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Received — 15 September 2026 ⏭

Tracing and Coordinating Cross-Layer Influence for Multimodal Model Merging

✇cs.AI, q-bio.NC updates on arXiv.org
By: Pengyang Zhou · Xiaobin Tu · Zhengxi Liu · Rongkun Xue · Haochen Li · Miancan Liu · Ziyuan Chen · Yinggui Wang · Jinkui Ren · Xiantao Zhang
14 September 2026 at 12:00
arXiv:2609.12897v1 Announce Type: new Abstract: Multimodal model merging aims to consolidate task experts into a single model that retains their complementary capabilities. Most unimodal model merging methods combine expert updates within individual layers, and multimodal approaches largely follow this design. However, an expert update changes the representations passed to subsequent layers, allowing its influence to propagate across depth and affect how visual and textual information interact. When visual and language updates are combined, later updates act on inputs already modified by earlier ones, coupling their effects. This poses two challenges: (1) how to characterize the multimodal influence of individual expert updates across depth, and (2) how to jointly combine expert updates based on their multimodal influence. To address these challenges, we propose TAC-Merge for tracing and coordinating cross-layer influence in multimodal model merging. It contains two modules, i.e., multimodal influence mapping (MIM) and coupled merge control (CMC). MIM constructs graphs of update effects and uses Ricci curvature together with expert predictions to define a shared fusion objective. CMC models interactions among coefficient adjustments and jointly optimizes regional weights to synthesize one shared model. Experiments across diverse multimodal tasks demonstrate the effectiveness of TAC-Merge in consolidating complementary expert capabilities and supporting generalization to unseen tasks.

InRTL: Effective Intra-Inter Interaction Learning for Relational Tables

✇cs.AI, q-bio.NC updates on arXiv.org
By: Weichen Li · Ken Zhong · Zheng Wang · Li Pan · Jianhua Li
14 September 2026 at 12:00
arXiv:2609.12712v1 Announce Type: cross Abstract: Relational table learning has recently emerged as an important research direction for modeling multiple tables connected through primary key-foreign key (PK-FK) relationships. Despite recent advances, a principled modeling framework tailored to this task remains underexplored. In this paper, we propose Intra-Inter Relational Table Learning (InRTL), a unified framework that explicitly models dependencies both within and across relational tables. Specifically, InRTL formalizes two complementary interaction patterns: intra-table interactions, describing associations among rows within the same table, and inter-table interactions, describing dependencies between rows across PK-FK-linked tables. To model these dependencies, we develop a column-aware table encoder to generate initial row representations, followed by Transformer-based self-attention and cross-attention modules for intra-table and inter-table learning, respectively. To further improve scalability, InRTL incorporates linearized attention and heterogeneous graph neural networks to simplify the self-attention and cross-attention operations. Extensive experiments on ten datasets covering 24 real-world tasks demonstrate the effectiveness of our approach. Code is available at https://github.com/W1nterFloW/InRTL.

Behavior Quotient Learning for Low-Rank Adaptation of LLM Agents

✇cs.AI, q-bio.NC updates on arXiv.org
By: Pengyang Zhou · Xiaobin Tu · Zhengxi Liu · Rongkun Xue · Haochen Li · Miancan Liu · Ziyuan Chen · Yinggui Wang · Jinkui Ren · Xiantao Zhang
14 September 2026 at 12:00
arXiv:2609.12896v1 Announce Type: cross Abstract: LLM-based agents rely on heterogeneous interaction capabilities to accomplish complex tasks. Existing approaches often distribute these capabilities across multiple LoRA adapters, which increases adapter storage requirements and introduces routing overhead during inference. A single LoRA avoids this overhead, but learning from diverse agent trajectories under a fixed rank budget presents two challenges. First, trajectories with different interaction traces and parameter gradients can induce equivalent changes in decision distributions, causing repeated updates to overemphasize redundant behavioral changes. Second, an aggregated update may exceed the rank budget of the adapter, and approximating it in weight space can distort the decision changes that it is intended to produce. We propose BQ-LoRA, a low-rank adaptation framework that organizes trajectory updates through a local behavior quotient manifold. It contains two modules, i.e., behavior quotient balancing (BQB) and decision preserving compression (DPC). BQB constructs the quotient manifold from decision distributions and reweights trajectory update directions according to their local density in the quotient tangent space. DPC projects the balanced gradient onto the intrinsic fixed rank tangent space and refactorizes the resulting target by jointly controlling effective weight error and distortion of decision distributions. Experiments on AppWorld and BrowseComp-Plus compare BQ-LoRA with standard LoRA and recent low-rank adaptation methods, while separate ablations evaluate the complementary contributions of both components.

CLAP: Cross-Embodiment Video World Models are Zero-Shot Physical Simulators

✇cs.AI, q-bio.NC updates on arXiv.org
By: Kechen Liu · Ola Shorinwa
14 September 2026 at 12:00
arXiv:2608.27406v2 Announce Type: replace-cross Abstract: State-of-the-art action-conditioned video models are typically restricted to a single robot embodiment, preventing them from leveraging the vast corpus of heterogeneous video data that contains rich signals for learning generalizable physics. To bridge this gap, we introduce CLAP, a framework for cross-embodiment action-conditioned video generation capable of being trained on diverse, internet-scale videos across human and robotic agents. CLAP is grounded in the insight that universal physical laws govern spatiotemporal dynamics regardless of the actor. However, cross-embodiment learning is non-trivial because action representations vary sharply across robot platforms and are typically absent in human videos. CLAP addresses this fundamental challenge through the following core contributions. First, CLAP reconciles disparate action spaces using end-effector poses, language instructions, and latent actions. Second, to resolve their individual limitations, CLAP introduces a curriculum-based cross-embodiment learning recipe that first learns foundational physical priors across unlabeled video data using latent actions and subsequently grounds them in end-effector action spaces for zero-shot deployment to real-world tasks. Crucially, CLAP approaches or surpasses state-of-the-art single-embodiment video models in challenging environments like DROID. These performance advantages compound via few-shot adaptation to establish a novel paradigm for training single-embodiment video world models. Ultimately, CLAP delivers the most comprehensive suite of action-conditioned video world models to date - spanning diverse action-conditioning spaces (end-effector, language, and latent) and robot morphologies (including cross-embodiment, DROID, Bridge, bimanual YAM robots, and G1 humanoids). We open-source all code and models. Project Website at https://omni-clap.github.io .
Received — 10 September 2026 ⏭

Adaptive Entangled Game Modules in Artificial General Intelligence

✇cs.AI, q-bio.NC updates on arXiv.org
By: Haochen Li · Xinshuai Guo · Jingdong Ouyang · Wei Zhang · Leilei Shi
10 September 2026 at 12:00
arXiv:2609.09226v1 Announce Type: new Abstract: We introduce a probability-wave framework for modeling the collective behavior of interacting adaptive agents, deriving testable eigenmodes through a generalized behavioral intelligence (GBI) nonlocal probability-wave equation. This framework captures a broad range of human intelligence behaviors with analytical mechanisms and offers an indirect method to examine the Liu-Chen-Ao (LCA) hypothesis of nonlocal entangled nerve fibers in the brain through collective trader behaviors. Our empirical analysis of Chinese intraday stock market data demonstrates that adaptive entangled game modes explain 82-94% (89% overall) of observed decision patterns, a sharp contrast to the predictions of neoclassical finance based on independent rational agents. Moreover, 2-12% of behaviors show adaption to intraday news, events, and environments, characterized by dual equilibrium states and abrupt reference point shifts, while purely independent modes occur in less than 5% of cases. These findings empirically support the LCA hypothesis, as observable trading behaviors reflect underlying brain mechanisms and internal intelligence decision-making in behavioral psychology. Our results highlight the necessity of incorporating adaptive entangled game modules into artificial general intelligence (AGI) architectures, addressing the limitations of conventional artificial neural network (ANN)-based AI, which relies on trillions of opaque parameters. By integrating ANN-based AI with probability-wave-based entangled-brain simulations, machine learning can enrich AGI foundation models (FMs) and facilitate the development of human-like processing units (HPUs) that leverage brain-inspired mechanisms. Such HPUs may ultimately create more compact, efficient, and robust AGI systems, particularly for embodied intelligence and robotics.

What Should an Agent Forget? Separating What Is Stored from What Is Used

✇cs.AI, q-bio.NC updates on arXiv.org
By: Yuhang Li · Yuchen Li
10 September 2026 at 12:00
arXiv:2609.10263v1 Announce Type: new Abstract: Persistent language agents need stored experience to remain available across time, while each answer requires evidence suited to a particular question. A superseded fact can mislead a current-state answer and still be essential for a historical query. We present RD-Forget, a training-free framework that separates what an agent stores from what it uses. A retained source archive preserves observations, and a query-conditioned memory view controls their influence on the current answer. A frozen language-model curator extracts relevant evidence, groups facts into semantic slots, and preserves the relations needed for multi-hop reasoning. Same-slot replacement links suppress superseded values in current-state contexts, while intent-aware retrieval makes earlier evidence eligible again. A rate-distortion formulation guides construction of the answer-time view within a memory budget. Experiments span conversational memory, knowledge updating, fact consolidation, long-context reasoning, and personalization under a shared answering pipeline. The results associate accurate answers with both query-relevant evidence construction and control over obsolete alternatives. Configurations without forgetting or query conditioning have the largest score deficits, while slot grouping, historical access, and relation preservation contribute complementary functions. Retaining history while selectively controlling its use offers a practical way to accommodate changing facts and future questions.

EEGBind: Detecting Source-Level Interictal Epileptiform Discharges via EEG-Centric Multimodal Binding

✇cs.AI, q-bio.NC updates on arXiv.org
By: Muchen Li · Anglin Liu · Xuetian Gao · Ruijian Xu · Jintai Chen
10 September 2026 at 12:00
arXiv:2609.09728v1 Announce Type: cross Abstract: Source-level analysis of interictal epileptiform discharges (IEDs) is relevant to presurgical evaluation and treatment planning because it helps characterize where epileptiform activity is likely to arise. Beyond detecting whether an IED is present, this setting requires assigning IED-positive activity to clinically meaningful brain-region categories. This setting is challenging because source-region evidence in short electroencephalography (EEG) windows can be subtle, partial, and affected by subject variability, class imbalance, and imperfect multimodal context. We present EEGBind, an EEG-centric multimodal binding framework for five-class source-level IED classification. EEGBind treats EEG as the primary modality and binds synchronized video-context features around an EEG-centric representation. Instead of relying on early or overly strong multimodal fusion, which may perturb the source-sensitive EEG representation, EEGBind uses video context as auxiliary evidence for robust classification. A view-consistent repair stage is further used to improve hidden-set robustness while preserving the learned source-class boundary. On the NeuroMM 2026 Grand Challenge Track 3 NMM-Source-IED benchmark, EEGBind achieves 0.8395 on weighted-F1 and outperforms strong competitors. These results support EEG-centric multimodal binding as a practical strategy for source-level IED classification. The open-source code is available at https://github.com/HKUSTGZ-ML4Health-Lab/NeuroMM2026_IED_Detection.

Genomics and social practices at Mogou and other Gansu sites during prehistoric trans-Eurasian exchange

✇Cell
By: Han Shi · E. Andrew Bennett · Guoke Chen · Hui Wang · Tianyi Wang · Peng Cao · Ruilin Mao · Fan Bai · Qingyan Dai · Feng Liu · Xiaotian Feng · Yongan Wang · Chong Yao · Jing Wu · Wenjun Wang · Ming Zhang · Tianxiang Liu · Jingkun Ran · Yue-Chen Liu · Yuan Liu · Dan Ju · Chuyan Li · Hongwei Hou · Xinyi Liu · Qiaomei Fu
3 September 2026 at 08:00
Ancient DNA from 149 individuals at 11 sites in Gansu, China, dated to around 4,700–3,000 years ago, reveals human population history during early transcontinental exchanges of agriculture and technology, as well as contemporary social practices, at the large Mogou cemetery.

Macrophage spatiotemporal plasticity in pulmonary diseases: decoding the niche at single-cell resolution

✇Pulmonary nodule
By: Chenchen Lin · Shaohui Huang · Li Yang · Ziqi Wang · Huanhuan Zhou · Quncheng Zhang · Xiaoju Zhang
3 July 2026 at 18:00

Front Immunol. 2026 Jun 18;17:1855906. doi: 10.3389/fimmu.2026.1855906. eCollection 2026.

ABSTRACT

Pulmonary gas exchange and host defense depend on the dynamic coordination of resident and recruited macrophage populations. Historically, macrophage functions have often been interpreted through the classic M1/M2 dichotomy; however, this binary framework does not capture the heterogeneity and context-dependent plasticity of macrophage states within the lung microenvironment. Advances in single-cell RNA sequencing and spatial multi-omics have substantially refined our understanding of this complex macrophage network. Here, we synthesize evidence from human studies and experimental models to summarize macrophage functional states in homeostasis and across chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, pulmonary hypertension, acute lung injury/acute respiratory distress syndrome, and lung cancer. We highlight how macrophage transcriptional programs are shaped by ontogeny, tissue niche, and epigenetic-metabolic regulation, and how these programs are linked to disease-specific remodeling of the pulmonary microenvironment. Across diverse respiratory diseases, persistent tissue injury and microenvironmental stress remodel resident macrophage programs and are frequently accompanied by the expansion and context-dependent differentiation of recruited monocyte-derived macrophages. These macrophage states are associated with inflammatory amplification, epithelial and endothelial barrier dysfunction, extracellular matrix remodeling, and tumor immune evasion. Ligand-receptor and spatial analyses further identify candidate communication axes linking macrophages with stromal, epithelial, endothelial, and immune cells, some of which appear partially conserved across disease contexts. Emerging macrophage-targeted strategies are increasingly being explored beyond broad depletion, with growing interest in context-specific reprogramming and niche modulation, including antibody-based, nanocarrier-mediated, and engineered-cell approaches. Decoding the spatiotemporal trajectories and cell-cell communication networks of specific macrophage subsets, while considering tissue context, species differences, and levels of experimental support, may help clarify mechanisms of tissue remodeling, therapeutic resistance, and macrophage-targeted intervention in complex pulmonary diseases.

PMID:42396453 | PMC:PMC13322945 | DOI:10.3389/fimmu.2026.1855906

Received — 27 May 2026 ⏭

A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development

✇(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Qian Tang · Chen Lian · Xinyan Han · Xuhan Zhang · Zihan Wang · Boyu Wang · Taoyu Zhu · Xinrui Lin · Xiaolei Wang · Yaping Xu · Manyu Xiao · Zijin Wang · Junming Li · Silin Chen · Yunze Wang · Yufei Liu · Songsong Li · Zuolin Shen · Xi Lu · Xueqi Han · Yilu Zhou · Mingyang Xiao · Jiayi Ran · Xiaoran Cao · Xinyi Xu · Hugo Sámano-Sánchez · Alfredo Rodríguez · Lian Wang · Shuifang Chen · Zhanyu Xu · Shirong Zhang · Nuo Yang · Yong Tang · Jian Liu
26 May 2026 at 18:00

Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.

ABSTRACT

Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development.

PMID:42189071 | DOI:10.1002/advs.75839

A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development

✇Omics In Lung
By: Qian Tang · Chen Lian · Xinyan Han · Xuhan Zhang · Zihan Wang · Boyu Wang · Taoyu Zhu · Xinrui Lin · Xiaolei Wang · Yaping Xu · Manyu Xiao · Zijin Wang · Junming Li · Silin Chen · Yunze Wang · Yufei Liu · Songsong Li · Zuolin Shen · Xi Lu · Xueqi Han · Yilu Zhou · Mingyang Xiao · Jiayi Ran · Xiaoran Cao · Xinyi Xu · Hugo Sámano-Sánchez · Alfredo Rodríguez · Lian Wang · Shuifang Chen · Zhanyu Xu · Shirong Zhang · Nuo Yang · Yong Tang · Jian Liu
26 May 2026 at 18:00

Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.

ABSTRACT

Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development.

PMID:42189071 | DOI:10.1002/advs.75839

Low-Cost Labels, Reliable Choices: Rollout-Calibrated Hyper-Heuristics for Job Shop Scheduling

✇cs.AI, q-bio.NC updates on arXiv.org
By: Junhao Wei · Yanxiao Li · Yifu Zhao · Zhenhong Peng · Baili Lu · Dexing Yao · Haochen Li · Qinbin He · Sio-Kei Im · Yapeng Wang · Xu Yang
26 May 2026 at 12:00
arXiv:2605.23957v1 Announce Type: new Abstract: Learning-assisted hyper-heuristics can select among dispatching rules while preserving the feasibility and interpretability of constructive Job Shop Scheduling Problem (JSSP) heuristics. Their main computational cost lies in label generation rather than model fitting, since each supervised label usually requires rolling out candidate rules from a partial schedule. We study this label-cost problem together with a reliability problem: a learned selector should not switch away from a strong default rule unless the predicted gain is credible. The proposed selector uses regret-normalized rollout labels, a contextual KNN uncertainty estimate, and a gate that acts only when the predicted improvement exceeds an uncertainty-adjusted margin. We also vary rollout depth and breadth to measure the cost-quality trade-off. On synthetic JSSP instances, the gated selector achieves the lowest mean RPD among learned selectors, remains close to the best fixed dispatching rule, and reduces Random-HH mean RPD by more than an order of magnitude.

MobileGym: A Verifiable and Highly Parallel Simulation Platform for Mobile GUI Agent Research

✇cs.AI, q-bio.NC updates on arXiv.org
By: Dingbang Wu · Rui Hao · Haiyang Wang · Shuzhe Wu · Han Xiao · Zhenghong Li · Bojiang Zhou · Zheng Ju · Zichen Liu · Lue Fan · Zhaoxiang Zhang
26 May 2026 at 12:00
arXiv:2605.26114v1 Announce Type: new Abstract: We present MobileGym, a browser-hosted, lightweight, fully controllable environment for everyday mobile use, targeting interaction fidelity without replicating proprietary backends. It enables two capabilities previously out of reach for everyday apps: verifiable outcome signals through deterministic state-based judging over structured JSON state, and scalable online RL through low-cost parallel rollouts. The full environment state is captured, configured, forked, and compared as structured JSON, and a single server can host hundreds of parallel instances, with about 400 MB memory per instance and about 3 s cold start. A layered state model and a declarative task-definition framework keep state programmability and task creation practical at scale, and a single programmatic judging mechanism delivers both deterministic evaluation verdicts and dense RL rewards. The accompanying MobileGym-Bench provides 416 parameterized task templates, including 256 test and 160 train templates, over 28 apps, with deterministic judges and a structured AnswerSheet protocol that avoids free-text matching failures. In a Sim-to-Real case study, GRPO on Qwen3-VL-4B-Instruct gains +12.8 percentage points on the 256-task test set, and on a 59-task real-device signal subset, real-device execution retains 95.1% of the simulation-side training gain. Project page: https://mobilegym.github.io.

Turning Stale Gradients into Stable Gradients: Coherent Coordinate Descent with Implicit Landscape Smoothing for Lightweight Zeroth-Order Optimization

✇cs.AI, q-bio.NC updates on arXiv.org
By: Chen Liang · Xiatao Sun · Qian Wang · Daniel Rakita
26 May 2026 at 12:00
arXiv:2605.14373v2 Announce Type: replace-cross Abstract: Zeroth-Order (ZO) optimization is pivotal for scenarios where backpropagation is unavailable, such as memory-constrained on-device learning and black-box optimization. However, existing methods face a stark trade-off: they are either sample-inefficient (e.g., standard finite differences) or suffer from high variance due to randomized estimation (e.g., random subspace methods). In this work, we propose Coherent Coordinate Descent (CoCD), a deterministic, sample-efficient, and budget-aware ZO optimizer. Theoretically, we formalize the notion of gradient coherence and demonstrate that CoCD is equivalent to Block Cyclic Coordinate Descent (BCCD) with ``warm starts,'' effectively converting historical (stale) gradients from a liability into a computational asset. This mechanism enables $O(1)$ query complexity per step while maintaining global descent directions. Furthermore, we derive error bounds revealing a counter-intuitive insight: larger finite-difference step sizes can induce an implicit smoothing effect on the optimization landscape by reducing the effective smoothness constant, thereby improving convergence stability. Experiments on MLP, CNN, and ResNet architectures (up to 270k parameters) demonstrate that CoCD significantly outperforms BCCD in terms of sample efficiency and convergence loss/accuracy, and exhibits superior stability over randomized ZO methods. Our results suggest that deterministic, structure-aware updates offer a superior alternative to randomization for lightweight ZO optimization.

AnyMo: Geometry-Aware Setup-Agnostic Modeling of Human Motion in the Wild

✇cs.AI, q-bio.NC updates on arXiv.org
By: Baiyu Chen · Zechen Li · Wilson Wongso · Lihuan Li · Xiachong Lin · Hao Xue · Benjamin Tag · Flora Salim
26 May 2026 at 12:00
arXiv:2605.22715v2 Announce Type: replace-cross Abstract: As wearable and mobile devices become increasingly embedded in daily life, they offer a practical way to continuously sense human motion in the wild. But inertial signals are highly dependent on the sensing setup, including body location, mounting position, sensor orientation, device hardware, and sampling protocol. This setup dependence makes it difficult to learn motion representations that transfer across devices and datasets, and limits the broader use of wearable IMUs beyond closed-set recognition. We introduce AnyMo, a geometry-aware framework for setup-agnostic human motion modeling. AnyMo uses physics-grounded IMU simulation over dense body-surface placements to generate diverse and plausible synthetic signals, pre-trains a graph encoder from paired synthetic placement views and masked partial observations, tokenizes multi-position IMU into full-body motion tokens, and aligns these tokens with an LLM for motion-language understanding. We evaluate AnyMo on three complementary tasks: zero-shot activity recognition across 14 unseen downstream datasets, cross-modal retrieval, and wearable IMU motion captioning, where it improves average Accuracy/F1/R@2 by 11.7\%/11.6\%/22.6\% on HAR, increases zero-shot IMU-to-text and text-to-IMU retrieval MRR by 15.9\% and 28.6\%, respectively, and improves zero-shot captioning BERT-F1 by 18.8\%. These results support AnyMo as a generalist model for wearable motion understanding in the wild. Project page: https://baiyuchen.com/project/AnyMo.

Cuproptosis causes meiotic metaphase I arrest by disrupting mitochondrial functions in oocytes

✇Cell Death Discovery nature.com science feeds
By: You-Hui Lu · Can Wang · Lei-Ning Chen · Li-Tao Yi · Ke Xu · Xu-Feng Li · Shu-Chen Liu · Xiao-Yi Chen · Yi-Xiao Li · Qing-Yuan Sun · Qiong Wang · Tie-Gang Meng
23 May 2026 at 08:00

Cell Death Discovery, Published online: 23 May 2026; doi:10.1038/s41420-026-03168-x

Cuproptosis causes meiotic metaphase I arrest by disrupting mitochondrial functions in oocytes

High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications

✇(Multiomics OR Omics) AND (Pancreatic)
By: Ke Xiao · Lin Gu · Jiayi Ma · Shanjie Rong · Xiongtao Yue · Yuechen Liu · Shiwei Liu · Fei Sun · Shu Zhang · Congyi Wang
19 May 2026 at 18:00

Chin Med J (Engl). 2026 May 19. doi: 10.1097/CM9.0000000000004098. Online ahead of print.

ABSTRACT

High-salt diet (HSD) has emerged as a prevalent environmental factor that exacerbates chronic inflammation and insulin resistance in obesity-associated type 2 diabetes (T2D) by modulating macrophage polarization, metabolic reprogramming, and epigenetic imprinting. Current evidence demonstrates that HSD activates p38/mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathways, by which it drives macrophage polarization toward a proinflammatory M1 phenotype while inducing a glycolysis-dominant metabolic shift, thereby establishing a persistent "metabolic memory". Moreover, HSD orchestrates metabolic memory in macrophages through coordinated epigenetic machinery, including histone modifications (Trimethylation of histone H3 at lysine 4 [H3K4me3] and Acetylation of histone H3 at lysine 27 [H3K27ac]), DNA methylation, and noncoding RNAs (e.g., long non-coding RNA MALAT1 and miR-155), leading to sustained inflammatory phenotypes. In multiple metabolic organs (e.g., adipose tissue, liver, pancreas, and gut), the HSD-macrophage axis aggravates systemic insulin resistance through shared proinflammatory signaling and other tissue-specific mechanisms. Most importantly, therapeutic strategies targeting the NLRP3 inflammasome, metabolic pathways, and epigenetic alterations offer novel approaches for managing metabolic inflammation. Future investigations are encouraged to leverage lineage tracing, single-cell sequencing, and spatial multi-omics technologies to advance the development of precision medicine for macrophage-associated metabolic disorders.

PMID:42156155 | DOI:10.1097/CM9.0000000000004098

The 2025 lung cancer landscape: advances in screening, molecular taxonomy and therapeutic strategy: a narrative review

✇Pulmonary nodule
By: Wenhai Fu · Xusen Zou · Tianrui He · Qi Cai · Peiling Chen · Bo Cheng · Yi Feng · Caichen Li · Feng Li · Jianfu Li · Huiting Wang · Shan Xiong · Wenjun Ye · Xin Zheng · Jianxing He · Wenhua Liang
15 April 2026 at 18:00

Transl Lung Cancer Res. 2026 Mar 23;15(3):62. doi: 10.21037/tlcr-2025-1-1477. Epub 2026 Mar 18.

ABSTRACT

BACKGROUND AND OBJECTIVE: In 2025, lung cancer research advanced rapidly across the disease continuum, from population-level risk assessment and screening to mechanistic studies of early carcinogenesis and therapeutic innovation in perioperative and metastatic settings. A key shift moved beyond a smoking-centred paradigm toward a multidimensional risk framework reflecting the growing burden among never-smokers and the roles of air pollution, occupational exposures, and systemic metabolic-inflammatory states. This narrative review aims to synthesize influential 2025 evidence across prevention, diagnosis, treatment, and survivorship, and to identify convergent themes and translational gaps relevant to clinical practice and policy.

METHODS: We performed a narrative synthesis of influential lung cancer studies published in major international journals in 2025. Evidence was organized along a clinically oriented pathway spanning carcinogenesis and screening, precision diagnosis, treatment optimization in resectable and advanced disease, and survivorship, emphasizing practice-informing trials, high-impact translational research, and implementation-relevant technologies.

KEY CONTENT AND FINDINGS: Lineage tracing, single-cell and spatial omics, and evolutionary inference refined concepts of field cancerization, clonal selection, and copy-number-driven fitness. In small-cell lung cancer, evidence further supported neuronal coupling and synapse-like programs as potentially tractable vulnerabilities. Clinically, low-dose computed tomography (CT) strategies and data-informed nodule thresholds aimed to balance under-detection against over-surveillance harms. In diagnostics, artificial intelligence (AI) models increasingly inferred molecular features from routine histopathology ("virtual molecular testing") and should be regarded as decision support requiring prospective validation, population calibration, and explicit failure-mode reporting. Multimodal approaches integrating imaging with circulating tumor DNA (ctDNA) improved feasibility in tissue-limited settings, but clinical utility remains contingent on assay standardization and pathway-level implementation. In resectable disease, longer follow-up consolidated neoadjuvant chemo-immunotherapy for selected patients, while ctDNA kinetics emerged as a candidate biomarker for response-adaptive escalation and de-escalation. In advanced non-small cell lung cancer (NSCLC), phase III evidence for antibody-drug conjugates and bispecific antibodies began reshaping sequencing, while highlighting challenges in toxicity, access, affordability, and immature overall survival in several programs.

CONCLUSIONS: The 2025 landscape reflects coordinated progress in risk conceptualization, biology, diagnostics, and therapeutics, yet gaps in validation, standardization, and real-world deliverability persist. Priorities include prospective evaluation of AI- and ctDNA-enabled pathways, toxicity-informed sequencing, and equitable implementation aligned with health-system capacity.

PMID:41982682 | PMC:PMC13071762 | DOI:10.21037/tlcr-2025-1-1477

Integrative fragmentomic and mutational signature profile of plasma cfDNA for early lung cancer detection

✇Omics In Lung
By: Jianxing He · Huiting Wang · Yi Feng · Jianfu Li · Peiling Chen · Xin Zheng · Wenhai Fu · Caichen Li · Hua Bao · Song Wang · Shuang Chang · Dongqin Zhu · Shanshan Yang · Yang Shao · Wen Zhong · Weisheng Guo · Rong Yin · Wenhua Liang
15 April 2026 at 18:00

NPJ Precis Oncol. 2026 Apr 15. doi: 10.1038/s41698-026-01416-y. Online ahead of print.

ABSTRACT

Detecting lung cancer effectively in the general population is essential for optimizing treatment outcomes and improving the 5-year survival rate. While low-dose computed tomography (LDCT) is the current standard, it has limitations in broader populations. We developed a blood-based multi-omics model using whole-genome cell-free DNA (cfDNA) features to distinguish lung cancer from non-cancer individuals. This study included 1600 patients and an equal number of non-cancer controls, divided into training and validation cohorts. The model achieved an area under the curve (AUC) of 95.59% for the training cohort and 95.74% for the validation cohort. The model consistently performed well across various cancer stages and histological subtypes. To further validate the performance of the model, an external validation cohort was utilized. Notably, it also effectively differentiated non-cancer samples from cancer samples in the external validation cohort, with 85.9% sensitivity and 94.78% specificity. Importantly, in simulated population screenings, our ctDNA assay outperformed both LDCT and a previously established method. This suggests its potential utility in wider lung cancer screening programs, possibly complementing the LDCT approach. In conclusion, our ctDNA assay emerges as a promising and highly sensitive tool for the early detection and categorization of lung cancer.

PMID:41986614 | DOI:10.1038/s41698-026-01416-y

Received — 8 April 2026 ⏭

A Multimodal Foundation Model of Spatial Transcriptomics and Histology for Biological Discovery and Clinical Prediction

✇cs.AI, q-bio.NC updates on arXiv.org
By: Jinxi Xiang · Siyu Hou · Yuchen Li · Ryan Quinton · Xiaoming Zhang · Feyisope Eweje · Xiangde Luo · Yijiang Chen · Zhe Li · Colin Bergstrom · Ted Kim · Sierra Willens · Francesca Maria Olguin · Matthew Abikenari · Andrew Heider · Sanjeeth Rajaram · Joel Neal · Maximilian Diehn · Xiang Zhou · Ruijiang Li
7 April 2026 at 12:00
arXiv:2604.03630v1 Announce Type: new Abstract: Spatial transcriptomics (ST) enables gene expression mapping within anatomical context but remains costly and low-throughput. Hematoxylin and eosin (H\&E) staining offers rich morphology yet lacks molecular resolution. We present \textbf{\ours} (\textbf{S}patial \textbf{T}ranscriptomics and hist\textbf{O}logy \textbf{R}epresentation \textbf{M}odel), a foundation model trained on 1.2 million spatially resolved transcriptomic profiles with matched histology across 18 organs. Using a hierarchical architecture integrating morphological features, gene expression, and spatial context, STORM bridges imaging and omics through robust molecular--morphological representations. STORM enhances spatial domain discovery, producing biologically coherent tissue maps, and outperforms existing methods in predicting spatial gene expression from H\&E images across 11 tumor types. The model is platform-agnostic, performing consistently across Visium, Xenium, Visium HD, and CosMx. Applied to 23 independent cohorts comprising 7,245 patients, STORM significantly improves immunotherapy response prediction and prognostication over established biomarkers, providing a scalable framework for spatially informed discovery and clinical precision medicine.
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