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On-premise medical AI agents for reliable clinical decision-making

✇Nature Medicine
By: Li Zhang · Georg Wölflein · Dyke Ferber · Junhao Liang · Zunamys I. Carrero · Xuewei Wu · Julien Vibert · Jan Clusmann · Lino Möhrmann · Elena E. Möhrmann · Catharina Wichmann · Fabian Wolf · Tim Lenz · Jakob Nikolas Kather

Nature Medicine, Published online: 15 September 2026; doi:10.1038/s41591-026-04609-x

An autonomous clinical AI agent enhances decision-making through on-premise deployment and reliability metrics, achieving high diagnostic accuracy and selective autonomy.
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A Mitochondrial-Related Gene Signature for Diagnosis and Immune Microenvironment Modulation in Lung Cancer and Venous Thromboembolism

✇Omics In Lung
By: Xue Li Zhang · Ai Li Gao · Zhan Ju Liu

World J Oncol. 2026 Sep 4;17(5):683-704. doi: 10.14740/wjon2815. eCollection 2026 Oct.

ABSTRACT

BACKGROUND: Lung cancer (LC) and venous thromboembolism (VTE) are closely associated, with VTE contributing to morbidity and mortality among patients with LC. We aimed to identify and characterize a mitochondrial-related transcriptomic signature shared between LC and VTE and to explore its association with immune microenvironment features.

METHODS: We applied a multiomics approach focused on mitochondrial-related signaling pathways. Publicly available transcriptomic datasets were analyzed using differential expression profiling and weighted gene co-expression network analysis to identify key regulatory genes. These genes were intersected with a mitochondrial gene set and subjected to functional enrichment analysis. Least absolute shrinkage and selection operator (LASSO) regression was used to identify candidate diagnostic genes validation. Immune cell infiltration was quantified, and associated regulatory mechanisms were explored.

RESULTS: Thirty-nine shared crosstalk genes were identified and were primarily enriched in mitochondrial metabolic processes. LASSO regression identified a five-gene candidate signature (ACAA1, HSD17B10, MTIF2, THOP1, and PDE2A). The model exhibited promising discriminatory performance (area under the curve > 0.9 in LC dataset and 0.7-0.9 in VTE dataset). These genes were significantly dysregulated and were associated with altered immune cell infiltration, particularly in dendritic cell and T cell subsets.

CONCLUSION: We identified a mitochondrial-related gene signature reflecting shared transcriptomic correlates between LC and VTE. The signature showed variable performance across disease contexts and correlative associations with immune features, supporting its role as a candidate biomarker for further investigation. Prospective validation in independent clinical cohorts is required before any translational application.

PMID:42730163 | PMC:PMC13568737 | DOI:10.14740/wjon2815

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A Mitochondrial-Related Gene Signature for Diagnosis and Immune Microenvironment Modulation in Lung Cancer and Venous Thromboembolism

✇(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Xue Li Zhang · Ai Li Gao · Zhan Ju Liu

World J Oncol. 2026 Sep 4;17(5):683-704. doi: 10.14740/wjon2815. eCollection 2026 Oct.

ABSTRACT

BACKGROUND: Lung cancer (LC) and venous thromboembolism (VTE) are closely associated, with VTE contributing to morbidity and mortality among patients with LC. We aimed to identify and characterize a mitochondrial-related transcriptomic signature shared between LC and VTE and to explore its association with immune microenvironment features.

METHODS: We applied a multiomics approach focused on mitochondrial-related signaling pathways. Publicly available transcriptomic datasets were analyzed using differential expression profiling and weighted gene co-expression network analysis to identify key regulatory genes. These genes were intersected with a mitochondrial gene set and subjected to functional enrichment analysis. Least absolute shrinkage and selection operator (LASSO) regression was used to identify candidate diagnostic genes validation. Immune cell infiltration was quantified, and associated regulatory mechanisms were explored.

RESULTS: Thirty-nine shared crosstalk genes were identified and were primarily enriched in mitochondrial metabolic processes. LASSO regression identified a five-gene candidate signature (ACAA1, HSD17B10, MTIF2, THOP1, and PDE2A). The model exhibited promising discriminatory performance (area under the curve > 0.9 in LC dataset and 0.7-0.9 in VTE dataset). These genes were significantly dysregulated and were associated with altered immune cell infiltration, particularly in dendritic cell and T cell subsets.

CONCLUSION: We identified a mitochondrial-related gene signature reflecting shared transcriptomic correlates between LC and VTE. The signature showed variable performance across disease contexts and correlative associations with immune features, supporting its role as a candidate biomarker for further investigation. Prospective validation in independent clinical cohorts is required before any translational application.

PMID:42730163 | PMC:PMC13568737 | DOI:10.14740/wjon2815

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DiffLUT-Net: Differentiable Training of FPGA LUT Networks with Learnable Connectivity

✇cs.AI, q-bio.NC updates on arXiv.org
By: Jiaqi Ye · Xinrui Gong · Jingcun Wang · Olga Kondrateva · Bing Li · Grace Li Zhang
arXiv:2609.09254v1 Announce Type: cross Abstract: Field-programmable gate arrays (FPGAs) enable efficient neural-network inference, but most deployment flows either accelerate multiply-accumulate operations or convert pretrained quantized models into lookup tables (LUTs). We present DiffLUT-Net, an FPGA-native network connected by six-input LUTs that are trained from scratch. We jointly learn the 64 truth-table entries of a LUT and the source to each of its six input ports using a differentiable LUT function relaxation and hardware source selection. After training, the truth tables and connections are discretized, unused logic can be pruned, and the network is exported directly as synthesizable Verilog. Across five benchmarks, DiffLUT-Net achieves favorable accuracy-resource trade-offs. These results demonstrate the effectiveness of jointly learning LUT functions and sparse connectivity for compact FPGA-native inference. The code is available at https://github.com/TUDa-HWAI/DiffLUT-Network.
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Lipotoxicity-induced ER-mitochondrial hypercoupling activates the mtDNA-cGAS-STING-NF-κB axis to drive follicular arrest in metabolically compromised PCOS

✇Cell Death Discovery nature.com science feeds
By: Mingrui Xue · Qi Zhu · Shuli Zhang · Guangzong Zhao · Xiaoqi Hong · Di Pang · Yue Xu · Xiaolu Li · Yuxin Liu · Ying Li · Qiucheng Jia · Sisi Xu · Hongshan Ge

Cell Death Discovery, Published online: 08 September 2026; doi:10.1038/s41420-026-03339-w

Lipotoxicity-induced ER-mitochondrial hypercoupling activates the mtDNA-cGAS-STING-NF-κB axis to drive follicular arrest in metabolically compromised PCOS
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Multiomic characterization of malignant pulmonary nodules and development of a methylation-based diagnostic Model

✇Pulmonary nodule
By: Wei Zhou · Tongji Xie · Qingjun Wu · Mengmeng Song · Jianzhen Weng · Jieli Zhang · Xuan Gao · Min Zheng · Zheng Wang · Yunzhi Zhou · Yanming Li

J Transl Med. 2026 Jun 8;24(1):776. doi: 10.1186/s12967-026-08382-w.

ABSTRACT

BACKGROUND: The molecular distinction between benign and malignant pulmonary nodules remains a significant diagnostic challenge. While genomic drivers are well studied, multiomic integration of the epigenetic-transcriptional landscape and its translation into noninvasive tools are lacking.

METHODS: We performed a multiomic characterization (genomic, epigenomic, and transcriptomic) of 158 pulmonary nodules. Unsupervised factor analysis integrated these layers to identify core regulatory axes. A 9-gene cell-free DNA (cfDNA) methylation classifier was developed and validated in blood and tissue cohorts.

RESULTS: Genomic profiling revealed EGFR mutations (exclusive to malignant nodules) and MYC amplification as fundamental initiators of malignancy. Multiomic factor analysis (Factor 1) revealed profound genetic‒epigenetic synergy, in which these alterations dictate a permissive methylome, leading to aberrant epigenetic programming of chromatin accessibility, as well as epigenetic-transcriptional effects: hypomethylation at the promoters of cell cycle genes that augments their expression, and hypermethylation at immune related pathways gene loci that silences their transcription. This effect orchestrates formation of proproliferative (E2F target/G2M checkpoint) and "immune-cold" malignant phenotype, characterized by elevated Treg/CD8+ ratios and fibroblast recruitment. Notably, we observed a gradual accumulation of methylation aberrations along the premalignant-to-invasive continuum (adenocarcinoma in situ [AIS]→minimally invasive adenocarcinoma [MIA]→adenocarcinoma [ADC]), identifying progressive epigenetic dysregulation as a hallmark of tumor aggressiveness. Global methylome remodeling drives ADC progression through hypermethylation-mediated silencing of tumor suppressors (RASA3 and PPARG) and hypomethylation-activated oncogenic axes, specifically the GDF15 axis, which independently predict poor survival in patients with lung ADC in the TCGA cohort. We translated these tissue-derived insights into a 9-gene cfDNA methylation classifier, which achieved exceptional diagnostic accuracy across independent cohorts (training AUC = 1.00; test AUC = 0.93; tissue AUC = 0.96). Rooted in the biological "ground truth" of tissue dysregulation, this classifier functions specifically as a functional readout of the core cell cycle and proliferative pathways, offering a robust, noninvasive tool for the biology-informed risk assessment of pulmonary nodules.

CONCLUSIONS: This study delineates an epigenetic-transcriptional regulatory network that drives nodule malignancy. Our findings provide a robust theoretical foundation and a high-performance liquid biopsy tool for the precise, noninvasive diagnosis of pulmonary nodules.

PMID:42260586 | PMC:PMC13274191 | DOI:10.1186/s12967-026-08382-w

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Sirt1 sustains Sonic hedgehog signaling to promote medulloblastoma progression through regulating Gli3 processing

✇Oncogene - Issue - nature.com science feeds
By: Jian Hu · Chaonan Zheng · Yingying Feng · Yuhang Li · Panpan Pei · Man Yang · Yanghui Qu · Long-Tai Zheng · Li Zhang · Xue-Chu Zhen · Yuan Wang

Oncogene, Published online: 18 April 2026; doi:10.1038/s41388-026-03781-1

Sirt1 sustains Sonic hedgehog signaling to promote medulloblastoma progression through regulating Gli3 processing
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Comparative reversal learning reveals rigid adaptation in LLMs under non-stationary uncertainty

✇cs.AI, q-bio.NC updates on arXiv.org
By: Haomiaomiao Wang · Tom\'as E Ward · Lili Zhang
arXiv:2604.04182v1 Announce Type: new Abstract: Non-stationary environments require agents to revise previously learned action values when contingencies change. We treat large language models (LLMs) as sequential decision policies in a two-option probabilistic reversal-learning task with three latent states and switch events triggered by either a performance criterion or timeout. We compare a deterministic fixed transition cycle to a stochastic random schedule that increases volatility, and evaluate DeepSeek-V3.2, Gemini-3, and GPT-5.2, with human data as a behavioural reference. Across models, win-stay was near ceiling while lose-shift was markedly attenuated, revealing asymmetric use of positive versus negative evidence. DeepSeek-V3.2 showed extreme perseveration after reversals and weak acquisition, whereas Gemini-3 and GPT-5.2 adapted more rapidly but still remained less loss-sensitive than humans. Random transitions amplified reversal-specific persistence across LLMs yet did not uniformly reduce total wins, demonstrating that high aggregate payoff can coexist with rigid adaptation. Hierarchical reinforcement-learning (RL) fits indicate dissociable mechanisms: rigidity can arise from weak loss learning, inflated policy determinism, or value polarisation via counterfactual suppression. These results motivate reversal-sensitive diagnostics and volatility-aware models for evaluating LLMs under non-stationary uncertainty.
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Genetically encoded fluorescent reporters to visualize α-synuclein pathology in live brain

✇Cell
By: Li Zhang · Minhui Yu · Guoqing Chen · Siyuan Ge · Mengdi Wang · Xianying Zhang · Miao Zhao · Huating Gu · Meizhu Huang · Aixue Liu · Gengxin Ran · Zeyuan Liu · Tiepeng Liao · Qi Chen · Chenjian Miao · Yao Lu · Yibing Wang · Fengchao Wang · Zhihui Liu · Hongying Zhu · Qian Wu · Zhuan Zhou · Wei Xiong · Xiaoqun Wang · Peng Cao
The development of genetically encoded fluorescent reporters, along with their corresponding knock-in mouse lines for labeling α-Syn inclusions, enables diverse applications in studying the propagation and pathological effects of α-Syn inclusions in the live brain.
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METTL16 enhances proteasome inhibitor resistance in multiple myeloma by inhibiting eIF2α-PERK interaction and promoting PSMB5 translation

✇Oncogene - Issue - nature.com science feeds
By: Guanli Wang · Xuejie Gao · Hui Zhang · Ke Hu · Qilin Feng · Yujie Liu · Chaolu Hu · Shushan Guo · Dandan Yu · Shuaikang Chang · Xiaosong Wu · Xinyan Jia · Dong An · Yu Peng · Yi Tao · Haiyan Cai · Gege Chen · Li Zhang · Jumei Shi

Oncogene, Published online: 13 March 2026; doi:10.1038/s41388-026-03706-y

METTL16 enhances proteasome inhibitor resistance in multiple myeloma by inhibiting eIF2α-PERK interaction and promoting PSMB5 translation
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Rigidity in LLM Bandits with Implications for Human-AI Dyads

✇cs.AI, q-bio.NC updates on arXiv.org
By: Haomiaomiao Wang · Tom\'as E Ward · Lili Zhang
arXiv:2603.07717v1 Announce Type: new Abstract: We test whether LLMs show robust decision biases. Treating models as participants in two-arm bandits, we ran 20000 trials per condition across four decoding configurations. Under symmetric rewards, models amplified positional order into stubborn one-arm policies. Under asymmetric rewards, they exploited rigidly yet underperformed an oracle and rarely re-checked. The observed patterns were consistent across manipulations of temperature and top-p, with top-k held at the provider default, indicating that the qualitative behaviours are robust to the two decoding knobs typically available to practitioners. Crucially, moving beyond descriptive metrics to computational modelling, a hierarchical Rescorla-Wagner-softmax fit revealed the underlying strategies: low learning rates and very high inverse temperatures, which together explain both noise-to-bias amplification and rigid exploitation. These results position minimal bandits as a tractable probe of LLM decision tendencies and motivate hypotheses about how such biases could shape human-AI interaction.
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CauKer: Classification Time Series Foundation Models Can Be Pretrained on Synthetic Data

✇cs.AI, q-bio.NC updates on arXiv.org
By: Shifeng Xie · Vasilii Feofanov · Ambroise Odonnat · Lei Zan · Marius Alonso · Jianfeng Zhang · Themis Palpanas · Lujia Pan · Keli Zhang · Ievgen Redko
arXiv:2508.02879v3 Announce Type: replace-cross Abstract: Time series foundation models (TSFMs) have recently gained significant attention due to their strong zero-shot capabilities and widespread real-world applications. Such models typically require a computationally costly pre-training on large-scale, carefully curated collections of real-world sequences. To allow for a sample-efficient pre-training of TSFMs, we propose \textsc{CauKer}, a novel algorithm designed to generate diverse, causally coherent synthetic time series with realistic trends, seasonality, and nonlinear interactions. \textsc{CauKer} combines Gaussian Process (GP) kernel composition with Structural Causal Models (SCM) to produce data for sample-efficient pre-training of state-of-the-art classification TSFMs having different architectures and following different pre-training approaches. Additionally, our experiments reveal that \textsc{CauKer}-generated datasets exhibit clear scaling laws for both dataset size (10K to 10M samples) and model capacity (1M to 783M parameters), unlike real-world datasets, which display irregular scaling behavior. The source code is publicly available at https://github.com/ShifengXIE/CauKer.
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Agentic Peer-to-Peer Networks: From Content Distribution to Capability and Action Sharing

✇cs.AI, q-bio.NC updates on arXiv.org
By: Taotao Wang · Lizhao You · Jingwen Tong · Chonghe Zhao · Shengli Zhang
arXiv:2603.03753v1 Announce Type: cross Abstract: The ongoing shift of AI models from centralized cloud APIs to local AI agents on edge devices is enabling \textit{Client-Side Autonomous Agents (CSAAs)} -- persistent personal agents that can plan, access local context, and invoke tools on behalf of users. As these agents begin to collaborate by delegating subtasks directly between clients, they naturally form \emph{Agentic Peer-to-Peer (P2P) Networks}. Unlike classic file-sharing overlays where the exchanged object is static, hash-indexed content (e.g., files in BitTorrent), agentic overlays exchange \emph{capabilities and actions} that are heterogeneous, state-dependent, and potentially unsafe if delegated to untrusted peers. This article outlines the networking foundations needed to make such collaboration practical. We propose a plane-based reference architecture that decouples connectivity/identity, semantic discovery, and execution. Besides, we introduce signed, soft-state capability descriptors to support intent- and constraint-aware discovery. To cope with adversarial settings, we further present a \textit{tiered verification} spectrum: Tier~1 relies on reputation signals, Tier~2 applies lightweight canary challenge-response with fallback selection, and Tier~3 requires evidence packages such as signed tool receipts/traces (and, when applicable, attestation). Using a discrete-event simulator that models registry-based discovery, Sybil-style index poisoning, and capability drift, we show that tiered verification substantially improves end-to-end workflow success while keeping discovery latency near-constant and control-plane overhead modest.
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DICArt: Advancing Category-level Articulated Object Pose Estimation in Discrete State-Spaces

✇cs.AI, q-bio.NC updates on arXiv.org
By: Li Zhang · Mingyu Mei · Ailing Wang · Xianhui Meng · Yan Zhong · Xinyuan Song · Liu Liu · Rujing Wang · Zaixing He · Cewu Lu
arXiv:2602.19565v1 Announce Type: cross Abstract: Articulated object pose estimation is a core task in embodied AI. Existing methods typically regress poses in a continuous space, but often struggle with 1) navigating a large, complex search space and 2) failing to incorporate intrinsic kinematic constraints. In this work, we introduce DICArt (DIsCrete Diffusion for Articulation Pose Estimation), a novel framework that formulates pose estimation as a conditional discrete diffusion process. Instead of operating in a continuous domain, DICArt progressively denoises a noisy pose representation through a learned reverse diffusion procedure to recover the GT pose. To improve modeling fidelity, we propose a flexible flow decider that dynamically determines whether each token should be denoised or reset, effectively balancing the real and noise distributions during diffusion. Additionally, we incorporate a hierarchical kinematic coupling strategy, estimating the pose of each rigid part hierarchically to respect the object's kinematic structure. We validate DICArt on both synthetic and real-world datasets. Experimental results demonstrate its superior performance and robustness. By integrating discrete generative modeling with structural priors, DICArt offers a new paradigm for reliable category-level 6D pose estimation in complex environments.
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