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Biology subjects

Schwarz, E. L.

Publications and source records attributed to Schwarz, E. L..

2 recordsLinked to original sources

Mechanisms Driving Thoracic Aortic Aneurysm Stability

Thoracic aortic aneurysms (TAAs) arise from a combination of biological and mechanical factors. Current clinical guidelines use size and rate of expansion to stratify risk, but such metrics do not predict if an aneurysm will stabilize, grow, dissect, or rupture. Computational biomechanical models can provide insights into mechanisms of aneurysm behavior that would be difficult or impossible to capture in vivo. Here, we use a constrained mixture theory of growth and remodeling to simulate lesion progression while co-varying rate-dependent parameters that contribute to the natural history of aneurysm growth. This includes insults to the material structure and mechanosensitivity of the vessel. This framework successfully simulates clinically-relevant phenotypes, including cases where lesions with initially similar degrees of dilatation or rates of expansion diverge in behavior later in their progression. By capturing this spectrum of outcomes, our framework lays a foundation for more accurate, patient-specific risk prediction and future integration of machine learning tools to accelerate translation into clinical practice.

bioengineering↗

Postnatal Pulmonary Artery Development from Transcript to Tissue

Many congenital conditions and surgical interventions perturb the hemodynamics experienced by proximal pulmonary arteries during early postnatal development, thus leading to differential gene expression and associated changes in vascular structure and function. Among these, pathologic conditions include patent ductus arteriosus, pulmonary atresia and stenosis, and hypoxemia-induced pulmonary hypertension while surgical interventions include the placement of a Blalock-Taussig shunt as well as Glenn, Fontan, and Norwood procedures. Despite the significant morbidity associated with these diverse conditions, there has been little attention directed towards understanding natural postnatal development of pulmonary arteries from both biological and mechanical perspectives. With-out such information, we cannot truly understand the phenotype of the affected pulmonary artery, which is fundamental to improving diagnosis, treatment, and prognosis. In this paper, we present novel data from wild-type mice that document normal postnatal changes in select gene expression, vascular wall composition, and biomechanical properties of proximal pulmonary arteries. These findings enabled the establishment of a novel, data-informed computational model of pulmonary artery development capable of simulating outcomes in response to perturbations in the pulmonary artery hemodynamic environment.

bioengineering↗