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cs.AI, q-bio.NC updates on arXiv.org
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Context-CoT: Enhancing Context Learning via High-Quality Reasoning Synthesis
arXiv:2605.25354v1 Announce Type: new Abstract: While LLMs excel at reasoning over prompts using static pretrained knowledge, they struggle significantly with context learning-the ability to dynamically extract, internalize, and apply new knowledge from complex, task-specific contexts. Recent evaluations on the CL-Bench reveal a critical capability gap: frontier models solve only 17.2% of context-dependent tasks on average.
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cs.AI, q-bio.NC updates on arXiv.org
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AutoResearchClaw: Self-Reinforcing Autonomous Research with Human-AI Collaboration
arXiv:2605.20025v2 Announce Type: replace Abstract: Automating scientific discovery requires more than generating papers from ideas. Real research is iterative: hypotheses are challenged from multiple perspectives, experiments fail and inform the next attempt, and lessons accumulate across cycles. Existing autonomous research systems often model this process as a linear pipeline: they rely on single-agent reasoning, stop when execution fails, and do not carry experience across runs. We present
AutoResearchClaw: Self-Reinforcing Autonomous Research with Human-AI Collaboration
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Omics In Lung
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hUCMSC-exosomes attenuate acute lung injury by inhibiting ferroptosis in pulmonary microvascular endothelial cells through ribosomal protein RPS11 upregulation
J Nanobiotechnology. 2026 May 22. doi: 10.1186/s12951-026-04565-1. Online ahead of print.ABSTRACTBACKGROUND: Human umbilical cord mesenchymal stem cell-derived exosomes (hUCMSC-Exos) are a promising treatment for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), but traditional delivery methods have limitations. Therefore, this study presents a noninvasive therapeutic approach for ALI/ARDS, offering new mechanistic insights and identifying potential therapeutic targets.RESULTS:
hUCMSC-exosomes attenuate acute lung injury by inhibiting ferroptosis in pulmonary microvascular endothelial cells through ribosomal protein RPS11 upregulation
J Nanobiotechnology. 2026 May 22. doi: 10.1186/s12951-026-04565-1. Online ahead of print.
ABSTRACT
BACKGROUND: Human umbilical cord mesenchymal stem cell-derived exosomes (hUCMSC-Exos) are a promising treatment for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), but traditional delivery methods have limitations. Therefore, this study presents a noninvasive therapeutic approach for ALI/ARDS, offering new mechanistic insights and identifying potential therapeutic targets.
RESULTS: We established a nebulized LPS-induced ALI model that was characterized by diffuse lung injury and high homogeneity. Following inhalation, hUCMSC-Exos were observed to be internalized by pulmonary microvascular endothelial cells. Analysis revealed that hUCMSC-Exos alleviated ALI by reducing the severity of histological damage, pulmonary oedema, lung inflammation and ferroptosis. Additionally, hUCMSC-Exos improved the mitochondrial function of human pulmonary microvascular endothelial cells (HPMECs) via the transfer of mitochondrial components. Subsequent proteomic sequencing of mitochondria isolated from HPMECs receiving different treatments revealed the significant differential expression of ribosomal proteins among the groups. The most significantly upregulated protein, RPS11, was identified as a key mediator; its knockdown blocked the ability of hUCMSC-Exos to suppress ferroptosis and restore mitochondrial function in HPMECs. Mechanistically, hUCMSC-Exos exert their effects by enhancing mitochondria-encoded protein translation.
CONCLUSIONS: We report a mechanism whereby hUCMSC-Exos upregulate RPS11 to promote mitochondria-encoded protein translation, rescuing mitochondrial function, inhibiting ferroptosis in HPMECs, and ultimately alleviating ALI. Validated across multiple models and supported by multi-omics analyses, our findings collectively establish nebulized hUCMSC-Exos as a promising cell-free therapy targeting mitochondrial homeostasis in HPMECs for the treatment of ALI.
PMID:42174606 | DOI:10.1186/s12951-026-04565-1