study we showed that a CRISPR/Cas9-mediated knock out of VHL in the RENCA model leads to morphologic and molecular changes indicative of EMT, which in turn drives increased metastasis to the lungs. RENCA cells deficient in HIF-1α failed to undergo EMT changes upon VHL knockout. RNA-seq revealed several HIF-1α-regulated genes that are upregulated in our VHL knockout cells and whose overexpression signifies an aggressive form of ccRCC in the cancer genome atlas (TCGA) database. Independent validation in a new clinical dataset confirms the upregulation of these genes in ccRCC samples compared to adjacent normal tissue. Our findings indicate that loss of VHL could be driving tumour cell dissemination through stabilization of HIF-1α in RCC. A better understanding of the mechanisms involved in this phenomenon can guide the search for more effective treatments to combat mRCC

Role of FIP200 in cardiac and liver development and its regulation of TNFα and TSC–mTOR signaling pathways

Focal adhesion kinase family interacting protein of 200 kD (FIP200) has been shown to regulate diverse cellular functions such as cell size, proliferation, and migration in vitro. However, the function of FIP200 in vivo has not been investigated. We show that targeted deletion of FIP200 in the mouse led to embryonic death at mid/late gestation associated with heart failure and liver degeneration. We found that FIP200 knockout (KO) embryos show reduced S6 kinase activation and cell size as a result of increased tuberous sclerosis complex function. Furthermore, FIP200 KO embryos exhibited significant apoptosis in heart and liver. Consistent with this, FIP200 KO mouse embryo fibroblasts and liver cells showed increased apoptosis and reduced c-Jun N-terminal kinase phosphorylation in response to tumor necrosis factor (TNF) α stimulation, which might be mediated by FIP200 interaction with apoptosis signal–regulating kinase 1 (ASK1) and TNF receptor–associated factor 2 (TRAF2), regulation of TRAF2–ASK1 interaction, and ASK1 phosphorylation. Together, our results reveal that FIP200 functions as a regulatory node to couple two important signaling pathways to regulate cell growth and survival during mouse embryogenesis