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Scaling up Energy-Aware Multi-Agent Reinforcement Learning for Mission-Oriented Drone Networks with Individual Reward

arXiv:2605.24992v1 Announce Type: cross Abstract: Multi-agent reinforcement learning (MARL) has shown wide applicability in collaborative systems such as autonomous driving and smart cities for its ability of learning through interaction. With the recent development of drone networks, researchers have also applied MARL to address the trajectory planning problems. However, the dynamic environment and the limited battery capacity are still challenging for using MARL to achieve efficient collaborative task execution. In this paper, we propose an energy-aware MARL model as an attempt to tackle these challenges, leveraging Deep Q-Networks (DQN) with \emph{individual reward functions} driven by the task execution progress and the remaining battery of drones. We conduct a set of simulation studies for the proposed mode and compare it with the shared reward MARL~\cite{Li2022MARL} to explore the impact of credit assignment in MARL. The results indicate that our proposed model can achieve at least 80\% success rate regardless of the task locations and lengths. Similar to the shared reward mode, the individual reward mode can achieve a better success rate when the task density is high, and it can hit nearly a 100\% success rate when task density gets close to 40\%. The true advantage of our proposed model with individual reward is revealed when scaling up the environment. The comparison to the shared reward MARL shows that the our proposed model is more robust towards the change of the environment size and agent numbers. It can achieve higher success rate with fewer steps due to the clarity of the goal which improves energy efficiency even better.
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Multi-omics Analysis Reveals the Protection of a Quadruple Probiotic Mixture in Experimental Autoimmune Hepatitis

Probiotics Antimicrob Proteins. 2026 May 23. doi: 10.1007/s12602-026-11062-2. Online ahead of print.

ABSTRACT

Autoimmune hepatitis (AIH) is a chronic progressive inflammatory liver disease with a rising global incidence. The treatment of AIH remains challenging because first-line drugs show limited efficacy and systemic side effects. Gut microbiota plays a crucial role in the pathogenesis of AIH, leading to growing interest in developing probiotic-based therapies. In this study, we used multi-omics analysis to investigate the therapeutic effects of a quadruple probiotic mixture (Probiotic-quad) consisting of Bifidobacterium infantis, Lactobacillus acidophilus, Enterococcus faecalis, and Bacillus cereus in a well-established chronic AIH murine model. Our results showed that Probiotic-quad treatment significantly alleviated AIH progression, as evidenced by lower serum liver enzyme levels, ameliorated hepatic inflammatory infiltration and histopathological damage. Metagenomic sequencing results showed that gut dysbiosis in AIH mice was partially reversed after Probiotic-quad administration. Additionally, the integrity of the intestinal epithelial barrier was restored, accompanied by a reduction in serum lipopolysaccharide levels. Untargeted metabolomic and transcriptomic analysis revealed that Probiotic-quad treatment was linked to alterations in hepatic metabolism, including the citrate cycle and tryptophan metabolism, and was associated with reduced activation of the NF-κB and NOD-like receptor signaling pathways. These findings suggest that Probiotic-quad treatment ameliorates AIH severity and is potentially associated with changes in hepatic immune responses, metabolism, gut microbiota, and intestinal barrier function, highlighting its potential as an adjuvant therapy for AIH.

PMID:42176246 | DOI:10.1007/s12602-026-11062-2

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A pathogen lncRNA secreted into rice sequesters a host miRNA for virulence

Nature, Published online: 20 May 2026; doi:10.1038/s41586-026-10572-x

A fungal long non-coding RNA from Magnaporthe oryzae translocates into rice cells to sequester a host microRNA that normally represses PKR1, a negative immunity regulator, thereby facilitating infection and revealing a widespread RNA-based pathogen–host interaction mechanism.
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GPNMB Drives Brain Metastasis by Sculpting a Pathological Endothelial-Immune Interactome

Cancer Discov. 2026 Apr 15. doi: 10.1158/2159-8290.CD-25-1663. Online ahead of print.

ABSTRACT

Brain metastases (BM) remain a devastating disease with dismal prognosis. How circulating tumor cells (CTCs) penetrate the blood brain barrier (BBB) and reprogram the brain microenvironment remain unclear. Using spatially resolved multi-omic profiling of CTCs and brain metastases, integrated with experimental and clinical analyses, we identified Glycoprotein Non-Metastatic Melanoma Protein B (GPNMB) as a CTC-secreted driver of vascular disruption and brain colonization. CBX3 upregulation induced GPNMB expression, which bound endothelial EGFR, triggering CBL-mediated ubiquitination and degradation. Attenuated EGFR signaling suppressed FTO and disrupted endothelial junctions via YTHDF2-dependent TJP1 m6A methylation. Remarkably, GPNMB-induced BBB remodeling promoted immune infiltration via CXCL12-CXCR4 axis, and induced time course-dependent T cell exhaustion within the brain microenvironment. Clinically, elevated CBX3⁺GPNMB⁺ CTCs and plasma CXCL12 were significantly associated with BM progression in lung cancer and melanoma. Therapeutically, dual blockade of GPNMB and PD1 enhanced anti-BM efficacy in mice, unveiling GPNMB as a promising target for precision immunotherapy.

PMID:41973996 | DOI:10.1158/2159-8290.CD-25-1663

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Transplantation of encapsulated mitochondria alleviates dysfunction in mitochondrial and Parkinson’s disease models

A mitochondrial transplantation approach rescues mitochondrial deficiency and prevents mitochondrial DNA depletion syndrome, Leigh syndrome, and Parkinson’s disease in cellular and mouse models.
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Respiratory viral infections prime accelerated lung cancer growth

Severe COVID-19 is associated with an increased subsequent risk of lung cancer. Viral pneumonia induces durable lung epigenetic imprinting that promotes tumor-supportive neutrophils and impairs T cell immunity, which is reversible with combined CXCR2 inhibition and PD-L1 blockade.
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