Biology subjects

Myers, K. J.

Publications and source records attributed to Myers, K. J..

3 recordsLinked to original sources

bioRxiv2025

An image-based biophysical model of the lung to investigate the effect of pulmonary surfactant on lung function

Lung biomechanics aims to understand the structure-function relationship in the lung under normal and pathological conditions. Pulmonary surfactant has a key structural role in lung function with a significant contribution to the mechanical response of the lungs during respiration. Pulmonary surfactant dynamically regulates surface tension at the air-liquid interface to decrease stiffness during respiration and prevent alveolar collapse during lower volumes. Many lung injuries involve alterations to the contribution of surfactants to lung function. We developed a novel biophysical model using a poroelastic formulation that incorporates pulmonary surfactant dynamics and aims to quantify the contribution of the pulmonary surfactant toward lung compliance. The effect of pulmonary surfactant was modeled as a surface energy function, and the surface behavior was converted to bulk behavior by assuming uniform spherical alveoli. The model was used to simulate respiration and investigate the effect of altered surface tension caused by surfactant dysfunction. The model captured the characteristic sigmoidal inspiratory pressure-volume curve and hysteresis observed during clinical measurements. In addition, the model predicted the expected behavior in surfactant dysfunction in lung injuries. We expect this work to serve as an essential step towards de-convoluting and predicting the contributions of the lung parenchyma and pulmonary surfactant to global and regional lung compliance in health and disease.

biophysics↗

bioRxiv2024

Dissecting contributions of pulmonary arterial remodeling to right ventricular afterload in pulmonary hypertension

Pulmonary hypertension (PH) is defined as an elevation in the right ventricle (RV) afterload, characterized by increased hemodynamic pressure in the main pulmonary artery (PA). Elevations in RV afterload increase RV wall stress, resulting in RV remodeling and potentially RV failure. From a biomechanical standpoint, the primary drivers for RV afterload elevations include increases in pulmonary vascular resistance (PVR) in the distal vasculature and decreases in vessel compliance in the proximal PA. However, the individual contributions of the various vascular remodeling events toward the progression of PA pressure elevations and altered vascular hemodynamics remain elusive. In this study, we used a subject-specific one-dimensional (1D) fluid-structure interaction (FSI) model to investigate the alteration of pulmonary hemodynamics in PH and to quantify the contributions of vascular stiffening and increased resistance towards increased main pulmonary artery (MPA) pressure. We used a combination of subject-specific hemodynamic measurements, ex-vivo mechanical testing of arterial tissue specimens, and ex-vivo X-ray micro-tomography imaging to develop the 1D-FSI model and dissect the contribution of PA remodeling events towards alterations in the MPA pressure waveform. Both the amplitude and pulsatility of the MPA pressure waveform were analyzed. Our results indicated that increased distal resistance has the greatest effect on the increase in maximum MPA pressure, while increased stiffness caused significant elevations in the characteristic impedance. The method presented in this study will serve as an essential step toward understanding the complex interplay between PA remodeling events that leads to the most severe adverse effect on RV dysfunction.

bioengineering↗

bioRxiv2024

Complete spatiotemporal quantification of cardiac motion in mice through enhanced acquisition and super-resolution reconstruction

The quantification of cardiac motion using cardiac magnetic resonance imaging (CMR) has shown promise as an early-stage marker for cardiovascular diseases. Despite the growing popularity of CMR-based myocardial strain calculations, measures of complete spatiotemporal strains (i.e., three-dimensional strains over the cardiac cycle) remain elusive. Complete spatiotemporal strain calculations are primarily hampered by poor spatial resolution, with the rapid motion of the cardiac wall also challenging the reproducibility of such strains. We hypothesize that a super-resolution reconstruction (SRR) framework that leverages combined image acquisitions at multiple orientations will enhance the reproducibility of complete spatiotemporal strain estimation. Two sets of CMR acquisitions were obtained for five wild-type mice, combining short-axis scans with radial and orthogonal long-axis scans. Super-resolution reconstruction, integrated with tissue classification, was performed to generate full four-dimensional (4D) images. The resulting enhanced and full 4D images enabled complete quantification of the motion in terms of 4D myocardial strains. Additionally, the effects of SRR in improving accurate strain measurements were evaluated using an in-silico heart phantom. The SRR framework revealed near isotropic spatial resolution, high structural similarity, and minimal loss of contrast, which led to overall improvements in strain accuracy. In essence, a comprehensive methodology was generated to quantify complete and reproducible myocardial deformation, aiding in the much-needed standardization of complete spatiotemporal strain calculations.

bioengineering↗