Jacob Samuel Brenner

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.

This study investigates complement activation on nanoparticle surfaces, showing it exhibits criticality with diverging order parameters and a transport-limited mechanism.

This study shows that targeting DNA-LNPs to endothelial cells enhances transgene expression magnitude, duration, and specificity in target organs.

This paper identifies that lipid nanoparticle-induced inflammation arises from endosomal membrane damage and proposes strategies to mitigate it through galectin inhibition or ESCRT-recruiting lipids.

This study develops lipid nanoparticles co-loaded with anti-inflammatory lipids to reduce inflammation from DNA delivery, enabling prolonged transgene expression.

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