R. Pandey

The paper develops a mathematical model to show how NFκB and IRF-3 co-regulate IFNβ expression during viral infections, with NFκB driving immediate response and IRF-3 causing delayed but persistent expression.

This study identifies shared genetic and regulatory mechanisms between AML and BC CML, highlighting common genes and pathways that may serve as therapeutic targets.

The paper constructs a network and mathematical model of IL-36-mediated cell interactions to show that increased IL-36 leads to keratinocyte hyper-proliferation and Psoriasis, with potential for switch-like behavior and treatment strategies.