A wearable multi-modal acoustic system for breathing analysis.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide with over 3 × 106 deaths in 2019. Such an alarming figure becomes frightening when combined with the number of lost lives resulting from COVID-caused respiratory failure. Because COPD exacerbations identified early can commonly be treated at home, early symptom detections may enable a major reduction of COPD patient readmission and associated healthcare costs; this is particularly important during pandemics such as COVID-19 in which healthcare facilities are overwhelmed. The standard adjuncts used to assess lung function (e.g., spirometry, plethysmography, and CT scan) are expensive, time consuming, and cannot be used in remote patient monitoring of an acute exacerbation. In this paper, a wearable multi-modal system for breathing analysis is presented, which can be used in quantifying various airflow obstructions. The wearable multi-modal electroacoustic system employs a body area sensor network with each sensor-node having a multi-modal sensing capability, such as a digital stethoscope, electrocardiogram monitor, thermometer, and goniometer. The signal-to-noise ratio (SNR) of the resulting acoustic spectrum is used as a measure of breathing intensity. The results are shown from data collected from over 35 healthy subjects and 3 COPD subjects, demonstrating a positive correlation of SNR values to the health-scale score.

Smart Multimodal Telehealth-IoT System for COVID-19 Patients.

The COVID-19 pandemic has highlighted how the healthcare system could be overwhelmed. Telehealth stands out to be an effective solution, where patients can be monitored remotely without packing hospitals and exposing healthcare givers to the deadly virus. This article presents our Intel award winning solution for diagnosing COVID-19 related symptoms and similar contagious diseases. Our solution realizes an Internet of Things system with multimodal physiological sensing capabilities. The sensor nodes are integrated in a wearable shirt (vest) to enable continuous monitoring in a noninvasive manner; the data are collected and analyzed using advanced machine learning techniques at a gateway for remote access by a healthcare provider. Our system can be used by both patients and quarantined individuals. The article presents an overview of the system and briefly describes some novel techniques for increased resource efficiency and assessment fidelity. Preliminary results are provided and the roadmap for full clinical trials is discussed.

Enabling effective breathing sound analysis for automated diagnosis of lung diseases.

With the emergence of the COVID-19 pandemic, early diagnosis of lung diseases has attracted growing attention. Generally, monitoring the breathing sound is the traditional means for assessing the status of a patient's respiratory health through auscultation; for that a stethoscope is one of the clinical tools used by physicians for diagnosis of lung disease and anomalies. On the other hand, recent technological advances have made telehealth systems a practical and effective option for health status assessment and remote patient monitoring. The interest in telehealth solutions have further grown with the COVID-19 pandemic. These telehealth systems aim to provide increased safety and help to cope with the massive growth in healthcare demand. Particularly, employing acoustic sensors to collect breathing sound would enable real-time assessment and instantaneous detection of anomalies. However, existing work focuses on autonomous determination of respiratory rate which is not suitable for anomaly detection due to inability to deal with noisy data recording. This paper presents a novel approach for effective breathing sound analysis. We promote a new segmentation mechanism of the captured acoustic signals to identify breathing cycles in recorded sound signals. A scoring scheme is applied to qualify the segment based on the targeted respiratory illness by the overall breathing sound analysis. We demonstrate the effectiveness of our approach via experiments using published COPD datasets.

Spiral waves and reentry dynamics in an in vitro model of the healed infarct border zone.

RATIONALE: Reentry underlies most ventricular tachycardias (VTs) seen postmyocardial infarction (MI). Mapping studies reveal that the majority of VTs late post-MI arise from the infarct border zone (IBZ). OBJECTIVE: To investigate reentry dynamics and the role of individual ion channels on reentry in in vitro models of the "healed" IBZ. METHODS AND RESULTS: We designed in vitro models of the healed IBZ by coculturing skeletal myotubes with neonatal rat ventricular myocytes and performed optical mapping at high temporal and spatial resolution. In culture, neonatal rat ventricular myocytes mature to form striated myocytes and electrically uncoupled skeletal myotubes simulate fibrosis seen in the healed IBZ. High resolution mapping revealed that skeletal myotubes produced localized slowing of conduction velocity (CV), increased dispersion of CV and directional-dependence of activation delay without affecting myocyte excitability. Reentry was easily induced by rapid pacing in cocultures; treatment with lidocaine, a Na(+) channel blocker, significantly decreased reentry rate and CV, increased reentry path length and terminated 30% of reentrant arrhythmias (n=18). In contrast, nitrendipine, an L-type Ca(2+) channel blocker terminated 100% of reentry episodes while increasing reentry cycle length and path length and decreasing reentry CV (n=16). K(+) channel blockers increased reentry action potential duration but infrequently terminated reentry (n=12). CONCLUSIONS: Cocultures reproduce several architectural and electrophysiological features of the healed IBZ. Reentry termination by L-type Ca(2+) channel, but not Na(+) channel, blockers suggests a greater Ca(2+)-dependence of propagation. These results may help explain the low efficacy of pure Na(+) channel blockers in preventing and terminating clinical VTs late after MI.

Cell cycle activation linked to neuronal cell death initiated by DNA damage.

Increasing evidence indicates that neurodegeneration involves the activation of the cell cycle machinery in postmitotic neurons. However, the purpose of these cell cycle-associated events in neuronal apoptosis remains unknown. Here we tested the hypothesis that cell cycle activation is a critical component of the DNA damage response in postmitotic neurons. Different genotoxic compounds (etoposide, methotrexate, and homocysteine) induced apoptosis accompanied by cell cycle reentry of terminally differentiated cortical neurons. In contrast, apoptosis initiated by stimuli that do not target DNA (staurosporine and colchicine) did not initiate cell cycle activation. Suppression of the function of ataxia telangiectasia mutated (ATM), a proximal component of DNA damage-induced cell cycle checkpoint pathways, attenuated both apoptosis and cell cycle reentry triggered by DNA damage but did not change the fate of neurons exposed to staurosporine and colchicine. Our data suggest that cell cycle activation is a critical element of the DNA damage response of postmitotic neurons leading to apoptosis.

Spiral wave attachment to millimeter-sized obstacles.

BACKGROUND: Functional reentry in the heart takes the form of spiral waves. Drifting spiral waves can become pinned to anatomic obstacles and thus attain stability and persistence. Lidocaine is an antiarrhythmic agent commonly used to treat ventricular tachycardia clinically. We examined the ability of small obstacles to anchor spiral waves and the effect of lidocaine on their attachment. METHODS AND RESULTS: Spiral waves were electrically induced in confluent monolayers of cultured, neonatal rat cardiomyocytes. Small, circular anatomic obstacles (0.6 to 2.6 mm in diameter) were situated in the center of the monolayers to provide an anchoring site. Eighty reentry episodes consisting of at least 4 revolutions were studied. In 36 episodes, the spiral wave attached to the obstacle and became stationary and sustained, with a shorter reentry cycle length and higher rate. Spiral waves could attach to obstacles as small as 0.6 mm, with a likelihood for attachment that increased with obstacle size. After attachment, both conduction velocity of the wave-front tip and wavelength near the obstacle adapted from their pre-reentry values and increased linearly with obstacle size. In contrast, reentry cycle length did not correlate significantly with obstacle size. Addition of lidocaine 90 mumol/L depressed conduction velocity, increased reentry cycle length, and caused attached spiral waves to become quasi- attached to the obstacle or terminate. CONCLUSIONS: Anchored spiral waves exhibit properties of both unattached spiral waves and anatomic reentry. Their behavior may be representative of functional reentry dynamics in cardiac tissue, particularly in the setting of monomorphic tachyarrhythmias.

Folate deficiency inhibits proliferation of adult hippocampal progenitors.

Neurogenesis in the adult hippocampus may play important roles in learning and memory, and in recovery from injury. As recent findings suggest, the perturbance of homocysteine/folate or one-carbon metabolism can adversely affect both the developing and the adult brain, and increase the risk of neural tube defects and Alzheimer's disease. We report that dietary folic acid deficiency dramatically increased blood homocysteine levels and significantly reduced the number of proliferating cells in the dentate gyrus of the hippocampus in adult mice. In vitro, the perturbance of one-carbon metabolism repressed proliferation of cultured embryonic multipotent neuroepithelial progenitor cells and affected cell cycle distribution. Our results suggest that dietary folate deficiency inhibits proliferation of neuronal progenitor cells in the adult brain and thereby affects neurogenesis.