During music rehearsals, students and teachers are regularly exposed to unsafe sound levels; hearing loss is a major concern among musicians. By providing real time feedback to music instructors, we can persuade them to modify their teaching methods to achieve safe listening conditions. To accomplish this, we created a user-friendly dashboard that displays the cumulative sound energy being collected in real-time. Since there are few standards for limiting music exposure, we used NIOSH standards for industrial noise exposure as the permissible exposure limit (PEL). Circular dials on the dashboard were programmed to display the amount of exposure relative to the PEL. To aid in identifying the type of exposure, each dial represents the amount of sound accumulation in a band of frequencies relative to typical human speech: below (15Hz–85 Hz), at (85Hz–252 Hz), and above (242Hz–24 675 Hz). The dashboard also displays an equalizer representing the instantaneous microphone input. After each session, the cumulative exposure data can be sent out in email format. Inexpensive and convenient to use, this dashboard will enable music instructors to make informed decisions on how to best modify their teaching approaches to reduce the risk of hearing loss.
Pulmonary vascular remodeling is the key structural abnormality in pulmonary hypertension (PH). Mechanistic target of rapamycin (mTOR) has long been suspected to play a role in the development of pulmonary vascular remodeling. However, underlying cellular and molecular mechanisms leading to this pathophysiological condition remain incompletely understood. To elucidate the crosstalk between lung mesenchyme with activated mTOR and endothelial cells (ECs), we focused on a monogenic lung disease, pulmonary lymphangioleiomyomatosis (LAM). LAM is a progressive cystic lung disease caused by a mutational inactivation of tuberous sclerosis complex (TSC1/TSC2), which results in constitutive mTOR activation in mesenchymal LAM cells. ECs derived from LAM lung explants showed increased proliferation, migration, and defective angiogenesis compared to age- and sex-matched ECs from control human lung. In LAM cells, we found increased WNT2 ligand expression. We also identified corresponding Frizzled 4 (FZD) receptors on ECs isolated from distal LAM lung, suggesting cellular crosstalk between LAM cells and ECs. In endothelial-fibroblast cocultures, treatment of normal ECs with WNT2 ligands recapitulated LAM EC phenotype and morphology. We observed transcriptomic upregulation in metabolic, angiogenic and growth pathways in ECs of young mice, while 1-year-old Tsc2KO mice spontaneously developed pulmonary vascular remodeling with concurrent elevation in right ventricular systolic pressure. Our study demonstrates that LAM cells are not just a pathological mesenchymal cell state but a signaling hub that contributes to dysregulated cellular response in the surrounding vasculature, eventual pulmonary vascular remodeling and PH.
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