Special Transition and Extraordinary Phase on the Surface of a Two-Dimensional Quantum Heisenberg Antiferromagnet

Continuous phase transitions exhibit richer critical phenomena on the surface than in the bulk, because distinct surface universality classes can be realized at the same bulk critical point by tuning the surface interactions. The exploration of surface critical behavior provides a window looking into higher-dimensional boundary conformal field theories. In this work, we study the surface critical behavior of a two-dimensional (2D) quantum critical Heisenberg model by tuning the surface coupling strength, and discover a direct special transition on the surface from the ordinary phase into an extraordinary phase. The extraordinary phase has a long-range antiferromagnetic order on the surface, in sharp contrast to the logarithmically decaying spin correlations in the 3D classical O(3) model. The special transition point has a new set of critical exponents, $y_{s}=0.86(4)$ and $\eta_{\parallel}=-0.32(1)$, which are distinct from the special transition of the classical O(3) model and indicate a new surface universality class of the 3D O(3) Wilson-Fisher theory.Comment: 5 pages, 3 figures; v2: substantially revised, new fitting form in extraordinary phas

Rab7 GTPase controls lipid metabolic signaling in myeloid-derived suppressor cells

Lysosomal acid lipase (LAL) is a critical neutral lipid metabolic enzyme that regulates metabolic reprogramming in myeloid-derived suppressor cells (MDSCs) through over-activation of mammalian target of rapamycin (mTOR). Affymetrix GeneChip microarray analysis of MDSCs from LAL deficient mouse (lal-/-) revealed upregulation of Rab7 GTPase protein, which belongs to a superfamily of small-molecular-weight GTPase known to regulate intracellular membrane trafficking from early to late endosomes and lysosomes. Here, the physical protein-protein interaction between Rab7 GTPase and mTOR has been detected by co-immunoprecipitation in the cell extract of wild type HD1A and lal-/- MDSC-like HD1B myeloid cell lines. The GST pull down assay using the recombinant GST-Rab7 GTPase fusion protein showed that Rab7 GTPase interacts with the mTOR N-terminal heat repeat domain. Rab7 GTPase siRNA knocking down reversed the altered lysosome/mTOR distribution and expression levels in HD1B cells. Rab7 GTPase siRNA knocking down in isolated bone marrow lal-/- MDSCs or HD1B cells not only reduced over-activation of mTOR and its downstream effector S6, but also decreased glucose consumption, decreased ROS over-production, and increased healthy mitochondria by membrane potential measurement. Inhibition of Rab7 GTPase led to reduced lal-/- MDSCs differentiation from bone marrow Lin- progenitor cells, reduced lal-/- MDSCs trans-endothelial migration, and reversed lal-/- MDSCs suppression of T cell proliferation. Furthermore, inhibition of Rab7 GTPase reduced lal-/- MDSCs ability to stimulate tumor cell proliferation in vitro, tumor growth in vivo, and tumor invasion. Together, these results showed that Rab7 GTPase is critically involved in MDSCs homeostasis and pathogenic functions

Multitask Active Learning for Graph Anomaly Detection

In the web era, graph machine learning has been widely used on ubiquitous graph-structured data. As a pivotal component for bolstering web security and enhancing the robustness of graph-based applications, the significance of graph anomaly detection is continually increasing. While Graph Neural Networks (GNNs) have demonstrated efficacy in supervised and semi-supervised graph anomaly detection, their performance is contingent upon the availability of sufficient ground truth labels. The labor-intensive nature of identifying anomalies from complex graph structures poses a significant challenge in real-world applications. Despite that, the indirect supervision signals from other tasks (e.g., node classification) are relatively abundant. In this paper, we propose a novel MultItask acTIve Graph Anomaly deTEction framework, namely MITIGATE. Firstly, by coupling node classification tasks, MITIGATE obtains the capability to detect out-of-distribution nodes without known anomalies. Secondly, MITIGATE quantifies the informativeness of nodes by the confidence difference across tasks, allowing samples with conflicting predictions to provide informative yet not excessively challenging information for subsequent training. Finally, to enhance the likelihood of selecting representative nodes that are distant from known patterns, MITIGATE adopts a masked aggregation mechanism for distance measurement, considering both inherent features of nodes and current labeled status. Empirical studies on four datasets demonstrate that MITIGATE significantly outperforms the state-of-the-art methods for anomaly detection. Our code is publicly available at: https://github.com/AhaChang/MITIGATE.Comment: Preprint. Under review. Code available at https://github.com/AhaChang/MITIGAT

Novel PAX9 compound heterozygous variants in a Chinese family with non-syndromic oligodontia and genotype-phenotype analysis of PAX9 variants

Studies have reported that >91.9% of non-syndromic tooth agenesis cases are caused by seven pathogenic genes. Objective: To report novel heterozygous PAX9 variants in a Chinese family with non-syndromic oligodontia and summarize the reported genotype-phenotype relationship of PAX9 variants. Methodology: We recruited 28 patients with non-syndromic oligodontia who were admitted to the Hospital of Stomatology Hebei Medical University (China) from 2018 to 2021. Peripheral blood was collected from the probands and their core family members for whole-exome sequencing (WES) and variants were verified by Sanger sequencing. Bioinformatics tools were used to predict the pathogenicity of the variants. SWISS-MODEL homology modeling was used to analyze the three-dimensional structural changes of variant proteins. We also analyzed the genotype-phenotype relationships of PAX9 variants. Results: We identified novel compound heterozygous PAX9 variants (reference sequence NM_001372076.1) in a Chinese family with non-syndromic oligodontia: a new missense variant c.1010C>A (p.T337K) in exon 4 and a new frameshift variant c.330_331insGT (p.D113Afs*9) in exon 2, which was identified as the pathogenic variant in this family. This discovery expands the known variant spectrum of PAX9; then, we summarized the phenotypes of non-syndromic oligodontia with PAX9 variants. Conclusion: We found that PAX9 variants commonly lead to loss of the second molars