The goal of my research program is to understand the pathogenic mechanisms of ventilator-induced lung injury (VILI) in order to develop personalized closed-loop ventilation systems to improve survival in acute respiratory distress syndrome (ARDS). This condition results in approximately 75,000 deaths per year, exceeding the mortality due to breast or prostate cancer. My interests lie in the delicate lung parenchymal tissue where surface tension forces and fluid-structure interactions play an important role in maintaining normal lung mechanics. To understand how the dynamic properties of the alveoli and small airways change during ARDS and VILI, we employ titratable in vivo models of lung injury. Precise measurements of lung structure and function in these experiments have provided important insights into the ventilation-induced mechanical forces that cause epithelial cell damage, blood-air barrier disruption, and degeneration in lung function. To explain how applied ventilation alters the pulmonary microenvironment, which increases stress and leads to injury, we utilize numerical models implemented on high performance computing clusters. These simulations allow prediction of the microscale forces and the organ-scale mechanical consequences resulting from different modes of mechanical ventilation.