We present PhysBrain 1.5, a unified model for understanding physical environments, generating actions, and predicting future states. Motivated by the physical loop of observation, interaction, and environmental change, we bring these capabilities into a common learning framework. Starting from a general vision--language model, we encode language responses, end-effector motion, and dense visual targets as discrete sequences and jointly optimize them with autoregressive next-token prediction. Pre-training draws its embodied supervision entirely from human interaction videos, using task-centered episodes to pair semantic and spatial context with recovered motion and subsequent observations. We then adapt the model through supervised fine-tuning on a mixture of human demonstrations, robot trajectories, and simulated experience. Across 28 embodied understanding benchmarks, our 8B model achieves an average score of 72.5, setting a new open-source state of the art and performing on par with leading proprietary models such as GPT-6-Astra and Gemini 3.6 Flash. It achieves the best open-source results on 14 benchmarks while retaining general multimodal capabilities. Beyond these understanding evaluations, qualitative examples show the model's ability to produce end-effector trajectories and predict future scenes through spatially aligned RGB, depth, and robot-mask outputs.
DeepCybo Team, Yue Bin, Hai-Peng Cao et al.· 0 citations
BACKGROUND
Heart failure is driven by pathological remodeling in which inflammation and mitochondrial dysfunction reinforce each other, yet the molecules that coordinate this interplay remain poorly defined. Netrin-3 is a guidance cue with no known function in the heart. We asked whether Netrin-3 acts in cardiomyocytes to affect mitochondrial integrity under inflammatory stress.
METHODS
We used neonatal rat cardiomyocytes treated with nigericin to activate the NLRP3 inflammasome. Netrin-3 was overexpressed via adenovirus or knocked down by siRNA. Its subcellular distribution was tracked by fractionation and by immunofluorescence. Mitochondrial morphology, Drp1 Ser616 phosphorylation, Mfn2 protein levels, and ROS production were quantified. Inflammasome activation was evaluated through caspase-1 cleavage, ASC speck formation, and IL-1β release. In mice with transverse aortic constriction, we delivered AAV9-shNetrin-3 or a neutralizing antibody and assessed cardiac function, tissue histology, and molecular markers.
RESULTS
NLRP3 activation increased Netrin-3 expression and its mitochondrial fraction content, a pattern supported by immunofluorescence colocalization with TOM20. Netrin-3 overexpression was associated with greater mitochondrial fragmentation, higher Drp1 phosphorylation, lower Mfn2, and increased mitochondrial ROS. Netrin-3 knockdown had the opposite effects on these parameters. ROS scavenging with N-acetylcysteine or MitoTEMPO attenuated the Netrin-3-associated increases in caspase-1 cleavage and IL-1β secretion. In pressure-overloaded hearts, Netrin-3 was upregulated; its genetic or pharmacological inhibition correlated with improved ejection fraction and reduced hypertrophy, fibrosis, and macrophage infiltration.
CONCLUSION
These observations support a model in which Netrin-3 participates in coupling inflammasome signaling to mitochondrial alterations through a ROS-dependent route. Whether Netrin-3 inhibition has therapeutic value in heart failure warrants further investigation.
Biao Li, Hao-Yang Ge, Xi-Wei Chen et al.· International Immunopharmaco...· 0 citations
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