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Hierarchical Reference Sets for Robust Unsupervised Detection of Scattered and Clustered Outliers

arXiv:2603.12847v1 Announce Type: cross Abstract: Most real-world IoT data analysis tasks, such as clustering and anomaly event detection, are unsupervised and highly susceptible to the presence of outliers. In addition to sporadic scattered outliers caused by factors such as faulty sensor readings, IoT systems often exhibit clustered outliers. These occur when multiple devices or nodes produce similar anomalous measurements, for instance, owing to localized interference, emerging security threats, or regional false alarms, forming micro-clusters. These clustered outliers can be easily mistaken for normal behavior because of their relatively high local density, thereby obscuring the detection of both scattered and contextual anomalies. To address this, we propose a novel outlier detection paradigm that leverages the natural neighboring relationships using graph structures. This facilitates multi-perspective anomaly evaluation by incorporating reference sets at both local and global scales derived from the graph. Our approach enables the effective recognition of scattered outliers without interference from clustered anomalies, whereas the graph structure simultaneously helps reflect and isolate clustered outlier groups. Extensive experiments, including comparative performance analysis, ablation studies, validation on downstream clustering tasks, and evaluation of hyperparameter sensitivity, demonstrate the efficacy of the proposed method. The source code is available at https://github.com/gordonlok/DROD.

OpenVision 3: A Family of Unified Visual Encoder for Both Understanding and Generation

arXiv:2601.15369v2 Announce Type: replace-cross Abstract: This paper presents a family of advanced vision encoder, named OpenVision 3, that learns a single, unified visual representation that can serve both image understanding and image generation. Our core architecture is simple: we feed VAE-compressed image latents to a ViT encoder and train its output to support two complementary roles. First, the encoder output is passed to the ViT-VAE decoder to reconstruct the original image, encouraging the representation to capture generative structure. Second, the same representation is optimized with contrastive learning and image-captioning objectives, strengthening semantic features. By jointly optimizing reconstruction- and semantics-driven signals in a shared latent space, the encoder learns representations that synergize and generalize well across both regimes. We validate this unified design through extensive downstream evaluations with the encoder frozen. For generation, we test it under the RAE framework: ours substantially surpasses the standard CLIP-based encoder (e.g., gFID: 1.87 vs. 2.54 on ImageNet). For multimodal understanding, we plug the encoder into the LLaVA-1.5 and LLaVA-NeXT framework: it performs comparably with a standard CLIP vision encoder (e.g., 63.3 vs. 61.2 on SeedBench, and 59.2 vs. 58.1 on GQA). We provide empirical evidence that generation and understanding are mutually beneficial in our architecture, while further underscoring the critical role of the VAE latent space. We hope this work can spur future research on unified modeling.

FNDC1 Competitively Binds Gbeta2 to Suppress the beta-Catenin-Destruction Complex and Promote Gastric Cancer Malignancy

11 March 2026 at 18:00

FASEB J. 2026 Mar 31;40(6):e71634. doi: 10.1096/fj.202503587R.

ABSTRACT

Gastric cancer (GC) is a leading cause of cancer-related deaths and has high recurrence rate. Although fibronectin domain-containing protein 1 (FNDC1) is implicated in GC progression, its molecular mechanisms remain unclear. Multi-omics analyses (TCGA, GEO datasets) were used to assess FNDC1 expression and clinical correlation. In vitro (cell proliferation, invasion, EMT markers) and in vivo (xenograft) experiments, combined with molecular assays (Co-IP, WB, ChIP), explored FNDC1's function and mechanism. FNDC1 was significantly upregulated in GC, correlating with advanced clinicopathological features and poor prognosis. Knockdown of FNDC1 suppressed GC cell proliferation, invasion, and metastasis by inhibiting EMT and Wnt/Ξ²-catenin signaling. Mechanistically, FNDC1 competitively bound the WD5 domain (residues 224-254) of GΞ²2, disrupting GΞ²Ξ³-Dvl1 interaction. This prevented Dvl1 degradation, promoted Axin1 ubiquitination, and destabilized the Ξ²-catenin-destruction complex (GSK3 Ξ²-APC-Axin1), leading to Ξ²-catenin accumulation and Wnt pathway activation. FNDC1 drives GC malignancy by targeting the GΞ²2-Dvl1 axis to activate Wnt/Ξ²-catenin signaling, suggesting FNDC1 as a novel prognostic biomarker and therapeutic target.

PMID:41808415 | PMC:PMC12976582 | DOI:10.1096/fj.202503587R

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