Jia Nong

This paper identifies pulmonary neutrophils as the primary target of Abraxane in lung cancer and shows that its efficacy depends on complement pathway-mediated lung uptake.

The paper develops a 3D MASH liver fibrosis model using patient-derived organoids and shows that YAP1 knockdown reduces fibrosis by inducing myofibroblast senescence.

The paper identifies a critical threshold in complement activation based on surface density, showing percolation-type behavior in immune responses to materials.

This paper introduces multi-stage-mixing (MSM) to control lipid nanoparticle (LNP) supramolecular structure, creating a core-then-shell arrangement that significantly improves mRNA and DNA-LNP performance.

The paper shows that lung marginated neutrophils effectively uptake endothelial-targeted nanoparticles, suggesting they are part of the reticuloendothelial system.