Robust Mesh Denoising via Triple Sparsity

Mesh denoising is to recover high quality meshes from noisy inputs scanned from the real world. It is a crucial step in geometry processing, computer vision, computer-aided design, etc. Yet, state-of-the-art denoising methods still fall short of handling meshes containing both sharp features and fine details. Besides, some of the methods usually introduce undesired staircase effects in smoothly curved regions. These issues become more severe when a mesh is corrupted by various kinds of noise, including Gaussian, impulsive, and mixed Gaussian⁻impulsive noise. In this paper, we present a novel optimization method for robustly denoising the mesh. The proposed method is based on a triple sparsity prior: a double sparse prior on first order and second order variations of the face normal field and a sparse prior on the residual face normal field. Numerically, we develop an efficient algorithm based on variable-splitting and augmented Lagrange method to solve the problem. The proposed method can not only effectively recover various features (including sharp features, fine details, smoothly curved regions, etc), but also be robust against different kinds of noise. We testify effectiveness of the proposed method on synthetic meshes and a broad variety of scanned data produced by the laser scanner, Kinect v1, Kinect v2, and Kinect-fusion. Intensive numerical experiments show that our method outperforms all of the compared select-of-the-art methods qualitatively and quantitatively

Mining Frequent Trajectory Using FP-tree in GPS Data ⋆

Pervasiveness of location-acquisition technologies makes it convenient to collect the movement data of moving objects, and the spatial-temporal information contained implicitly in the historical trajectories unveils important knowledge about movement behaviors. This paper presents a novel frequent trajectory mining method using FP-Tree Most existing approaches transform trajectories into sequences of popular region-ids using a statically predefined grid of cells with the same size, and then merge popular cells into larger popular regions. However, due to the size of these popular regions have not been limited, the movements of objects in the region may be lost. And predefined grid may be lack of adaptability. This study defines a Boundary Function to limit the maximum size of the popular regions and selects the size of the grid dynamically by defining a distance threshold d. Then, an improved FP-Tree algorithm is proposed to mine frequent trajectories. The experimental results show our method is efficient

Cloning, Synthesis and Functional Characterization of a Novel α-Conotoxin Lt1.3

α-Conotoxins (α-CTxs) are small peptides composed of 11 to 20 amino acid residues with two disulfide bridges. Most of them potently and selectively target nicotinic acetylcholine receptor (nAChR) subtypes, and a few were found to inhibit the GABAB receptor (GABABR)-coupled N-type calcium channels (Cav2.2). However, in all of α-CTxs targeting both receptors, the disulfide connectivity arrangement “C1-C3, C2-C4” is present. In this work, a novel α4/7-CTx named Lt1.3 (GCCSHPACSGNNPYFC-NH2) was cloned from the venom ducts of Conus litteratus (C. litteratus) in the South China Sea. Lt1.3 was then chemically synthesized and two isomers with disulfide bridges “C1-C3, C2-C4” and “C1-C4, C2-C3” were found and functionally characterized. Electrophysiological experiments showed that Lt1.3 containing the common disulfide bridges “C1-C3, C2-C4” potently and selectively inhibited α3β2 nAChRs and not GABABR-coupled Cav2.2. Surprisingly, but the isomer with the disulfide bridges “C1-C4, C2-C3” showed exactly the opposite inhibitory activity, inhibiting only GABABR-coupled Cav2.2 and not α3β2 nAChRs. These findings expand the knowledge of the targets and selectivity of α-CTxs and provide a new structural motif to inhibit the GABABR-coupled Cav2.2

Non-driver mutations in myeloproliferative neoplasm-associated myelofibrosis

Abstract We studied non-driver mutations in 62 subjects with myeloproliferative neoplasm (MPN)-associated myelofibrosis upon diagnosis, including 45 subjects with primary myelofibrosis (PMF) and 17 with post-polycythemia vera or post-essential thrombocythemia myelofibrosis (post-PV/ET MF). Fifty-eight subjects had ≥1 non-driver mutation upon diagnosis. Mutations in mRNA splicing genes, especially in U2AF1, were significantly more frequent in PMF than in post-PV/ET MF (33 vs. 6%; P = 0.015). There were also striking differences in clonal architecture. These data indicate different genomic spectrums between PMF and post-PV/ET MF

Case of cryptic TNIP1::PDGFRB rearrangement presenting with myelodysplastic syndrome achieved hematologic and cytogenetic remission with low-dose imatinib plus decitabine therapy

For a long time, FIP1L1::PDGFRA fusion seems to be the only cryptic rearrangement of myeloid/lymphoid neoplasm with tyrosine kinase gene fusions. Recently, with the wide application of RNA sequencing, more cryptic rearrangements of other TK genes have been identified, especially the PDGFRB. Here we report a case of myelodysplastic syndrome with severe thrombocytopenia. Conventional karyotype analysis revealed a t (5;19) (q33; p13.2) but no PDGFRB rearrangement was detected by the PDGFRB break-apart probe. The TNIP1::PDGFRB fusion was eventually found by RNA sequencing, leading us to treat with low-dose imatinib plus decitabine, and the patient achieved hematologic improvement and cytogenetic remission

Expression of PD-1 mitigates phagocytic activities TAM in osteosarcoma

The high expression of programmed death 1 (PD-1) is a hallmark of T cell exhaustion, consequently inhibiting the anti-tumor immunity, tumor-associated macrophages (TAMs) aggravate Osteosarcoma (OS) progression. However, PD-1 expression on TAMs in OS metastasis remains unclear. Here, we used scRNA-Seq of 15500 individual cells from human OS lung metastatic lesion, identified thirteen major cell clusters. Our data revealed that tumor-infiltrating lymphocytes (TILs) OS lung metastatic accompanied by accumulation of exhausted T cells and regulatory T cells (Tregs). CD3+ T cells from human OS lung metastatic exhibited lower proliferation than in primary tissue. Importantly, TAMs mainly comprise immunosuppressive M2 phenotype in OS metastasis. Mechanistically, we found that PD-1 of TAMs inhibits the phagocytic potency, further promoting the progression of OS metastasis. Therefore, the study provides a strong technical support for OS immunotherapy based on PD-1 inhibitors