Publications by authors named "Thien-Khoi Phung"

Mechanical forces are essential for the function of key organs, including the bladder, bowel, heart, and lung<1/sup>. These organs often encounter excessive or dysregulated mechanical forces, which are associated with pathological conditions. However, the key regulators of mechanotransduction remain poorly understood.

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Background: Rhinovirus (RV) infection of airway epithelial cells triggers asthma exacerbations, during which airway smooth muscle (ASM) excessively contracts. Due to ASM contraction, airway epithelial cells become mechanically compressed. We previously reported that compressed human bronchial epithelial (HBE) cells are a source of endothelin-1 (ET-1) that causes ASM contraction.

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Under homeostatic conditions, epithelial cells remain non-migratory. However, during embryonic development and pathological conditions, they become migratory. The mechanism underlying the transition of the epithelial layer between non-migratory and migratory phases is a fundamental question in biology.

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Histological and lineage immunofluorescence examination revealed that healthy conducting airways of humans and animals harbor sporadic poorly differentiated epithelial patches mostly in the dorsal noncartilage regions that remarkably manifest squamous differentiation. analysis demonstrated that this squamous phenotype is not due to intrinsic functional change in underlying airway basal cells. Rather, it is a reversible physiological response to persistent Wnt signaling stimulation during differentiation.

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Aberrant remodeling of the asthmatic airway is not well understood but is thought to be attributable in part to mechanical compression of airway epithelial cells. Here, we examine compression-induced expression and secretion of the extracellular matrix protein tenascin C (TNC) from well-differentiated primary human bronchial epithelial (HBE) cells grown in an air-liquid interface culture. We measured mRNA expression using RT-qPCR and secreted TNC protein using Western blotting and ELISA.

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Cardiac resynchronization therapy (CRT) is an effective therapy for patients who suffer from heart failure and ventricular dyssynchrony such as left bundle branch block (LBBB). When it works, it reverses adverse left ventricular (LV) remodeling and the progression of heart failure. However, CRT response rate is currently as low as 50-65%.

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In asthma, progressive structural changes of the airway wall are collectively termed airway remodelling. Despite its deleterious effect on lung function, airway remodelling is incompletely understood. As one of the important causes leading to airway remodelling, here we discuss the significance of mechanical forces that are produced in the narrowed airway during asthma exacerbation, as a driving force of airway remodelling.

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Creating patient-specific models of the heart is a promising approach for predicting outcomes in response to congenital malformations, injury, or disease, as well as an important tool for developing and customizing therapies. However, integrating multimodal imaging data to construct patient-specific models is a nontrivial task. Here, we propose an approach that employs a prolate spheroidal coordinate system to interpolate information from multiple imaging datasets and map those data onto a single geometric model of the left ventricle (LV).

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Airway narrowing due to hyperresponsiveness severely limits gas exchange in patients with asthma. Imaging studies in humans and animals have shown that bronchoconstriction causes patchy patterns of ventilation defects throughout the lungs, and several computational models have predicted that these regions are due to constriction of smaller airways. However, these imaging approaches are often limited in their ability to capture dynamic changes in small airways, and the patterns of constriction are heterogeneous.

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Background: Atrial fibrillation (AF) is often treated with catheter ablation, which induces scar formation to isolate misfiring electrical signals in the left atrium. Successful ablation restores sinus rhythm at the cost of replacing viable myocardium with scar. The impact of ablation scar on mechanical function of the left atrium is poorly understood.

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