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Profiling-Driven Adaptive Distributed Transformer Inference on Embedded Edge Deployment
AgentArk: Distilling Multi-Agent Intelligence into a Single LLM Agent
Safety in Embodied AI: A Survey of Risks, Attacks, and Defenses
PRXL2B facilitates the progression of hepatocellular carcinoma and the therapeutic efficacy of oncolytic adenovirus H101 through the PI3K/AKT/PD-L1 axis
Biosci Trends. 2026 May 21. doi: 10.5582/bst.2026.01000. Online ahead of print.
ABSTRACT
Oncolytic adenovirus H101 has shown antitumor activity in hepatocellular carcinoma (HCC), but the molecular determinants of treatment response remain unclear. In this study, a Hepa1-6 subcutaneous tumor model was established in C57BL/6 mice and treated with intratumoral H101, followed by integrated transcriptomic and proteomic analyses to identify candidate genes associated with H101 response. PRXL2B was selected for further investigation using public multi-omics datasets, tissue microarray-based immunohistochemistry, in vitro functional assays, mechanistic analyses, and in vivo validation experiments. Integrated multi-omics analyses identified PRXL2B as a candidate gene downregulated after H101 treatment. Public datasets and tissue-based validation further showed that PRXL2B was upregulated in HCC tissues. In MHCC97H and HCCLM3 cells, PRXL2B knockdown inhibited proliferation, migration, and invasion, promoted apoptosis and cell-cycle arrest, and enhanced the antitumor effect of H101. Mechanistically, PRXL2B silencing reduced AKT phosphorylation and PD-L1 expression. In vivo, PRXL2B knockdown suppressed tumor growth, and the combination of PRXL2B knockdown and H101 produced the strongest antitumor effect. These findings indicate that PRXL2B promotes malignant phenotypes in HCC and may modulate H101 efficacy through the PI3K/AKT/PD-L1 axis. Targeting PRXL2B may therefore represent a potential strategy to enhance the therapeutic efficacy of oncolytic virus therapy in HCC.
PMID:42161529 | DOI:10.5582/bst.2026.01000
High-throughput strategy for targeting MDM2 in uveal melanoma to reverse radiation therapy resistance
Cell Death Discovery, Published online: 11 April 2026; doi:10.1038/s41420-026-02970-x
High-throughput strategy for targeting MDM2 in uveal melanoma to reverse radiation therapy resistanceGA-GS: Generation-Assisted Gaussian Splatting for Static Scene Reconstruction
Protective Effects of the Ethyl Acetate Fraction from Madeng'ai on Lipopolysaccharide-Induced Acute Lung Injury in Mice: Insights from Integrated Multi-Omics Analysis
J Ethnopharmacol. 2026 Apr 4:121650. doi: 10.1016/j.jep.2026.121650. Online ahead of print.
ABSTRACT
ETHNOPHARMACOLOGICAL RELEVANCE: Madeng'ai (MDA) is a traditional medicinal plant of the Dong ethnic group. Its roots have been widely used in folk medicine for clearing heat and removing toxins, alleviating swelling and relieving pain, dispersing blood stasis and arresting bleeding, as well as promoting wound healing. It is taxonomically classified as a variety of Potentilla freyniana Bornm.
AIM OF THE STUDY: Acute lung injury (ALI) is a life-threatening pulmonary disorder associated with high mortality, underscoring the urgent need to explore novel therapeutic strategies. This study aimed to evaluate the protective effects of the ethyl acetate fraction of MDA (MEA) against LPS-induced ALI in mice and to investigate its underlying mechanisms.
MATERIALS AND METHODS: LC-MS/MS was employed to tentatively identify the bioactive components of MEA. A mouse model of ALI was established by LPS induction. The protective effects of MEA were evaluated through assessments of lung histopathology, inflammatory cytokine levels, and oxidative stress markers. The underlying mechanisms were systematically investigated by integrating transcriptomics, metabolomics, network pharmacology, molecular docking, and Western blotting.
RESULTS: MEA significantly attenuated LPS-induced pulmonary pathological lesions, pulmonary edema, and excessive inflammatory responses in ALI mice. Comprehensive bioinformatics analyses predicted potential mechanisms involving oxidative stress and the regulation of metabolic pathways. Experimental validation via Western blotting confirmed that MEA inhibited TLR4-mediated inflammatory signaling and modulated the PI3K/AKT pathway, thereby exerting multi-pathway protective effects against ALI.
CONCLUSIONS: Collectively, this study confirms that MEA, as a traditional herbal extract, holds potential as an adjuvant therapeutic agent for ALI, providing experimental evidence for the modernization and development of ethnic medicines.
PMID:41941987 | DOI:10.1016/j.jep.2026.121650
Protective Effects of the Ethyl Acetate Fraction from Madeng'ai on Lipopolysaccharide-Induced Acute Lung Injury in Mice: Insights from Integrated Multi-Omics Analysis
J Ethnopharmacol. 2026 Apr 4:121650. doi: 10.1016/j.jep.2026.121650. Online ahead of print.
ABSTRACT
ETHNOPHARMACOLOGICAL RELEVANCE: Madeng'ai (MDA) is a traditional medicinal plant of the Dong ethnic group. Its roots have been widely used in folk medicine for clearing heat and removing toxins, alleviating swelling and relieving pain, dispersing blood stasis and arresting bleeding, as well as promoting wound healing. It is taxonomically classified as a variety of Potentilla freyniana Bornm.
AIM OF THE STUDY: Acute lung injury (ALI) is a life-threatening pulmonary disorder associated with high mortality, underscoring the urgent need to explore novel therapeutic strategies. This study aimed to evaluate the protective effects of the ethyl acetate fraction of MDA (MEA) against LPS-induced ALI in mice and to investigate its underlying mechanisms.
MATERIALS AND METHODS: LC-MS/MS was employed to tentatively identify the bioactive components of MEA. A mouse model of ALI was established by LPS induction. The protective effects of MEA were evaluated through assessments of lung histopathology, inflammatory cytokine levels, and oxidative stress markers. The underlying mechanisms were systematically investigated by integrating transcriptomics, metabolomics, network pharmacology, molecular docking, and Western blotting.
RESULTS: MEA significantly attenuated LPS-induced pulmonary pathological lesions, pulmonary edema, and excessive inflammatory responses in ALI mice. Comprehensive bioinformatics analyses predicted potential mechanisms involving oxidative stress and the regulation of metabolic pathways. Experimental validation via Western blotting confirmed that MEA inhibited TLR4-mediated inflammatory signaling and modulated the PI3K/AKT pathway, thereby exerting multi-pathway protective effects against ALI.
CONCLUSIONS: Collectively, this study confirms that MEA, as a traditional herbal extract, holds potential as an adjuvant therapeutic agent for ALI, providing experimental evidence for the modernization and development of ethnic medicines.
PMID:41941987 | DOI:10.1016/j.jep.2026.121650
Captioning Daily Activity Images in Early Childhood Education: Benchmark and Algorithm
JFTA-Bench: Evaluate LLM's Ability of Tracking and Analyzing Malfunctions Using Fault Trees
SortedRL: Accelerating RL Training for LLMs through Online Length-Aware Scheduling
SARE: Sample-wise Adaptive Reasoning for Training-free Fine-grained Visual Recognition
Precipitation observing network gaps limit climate change impact assessment
Nature, Published online: 25 March 2026; doi:10.1038/s41586-026-10300-5
At present, only 13.4% of the global land surface meets the World Meteorological Organization requirements for annual precipitation monitoring.Human-specific features of the cerebellum and ZP2-regulated synapse development
Evaluation Faking: Unveiling Observer Effects in Safety Evaluation of Frontier AI Systems
Effects of Digital Health Interventions on Functional and Psychological Outcomes in Older Patients With Hip Fractures: Systematic Review and Meta-Analysis of Randomized Controlled Trials
Rel-MOSS: Towards Imbalanced Relational Deep Learning on Relational Databases
Dexamethasone promotes neutrophil ROS-mediated tumor killing through the glucocorticoid receptor
Oncogene, Published online: 06 March 2026; doi:10.1038/s41388-026-03708-w
Dexamethasone promotes neutrophil ROS-mediated tumor killing through the glucocorticoid receptor