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LifeFuse-Mem: Lifecycle-Aware State Fusion Against Temporary Overwriting for Long-Term Memory
Ammonium tetrathiomolybdate improves auditory and vestibular function after gentamicin exposure via the NRF2–GPX4 axis
The DreAM-plus integrative RNA switch enhances transient AAV expression and reduces side effects of gene editing
Multi-Omics and Molecular Simulation Identify KIF11 as a Candidate Direct Target of Resveratrol in Hepatocellular Carcinoma
J Hepatocell Carcinoma. 2026 Aug 26;13:615781. doi: 10.2147/JHC.S615781. eCollection 2026.
ABSTRACT
OBJECTIVE: Hepatocellular carcinoma (HCC) has poor prognosis and variable immunotherapy response. Resveratrol exhibits anti-HCC activity, but its direct targets and association with immunotherapy response are unclear. This study identifies core resveratrol targets in HCC and evaluates their prognostic and predictive value.
METHODS: Resveratrol targets were intersected with TCGA-LIHC differentially expressed genes. A prognostic risk model was built using LASSO-Cox regression. Drug-target binding was assessed by molecular dynamics simulations and qRT-PCR. Single-cell and spatial transcriptomics, cell-cell communication, and a pan-immunotherapy cohort were used to investigate KIF11. An HCC mouse model validated immunomodulatory effects via flow cytometry.
RESULTS: Thirty-four resveratrol-associated targets were identified, enriched in metabolism pathways. A nine-gene risk model showed robust prognostic performance. Resveratrol stably binds to KIF11's ATP-binding pocket. KIF11 is overexpressed in malignant hepatocytes and proliferating T cells; KIF11⁺ cells orchestrate VEGF-mediated microenvironment remodeling. High KIF11 expression correlated with poor prognosis but predicted superior survival in the immunotherapy cohort, a phenomenon attributed to the observation that KIF11-high tumors exhibit both enhanced immunogenicity and active immunosuppression. In vivo, resveratrol enhanced CD8⁺ T cell infiltration, proliferation, effector function, and central memory T cells, while reducing Tregs.
CONCLUSION: KIF11 drives HCC progression and predicts immunotherapy response. It is a candidate direct resveratrol target and a potential biomarker for patient stratification in immune checkpoint therapy, although further experimental validation is warranted.
PMID:42670538 | PMC:PMC13526380 | DOI:10.2147/JHC.S615781
Activation of methionine metabolism mediated by HNF4α confers ferroptosis resistance in hepatocellular carcinoma
Cell Death Discovery, Published online: 26 May 2026; doi:10.1038/s41420-026-03165-0
Activation of methionine metabolism mediated by HNF4α confers ferroptosis resistance in hepatocellular carcinomaFDX1 as a predictive biomarker and therapeutic target for lymph node metastasis in gastric cancer
Clin Exp Med. 2026 May 10. doi: 10.1007/s10238-026-02160-0. Online ahead of print.
ABSTRACT
The prognostic values of cuproptosis-related genes (CRGs) in gastric cancer with lymph node metastasis (GCLM), especially in the tumor immune microenvironment (TIME), remain unclear. We analyzed the expression, mutation, immunity, drug sensitivity, and prognostic value of CRGs in GCLM using TCGA and GEO cohorts. Consensus clustering was performed to identify CRG subtypes, with differences characterized by multi-omics analysis. A CRG-based prognostic risk score and immune score were constructed for individualized assessment, and the role of CRGs was validated through in vitro and in vivo experiments. Consensus clustering revealed that CRGs were significantly enriched in biological processes related to mitosis and energy metabolism, as well as in immune-related and cancer-associated pathways. Four distinct CRG subtypes were identified, showing marked differences in expression profiles, prognosis, genetic alterations, TIME, and chemotherapeutic drug sensitivity. We developed an exploratory CRG-based prognostic risk score for preliminary individualized assessment, and the functional relevance of CRGs in GCLM was further validated through in vitro experiments. Among these, FDX1, LIAS, DLAT, MTF1, and GLS were identified as key determinants of overall survival in patients with GCLM, with FDX1 emerging as a potential independent prognostic factor. Notably, upregulation of FDX1 significantly suppressed lymph node metastasis of gastric cancer cells in a mouse popliteal lymph node metastasis model. Our data uncovers FDX1 might be a potential favorable prognostic factors in GCLM patients. These findings may improve our understanding of CRGs in GCLM and provide new in-sights for assessing prognosis and developing more effective treatment strategies.
PMID:42107026 | DOI:10.1007/s10238-026-02160-0
Molecular basis for methylation-sensitive editing by Cas9
Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10384-z
ThermoCas9, a genome-editing enzyme that is sensitive to the DNA methylation status of the target locus, is characterized and shows promise for targeting hypomethylated DNA regions in cancer cells.Beyond Retrieval: Modeling Confidence Decay and Deterministic Agentic Platforms in Generative Engine Optimization
InsTraj: Instructing Diffusion Models with Travel Intentions to Generate Real-world Trajectories
InferenceEvolve: Towards Automated Causal Effect Estimators through Self-Evolving AI
Domain-Contextualized Inference: A Computable Graph Architecture for Explicit-Domain Reasoning
APPA: Adaptive Preference Pluralistic Alignment for Fair Federated RLHF of LLMs
Scalable homology detection with ERAST
Nature Biotechnology, Published online: 01 April 2026; doi:10.1038/s41587-026-03051-1
ERAST speeds up homology search and provides a vector database for 1 billion biological sequences.Pathogenesis and immune regulation of rheumatoid arthritis-associated interstitial lung disease: from basic research to clinical implications
Front Immunol. 2026 Mar 13;17:1770348. doi: 10.3389/fimmu.2026.1770348. eCollection 2026.
ABSTRACT
Interstitial lung disease (ILD) is one of the most common extra-articular manifestations of rheumatoid arthritis (RA). Some patients with RA-ILD may develop progressive pulmonary fibrosis, leading to severe impairment of lung function and respiratory failure, which impacts quality of life and can even be life-threatening. This review identified genetic susceptibility, environmental factors, and immune dysregulation as key contributors to the etiology and pathogenesis of RA-ILD. We highlight that autoantibodies, adaptive immune abnormalities, and tertiary lymphoid organ formation significantly drive pulmonary inflammation and fibrosis, while pro-inflammatory cytokines and epithelial-mesenchymal transition (EMT) further contribute to lung tissue injury. Current treatment options, including glucocorticoids, immunosuppressants, and antifibrotic agents such as nintedanib and pirfenidone, are often limited by substantial side effects. Additionally, emerging therapies like JAK inhibitors, CAR-T cells, and the upcoming phosphodiesterase-4B inhibitor, nerandomilast, show promise, but no curative treatment exists to date. Future research could focus on multi-omics technologies and conducting multicenter clinical trials to establish therapeutic targets and advance precision medicine for RA-ILD.
PMID:41909710 | PMC:PMC13021622 | DOI:10.3389/fimmu.2026.1770348
High-temperature memristors enabled by interfacial engineering
Detecting Miscitation on the Scholarly Web through LLM-Augmented Text-Rich Graph Learning
Towards AI Search Paradigm
TRIM27-controlled endothelium-derived exosomes play a central role in podocyte injury in diabetic kidney disease
Cell Death Discovery, Published online: 07 March 2026; doi:10.1038/s41420-026-02953-y
TRIM27-controlled endothelium-derived exosomes play a central role in podocyte injury in diabetic kidney disease