Stud Health Technol Inform
February 2024
In partnership with clinician advisors, a text-based program, BeWell, was co-created to support clinician well-being at a Canadian mental health hospital. This paper briefly describes the process of designing BeWell with clinician advisors and highlights key lessons learned in engaging clinicians as advisors in the design and development of a digital health intervention. The lessons learned can serve as best practices for health systems, organizations, and researchers to consider when engaging clinicians in the design, development, and implementation of digital health interventions.
View Article and Find Full Text PDFExercise-induced increases in pulmonary blood flow normally increase pulmonary arterial pressure only minimally, largely due to a reserve of pulmonary capillaries that are available for recruitment to carry the flow. In pulmonary arterial hypertension, due to precapillary arteriolar obstruction, such recruitment is greatly reduced. In exercising pulmonary arterial hypertension patients, pulmonary arterial pressure remains high and may even increase further.
View Article and Find Full Text PDFPulmonary arterial pressure rises minimally during exercise. The pulmonary microcirculation accommodates increasing blood flow recruitment of pulmonary capillaries and, at higher flows, by distention of already perfused capillaries. The flow transition range between recruitment and distention has not been studied or compared across mammalian species, including humans.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
September 2019
Placentophagia (consuming the placenta) has historically not been a common practice among humans. Over the past few decades the practice has gained attention as more women, particularly educated, middle-class, White American women, choose to partake in this practice. Purported benefits of placentophagia include pain relief, increased breast milk production, and decreased risk of postpartum depression; however, there is a lack of evidence to support these claims.
View Article and Find Full Text PDFA custom code for molecular dynamics simulations has been designed to run on CUDA-enabled NVIDIA graphics processing units (GPUs). The double-precision code simulates multicomponent fluids, with intramolecular and intermolecular forces, coarse-grained and atomistic models, holonomic constraints, Nosé-Hoover thermostats, and the generation of distribution functions. Algorithms to compute Lennard-Jones and Gay-Berne interactions, and the electrostatic force using Ewald summations, are discussed.
View Article and Find Full Text PDFAims: Increased endothelin-1 (ET-1) is a hallmark of pulmonary arterial hypertension (PAH), and contributes to its pathogenesis. The factors controlling ET-1 in PAH are poorly understood. Combined with other stimuli, vascular endothelial growth factor (VEGF) blockade results in PAH-like lesions in animal models, and has been associated with PAH in humans.
View Article and Find Full Text PDFBackground: Many cases of pulmonary arterial hypertension (PAH) are heritable and related to gene mutations in bone morphogenic receptor-2 (BMPR2). These patients consequently may have a signaling imbalance within the transforming growth factor beta (TGFβ) receptor superfamily. The causes of increased endothelin-1 (ET-1), which contributes to PAH, are unknown, and we therefore studied the contribution of various BMPs and their receptors on ET-1 production in vitro, after knockdown of BMPR2 in human pulmonary microvascular endothelial cells (HMVEC-LBl).
View Article and Find Full Text PDFAbnormalities of signalling for the transforming growth factor beta (TGFβ) family of peptides, including bone morphogenic proteins (BMP), have been described in heritable pulmonary arterial hypertension (PAH). TGFβ can modulate synthesis of the vasoconstrictor and mitogen, endothelin-1 (ET-1), a mediator that contributes to the pathogenesis of PAH. BMP-9 is a circulating peptide recently recognized to affect endothelial function.
View Article and Find Full Text PDFBackground: Altered endothelial cell (EC)-derived mediator levels, including increased endothelin-1 (ET-1), are hallmarks of human pulmonary arterial hypertension (PAH). Gene mutations for receptors for bone morphogenic proteins (BMP), or transforming growth factor-beta (TGF-beta) cause heritable PAH. The effects of BMPs and TGF-beta on ET-1 production by human pulmonary microvascular EC (HMVEC-LBl) are unknown.
View Article and Find Full Text PDFBackground: Chronic thromboembolic pulmonary hypertension (CTEPH) causes physical plugging of large pulmonary arteries as well as a distal micro-vasculopathy. Pulmonary endothelium is an active metabolic tissue in normal humans. The effects of CTEPH on pulmonary endothelial metabolism are unknown.
View Article and Find Full Text PDFObjective: Pulmonary endothelial dysfunction is intertwined with the development and progression of pulmonary arterial hypertension (PAH). Pulmonary endothelium is an active metabolic tissue in healthy human subjects. This study was undertaken to determine the effects of PAH on pulmonary endothelial angiotensin-converting enzyme (ACE) activity and to identify differences between common PAH types, i.
View Article and Find Full Text PDFStudy Objectives: Endothelin (ET)-1 is a mediator of vascular remodeling seen in human pulmonary hypertension (PH), and it is normally cleared via endothelial ET-B receptors. Increased levels of ET-1 are found in precapillary PH, partly from increased synthesis. We hypothesized that the endothelial dysfunction and vascular remodeling seen in human precapillary PH would also reduce ET-1 clearance.
View Article and Find Full Text PDF