A multiphasic model for determination of mouse ascending thoracic aorta mass transport properties with and without aneurysm.

Thoracic aortic aneurysms (TAAs) are associated with aortic wall remodeling that affects transmural transport or the movement of fluid and solute across the wall. In previous work, we used a Fbln4 (MU) mouse model to investigate transmural transport changes as a function of aneurysm severity. We compared wild-type (WT), MU with no aneurysm (MU-NA), MU with aneurysm (MU-A), and MU with an additional genetic mutation that led to increased aneurysm penetrance (MU-XA).

Measurement of relative motion of the brain and skull in the mini-pig in-vivo.

The mechanical role of the skull-brain interface is critical to the pathology of concussion and traumatic brain injury (TBI) and may evolve with age. Here we characterize the skull-brain interface in juvenile, female Yucatan mini-pigs from 3 to 6 months old using techniques from magnetic resonance elastography (MRE). The displacements of the skull and brain were measured by a motion-sensitive MR imaging sequence during low-amplitude harmonic motion of the head.

Changes in transmural mass transport correlate with ascending thoracic aortic aneurysm diameter in a fibulin-4 E57K knockin mouse model.

Thoracic aortic aneurysm is characterized by dilation of the aortic diameter by greater than 50%, which can lead to dissection or rupture. Common histopathology includes extracellular matrix remodeling that may affect transmural mass transport, defined as the movement of fluids and solutes across the wall. We measured in vitro ascending thoracic aorta mass transport in a mouse model with partial aneurysm phenotype penetration due to a mutation in the extracellular matrix protein fibulin-4 [, referred to as MU-A (aneurysm) or MU-NA (no aneurysm)].