Cell culture process development and scale-up, Cell culture kinetic modeling and CFD modeling

Multiscale mathematical modeling of cell migration and wound healing to understand cell migration behavior in a wound healing process. Hybrid stochastic-deterministic spatiotemporal model has been used to characterize the cell migration phenomenon in response to a chemical gradient.

Successfully built an improved version of the multi-scale mechanistic model of the immune system for immunogenicity risk prediction of therapeutic protein products or drugs. Performed PKPD modeling using Phoenix WinNonlin & SimBiology to obtain PK parameters used in the immunogenicity model.Generated hypotheses on immune systems biology based on the model analysis. Conducted T cell proliferation assay, dendritic cell activation assay and flow cytometry to collect necessary data for model refinement or model validations.

PhD thesis "Quantitative analysis of Akt/mTOR signaling network". • Collected detailed kinetic protein phosphorylation data of mTOR pathway.• Identified PI3K/Akt as the dominant pathway of mTOR activation in NIH3T3 fibroblasts.• Discovered a novel phenomenon "activation by deactivation of a negative regulator" that regulates mTOR activity by Akt through TSC2/Rheb and PRAS40 pathways.• Developed a quantitative data driven mathematical model of PI3K/Akt/mTOR pathway. The model allowed us to discover the equal contribution of TSC2/Rheb and PRAS40 proteins in mTOR regulation. Validated the model predictions with necessary protein knockdown experiments. • Discovered that Akt exerts feedforward control of mTORC1 activity via a "see-saw" regulation mechanism.

Taught chemical engineering undergraduate fundamental courses.

Taught chemical engineering undergraduate fundamental courses and lab courses. Involved in design verification projects of several refinery plants.