Jay D. Humphrey

The paper develops an optimized model of endothelial signaling using ODEs, showing that most responses can be captured with shared parameters, with only a few reactions needing specific parameterization.

This study shows that blocking lysyl oxidase in Marfan syndrome mice under hypertension worsens aortic disease, highlighting the protective role of collagen cross-linking.

The paper presents data on normal postnatal development of pulmonary arteries in mice and develops a computational model to simulate responses to hemodynamic perturbations.

The paper investigates how hydraulic fracturing in aortic dissection causes medial damage beyond the false lumen, leading to structural weakening of the aortic wall.

This study investigates how increased medial collagen affects aortic resilience against mural delamination by analyzing pressure responses in human aortic specimens under different conditions.

This study quantifies how axial stretch, injection rate, and needle gauge influence intramural delamination in porcine aortas, revealing a hydraulic fracture mechanism in layered tissue.

The paper investigates age-related changes in proximal pulmonary artery mechanics in mouse models, finding increased stiffness and collagen reorientation linked to aging biomarkers and cellular senescence.

This paper develops a biomechanical framework to optimize the design of a pulsatile Fontan conduit for congenital heart defect palliation, focusing on microstructure and material properties to achieve desired hemodynamic performance.

This paper develops a computational biomechanical model to simulate thoracic aortic aneurysm progression and predict outcomes like stabilization or rupture.

This study introduces CausaLink, a cross-scale causal mapping framework that identifies Mgl2 macrophages as key regulators of balanced arterial development using single-cell transcriptomics and organoid validation.

The paper investigates growth arrest in thoracic aortic aneurysms of aging Marfan mice, identifying gene expression and proteomic changes that may contribute to disease stabilization.

This study examines hypoxia-induced cardiopulmonary remodeling in mice, finding that pulmonary artery stiffening due to collagen remodeling precedes and correlates with cardiac and lung dysfunction, with partial recovery observed after normoxia.

This study shows that disrupting TGFβ signaling in adult mice makes the aorta susceptible to hypertension-induced dissection, even from short-term blood pressure increases.

The paper identifies differential proteoglycan dynamics in umbilical artery and vein as the mechanism ensuring rapid arterial closure and venous patency at birth.