Boron-Nitrogen Lewis Pairs in the Assembly of Supramolecular Macrocycles, Molecular Cages, Polymers, and 3D Materials.

Covering an exceptionally wide range of bond strengths, the dynamic nature and facile tunability of dative B-N bonds is highly attractive when it comes to the assembly of supramolecular polymers and materials. This Minireview offers an overview of advances in the development of functional materials where Lewis pairs (LPs) play a key role in their assembly and critically influence their properties. Specifically, we describe the reversible assembly of linear polymers with interesting optical, electronic and catalytic properties, discrete macrocycles and molecular cages that take up diverse guest molecules and undergo structural changes triggered by external stimuli, covalent organic frameworks (COFs) with intriguing interlocked structures that can embed and separate gases such as CO2 and acetylene, and soft polymer networks that serve as recyclable, self-healing, and responsive thermosets, gels and elastomeric materials.

Inhibition of ox-LDL-induced endothelial cell injury by LINC02381 knockdown through the microRNA-491-5p/transcription factor 7 axis.

Atherosclerosis (AS) is a complex multifactorial and chronic inflammatory vascular disease that contributes to the development of cardiovascular diseases. Abnormal cellular proliferation in human umbilical vein endothelial cells (HUVECs) is a crucial element in AS development. In this study, we investigated the potential role of the long noncoding RNA LINC02381/microRNA (miR)-491-5p/transcription factor 7 (TCF7) axis in regulating HUVEC injury in 30 participants suffering from AS and 30 healthy control participants. We established an in vitro model of AS in HUVECs using oxidized low-density lipoprotein (ox-LDL), and measured cellular mRNA and protein levels of LINC02381, miR-491-5p, and TCF7 in serum samples using reverse transcription-quantitative polymerase chain reaction and Western blotting assays. We evaluated cell viability, apoptosis, and inflammation using Cell Counting Kit-8, flow cytometry, and enzyme-linked immunosorbent assays, respectively. Moreover, we analyzed apoptosis-related protein expression using western blotting analysis and determined the association between miR-491-5p and LINC02381 or TCF7 using dual-luciferase reporter assay, RNA pull-down, and rescue experiments. We observed that LINC02381 was elevated, while miR-491-5p was downregulated in serum samples from participants with AS and in ox-LDL-treated HUVECs. LINC02381 knockdown was protective against HUVEC injury via miR-491-5p inhibition, which is its downstream target. Rescue experiments further demonstrated that miR-491-5p alleviated HUVEC injury by modulating TCF7. Thus, LINC02381 knockdown ameliorated HUVEC injury by regulating the miR-491-5p/TCF7 axis, which provides new insights into AS treatment strategies.

By modulating miR-525-5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis.

BACKGROUND: Deep vein thrombosis (DVT) is a vascular disease that has no effective treatment at present. Endothelial cells play a crucial role in the processes vasoconstriction, platelet activation, and blood coagulation and are an integral part of the vascular response to injury resulting in thrombus formation. OBJECTIVE: The aim of this study was to investigate the roles and mechanisms of long noncoding RNA LINC00659 (LINC00659) in endothelial cells. METHODS: The functions of LINC00659 and miR-525-5p on endothelial cells were explored by cell transfection assays, and the expression levels of LINC00659, miR-525-5p, and Bax in human umbilical vein endothelial cells (HUVECs) were assessed with reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR). Binding sites of LINC00659 and miR-525-5p were subsequently analyzed with bioinformatics software, and validated with dual-luciferase reporter gene assay. Effects of LINC00659 and miR-525-5p on proliferation and apoptosis of HUVECs were detected with MTT (3-(45)-dimethylthiahiazo (-z-y1)-35-di-phenytetrazoliumromide) assay and flow cytometry. RT-qPCR and western blot analysis were used to evaluate the mRNA and protein levels of apoptosis-related markers Bcl-2 and Bax in HUVECs. RESULTS: LINC00659 directly targeted and negatively regulated miR-525-5p, and Bax was a target of miR-525-5p. Upregulation of LINC00659 could inhibit proliferation and promote apoptosis of HUVECs, while the silencing of LINC00659 could increase the viability of HUVECs and inhibit apoptosis via upregulating miR-525-5p. Further mechanistic studies revealed miR-525-5p could negatively regulate Bax in HUVECs, and increased the viability of HUVECs and inhibited apoptosis by downregulating Bax expression. CONCLUSION: LINC00659 played an important role in DVT by regulating the apoptosis of vascular endothelial cells through regulating miR-525-5p/Bax axis.

OrthoAligner: Image-Based Teeth Alignment Prediction via Latent Style Manipulation.

In this article, we present OrthoAligner, a novel method to predict the visual outcome of orthodontic treatment in a portrait image. Unlike the state-of-the-art method, which relies on a 3D teeth model obtained from dental scanning, our method generates realistic alignment effects in images without requiring additional 3D information as input and thus making our system readily available to average users. The key of our approach is to employ the 3D geometric information encoded in an unsupervised generative model, i.e., StyleGAN in this article. Instead of directly conducting translation in the image space, we embed the teeth region extracted from a given portrait to the latent space of the StyleGAN generator and propose a novel latent editing method to discover a geometrically meaningful editing path that yields the alignment process in the image space. To blend the edited mouth region with the original portrait image, we further introduce a BlendingNet to remove boundary artifacts and correct color inconsistency. We also extend our method to short video clips by propagating the alignment effects across neighboring frames. We evaluate our method in various orthodontic cases, compare it to the state-of-the-art and competitive baselines, and validate the effectiveness of each component.

TeethGNN: Semantic 3D Teeth Segmentation With Graph Neural Networks.

In this paper, we present TeethGNN, a novel 3D tooth segmentation method based on graph neural networks (GNNs). Given a mesh-represented 3D dental model in non-euclidean domain, our method outputs accurate and fine-grained separation of each individual tooth robust to scanning noise, foreign matters (e.g., bubbles, dental accessories, etc.), and even severe malocclusion. Unlike previous CNN-based methods that bypass handling non-euclidean mesh data by reshaping hand-crafted geometric features into regular grids, we explore the non-uniform and irregular structure of mesh itself in its dual space and exploit graph neural networks for effective geometric feature learning. To address the crowded teeth issues and incomplete segmentation that commonly exist in previous methods, we design a two-branch network, one of which predicts a segmentation label for each facet while the other regresses each facet an offset away from its tooth centroid. Clustering are later conducted on offset-shifted locations, enabling both the separation of adjoining teeth and the adjustment of incompletely segmented teeth. Exploiting GNN for directly processing mesh data frees us from extracting hand-crafted feature, and largely speeds up the inference procedure. Extensive experiments have shown that our method achieves the new state-of-the-art results for teeth segmentation and outperforms previous methods both quantitatively and qualitatively.

Human Bas-Relief Generation From a Single Photograph.

We present a semi-automatic method for producing human bas-relief from a single photograph. Given an input photo of one or multiple persons, our method first estimates a 3D skeleton for each person in the image. SMPL models are then fitted to the 3D skeletons to generate a 3D guide model. To align the 3D guide model with the image, we compute a 2D warping field to non-rigidly register the projected contours of the guide model with the body contours in the image. Then the normal map of the 3D guide model is warped by the 2D deformation field to reconstruct an overall base shape. Finally, the base shape is integrated with a fine-scale normal map to produce the final bas-relief. To tackle the complex intra- and inter-body interactions, we design an occlusion relationship resolution method that operates at the level of 3D skeletons with minimal user inputs. To tightly register the model contours to the image contours, we propose a non-rigid point matching algorithm harnessing user-specified sparse correspondences. Experiments demonstrate that our human bas-relief generation method is capable of producing perceptually realistic results on various single-person and multi-person images, on which the state-of-the-art depth and pose estimation methods often fail.

Nonconvex Low-Rank Kernel Sparse Subspace Learning for Keyframe Extraction and Motion Segmentation.

By exploiting the kernel trick, the sparse subspace model is extended to the nonlinear version with one or a combination of predefined kernels, but the high-dimensional space induced by predefined kernels is not guaranteed to be able to capture the features of the nonlinear data in theory. In this article, we propose a nonconvex low-rank learning framework in an unsupervised way to learn a kernel to replace the predefined kernel in the sparse subspace model. The learned kernel by a nonconvex relaxation of rank can better exploiting the low-rank property of nonlinear data to induce a high-dimensional Hilbert space that more closely approaches the true feature space. Furthermore, we give a global closed-form optimal solution of the nonconvex rank minimization and prove it. Considering the low-rank and sparseness characteristics of motion capture data in its feature space, we use them to verify the better representation of nonlinear data with the learned kernel via two tasks: keyframe extraction and motion segmentation. The performances on both tasks demonstrate the advantage of our model over the sparse subspace model with predefined kernels and some other related state-of-art methods.

Nonlinear Low-Rank Matrix Completion for Human Motion Recovery.

Human motion capture data has been widely used in many areas, but it involves a complex capture process and the captured data inevitably contains missing data due to the occlusions caused by the actor's body or clothing. Motion recovery, which aims to recover the underlying complete motion sequence from its degraded observation, still remains as a challenging task due to the nonlinear structure and kinematics property embedded in motion data. Low-rank matrix completion based methods have shown promising performance in short-time-missing motion recovery problems. However, low-rank matrix completion, which is designed for linear data, lacks the theoretic guarantee when applied to the recovery of nonlinear motion data. To overcome this drawback, we propose a tailored nonlinear matrix completion model for human motion recovery. Within the model, we first learn a combined low-rank kernel via multiple kernel learning. By exploiting the learned kernel, we embed the motion data into a high dimensional Hilbert space where motion data is of desirable low-rank and we then use the low-rank matrix completion to recover motions. In addition, we add two kinematic constraints to the proposed model to preserve the kinematics property of human motion. Extensive experiment results and comparisons with five other state-of-the-art methods demonstrate the advantage of the proposed method.

WWC3 inhibits intimal proliferation following vascular injury via the Hippo signaling pathway.

The Hippo signaling pathway is involved in the formation and development of the cardiovascular system. In the present study, the effects of WWC family member 3 (WWC3) on vascular smooth muscle cells (VSMCs) following injury were investigated, in addition to the associated mechanisms underlying this process. Platelet­derived growth factor BB (PDGF­BB) was used as a cell injury factor, and rats with balloon injuries were used as a model of carotid intimal injury. Furthermore, the expression levels of WWC3 in VSMCs and arteries post­injury were investigated, in addition to the effect of WWC3 on the proliferation and migration of VSMCs. The results demonstrated that following injury, WWC3 expression was suppressed in VSMCs and the rat carotid artery, and the activity of the Hippo signaling pathway was significantly downregulated. In addition, the expression of YY1­associated protein­1 (YAP) and a number of its downstream target genes, including connective tissue growth factor (CTGF), were enhanced, thus enhancing the proliferation and migration of VSMCs. Knockdown of WWC3 suppressed the levels of large tumor suppressor kinase 1 (LATS1) expression and YAP phosphorylation, and the expression of YAP, CTGF and cyclin E was subsequently enhanced, thus promoting cell proliferation and migration. Similar results were obtained following overexpression of WWC3. Treatment with PDGF­BB was revealed to suppress the proliferation and migration of VSMCs transfected with the WWC3 plasmid, compared with VSMCs transfected with an empty vector. The present study demonstrated that WWC3 may interact with LATS1 in order to upregulate the Hippo signaling pathway via co­immunoprecipitation and enhancement of the phosphorylation of LATS1, in addition to the corresponding suppression of the nuclear import of YAP. However, VSMCs transfected with WWC3 plasmid with a deletion of the WW domain fail to exhibit this effect. These results suggested that WWC3 expression is downregulated in VSMCs during neointimal hyperplasia following injury (PDGF­BB stimulation or balloon injury). WWC3 upregulates the activity of the Hippo signaling pathway, and weakens the proliferation and migration of VSMCs. Furthermore, the results of the present study suggested that WWC3 may interact with LATS1 to promote the phosphorylation of YAP and reduce its nuclear translocation, upregulate the activity of the Hippo pathway, and suppress the proliferation and migration of VSMCs following injury.