Results 161 to 170 of about 2,672,563 (309)
After ischemic stroke, injured neurons transfer circMagi1 to endothelial cells through extracellular vesicles. Within endothelial cells, circMagi1 binds ANXA2 and enhances its engagement with TRIM65, promoting ANXA2 ubiquitination and proteasomal degradation to constrain angiogenic repair.
Youkun Bi +16 more
wiley +1 more source
Exploring the application value of preoperative femoral artery and vein cannulation in redo cardiac surgery. [PDF]
Yu YH +5 more
europepmc +1 more source
A HER3‐targeted sonogenetic lipid nanoparticle platform is developed for triple‐negative breast cancer therapy. An AI‐designed miniprotein inhibits HER3 signaling, while TRPV4 and NFAT‐responsive IL‐15 plasmids enable ultrasound‐controlled calcium signaling and cytokine expression. The system induces Ca2+ overload, ROS generation, mitochondrial damage,
Junya Song +6 more
wiley +1 more source
Extrusion‐based 3D printing of silicones and discrete electronic components are combined to create cortical implants for rodents that integrate thermal neuromodulation and electrical recording. Linked to an autonomous auxiliary driver unit, the system enables rapid, stable and localized hypothermia alongside ECoG recording.
Spencer Ryan Moore +6 more
wiley +1 more source
A Gut‐Brain Axis Underlying Succinate‐Associated Compulsive‐Like Behavior
Gut‐derived succinate is associated with an excitatory‐inhibitory imbalance in dmPFC glutamatergic neurons, involving microglial SUCNR1 activation and vagal afferent signaling via upregulated gut 5‐HT4 receptors along the DVC‐CeA‐dmPFC circuit, changes that are linked to excessive compulsive‐like behavior.
Yi Li +12 more
wiley +1 more source
Graphical illustration of 68Ga‐GZB PET/CT imaging reveals immune dynamics post‐EGFR‐TKI resistance in NSCLC; Lgmn+ macrophages‐derived Lgmn‐containing extracellular vesicles inhibit glycolysis, induce CD8+ T cell exhaustion, and targeting Lgmn restores immunotherapy sensitivity.
Dongliang Wang +9 more
wiley +1 more source
Disuse‐induced muscle atrophy is driven by a non‐metabolic, nuclear function of the enzyme PFKFB3. Acting as a scaffold, PFKFB3 facilitates Nedd4‐mediated ubiquitination and degradation of the anti‐atrophy transcription factor JunB. Inhibiting this novel PFKFB3–Nedd4–JunB signaling axis stabilizes JunB and alleviates muscle wasting, revealing a highly ...
Mengjun Ma +12 more
wiley +1 more source

