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Received β€” 26 March 2026 ⏭

Toward Faithful Segmentation Attribution via Benchmarking and Dual-Evidence Fusion

βœ‡cs.AI, q-bio.NC updates on arXiv.org
By: Abu Noman Md Sakib Β· OFM Riaz Rahman Aranya Β· Kevin Desai Β· Zijie Zhang
25 March 2026 at 12:00
arXiv:2603.22624v1 Announce Type: cross Abstract: Attribution maps for semantic segmentation are almost always judged by visual plausibility. Yet looking convincing does not guarantee that the highlighted pixels actually drive the model's prediction, nor that attribution credit stays within the target region. These questions require a dedicated evaluation protocol. We introduce a reproducible benchmark that tests intervention-based faithfulness, off-target leakage, perturbation robustness, and runtime on Pascal VOC and SBD across three pretrained backbones. To further demonstrate the benchmark, we propose Dual-Evidence Attribution (DEA), a lightweight correction that fuses gradient evidence with region-level intervention signals through agreement-weighted fusion. DEA increases emphasis where both sources agree and retains causal support when gradient responses are unstable. Across all completed runs, DEA consistently improves deletion-based faithfulness over gradient-only baselines and preserves strong robustness, at the cost of additional compute from intervention passes. The benchmark exposes a faithfulness-stability tradeoff among attribution families that is entirely hidden under visual evaluation, providing a foundation for principled method selection in segmentation explainability. Code is available at https://github.com/anmspro/DEA.

Mind Your HEARTBEAT! Claw Background Execution Inherently Enables Silent Memory Pollution

βœ‡cs.AI, q-bio.NC updates on arXiv.org
By: Yechao Zhang Β· Shiqian Zhao Β· Jie Zhang Β· Gelei Deng Β· Jiawen Zhang Β· Xiaogeng Liu Β· Chaowei Xiao Β· Tianwei Zhang
25 March 2026 at 12:00
arXiv:2603.23064v2 Announce Type: cross Abstract: We identify a critical security vulnerability in mainstream Claw personal AI agents: untrusted content encountered during heartbeat-driven background execution can silently pollute agent memory and subsequently influence user-facing behavior without the user's awareness. This vulnerability arises from an architectural design shared across the Claw ecosystem: heartbeat background execution runs in the same session as user-facing conversation, so content ingested from any external source monitored in the background (including email, message channels, news feeds, code repositories, and social platforms) can enter the same memory context used for foreground interaction, often with limited user visibility and without clear source provenance. We formalize this process as an Exposure (E) $\rightarrow$ Memory (M) $\rightarrow$ Behavior (B) pathway: misinformation encountered during heartbeat execution enters the agent's short-term session context, potentially gets written into long-term memory, and later shapes downstream user-facing behavior. We instantiate this pathway in an agent-native social setting using MissClaw, a controlled research replica of Moltbook. We find that (1) social credibility cues, especially perceived consensus, are the dominant driver of short-term behavioral influence, with misleading rates up to 61%; (2) routine memory-saving behavior can promote short-term pollution into durable long-term memory at rates up to 91%, with cross-session behavioral influence reaching 76%; (3) under naturalistic browsing with content dilution and context pruning, pollution still crosses session boundaries. Overall, prompt injection is not required: ordinary social misinformation is sufficient to silently shape agent memory and behavior under heartbeat-driven background execution.

Generalizable Heuristic Generation Through LLMs with Meta-Optimization

βœ‡cs.AI, q-bio.NC updates on arXiv.org
By: Yiding Shi Β· Jianan Zhou Β· Wen Song Β· Jieyi Bi Β· Yaoxin Wu Β· Zhiguang Cao Β· Jie Zhang
25 March 2026 at 12:00
arXiv:2505.20881v2 Announce Type: replace-cross Abstract: Heuristic design with large language models (LLMs) has emerged as a promising approach for tackling combinatorial optimization problems (COPs). However, existing approaches often rely on manually predefined evolutionary computation (EC) heuristic-optimizers and single-task training schemes, which may constrain the exploration of diverse heuristic algorithms and hinder the generalization of the resulting heuristics. To address these issues, we propose Meta-Optimization of Heuristics (MoH), a novel framework that operates at the optimizer level, discovering effective heuristic-optimizers through the principle of meta-learning. Specifically, MoH leverages LLMs to iteratively refine a meta-optimizer that autonomously constructs diverse heuristic-optimizers through (self-)invocation, thereby eliminating the reliance on a predefined EC heuristic-optimizer. These constructed heuristic-optimizers subsequently evolve heuristics for downstream tasks, enabling broader heuristic exploration. Moreover, MoH employs a multi-task training scheme to promote its generalization capability. Experiments on classic COPs demonstrate that MoH constructs an effective and interpretable meta-optimizer, achieving state-of-the-art performance across various downstream tasks, particularly in cross-size settings. Our code is available at: https://github.com/yiding-s/MoH.

Protein phosphatase 2A methylation state impacts Ξ±-synucleinopathy in mouse models

βœ‡Cell Death Discovery nature.com science feeds
By: Santhosh Maddila Β· Kambiz Hassanzadeh Β· Jun Liu Β· Jie Zhang Β· Faheem Ullah Β· Russell E. Nichols Β· M. Maral Mouradian
24 March 2026 at 08:00

Cell Death Discovery, Published online: 24 March 2026; doi:10.1038/s41420-026-03045-7

Protein phosphatase 2A methylation state impacts Ξ±-synucleinopathy in mouse models

NUP85 as a Pan-Cancer Immune Biomarker: Integrated Multi Omics and Functional Analyses Reveal Its Role in Tumor Prognosis

βœ‡(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Weihao Kong Β· Ying Hu Β· Kangjie Zhang Β· Zhipeng Zhu Β· Yajun Zou Β· Long Teng Β· Xingyu Wang Β· Jianlin Zhang
23 March 2026 at 18:00

Immunotargets Ther. 2026 Mar 17;15:541852. doi: 10.2147/ITT.S541852. eCollection 2026.

ABSTRACT

PURPOSE: NUP85 encodes protein components of the Nup107-160 subunit of the nuclear pore complex, belonging to the Nucleoporins (NUPs) family, potentially implicating its role in human cancer. This study aims to elucidate the potential involvement of NUP85 in cancer pathogenesis.

METHODS: Leveraging data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), Clinical Proteomic Tumor Analysis Consortium (CPTAC), Cancer Cell Line Encyclopedia (CCLE), Human Protein Atlas (HPA), Gene Expression Profiling Interactive Analysis (GEPIA), CellMiner, and GeneMANIA databases, we investigated the role of NUP85 across various tumors. Correlations between NUP85 expression and pathological stage, histological grade, survival, immune infiltration, tumor mutational burden (TMB), microsatellite instability (MSI), drug resistance, DNA methylation, copy number variation (CNV), and single-cell expression were analyzed. Gene functional enrichment analysis was conducted to explore NUP85-associated pathways. Molecular biology experiments including Western blotting, flow cytometry, trans-well migration, and invasion assays were performed to validate NUP85's oncogenic role in lung adenocarcinoma (LUAD) and oral squamous cell carcinoma (OSCC) cell lines.

RESULTS: Our findings reveal up-regulated expression of NUP85 in most tumor tissues, with significant correlations observed with pathological stage, survival, immune infiltration, TMB, MSI, drug resistance, DNA methylation, and CNV. Molecular biology experiments confirm NUP85's tumor-promoting role in LUAD and OSCC cell lines. Single-cell sequencing data suggest elevated NUP85 expression primarily in proliferative T cells (Tprolif).

CONCLUSION: NUP85 emerges as a potential tumor marker associated with tumor immunity and poor prognosis. These insights offer avenues for the development of novel therapeutic targets and anti-neoplastic drugs.

PMID:41869435 | PMC:PMC13005628 | DOI:10.2147/ITT.S541852

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