Predicting the Silent Majority on Graphs: Knowledge Transferable Graph Neural Network

Graphs consisting of vocal nodes ("the vocal minority") and silent nodes ("the silent majority"), namely VS-Graph, are ubiquitous in the real world. The vocal nodes tend to have abundant features and labels. In contrast, silent nodes only have incomplete features and rare labels, e.g., the description and political tendency of politicians (vocal) are abundant while not for ordinary people (silent) on the twitter's social network. Predicting the silent majority remains a crucial yet challenging problem. However, most existing message-passing based GNNs assume that all nodes belong to the same domain, without considering the missing features and distribution-shift between domains, leading to poor ability to deal with VS-Graph. To combat the above challenges, we propose Knowledge Transferable Graph Neural Network (KT-GNN), which models distribution shifts during message passing and representation learning by transferring knowledge from vocal nodes to silent nodes. Specifically, we design the domain-adapted "feature completion and message passing mechanism" for node representation learning while preserving domain difference. And a knowledge transferable classifier based on KL-divergence is followed. Comprehensive experiments on real-world scenarios (i.e., company financial risk assessment and political elections) demonstrate the superior performance of our method. Our source code has been open sourced.Comment: Paper was accepted by WWW202

Make Heterophily Graphs Better Fit GNN: A Graph Rewiring Approach

Graph Neural Networks (GNNs) are popular machine learning methods for modeling graph data. A lot of GNNs perform well on homophily graphs while having unsatisfactory performance on heterophily graphs. Recently, some researchers turn their attention to designing GNNs for heterophily graphs by adjusting the message passing mechanism or enlarging the receptive field of the message passing. Different from existing works that mitigate the issues of heterophily from model design perspective, we propose to study heterophily graphs from an orthogonal perspective by rewiring the graph structure to reduce heterophily and making the traditional GNNs perform better. Through comprehensive empirical studies and analysis, we verify the potential of the rewiring methods. To fully exploit its potential, we propose a method named Deep Heterophily Graph Rewiring (DHGR) to rewire graphs by adding homophilic edges and pruning heterophilic edges. The detailed way of rewiring is determined by comparing the similarity of label/feature-distribution of node neighbors. Besides, we design a scalable implementation for DHGR to guarantee high efficiency. DHRG can be easily used as a plug-in module, i.e., a graph pre-processing step, for any GNNs, including both GNN for homophily and heterophily, to boost their performance on the node classification task. To the best of our knowledge, it is the first work studying graph rewiring for heterophily graphs. Extensive experiments on 11 public graph datasets demonstrate the superiority of our proposed methods.Comment: 11 page

Classification of Geological Samples Based on Soft Independent Modeling of Class Analogy Using Laser-Induced Breakdown Spectroscopy

Laser-induced breakdown spectroscopy with soft independent modeling of class analogy is used in the identification of a large number of unprocessed geological samples having similar components in this study. Considering a variety of data from different samples, representative spectral regions representing the major components were extracted. In addition, principal component analysis was applied to remove noninformative variables from the spectrum. The unclassification rate, misclassification rate, and average correct classification rate for 25 types of geological samples were 1.2%, 4.7%, and 94.1%, respectively. These results suggest that laser-induced breakdown spectroscopy using soft independent modeling of class analogy can be used to identify a wide variety of geological samples. Furthermore, we found that this approach can be used to identify spectral differences among similar sample types because of matrix effects and the trace element impurities

miR-185-5p / ATG101 axis alleviated intestinal barrier damage in intestinal ischemia reperfusion through autophagy

Objective: Intestinal ischemia-reperfusion (II/R) is a common pathological injury in clinic, and the systemic inflammatory response it causes will lead to multiple organ damage and functional failure. miR-185-5p has been reported to be a regulator of inflammatory response and autophagy, but whether it participates in the regulation of autophagy in II/R is still unclear. Therefore, we aimed to explore the mechanism of miR-185-5p regulating intestinal barrier injury in (II/R). Methods: Caco-2 cells was induced by oxygen-glucose deprivation/reoxygenation (OGD/R) to establish II/R model. The superior mesenteric artery of C57BL/6 mice was clamped for 45 min and then subjected to reperfusion for 4 h for the establishment of II/R mice model. miR-185-5p mimic, miR-185-5p inhibitor, pcDNA-autophagy-related 101 (ATG101) were respectively transfected into Caco-2 cells. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to assess miR-185-5p expression. Western blot detected the level of ATG101 and tight junction-associated proteins ZO1, Occludin, E-cadherin, β-catenin, as well as autophagy markers ATG5, ATG12, LC3Ⅰ/Ⅱ, Beclin1 and SQSTM1. Transepithelial electrical resistance (TEER) values was detected by a resistance meter. FITC-Dextran was performed to measure cell permeability. 5-ethynyl-2’-deoxyuridine (EDU) staining measured cell proliferation. Transmission electron microscope was conducted to observe autophagosomes. Hematoxylin & eosin (H&E) staining observed the damage of mice intestinal. Immunohistochemistry (IHC) measured the percentage of ki67 positive cells. TdT-mediated dUTP nick-end labeling (TUNEL) assay assessed cell apoptosis in intestinal tissues of II/R. Dual-luciferase assay verified the targeting relationship between miR-185-5p and ATG101.Results miR-185-5p was overexpressed in OGD/R-induced Caco-2 cells and intestinal tissues of II/R mice. Knocking down miR-185-5p markedly promoted autophagy and TEER values, reduced cell permeability, and alleviated intestinal barrier damage. ATG101 was a target of miR-185-5p, and overexpression of ATG101 promoted autophagy and dampened OGD/R-induced intestinal barrier damage. Overexpression of miR-185-5p reversed the effect of overexpressed ATG101 on OGD/R-induced Caco-2 cells. Conclusion: Knockdown of miR-185-5p enhanced autophagy and alleviated II/R intestinal barrier damage by targeting ATG101

Haploinsufficiency of Sox9 results in defective cartilage primordia and premature skeletal mineralization

In humans, SOX9 heterozygous mutations cause the severe skeletal dysmorphology syndrome campomelic dysplasia. Except for clinical descriptions, little is known about the pathogenesis of this disease. We have generated heterozygous Sox9 mutant mice that phenocopy most of the skeletal abnormalities of this syndrome. The Sox9(+/−) mice died perinatally with cleft palate, as well as hypoplasia and bending of many skeletal structures derived from cartilage precursors. In embryonic day (E)14.5 heterozygous embryos, bending of radius, ulna, and tibia cartilages was already prominent. In E12.5 heterozygotes, all skeletal elements visualized by using Alcian blue were smaller. In addition, the overall levels of Col2a1 RNA at E10.5 and E12.5 were lower than in wild-type embryos. We propose that the skeletal abnormalities observed at later embryonic stages were caused by delayed or defective precartilaginous condensations. Furthermore, in E18.5 embryos and in newborn heterozygotes, premature mineralization occurred in many bones, including vertebrae and some craniofacial bones. Because Sox9 is not expressed in the mineralized portion of the growth plate, this premature mineralization is very likely the consequence of allele insufficiency existing in cells of the growth plate that express Sox9. Because the hypertrophic zone of the heterozygous Sox9 mutants was larger than that of wild-type mice, we propose that Sox9 also has a role in regulating the transition to hypertrophic chondrocytes in the growth plate. Despite the severe hypoplasia of cartilages, the overall organization and cellular composition of the growth plate were otherwise normal. Our results suggest the hypothesis that two critical steps of the chondrocyte differentiation pathway are sensitive to Sox9 dosage. First, an early step presumably at the stage of mesenchymal condensation of cartilage primordia, and second, a later step preceding the transition of chondrocytes into hypertrophic chondrocytes

Hydrogen-Bonded Organic Frameworks Based Mixed-Matrix Membranes with Low Temperature Antiviral Activity

Hydrogen-bonded organic frameworks (HOFs) are a type of porous molecular crystal consisting of multiple rigid large π-conjugated structures. They hold great potential as photosensitive antiviral materials due to their solution processability. Moreover, HOFs can easily bind to polymeric matrices, making them a flexible and green option for low-temperature antiviral materials. In this study, we fabricated a series of HOF@polymer mixed-matrix membranes (MMMs) by a solution casting technique for low temperature antiviral applications. The incorporation of HOF-101 crystals into poly vinylidene difluoride (PVDF) membranes can enhance their mechanical strength by at least 20%. The unique one-dimensional pore channels of HOF-101 enable the MMMs to have increased exposure to oxygen, providing the potential for enhanced generation of singlet oxygen (1O2). The 1O2 generated by 1 wt % HOF-101@PVDF MMMs at 263 K was observed to be more than 40% higher compared to that at 298 K. The excellent 1O2 generation efficiency allowed the MMMs to maintain their virucidal efficacy by more than 99% and 95% against vesicular stomatitis virus and herpes simplex virus type 1, respectively, at low temperatures