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Cell
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An activated wheat CCG10-NLR immune receptor forms an octameric resistosome
An activated CCG10-NLR WAI3 plant immune receptor forms an octameric resistosome, which induces calcium influx and immune responses through a unique channel architecture.
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Genetic mutation and dysfunction of AT2 cells drive B(a)P/LPS-induced inflammation-related lung tumorigenesis: evidence and mechanism of autophagy
Acta Biochim Biophys Sin (Shanghai). 2026 Mar 25. doi: 10.3724/abbs.2025238. Online ahead of print.ABSTRACTThe environmental pollutant benzo(a)pyrene (B(a)P), a representative polycyclic aromatic hydrocarbon (PAH), is a recognized carcinogen, and chronic pulmonary inflammation is closely associated with lung carcinogenesis. Although alveolar type 2 (AT2) cells are the origin of lung adenocarcinoma, the genetic and functional changes in AT2 cells and the mechanisms involved in inflammation-relate
Genetic mutation and dysfunction of AT2 cells drive B(a)P/LPS-induced inflammation-related lung tumorigenesis: evidence and mechanism of autophagy
Acta Biochim Biophys Sin (Shanghai). 2026 Mar 25. doi: 10.3724/abbs.2025238. Online ahead of print.
ABSTRACT
The environmental pollutant benzo(a)pyrene (B(a)P), a representative polycyclic aromatic hydrocarbon (PAH), is a recognized carcinogen, and chronic pulmonary inflammation is closely associated with lung carcinogenesis. Although alveolar type 2 (AT2) cells are the origin of lung adenocarcinoma, the genetic and functional changes in AT2 cells and the mechanisms involved in inflammation-related lung tumorigenesis have not been elucidated. Here, C57BL/6J mice are exposed to B(a)P and the inflammatory irritant lipopolysaccharide (LPS) to establish a model of inflammation-related lung tumorigenesis. Single-cell RNA sequencing is performed on lung tissues. DNA mutations in AT2 cells are analyzed via whole-exome sequencing. The protein expression of AT2 cells in lung cancer tissue is determined by immunofluorescence staining. The results reveal that LPS promotes B(a)P-induced lung tumorigenesis; in the whole lungs of B(a)P/LPS, a decreased proportion, altered differentiation trajectory, and increased gene mutation number in AT2 cells are observed. Additionally, in B(a)P/LPS-treated lung cancer tissue, the levels of γ-H2AX DNA damage and the proliferation marker Ki67 in AT2 cells are increased, whereas the levels of differentiation markers are decreased. Single-cell RNA transcriptomics reveals that the autophagy-related genes Foxo3 and Ppp2r5, which are enriched in the PI3K-Akt pathway, and the autophagy-related genes in AT2 cells in lung cancer are decreased in the B(a)P/LPS group. Thus, chronic inflammation promotes DNA damage, gene mutation and dysfunction in AT2 cells, and decreased autophagy in AT2 cells may be an important mechanism for inflammation-related lung tumorigenesis.
PMID:41952558 | DOI:10.3724/abbs.2025238
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cs.AI, q-bio.NC updates on arXiv.org
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Multimodal Continual Learning with MLLMs from Multi-scenario Perspectives
arXiv:2511.18507v3 Announce Type: replace-cross Abstract: Multimodal large language models (MLLMs) deployed on devices must adapt to continuously changing visual scenarios such as variations in background and perspective, to effectively perform complex visual tasks. To investigate catastrophic forgetting under real-world scenario shifts, we construct a multimodal visual understanding dataset (MSVQA), covering four distinct scenarios and perspectives: high-altitude, underwater, low-altitude, and
Multimodal Continual Learning with MLLMs from Multi-scenario Perspectives
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cs.AI, q-bio.NC updates on arXiv.org
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Silent Inconsistency in Data-Parallel Full Fine-Tuning: Diagnosing Worker-Level Optimization Misalignment
arXiv:2602.14462v1 Announce Type: cross Abstract: Data-parallel (DP) training with synchronous all-reduce is a dominant paradigm for full-parameter fine-tuning of large language models (LLMs). While parameter synchronization guarantees numerical equivalence of model weights after each iteration, it does not necessarily imply alignment of worker-level optimization dynamics before gradient aggregation. This paper identifies and studies this latent mismatch, termed \emph{silent inconsistency}, whe