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Many congratulations to Yu Hu who passed her PhD viva. During her PhD, Yu developed an organ-on-a-chip model of the human coronary artery incorporating endothelial cells, smooth muscle cells and circulating immune cells. The organ-chips were subjected to pulsatile dilation and fluid shear stress causing cellular reorganisation as seen in vivo. Introduction of pro-inflammatory cytokines induced a robust inflammatory response which was upregulated in areas with lower levels of either tensile strain or shear stress. This again replicated the increased inflammation observed in vivo around bifurcations and areas of reduced flow.

Yu's thesis also explored the mechanism through which low shear stress primes endothelial cells to be more susceptible to inflammation. She showed that this was associated with changes in YAP and primary expression. Increased cilia and associated intraflagellar transport protein, IFT88, were observed in response to lower levels of shear stress. Knock down of IFT88 replicated the anti-inflammatory effect of high shear stress.

Yu was supervised by Prof Martin Knight and has already published one paper with a second in revision:

• Pulsatile low shear stress increases susceptibility to endothelial inflammation via upregulation of IFT and activation of YAP. Hou Y Screen HRC Knight MM. (2025) Apl Bioengineering, vol. 9 (2)